Evaluating Factors Impacting Hidradenitis Suppurativa Disease Severity in Patients With Darker Skin Types

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Evaluating Factors Impacting Hidradenitis Suppurativa Disease Severity in Patients With Darker Skin Types

Hidradenitis suppurativa (HS) is a debilitating chronic skin disease that often affects apocrinebearing regions of the skin such as the axillae, perineum, and groin.1 Although current research on the etiology and pathogenesis of HS is limited, the disease is known to have a considerable psychosocial impact on patient quality of life.

Clinically, HS lesions manifest as tender subcutaneous nodules that rupture to form painful and deep dermal abscesses.2 These lesions typically develop due to hair follicle occlusion, followed by a cyclic process of inflammation, healing, re-inflammation, and scarring. Often, they are mistaken for cysts or a simple abscess in the early stages of the disease, leading to a delay in diagnosis.1 Disease severity is categorized based on Hurley staging: stage 1 involves abscess formation without scarring; stage 2 involves limited sinus tracts and recurrent abscesses with scarring and/or multiple separated lesions; and stage 3 is the most advanced stage, with diffuse involvement or multiple interconnected sinus tracts across an area with scarring. The condition primarily is medically managed with antibiotics and immunomodulators, but patients who have refractory disease can benefit from surgical excision.1,2

The prevalence of HS in the United States ranges from 0.77% to 1.19%, and individuals who self-identify as Black have 3-fold higher odds of having this condition compared with all other racial groups.3-5 Black patients also are thought to have a greater number and size of apocrine glands compared with patients who self-identify as White, suggesting an anatomic predisposition to developing HS and greater disease severity.6 However, despite HS disproportionately impacting individuals with skin of color (SOC), the majority of published HS research includes predominantly White patient cohorts.5 There is insufficient research assessing HS epidemiology, comorbidities, and treatment responses in patients with SOC.

A 2020 review reported the notable lack of clinical trials that sufficiently examine systemic medication treatment response in HS patients with SOC.7 Of the 15 HS treatment trials published from 2000 to 2019, only 16.4% (138/840) of the patient population were of African descent.7 Clinical trials investigating the efficacy of adalimumab in reducing HS burden also did not adequately evaluate clinical response in patients with SOC. One clinical trial did not include any Black patients as part of the cohort,8 and in 3 other studies, 80% to 85% of the study participants self-identified as White.9 The current literature does not reflect the patient populations most affected by HS, as several studies have reported that 65% of patients diagnosed with HS in the United States annually are Black.5,7 These results emphasize the underrepresentation of SOC populations in the current HS literature and the need for more research that investigates the disease processes, comorbidities, and treatment outcomes of the diverse patient population impacted by HS.

Methods

Study Population and Data Extraction—Following a protocol reviewed and approved by the MedStar Health/Georgetown University institutional review board (IRB #00006783), a retrospective chart review of 31 adult patients with HS who underwent surgery at a regional verified burn center from April 2014 to April 2023 was conducted. The following variables were collected from the electronic medical record (EMR): baseline demographics including age, sex, body mass index (BMI), obesity status, race, ethnicity, Fitzpatrick skin type, smoking status, substance use, employment status, and family history of HS; HS-specific details including Hurley staging, affected areas, and age at initial diagnosis; comorbidities such as dermatologic conditions, autoimmune disorders, infectious diseases, cardiovascular and associated diseases, ovarian disorders, gastrointestinal diseases, and othother common chronic comorbidities (psychiatric illness, kidney disease, type 2 diabetes [T2D], asthma, allergies, lymphedema, and inflammatory eye disease); and use of pharmacologics such as topical medications, oral antibiotics, immunomodulators, and steroids.

Study Definitions—Obesity was defined as both a continuous and categorical variable. Each patient’s BMI at the surgery date was recorded from the EMR as a continuous variable. Patients with obesity also had this condition listed under their complaints and problem list in the EMR, which was recorded as a categorical variable. Race and ethnicity were self-reported by patients. Comorbidity data, including T2D and hyperlipidemia, were defined by previously diagnosed diseases listed in the EMR. Pharmacologic medication data were included in the study if a patient was recommended/prescribed a medication and they had confirmed use of the medication in a subsequent office visit.

Statistical Analysis—Descriptive statistics were calculated for demographics, HS characteristics (eg, location, Hurley stage), and comorbidities. Continuous variables were presented as mean and standard deviation or median and interquartile range and were evaluated using a t test or Mann-Whitney U test when appropriate. Categorical variables were presented as frequencies and percentages and tested for associations using the X2 or Fisher exact test. Data analyses were performed using SAS software version 9.4 (SAS Institute Inc.).

Results

Thirty-one patients (17 females, 14 males; mean age, 40.9 years) were included in the study. Twenty-nine (93.5%) patients identified as Black. All study patients had at least 1 comorbidity. Obesity was diagnosed in 22 (71.0%) patients (mean BMI, 35.5 kg/m2). A total of 16 (51.6%) patients were current smokers, 3 (9.7%) were past smokers, 22 (71%) reported alcohol use, and 17 (54.8%) were active marijuana users. Only 3 (9.7%) patients had a family history of HS (Table 1).

CT115005140-Table1

Other common comorbidities associated with HS were anemia (64.5% [20/31]), a non–inflammatory bowel disease gastrointestinal disease (61.3% [19/31]), allergies (54.8% [17/31]), hypertension (41.9% [13/31]), cardiovascular disease (41.9% [13/31]), T2D (32.3% [10/31]), asthma (32.3% [10/31]), kidney disease (29.0% [9/31]), and atopic dermatitis (25.8% [8/31]). More than half (54.8% [17/31]) of patients were diagnosed with psychiatric illnesses, including depression, anxiety, bipolar depression, psychosis, anorexia, impulsive anger, hallucinations, delusion, attention deficit-hyperactivity disorder, and panic disorder (Table 2). Depression was diagnosed in 38.7% (12/31) of patients, and 22.6% (7/31) were diagnosed with anxiety.

CT115005140-Table2

The most common anatomic locations for HS were the right axilla (74.2% [23/31]), left axilla (74.2% [23/31]), groin (71% [22/31]), perineum (61.3% [19/31]), buttocks (41.9% [13/31]), and thigh (41.9% [13/31]). Other locations included the breast, lower back, posterior neck, dorsal foot, and scalp (all 3.2% [1/31])(Table 3). Twenty (64.5%) patients had Hurley staging recorded in the EMR. Seventeen (54.8%) were categorized as Hurley stage 3, and 3 (9.7%) were categorized as Hurley stage 2.

CT115005140-Table3

Twenty-nine (93.5%) patients were prescribed an oral antibiotic regimen. The most common oral antibiotics were clindamycin (35.5% [11/31]), doxycycline (35.5% [11/31]), rifampin (29% [9/31]), trimethoprim/sulfamethoxazole (22.6% [7/31]), and cephalexin (22.6% [7/31]). Of the patients who were prescribed rifampin, 87.5% (8/9) also were prescribed an adjunct oral clindamycin regimen. Twenty-nine percent (9/31) of patients were prescribed a biologic regimen; 22.6% (7/31) were prescribed adalimumab, 3.2% (1/31) were prescribed secukinumab, and 3.2% (1/31) were prescribed ustekinumab (Table 4).

CT115005140-Table4

Twenty-five (80.6%) patients were prescribed a topical treatment regimen, the most common being topical clindamycin (45.2% [14/31]). Other topical medications included triamcinolone (12.9% [4/31]), chlorhexidine gluconate wash (9.7% [3/31]), clobetasol (3.2% [1/31]), hydrocortisone (3.2% [1/31]), and hydroquinone (3.2% [1/31])(Table 4).

Other medical treatments for HS included metformin (25.8% [8/31]), spironolactone (16.1% [5/31]), and zinc supplements (12.9% [4/31]). Four patients (12.9%) were prescribed clindamycin plus rifampin as well as a combination of metformin, spironolactone, and/or zinc (Table 4).

Twenty-two (71.0%) patients had a history of receiving incision and drainage procedures as treatment for HS. All 31 patients underwent excisional surgery followed by appropriate reconstruction. The total number of excisional surgeries a single patient underwent for HS treatment ranged from 1 to 9, with a mean of 2 excisional surgeries per patient.

Comment

Our regional verified burn center in Washington, DC, serves a large population of patients with SOC, making it a unique and important sample to study for HS. Our results suggest that Black patients with HS may be at a higher risk for depression and anxiety. Twelve (38.7%) of our patients were diagnosed with depression, which is substantially higher than the 17% to 21% depression prevalence rate among all HS patients reported in meta-analyses.10,11 Additionally, 22.6% (7/31) of our patients were diagnosed with anxiety, which is higher than the 5% to 12% prevalence rate of anxiety among HS patients reported in meta-analyses.10,11 The stress of chronic disease management, psychosocial impact of living with HS, social stigma, sexual dysfunction, pain, and financial concerns make mental illness a debilitating yet common comorbidity for patients with HS. The results of our study suggest that anxiety and depression are highly prevalent among Black patients with HS. It is important to identify if this finding is due to the interplay of health care disparities and social determinants of health; the cause likely is multifactorial, as race and ethnicity may be potential predictors for increased disease severity. Hidradenitis suppurativa is known to be a major economic burden on patients, and race-dependent structural and societal inequalities may be influencing the increased prevalence of anxiety and depression among Black patients with HS.12 Therefore, clinicians must be vigilant for the signs and symptoms of mental illnesses to refer patients for psychiatric treatment when appropriate. Implementing self-report Patient Health Questionnaire-9, General Anxiety Disorder-7 depression and anxiety screening tools, and Dermatology Life Quality Index questionnaires at primary care and dermatology office visits may be a beneficial step toward identifying patients who could benefit from additional mental health resources.13

The patients included in our study predominantly self-identified as Black, and the current smoker prevalence rate was 51.6% (16/31). This percentage is lower than the smoking rates of other published HS studies conducted in predominantly White patient populations, which report up to a 76.5% smoking prevalence rate.14-16 One review article published in 2022 reported that approximately 90% of HS patients are current or former smokers.17 Additionally, a retrospective cohort analysis identifying HS cases among 3,924,310 tobacco smokers in the United States reported that tobacco smokers diagnosed with HS most commonly racially self-identified as White (66.2%).18 Tobacco chemicals and smoke can increase inflammatory cytokine levels, and the activation of nicotinic acetylcholine receptors surrounding pilosebaceous-apocrine units can increase follicular occlusion.14 While several studies1-3,14,19,20 support the strong correlation between tobacco smoking and HS, there are very few that specifically investigate the association between smoking and HS disease in SOC populations. It is possible that smoking rates may be lower in Black patients with HS compared with White patients with HS, which would suggest a multifactorial nature of HS disease pathophysiology. Future large, multicenter studies are needed that investigate smoking rates and HS disease severity in patients across various racial groups.

Prior research has shown a strong correlation between cigarette smoking and HS, but there is minimal data on the role of use of marijuana and other illicit drugs in HS disease pathophysiology.21 A total of 54.8% of our patients were active marijuana users with daily or weekly usage. Further research is needed to investigate whether marijuana use is linked with HS disease pathophysiology and severity or if patients with HS may be using marijuana to relieve pain, anxiety, and depression. Additional studies that survey the method of marijuana use (eg, joint, vape devices, or edibles) would clarify the relationship between not only HS and marijuana but also a potential link between disease severity and the process of inhaling large amounts of smoke vs a link with the active ingredients in the marijuana plant itself.

Approximately 61% (19/31) of our patients were diagnosed with a gastrointestinal disease in addition to HS. Current research reports the link between HS and inflammatory bowel disease, but few studies have investigated if a relationship exists between the gut microbiome and HS, as well as the incidence of general gastrointestinal disease among Black patients with HS.14,22 Our patients were diagnosed with gastrointestinal conditions such as colonic polyps, gastroesophageal reflux disease, benign neoplasms of the cecum and sigmoid colons, small bowel obstruction and perforation, biliary tract diseases, ileus, abdominal hernia, peritonitis, and diverticulosis. Further research is warranted to identify if there is a true relationship between gastrointestinal disease, the gut microbiome, and skin conditions such as HS.22 Biochemical research on the common genetic and inflammatory cytokine pathways involved in HS and gastrointestinal manifestations could help predict disease severity and management in HS patients with SOC.

Several research studies have reported the association between obesity and HS, likely due to adipose cells producing increased estrogen and leading to an estrogen-dominant hormone profile and increased local androgen production in adipose tissue.14,23,24 Antiandrogenic drugs such as finasteride and spironolactone lead to positive results in HS treatment compared to oral antibiotics alone.24 While 71.9% (22/31) of our patients were diagnosed with obesity, only 16.1% (5/31) were prescribed antiandrogen therapy such as spironolactone. It is unclear if this result reflects a health disparity due to insufficient insurance coverage and low prescribing rates or if there is patient hesitancy to taking antiandrogen medications. Additional clinical trials are needed to investigate the efficacy of antiandrogen therapies for HS. If proven to be efficacious, providers should consider adding these medications to the pharmacologic regimen of HS patients with SOC prior to recommending wide-excision surgeries. Furthermore, in addition to antiandrogen medication, weight-management interventions may be helpful in reducing HS disease. The results of a survey conducted in 35 HS patients who underwent bariatric surgery reported 48.6% (17/35) experienced complete disease remission after more than a 15% weight reduction.25,26 Investigating the impact of weight-management practices on disease severity would be helpful in outlining nonpharmacologic treatments for patients with HS.

Limitations

Our study was limited by the constraints of a retrospective chart review and small sample size. Retrospective chart reviews are susceptible to recall bias, variability in providers’ charting practices, and human error from data collectors. We acknowledge that a control group of non-HS patients should be the next step in furthering our research on HS disease comorbidities. Also, since 35.5% (11/31) of our patients did not have Hurley staging recorded in the EMR, it would be beneficial to conduct a future study comprehensive of all 3 Hurley stages. Since 93.5% (29/31) of the patients in our study racially identified as Black, having a control group of racially diverse HS patients would help further our understanding of HS pathophysiology. Lastly, since the inclusion criteria required patients to have undergone excisional surgery for HS, future studies that consider comorbidities among both surgical and nonsurgical patients with HS will aid in our understanding of HS patients with SOC.

Conclusion

The results of our study demonstrate a descriptive analysis of the demographics, most common comorbidities, lesion sites, pharmacologic treatments, and surgical profiles in patients with SOC who underwent surgical treatment for HS. Our data show that HS patients with SOC may be more likely to experience anxiety, depression, and gastrointestinal disease than other HS patients. Additionally, our patients had a high prevalence of marijuana use but lower prevalence of current cigarette use compared to studies conducted in predominantly White HS patient populations, emphasizing the multifactorial nature of HS pathophysiology. Furthermore, despite published research on the efficacy of immunomodulator therapy for HS, most of our HS patients with SOC underwent surgical intervention without first attempting biologic treatment regimens, indicating possible gaps in health care access for minority patients that may be impacting disease severity and outcomes. Studies such as this one that investigate disease pathophysiology and risk factors in SOC patient populations with HS are imperative in minimizing the health care disparity gap, improving disease outcomes, and providing more equitable health care for all patients.

References
  1. Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
  2. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60:539-563. doi:10.1016/j. jaad.2008.11.911
  3. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  4. Ingram JR, Jenkins-Jones S, Knipe DW, et al. Population-based Clinical Practice Research Datalink study using algorithm modelling to identify the true burden of hidradenitis suppurativa. Br J Dermatol. 2018;178:917-924. doi:10.1111/bjd.16101
  5. Lee DE, Clark AK, Shi VY. Hidradenitis suppurativa: disease burden and etiology in skin of color. Dermatology. 2017;233:456-461. doi:10.1159/000486741
  6. Brown-Korsah JB, McKenzie S, Omar D, et al. Variations in genetics, biology, and phenotype of cutaneous disorders in skin of color—part I: genetic, biologic, and structural differences in skin of color. J Am Acad Dermatol. 2022;87:1239-1258. doi:10.1016/j.jaad.2022.06.1193
  7. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  8. Arenbergerova M, Gkalpakiotis S, Arenberger P. Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy. Int J Dermatol. 2010;49:1445-1449. doi:10.1111/j.1365-4632.2010.04638.x
  9. Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
  10. Jalenques I, Ciortianu L, Pereira B, et al. The prevalence and odds of anxiety and depression in children and adults with hidradenitis suppurativa: systematic review and meta-analysis. J Am Acad Dermatol. 2020;83:542-553. doi:10.1016/j.jaad.2020.03.041
  11. Machado MO, Stergiopoulos V, Maes M, et al. Depression and anxiety in adults with hidradenitis suppurativa: a systematic review and meta-analysis. JAMA Dermatol. 2019;155:939-945. doi:10.1001 /jamadermatol.2019.0759
  12. Kilgour JM, Li S, Sarin KY. Hidradenitis suppurativa in patients of color is associated with increased disease severity and healthcare utilization: a retrospective analysis of 2 U.S. cohorts. JAAD Int. 2021;3:42-52. doi:10.1016/j.jdin.2021.01.007
  13. Rymaszewska JE, Krajewski PK, Szcze² ch J, et al. Depression and anxiety in hidradenitis suppurativa patients: a cross-sectional study among Polish patients. Postep Dermatol Alergol. 2023;40:35-39. doi:10.5114ada.2022.119080
  14. Johnston LA, Alhusayen R, Bourcier M, et al. Practical guidelines for managing patients with hidradenitis suppurativa: an update. J Cutan Med Surg. 2022;26(2 suppl):2S-24S. doi:10.1177/12034754221116115
  15. Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
  16. Seyed Jafari SM, Knüsel E, Cazzaniga S, et al. A retrospective cohort study on patients with hidradenitis suppurativa. Dermatology. 2018;234:71-78. doi:10.1159/000488344
  17. Lewandowski M, S´ wierczewska Z, Baran´ ska-Rybak W. Hidradenitis suppurativa: a review of current treatment options. Int J Dermatol. 2022;61:1152-1164. doi:10.1111/ijd.16115
  18. Garg A, Papagermanos V, Midura M, et al. Incidence of hidradenitis suppurativa among tobacco smokers: a population-based retrospective analysis in the U.S.A. Br J Dermatol. 2018;178:709-714. doi:10.1111/bjd.15939
  19. Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
  20. Tzellos T, Zouboulis CC. Which hidradenitis suppurativa comorbidities should I take into account? Exp Dermatol. 2022;31(suppl 1):29-32. doi:10.1111/exd.14633
  21. Metko D, Mehta S, Piguet V. Cannabis usage among patients with hidradenitis suppurativa: a scoping review. J Cutan Med Surg. 2024;28:307-308. doi:10.1177/12034754241238719
  22. Mahmud MR, Akter S, Tamanna SK, et al. Impact of gut microbiome on skin health: gut-skin axis observed through the lenses of therapeutics and skin diseases. Gut Microbes. 2022;14:2096995. doi:10.1080/194 90976.2022.2096995
  23. Mair KM, Gaw R, MacLean MR. Obesity, estrogens and adipose tissue dysfunction—implications for pulmonary arterial hypertension. Pulm Circ. 2020;10:2045894020952019. doi:10.1177/2045894020952023
  24. Abu Rached N, Gambichler T, Dietrich JW, et al. The role of hormones in hidradenitis suppurativa: a systematic review. Int J Mol Sci. 2022;23:15250. doi:10.3390/ijms232315250
  25. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016 /j.jaad.2019.02.067
  26. Choi ECE, Phan PHC, Oon HH. Hidradenitis suppurativa: racial and socioeconomic considerations in management. Int J Dermatol. 2022;61:1452-1457. doi:10.1111/ijd.16163
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Author and Disclosure Information

Kareena S. Garg and Drs. Pinto, Le, Moffatt, Shupp, and Carney are from the Firefighters’ Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, DC. Kareena S. Garg also is from the Georgetown University School of Medicine, Washington, DC. Drs. Moffatt, Shupp, and Carney also are from the Departments of Biochemistry and Molecular & Cellular Biology and Surgery, Georgetown University School of Medicine, Washington, DC. Dr. Shupp also is from the Department of Plastic and Reconstructive Surgery. Drs. Moffatt, Shupp, and Carney also are from The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, DC. Dr. Frey is from the Department of Dermatology, Howard University Hospital, Washington, DC.

The authors have no relevant financial disclosures to report.

Correspondence: Bonnie C. Carney, PhD, 110 Irving St NW, Suite 3B-55, Washington, DC 20010 ([email protected]).

Cutis. 2025 May;115(5):140-145. doi:10.12788/cutis.1209

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Kareena S. Garg and Drs. Pinto, Le, Moffatt, Shupp, and Carney are from the Firefighters’ Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, DC. Kareena S. Garg also is from the Georgetown University School of Medicine, Washington, DC. Drs. Moffatt, Shupp, and Carney also are from the Departments of Biochemistry and Molecular & Cellular Biology and Surgery, Georgetown University School of Medicine, Washington, DC. Dr. Shupp also is from the Department of Plastic and Reconstructive Surgery. Drs. Moffatt, Shupp, and Carney also are from The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, DC. Dr. Frey is from the Department of Dermatology, Howard University Hospital, Washington, DC.

The authors have no relevant financial disclosures to report.

Correspondence: Bonnie C. Carney, PhD, 110 Irving St NW, Suite 3B-55, Washington, DC 20010 ([email protected]).

Cutis. 2025 May;115(5):140-145. doi:10.12788/cutis.1209

Author and Disclosure Information

Kareena S. Garg and Drs. Pinto, Le, Moffatt, Shupp, and Carney are from the Firefighters’ Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, DC. Kareena S. Garg also is from the Georgetown University School of Medicine, Washington, DC. Drs. Moffatt, Shupp, and Carney also are from the Departments of Biochemistry and Molecular & Cellular Biology and Surgery, Georgetown University School of Medicine, Washington, DC. Dr. Shupp also is from the Department of Plastic and Reconstructive Surgery. Drs. Moffatt, Shupp, and Carney also are from The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, DC. Dr. Frey is from the Department of Dermatology, Howard University Hospital, Washington, DC.

The authors have no relevant financial disclosures to report.

Correspondence: Bonnie C. Carney, PhD, 110 Irving St NW, Suite 3B-55, Washington, DC 20010 ([email protected]).

Cutis. 2025 May;115(5):140-145. doi:10.12788/cutis.1209

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Hidradenitis suppurativa (HS) is a debilitating chronic skin disease that often affects apocrinebearing regions of the skin such as the axillae, perineum, and groin.1 Although current research on the etiology and pathogenesis of HS is limited, the disease is known to have a considerable psychosocial impact on patient quality of life.

Clinically, HS lesions manifest as tender subcutaneous nodules that rupture to form painful and deep dermal abscesses.2 These lesions typically develop due to hair follicle occlusion, followed by a cyclic process of inflammation, healing, re-inflammation, and scarring. Often, they are mistaken for cysts or a simple abscess in the early stages of the disease, leading to a delay in diagnosis.1 Disease severity is categorized based on Hurley staging: stage 1 involves abscess formation without scarring; stage 2 involves limited sinus tracts and recurrent abscesses with scarring and/or multiple separated lesions; and stage 3 is the most advanced stage, with diffuse involvement or multiple interconnected sinus tracts across an area with scarring. The condition primarily is medically managed with antibiotics and immunomodulators, but patients who have refractory disease can benefit from surgical excision.1,2

The prevalence of HS in the United States ranges from 0.77% to 1.19%, and individuals who self-identify as Black have 3-fold higher odds of having this condition compared with all other racial groups.3-5 Black patients also are thought to have a greater number and size of apocrine glands compared with patients who self-identify as White, suggesting an anatomic predisposition to developing HS and greater disease severity.6 However, despite HS disproportionately impacting individuals with skin of color (SOC), the majority of published HS research includes predominantly White patient cohorts.5 There is insufficient research assessing HS epidemiology, comorbidities, and treatment responses in patients with SOC.

A 2020 review reported the notable lack of clinical trials that sufficiently examine systemic medication treatment response in HS patients with SOC.7 Of the 15 HS treatment trials published from 2000 to 2019, only 16.4% (138/840) of the patient population were of African descent.7 Clinical trials investigating the efficacy of adalimumab in reducing HS burden also did not adequately evaluate clinical response in patients with SOC. One clinical trial did not include any Black patients as part of the cohort,8 and in 3 other studies, 80% to 85% of the study participants self-identified as White.9 The current literature does not reflect the patient populations most affected by HS, as several studies have reported that 65% of patients diagnosed with HS in the United States annually are Black.5,7 These results emphasize the underrepresentation of SOC populations in the current HS literature and the need for more research that investigates the disease processes, comorbidities, and treatment outcomes of the diverse patient population impacted by HS.

Methods

Study Population and Data Extraction—Following a protocol reviewed and approved by the MedStar Health/Georgetown University institutional review board (IRB #00006783), a retrospective chart review of 31 adult patients with HS who underwent surgery at a regional verified burn center from April 2014 to April 2023 was conducted. The following variables were collected from the electronic medical record (EMR): baseline demographics including age, sex, body mass index (BMI), obesity status, race, ethnicity, Fitzpatrick skin type, smoking status, substance use, employment status, and family history of HS; HS-specific details including Hurley staging, affected areas, and age at initial diagnosis; comorbidities such as dermatologic conditions, autoimmune disorders, infectious diseases, cardiovascular and associated diseases, ovarian disorders, gastrointestinal diseases, and othother common chronic comorbidities (psychiatric illness, kidney disease, type 2 diabetes [T2D], asthma, allergies, lymphedema, and inflammatory eye disease); and use of pharmacologics such as topical medications, oral antibiotics, immunomodulators, and steroids.

Study Definitions—Obesity was defined as both a continuous and categorical variable. Each patient’s BMI at the surgery date was recorded from the EMR as a continuous variable. Patients with obesity also had this condition listed under their complaints and problem list in the EMR, which was recorded as a categorical variable. Race and ethnicity were self-reported by patients. Comorbidity data, including T2D and hyperlipidemia, were defined by previously diagnosed diseases listed in the EMR. Pharmacologic medication data were included in the study if a patient was recommended/prescribed a medication and they had confirmed use of the medication in a subsequent office visit.

Statistical Analysis—Descriptive statistics were calculated for demographics, HS characteristics (eg, location, Hurley stage), and comorbidities. Continuous variables were presented as mean and standard deviation or median and interquartile range and were evaluated using a t test or Mann-Whitney U test when appropriate. Categorical variables were presented as frequencies and percentages and tested for associations using the X2 or Fisher exact test. Data analyses were performed using SAS software version 9.4 (SAS Institute Inc.).

Results

Thirty-one patients (17 females, 14 males; mean age, 40.9 years) were included in the study. Twenty-nine (93.5%) patients identified as Black. All study patients had at least 1 comorbidity. Obesity was diagnosed in 22 (71.0%) patients (mean BMI, 35.5 kg/m2). A total of 16 (51.6%) patients were current smokers, 3 (9.7%) were past smokers, 22 (71%) reported alcohol use, and 17 (54.8%) were active marijuana users. Only 3 (9.7%) patients had a family history of HS (Table 1).

CT115005140-Table1

Other common comorbidities associated with HS were anemia (64.5% [20/31]), a non–inflammatory bowel disease gastrointestinal disease (61.3% [19/31]), allergies (54.8% [17/31]), hypertension (41.9% [13/31]), cardiovascular disease (41.9% [13/31]), T2D (32.3% [10/31]), asthma (32.3% [10/31]), kidney disease (29.0% [9/31]), and atopic dermatitis (25.8% [8/31]). More than half (54.8% [17/31]) of patients were diagnosed with psychiatric illnesses, including depression, anxiety, bipolar depression, psychosis, anorexia, impulsive anger, hallucinations, delusion, attention deficit-hyperactivity disorder, and panic disorder (Table 2). Depression was diagnosed in 38.7% (12/31) of patients, and 22.6% (7/31) were diagnosed with anxiety.

CT115005140-Table2

The most common anatomic locations for HS were the right axilla (74.2% [23/31]), left axilla (74.2% [23/31]), groin (71% [22/31]), perineum (61.3% [19/31]), buttocks (41.9% [13/31]), and thigh (41.9% [13/31]). Other locations included the breast, lower back, posterior neck, dorsal foot, and scalp (all 3.2% [1/31])(Table 3). Twenty (64.5%) patients had Hurley staging recorded in the EMR. Seventeen (54.8%) were categorized as Hurley stage 3, and 3 (9.7%) were categorized as Hurley stage 2.

CT115005140-Table3

Twenty-nine (93.5%) patients were prescribed an oral antibiotic regimen. The most common oral antibiotics were clindamycin (35.5% [11/31]), doxycycline (35.5% [11/31]), rifampin (29% [9/31]), trimethoprim/sulfamethoxazole (22.6% [7/31]), and cephalexin (22.6% [7/31]). Of the patients who were prescribed rifampin, 87.5% (8/9) also were prescribed an adjunct oral clindamycin regimen. Twenty-nine percent (9/31) of patients were prescribed a biologic regimen; 22.6% (7/31) were prescribed adalimumab, 3.2% (1/31) were prescribed secukinumab, and 3.2% (1/31) were prescribed ustekinumab (Table 4).

CT115005140-Table4

Twenty-five (80.6%) patients were prescribed a topical treatment regimen, the most common being topical clindamycin (45.2% [14/31]). Other topical medications included triamcinolone (12.9% [4/31]), chlorhexidine gluconate wash (9.7% [3/31]), clobetasol (3.2% [1/31]), hydrocortisone (3.2% [1/31]), and hydroquinone (3.2% [1/31])(Table 4).

Other medical treatments for HS included metformin (25.8% [8/31]), spironolactone (16.1% [5/31]), and zinc supplements (12.9% [4/31]). Four patients (12.9%) were prescribed clindamycin plus rifampin as well as a combination of metformin, spironolactone, and/or zinc (Table 4).

Twenty-two (71.0%) patients had a history of receiving incision and drainage procedures as treatment for HS. All 31 patients underwent excisional surgery followed by appropriate reconstruction. The total number of excisional surgeries a single patient underwent for HS treatment ranged from 1 to 9, with a mean of 2 excisional surgeries per patient.

Comment

Our regional verified burn center in Washington, DC, serves a large population of patients with SOC, making it a unique and important sample to study for HS. Our results suggest that Black patients with HS may be at a higher risk for depression and anxiety. Twelve (38.7%) of our patients were diagnosed with depression, which is substantially higher than the 17% to 21% depression prevalence rate among all HS patients reported in meta-analyses.10,11 Additionally, 22.6% (7/31) of our patients were diagnosed with anxiety, which is higher than the 5% to 12% prevalence rate of anxiety among HS patients reported in meta-analyses.10,11 The stress of chronic disease management, psychosocial impact of living with HS, social stigma, sexual dysfunction, pain, and financial concerns make mental illness a debilitating yet common comorbidity for patients with HS. The results of our study suggest that anxiety and depression are highly prevalent among Black patients with HS. It is important to identify if this finding is due to the interplay of health care disparities and social determinants of health; the cause likely is multifactorial, as race and ethnicity may be potential predictors for increased disease severity. Hidradenitis suppurativa is known to be a major economic burden on patients, and race-dependent structural and societal inequalities may be influencing the increased prevalence of anxiety and depression among Black patients with HS.12 Therefore, clinicians must be vigilant for the signs and symptoms of mental illnesses to refer patients for psychiatric treatment when appropriate. Implementing self-report Patient Health Questionnaire-9, General Anxiety Disorder-7 depression and anxiety screening tools, and Dermatology Life Quality Index questionnaires at primary care and dermatology office visits may be a beneficial step toward identifying patients who could benefit from additional mental health resources.13

The patients included in our study predominantly self-identified as Black, and the current smoker prevalence rate was 51.6% (16/31). This percentage is lower than the smoking rates of other published HS studies conducted in predominantly White patient populations, which report up to a 76.5% smoking prevalence rate.14-16 One review article published in 2022 reported that approximately 90% of HS patients are current or former smokers.17 Additionally, a retrospective cohort analysis identifying HS cases among 3,924,310 tobacco smokers in the United States reported that tobacco smokers diagnosed with HS most commonly racially self-identified as White (66.2%).18 Tobacco chemicals and smoke can increase inflammatory cytokine levels, and the activation of nicotinic acetylcholine receptors surrounding pilosebaceous-apocrine units can increase follicular occlusion.14 While several studies1-3,14,19,20 support the strong correlation between tobacco smoking and HS, there are very few that specifically investigate the association between smoking and HS disease in SOC populations. It is possible that smoking rates may be lower in Black patients with HS compared with White patients with HS, which would suggest a multifactorial nature of HS disease pathophysiology. Future large, multicenter studies are needed that investigate smoking rates and HS disease severity in patients across various racial groups.

Prior research has shown a strong correlation between cigarette smoking and HS, but there is minimal data on the role of use of marijuana and other illicit drugs in HS disease pathophysiology.21 A total of 54.8% of our patients were active marijuana users with daily or weekly usage. Further research is needed to investigate whether marijuana use is linked with HS disease pathophysiology and severity or if patients with HS may be using marijuana to relieve pain, anxiety, and depression. Additional studies that survey the method of marijuana use (eg, joint, vape devices, or edibles) would clarify the relationship between not only HS and marijuana but also a potential link between disease severity and the process of inhaling large amounts of smoke vs a link with the active ingredients in the marijuana plant itself.

Approximately 61% (19/31) of our patients were diagnosed with a gastrointestinal disease in addition to HS. Current research reports the link between HS and inflammatory bowel disease, but few studies have investigated if a relationship exists between the gut microbiome and HS, as well as the incidence of general gastrointestinal disease among Black patients with HS.14,22 Our patients were diagnosed with gastrointestinal conditions such as colonic polyps, gastroesophageal reflux disease, benign neoplasms of the cecum and sigmoid colons, small bowel obstruction and perforation, biliary tract diseases, ileus, abdominal hernia, peritonitis, and diverticulosis. Further research is warranted to identify if there is a true relationship between gastrointestinal disease, the gut microbiome, and skin conditions such as HS.22 Biochemical research on the common genetic and inflammatory cytokine pathways involved in HS and gastrointestinal manifestations could help predict disease severity and management in HS patients with SOC.

Several research studies have reported the association between obesity and HS, likely due to adipose cells producing increased estrogen and leading to an estrogen-dominant hormone profile and increased local androgen production in adipose tissue.14,23,24 Antiandrogenic drugs such as finasteride and spironolactone lead to positive results in HS treatment compared to oral antibiotics alone.24 While 71.9% (22/31) of our patients were diagnosed with obesity, only 16.1% (5/31) were prescribed antiandrogen therapy such as spironolactone. It is unclear if this result reflects a health disparity due to insufficient insurance coverage and low prescribing rates or if there is patient hesitancy to taking antiandrogen medications. Additional clinical trials are needed to investigate the efficacy of antiandrogen therapies for HS. If proven to be efficacious, providers should consider adding these medications to the pharmacologic regimen of HS patients with SOC prior to recommending wide-excision surgeries. Furthermore, in addition to antiandrogen medication, weight-management interventions may be helpful in reducing HS disease. The results of a survey conducted in 35 HS patients who underwent bariatric surgery reported 48.6% (17/35) experienced complete disease remission after more than a 15% weight reduction.25,26 Investigating the impact of weight-management practices on disease severity would be helpful in outlining nonpharmacologic treatments for patients with HS.

Limitations

Our study was limited by the constraints of a retrospective chart review and small sample size. Retrospective chart reviews are susceptible to recall bias, variability in providers’ charting practices, and human error from data collectors. We acknowledge that a control group of non-HS patients should be the next step in furthering our research on HS disease comorbidities. Also, since 35.5% (11/31) of our patients did not have Hurley staging recorded in the EMR, it would be beneficial to conduct a future study comprehensive of all 3 Hurley stages. Since 93.5% (29/31) of the patients in our study racially identified as Black, having a control group of racially diverse HS patients would help further our understanding of HS pathophysiology. Lastly, since the inclusion criteria required patients to have undergone excisional surgery for HS, future studies that consider comorbidities among both surgical and nonsurgical patients with HS will aid in our understanding of HS patients with SOC.

Conclusion

The results of our study demonstrate a descriptive analysis of the demographics, most common comorbidities, lesion sites, pharmacologic treatments, and surgical profiles in patients with SOC who underwent surgical treatment for HS. Our data show that HS patients with SOC may be more likely to experience anxiety, depression, and gastrointestinal disease than other HS patients. Additionally, our patients had a high prevalence of marijuana use but lower prevalence of current cigarette use compared to studies conducted in predominantly White HS patient populations, emphasizing the multifactorial nature of HS pathophysiology. Furthermore, despite published research on the efficacy of immunomodulator therapy for HS, most of our HS patients with SOC underwent surgical intervention without first attempting biologic treatment regimens, indicating possible gaps in health care access for minority patients that may be impacting disease severity and outcomes. Studies such as this one that investigate disease pathophysiology and risk factors in SOC patient populations with HS are imperative in minimizing the health care disparity gap, improving disease outcomes, and providing more equitable health care for all patients.

Hidradenitis suppurativa (HS) is a debilitating chronic skin disease that often affects apocrinebearing regions of the skin such as the axillae, perineum, and groin.1 Although current research on the etiology and pathogenesis of HS is limited, the disease is known to have a considerable psychosocial impact on patient quality of life.

Clinically, HS lesions manifest as tender subcutaneous nodules that rupture to form painful and deep dermal abscesses.2 These lesions typically develop due to hair follicle occlusion, followed by a cyclic process of inflammation, healing, re-inflammation, and scarring. Often, they are mistaken for cysts or a simple abscess in the early stages of the disease, leading to a delay in diagnosis.1 Disease severity is categorized based on Hurley staging: stage 1 involves abscess formation without scarring; stage 2 involves limited sinus tracts and recurrent abscesses with scarring and/or multiple separated lesions; and stage 3 is the most advanced stage, with diffuse involvement or multiple interconnected sinus tracts across an area with scarring. The condition primarily is medically managed with antibiotics and immunomodulators, but patients who have refractory disease can benefit from surgical excision.1,2

The prevalence of HS in the United States ranges from 0.77% to 1.19%, and individuals who self-identify as Black have 3-fold higher odds of having this condition compared with all other racial groups.3-5 Black patients also are thought to have a greater number and size of apocrine glands compared with patients who self-identify as White, suggesting an anatomic predisposition to developing HS and greater disease severity.6 However, despite HS disproportionately impacting individuals with skin of color (SOC), the majority of published HS research includes predominantly White patient cohorts.5 There is insufficient research assessing HS epidemiology, comorbidities, and treatment responses in patients with SOC.

A 2020 review reported the notable lack of clinical trials that sufficiently examine systemic medication treatment response in HS patients with SOC.7 Of the 15 HS treatment trials published from 2000 to 2019, only 16.4% (138/840) of the patient population were of African descent.7 Clinical trials investigating the efficacy of adalimumab in reducing HS burden also did not adequately evaluate clinical response in patients with SOC. One clinical trial did not include any Black patients as part of the cohort,8 and in 3 other studies, 80% to 85% of the study participants self-identified as White.9 The current literature does not reflect the patient populations most affected by HS, as several studies have reported that 65% of patients diagnosed with HS in the United States annually are Black.5,7 These results emphasize the underrepresentation of SOC populations in the current HS literature and the need for more research that investigates the disease processes, comorbidities, and treatment outcomes of the diverse patient population impacted by HS.

Methods

Study Population and Data Extraction—Following a protocol reviewed and approved by the MedStar Health/Georgetown University institutional review board (IRB #00006783), a retrospective chart review of 31 adult patients with HS who underwent surgery at a regional verified burn center from April 2014 to April 2023 was conducted. The following variables were collected from the electronic medical record (EMR): baseline demographics including age, sex, body mass index (BMI), obesity status, race, ethnicity, Fitzpatrick skin type, smoking status, substance use, employment status, and family history of HS; HS-specific details including Hurley staging, affected areas, and age at initial diagnosis; comorbidities such as dermatologic conditions, autoimmune disorders, infectious diseases, cardiovascular and associated diseases, ovarian disorders, gastrointestinal diseases, and othother common chronic comorbidities (psychiatric illness, kidney disease, type 2 diabetes [T2D], asthma, allergies, lymphedema, and inflammatory eye disease); and use of pharmacologics such as topical medications, oral antibiotics, immunomodulators, and steroids.

Study Definitions—Obesity was defined as both a continuous and categorical variable. Each patient’s BMI at the surgery date was recorded from the EMR as a continuous variable. Patients with obesity also had this condition listed under their complaints and problem list in the EMR, which was recorded as a categorical variable. Race and ethnicity were self-reported by patients. Comorbidity data, including T2D and hyperlipidemia, were defined by previously diagnosed diseases listed in the EMR. Pharmacologic medication data were included in the study if a patient was recommended/prescribed a medication and they had confirmed use of the medication in a subsequent office visit.

Statistical Analysis—Descriptive statistics were calculated for demographics, HS characteristics (eg, location, Hurley stage), and comorbidities. Continuous variables were presented as mean and standard deviation or median and interquartile range and were evaluated using a t test or Mann-Whitney U test when appropriate. Categorical variables were presented as frequencies and percentages and tested for associations using the X2 or Fisher exact test. Data analyses were performed using SAS software version 9.4 (SAS Institute Inc.).

Results

Thirty-one patients (17 females, 14 males; mean age, 40.9 years) were included in the study. Twenty-nine (93.5%) patients identified as Black. All study patients had at least 1 comorbidity. Obesity was diagnosed in 22 (71.0%) patients (mean BMI, 35.5 kg/m2). A total of 16 (51.6%) patients were current smokers, 3 (9.7%) were past smokers, 22 (71%) reported alcohol use, and 17 (54.8%) were active marijuana users. Only 3 (9.7%) patients had a family history of HS (Table 1).

CT115005140-Table1

Other common comorbidities associated with HS were anemia (64.5% [20/31]), a non–inflammatory bowel disease gastrointestinal disease (61.3% [19/31]), allergies (54.8% [17/31]), hypertension (41.9% [13/31]), cardiovascular disease (41.9% [13/31]), T2D (32.3% [10/31]), asthma (32.3% [10/31]), kidney disease (29.0% [9/31]), and atopic dermatitis (25.8% [8/31]). More than half (54.8% [17/31]) of patients were diagnosed with psychiatric illnesses, including depression, anxiety, bipolar depression, psychosis, anorexia, impulsive anger, hallucinations, delusion, attention deficit-hyperactivity disorder, and panic disorder (Table 2). Depression was diagnosed in 38.7% (12/31) of patients, and 22.6% (7/31) were diagnosed with anxiety.

CT115005140-Table2

The most common anatomic locations for HS were the right axilla (74.2% [23/31]), left axilla (74.2% [23/31]), groin (71% [22/31]), perineum (61.3% [19/31]), buttocks (41.9% [13/31]), and thigh (41.9% [13/31]). Other locations included the breast, lower back, posterior neck, dorsal foot, and scalp (all 3.2% [1/31])(Table 3). Twenty (64.5%) patients had Hurley staging recorded in the EMR. Seventeen (54.8%) were categorized as Hurley stage 3, and 3 (9.7%) were categorized as Hurley stage 2.

CT115005140-Table3

Twenty-nine (93.5%) patients were prescribed an oral antibiotic regimen. The most common oral antibiotics were clindamycin (35.5% [11/31]), doxycycline (35.5% [11/31]), rifampin (29% [9/31]), trimethoprim/sulfamethoxazole (22.6% [7/31]), and cephalexin (22.6% [7/31]). Of the patients who were prescribed rifampin, 87.5% (8/9) also were prescribed an adjunct oral clindamycin regimen. Twenty-nine percent (9/31) of patients were prescribed a biologic regimen; 22.6% (7/31) were prescribed adalimumab, 3.2% (1/31) were prescribed secukinumab, and 3.2% (1/31) were prescribed ustekinumab (Table 4).

CT115005140-Table4

Twenty-five (80.6%) patients were prescribed a topical treatment regimen, the most common being topical clindamycin (45.2% [14/31]). Other topical medications included triamcinolone (12.9% [4/31]), chlorhexidine gluconate wash (9.7% [3/31]), clobetasol (3.2% [1/31]), hydrocortisone (3.2% [1/31]), and hydroquinone (3.2% [1/31])(Table 4).

Other medical treatments for HS included metformin (25.8% [8/31]), spironolactone (16.1% [5/31]), and zinc supplements (12.9% [4/31]). Four patients (12.9%) were prescribed clindamycin plus rifampin as well as a combination of metformin, spironolactone, and/or zinc (Table 4).

Twenty-two (71.0%) patients had a history of receiving incision and drainage procedures as treatment for HS. All 31 patients underwent excisional surgery followed by appropriate reconstruction. The total number of excisional surgeries a single patient underwent for HS treatment ranged from 1 to 9, with a mean of 2 excisional surgeries per patient.

Comment

Our regional verified burn center in Washington, DC, serves a large population of patients with SOC, making it a unique and important sample to study for HS. Our results suggest that Black patients with HS may be at a higher risk for depression and anxiety. Twelve (38.7%) of our patients were diagnosed with depression, which is substantially higher than the 17% to 21% depression prevalence rate among all HS patients reported in meta-analyses.10,11 Additionally, 22.6% (7/31) of our patients were diagnosed with anxiety, which is higher than the 5% to 12% prevalence rate of anxiety among HS patients reported in meta-analyses.10,11 The stress of chronic disease management, psychosocial impact of living with HS, social stigma, sexual dysfunction, pain, and financial concerns make mental illness a debilitating yet common comorbidity for patients with HS. The results of our study suggest that anxiety and depression are highly prevalent among Black patients with HS. It is important to identify if this finding is due to the interplay of health care disparities and social determinants of health; the cause likely is multifactorial, as race and ethnicity may be potential predictors for increased disease severity. Hidradenitis suppurativa is known to be a major economic burden on patients, and race-dependent structural and societal inequalities may be influencing the increased prevalence of anxiety and depression among Black patients with HS.12 Therefore, clinicians must be vigilant for the signs and symptoms of mental illnesses to refer patients for psychiatric treatment when appropriate. Implementing self-report Patient Health Questionnaire-9, General Anxiety Disorder-7 depression and anxiety screening tools, and Dermatology Life Quality Index questionnaires at primary care and dermatology office visits may be a beneficial step toward identifying patients who could benefit from additional mental health resources.13

The patients included in our study predominantly self-identified as Black, and the current smoker prevalence rate was 51.6% (16/31). This percentage is lower than the smoking rates of other published HS studies conducted in predominantly White patient populations, which report up to a 76.5% smoking prevalence rate.14-16 One review article published in 2022 reported that approximately 90% of HS patients are current or former smokers.17 Additionally, a retrospective cohort analysis identifying HS cases among 3,924,310 tobacco smokers in the United States reported that tobacco smokers diagnosed with HS most commonly racially self-identified as White (66.2%).18 Tobacco chemicals and smoke can increase inflammatory cytokine levels, and the activation of nicotinic acetylcholine receptors surrounding pilosebaceous-apocrine units can increase follicular occlusion.14 While several studies1-3,14,19,20 support the strong correlation between tobacco smoking and HS, there are very few that specifically investigate the association between smoking and HS disease in SOC populations. It is possible that smoking rates may be lower in Black patients with HS compared with White patients with HS, which would suggest a multifactorial nature of HS disease pathophysiology. Future large, multicenter studies are needed that investigate smoking rates and HS disease severity in patients across various racial groups.

Prior research has shown a strong correlation between cigarette smoking and HS, but there is minimal data on the role of use of marijuana and other illicit drugs in HS disease pathophysiology.21 A total of 54.8% of our patients were active marijuana users with daily or weekly usage. Further research is needed to investigate whether marijuana use is linked with HS disease pathophysiology and severity or if patients with HS may be using marijuana to relieve pain, anxiety, and depression. Additional studies that survey the method of marijuana use (eg, joint, vape devices, or edibles) would clarify the relationship between not only HS and marijuana but also a potential link between disease severity and the process of inhaling large amounts of smoke vs a link with the active ingredients in the marijuana plant itself.

Approximately 61% (19/31) of our patients were diagnosed with a gastrointestinal disease in addition to HS. Current research reports the link between HS and inflammatory bowel disease, but few studies have investigated if a relationship exists between the gut microbiome and HS, as well as the incidence of general gastrointestinal disease among Black patients with HS.14,22 Our patients were diagnosed with gastrointestinal conditions such as colonic polyps, gastroesophageal reflux disease, benign neoplasms of the cecum and sigmoid colons, small bowel obstruction and perforation, biliary tract diseases, ileus, abdominal hernia, peritonitis, and diverticulosis. Further research is warranted to identify if there is a true relationship between gastrointestinal disease, the gut microbiome, and skin conditions such as HS.22 Biochemical research on the common genetic and inflammatory cytokine pathways involved in HS and gastrointestinal manifestations could help predict disease severity and management in HS patients with SOC.

Several research studies have reported the association between obesity and HS, likely due to adipose cells producing increased estrogen and leading to an estrogen-dominant hormone profile and increased local androgen production in adipose tissue.14,23,24 Antiandrogenic drugs such as finasteride and spironolactone lead to positive results in HS treatment compared to oral antibiotics alone.24 While 71.9% (22/31) of our patients were diagnosed with obesity, only 16.1% (5/31) were prescribed antiandrogen therapy such as spironolactone. It is unclear if this result reflects a health disparity due to insufficient insurance coverage and low prescribing rates or if there is patient hesitancy to taking antiandrogen medications. Additional clinical trials are needed to investigate the efficacy of antiandrogen therapies for HS. If proven to be efficacious, providers should consider adding these medications to the pharmacologic regimen of HS patients with SOC prior to recommending wide-excision surgeries. Furthermore, in addition to antiandrogen medication, weight-management interventions may be helpful in reducing HS disease. The results of a survey conducted in 35 HS patients who underwent bariatric surgery reported 48.6% (17/35) experienced complete disease remission after more than a 15% weight reduction.25,26 Investigating the impact of weight-management practices on disease severity would be helpful in outlining nonpharmacologic treatments for patients with HS.

Limitations

Our study was limited by the constraints of a retrospective chart review and small sample size. Retrospective chart reviews are susceptible to recall bias, variability in providers’ charting practices, and human error from data collectors. We acknowledge that a control group of non-HS patients should be the next step in furthering our research on HS disease comorbidities. Also, since 35.5% (11/31) of our patients did not have Hurley staging recorded in the EMR, it would be beneficial to conduct a future study comprehensive of all 3 Hurley stages. Since 93.5% (29/31) of the patients in our study racially identified as Black, having a control group of racially diverse HS patients would help further our understanding of HS pathophysiology. Lastly, since the inclusion criteria required patients to have undergone excisional surgery for HS, future studies that consider comorbidities among both surgical and nonsurgical patients with HS will aid in our understanding of HS patients with SOC.

Conclusion

The results of our study demonstrate a descriptive analysis of the demographics, most common comorbidities, lesion sites, pharmacologic treatments, and surgical profiles in patients with SOC who underwent surgical treatment for HS. Our data show that HS patients with SOC may be more likely to experience anxiety, depression, and gastrointestinal disease than other HS patients. Additionally, our patients had a high prevalence of marijuana use but lower prevalence of current cigarette use compared to studies conducted in predominantly White HS patient populations, emphasizing the multifactorial nature of HS pathophysiology. Furthermore, despite published research on the efficacy of immunomodulator therapy for HS, most of our HS patients with SOC underwent surgical intervention without first attempting biologic treatment regimens, indicating possible gaps in health care access for minority patients that may be impacting disease severity and outcomes. Studies such as this one that investigate disease pathophysiology and risk factors in SOC patient populations with HS are imperative in minimizing the health care disparity gap, improving disease outcomes, and providing more equitable health care for all patients.

References
  1. Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
  2. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60:539-563. doi:10.1016/j. jaad.2008.11.911
  3. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  4. Ingram JR, Jenkins-Jones S, Knipe DW, et al. Population-based Clinical Practice Research Datalink study using algorithm modelling to identify the true burden of hidradenitis suppurativa. Br J Dermatol. 2018;178:917-924. doi:10.1111/bjd.16101
  5. Lee DE, Clark AK, Shi VY. Hidradenitis suppurativa: disease burden and etiology in skin of color. Dermatology. 2017;233:456-461. doi:10.1159/000486741
  6. Brown-Korsah JB, McKenzie S, Omar D, et al. Variations in genetics, biology, and phenotype of cutaneous disorders in skin of color—part I: genetic, biologic, and structural differences in skin of color. J Am Acad Dermatol. 2022;87:1239-1258. doi:10.1016/j.jaad.2022.06.1193
  7. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  8. Arenbergerova M, Gkalpakiotis S, Arenberger P. Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy. Int J Dermatol. 2010;49:1445-1449. doi:10.1111/j.1365-4632.2010.04638.x
  9. Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
  10. Jalenques I, Ciortianu L, Pereira B, et al. The prevalence and odds of anxiety and depression in children and adults with hidradenitis suppurativa: systematic review and meta-analysis. J Am Acad Dermatol. 2020;83:542-553. doi:10.1016/j.jaad.2020.03.041
  11. Machado MO, Stergiopoulos V, Maes M, et al. Depression and anxiety in adults with hidradenitis suppurativa: a systematic review and meta-analysis. JAMA Dermatol. 2019;155:939-945. doi:10.1001 /jamadermatol.2019.0759
  12. Kilgour JM, Li S, Sarin KY. Hidradenitis suppurativa in patients of color is associated with increased disease severity and healthcare utilization: a retrospective analysis of 2 U.S. cohorts. JAAD Int. 2021;3:42-52. doi:10.1016/j.jdin.2021.01.007
  13. Rymaszewska JE, Krajewski PK, Szcze² ch J, et al. Depression and anxiety in hidradenitis suppurativa patients: a cross-sectional study among Polish patients. Postep Dermatol Alergol. 2023;40:35-39. doi:10.5114ada.2022.119080
  14. Johnston LA, Alhusayen R, Bourcier M, et al. Practical guidelines for managing patients with hidradenitis suppurativa: an update. J Cutan Med Surg. 2022;26(2 suppl):2S-24S. doi:10.1177/12034754221116115
  15. Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
  16. Seyed Jafari SM, Knüsel E, Cazzaniga S, et al. A retrospective cohort study on patients with hidradenitis suppurativa. Dermatology. 2018;234:71-78. doi:10.1159/000488344
  17. Lewandowski M, S´ wierczewska Z, Baran´ ska-Rybak W. Hidradenitis suppurativa: a review of current treatment options. Int J Dermatol. 2022;61:1152-1164. doi:10.1111/ijd.16115
  18. Garg A, Papagermanos V, Midura M, et al. Incidence of hidradenitis suppurativa among tobacco smokers: a population-based retrospective analysis in the U.S.A. Br J Dermatol. 2018;178:709-714. doi:10.1111/bjd.15939
  19. Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
  20. Tzellos T, Zouboulis CC. Which hidradenitis suppurativa comorbidities should I take into account? Exp Dermatol. 2022;31(suppl 1):29-32. doi:10.1111/exd.14633
  21. Metko D, Mehta S, Piguet V. Cannabis usage among patients with hidradenitis suppurativa: a scoping review. J Cutan Med Surg. 2024;28:307-308. doi:10.1177/12034754241238719
  22. Mahmud MR, Akter S, Tamanna SK, et al. Impact of gut microbiome on skin health: gut-skin axis observed through the lenses of therapeutics and skin diseases. Gut Microbes. 2022;14:2096995. doi:10.1080/194 90976.2022.2096995
  23. Mair KM, Gaw R, MacLean MR. Obesity, estrogens and adipose tissue dysfunction—implications for pulmonary arterial hypertension. Pulm Circ. 2020;10:2045894020952019. doi:10.1177/2045894020952023
  24. Abu Rached N, Gambichler T, Dietrich JW, et al. The role of hormones in hidradenitis suppurativa: a systematic review. Int J Mol Sci. 2022;23:15250. doi:10.3390/ijms232315250
  25. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016 /j.jaad.2019.02.067
  26. Choi ECE, Phan PHC, Oon HH. Hidradenitis suppurativa: racial and socioeconomic considerations in management. Int J Dermatol. 2022;61:1452-1457. doi:10.1111/ijd.16163
References
  1. Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
  2. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60:539-563. doi:10.1016/j. jaad.2008.11.911
  3. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  4. Ingram JR, Jenkins-Jones S, Knipe DW, et al. Population-based Clinical Practice Research Datalink study using algorithm modelling to identify the true burden of hidradenitis suppurativa. Br J Dermatol. 2018;178:917-924. doi:10.1111/bjd.16101
  5. Lee DE, Clark AK, Shi VY. Hidradenitis suppurativa: disease burden and etiology in skin of color. Dermatology. 2017;233:456-461. doi:10.1159/000486741
  6. Brown-Korsah JB, McKenzie S, Omar D, et al. Variations in genetics, biology, and phenotype of cutaneous disorders in skin of color—part I: genetic, biologic, and structural differences in skin of color. J Am Acad Dermatol. 2022;87:1239-1258. doi:10.1016/j.jaad.2022.06.1193
  7. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  8. Arenbergerova M, Gkalpakiotis S, Arenberger P. Effective long-term control of refractory hidradenitis suppurativa with adalimumab after failure of conventional therapy. Int J Dermatol. 2010;49:1445-1449. doi:10.1111/j.1365-4632.2010.04638.x
  9. Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
  10. Jalenques I, Ciortianu L, Pereira B, et al. The prevalence and odds of anxiety and depression in children and adults with hidradenitis suppurativa: systematic review and meta-analysis. J Am Acad Dermatol. 2020;83:542-553. doi:10.1016/j.jaad.2020.03.041
  11. Machado MO, Stergiopoulos V, Maes M, et al. Depression and anxiety in adults with hidradenitis suppurativa: a systematic review and meta-analysis. JAMA Dermatol. 2019;155:939-945. doi:10.1001 /jamadermatol.2019.0759
  12. Kilgour JM, Li S, Sarin KY. Hidradenitis suppurativa in patients of color is associated with increased disease severity and healthcare utilization: a retrospective analysis of 2 U.S. cohorts. JAAD Int. 2021;3:42-52. doi:10.1016/j.jdin.2021.01.007
  13. Rymaszewska JE, Krajewski PK, Szcze² ch J, et al. Depression and anxiety in hidradenitis suppurativa patients: a cross-sectional study among Polish patients. Postep Dermatol Alergol. 2023;40:35-39. doi:10.5114ada.2022.119080
  14. Johnston LA, Alhusayen R, Bourcier M, et al. Practical guidelines for managing patients with hidradenitis suppurativa: an update. J Cutan Med Surg. 2022;26(2 suppl):2S-24S. doi:10.1177/12034754221116115
  15. Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
  16. Seyed Jafari SM, Knüsel E, Cazzaniga S, et al. A retrospective cohort study on patients with hidradenitis suppurativa. Dermatology. 2018;234:71-78. doi:10.1159/000488344
  17. Lewandowski M, S´ wierczewska Z, Baran´ ska-Rybak W. Hidradenitis suppurativa: a review of current treatment options. Int J Dermatol. 2022;61:1152-1164. doi:10.1111/ijd.16115
  18. Garg A, Papagermanos V, Midura M, et al. Incidence of hidradenitis suppurativa among tobacco smokers: a population-based retrospective analysis in the U.S.A. Br J Dermatol. 2018;178:709-714. doi:10.1111/bjd.15939
  19. Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
  20. Tzellos T, Zouboulis CC. Which hidradenitis suppurativa comorbidities should I take into account? Exp Dermatol. 2022;31(suppl 1):29-32. doi:10.1111/exd.14633
  21. Metko D, Mehta S, Piguet V. Cannabis usage among patients with hidradenitis suppurativa: a scoping review. J Cutan Med Surg. 2024;28:307-308. doi:10.1177/12034754241238719
  22. Mahmud MR, Akter S, Tamanna SK, et al. Impact of gut microbiome on skin health: gut-skin axis observed through the lenses of therapeutics and skin diseases. Gut Microbes. 2022;14:2096995. doi:10.1080/194 90976.2022.2096995
  23. Mair KM, Gaw R, MacLean MR. Obesity, estrogens and adipose tissue dysfunction—implications for pulmonary arterial hypertension. Pulm Circ. 2020;10:2045894020952019. doi:10.1177/2045894020952023
  24. Abu Rached N, Gambichler T, Dietrich JW, et al. The role of hormones in hidradenitis suppurativa: a systematic review. Int J Mol Sci. 2022;23:15250. doi:10.3390/ijms232315250
  25. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016 /j.jaad.2019.02.067
  26. Choi ECE, Phan PHC, Oon HH. Hidradenitis suppurativa: racial and socioeconomic considerations in management. Int J Dermatol. 2022;61:1452-1457. doi:10.1111/ijd.16163
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Evaluating Factors Impacting Hidradenitis Suppurativa Disease Severity in Patients With Darker Skin Types

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PRACTICE POINTS

  • Anxiety and depression are highly prevalent among Black patients with hidradenitis suppurativa (HS). Implementing self-report questionnaires at medical office visits are crucial to identifying patients who could benefit from additional psychiatric resources.
  • Hidradenitis suppurativa patients with skin of color may have a higher incidence of comorbid gastrointestinal disease than other HS patients.
  • Investigating the impact of weight-management practices on disease severity would be helpful in outlining nonpharmacologic treatments for patients with HS.
  • The patient cohort described here had a high prevalence of marijuana use but lower prevalence of current cigarette use compared to studies conducted in predominantly White HS patient populations, emphasizing the multifactorial nature of HS pathophysiology.
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Evaluating Access to Full-Body Skin Examinations in Los Angeles County, California

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Evaluating Access to Full-Body Skin Examinations in Los Angeles County, California

To the Editor:

Early skin cancer detection improves patient outcomes1; however, socioeconomic and racial disparities may impact access to dermatologic care.2 Although non-Hispanic White individuals have a high incidence of skin cancer, they experience higher melanoma-specific survival rates than non-White patients, who often receive later-stage diagnoses and experience higher mortality.2 Furthermore, racial/ ethnic minorities often face longer surgery wait times after diagnosis and have lower socioeconomic status (SES) and less favorable health insurance coverage, contributing to poorer outcomes.2,3

To examine access to full-body skin examinations (FBSEs) by board-certified dermatologists in Los Angeles (LA) County, California, we analyzed the availability of FBSEs based on racial demographics, income, and insurance type (Medicaid [Medi-Cal] vs private [Blue Cross Blue Shield (BCBS)]). Demographic data by zip code were obtained from the US Census Bureau.4 This validated metric highlights socioeconomic disparities and minimizes data gaps5,6 and was used to assess health care access among different population subgroups. Dermatologists’ contact information was obtained from the Find a Dermatologist page on the American Academy of Dermatology website and the listed phone numbers of their practice were used to contact them. Practices with board-certified dermatologists accepting new patients were included in the study; practices were not included if they had exclusive insurance plans; were pediatric, cosmetic, or research only; or were nonresponsive to calls. From August 2022 to September 2022, each practice was called twice within a 36-hour period—once by a simulated patient with Medi-Cal and once by a simulated patient with BCBS—and were asked about availability for new patient FBSE appointments and accepted insurance types. Data were analyzed using SAS software (SAS Institute Inc.).

Los Angeles County comprises 269 zip codes, of which 82 (30.5%) have dermatology practices. Of 213 total dermatologists in LA County listed on the American Academy of Dermatology website, 193 (90.6%) met preliminary criteria, and 169 (79.3%) were successfully contacted. Almost all (94.6% [160/169]) accepted new patients for FBSEs; of those, 63.1% (101/160) accepted only private insurance, 16.9% (27/160) accepted both private insurance and Medi-Cal, and 16.2% (26/160) did not accept any insurance. Racial predominance for each dermatology practice was analyzed by zip code (Table). Dermatologists included in our study were significantly more concentrated in predominantly non- Hispanic White areas of LA County vs predominantly Hispanic areas (P<.0001). Notably, the average income in predominantly non-Hispanic White zip codes ($114,757.74) was significantly higher than in predominantly Hispanic areas ($58,278.54)(P=.001)(Table).4

CT115005167-Table

In LA County, 40.1% (108/269) of zip codes have no racial majority, 28.2% (76/269) are predominantly Hispanic, 27.5% (74/269) are predominantly non-Hispanic White, 2.2% (6/269) are predominantly Black, and 1.9% (5/269) are predominantly Asian.4 There are no dermatologists in predominantly Black zip codes, 2 in predominantly Asian zip codes, 14 in predominantly Hispanic zip codes, 38 in zip codes with no racial majority, and 106 in predominantly non-Hispanic White zip codes. There are significantly more dermatologists in predominantly non-Hispanic White zip codes compared to predominantly Hispanic zip codes (P<.0001). In LA County, the average income in predominantly Asian, non-Hispanic White, and Hispanic zip codes was $93,594, $114,757.84, and $58,278.54, respectively, in 2021.4 The average income in predominantly non-Hispanic White zip codes was significantly higher than in predominantly Hispanic zip codes (P=.001). There were no income data available for predominantly Black zip codes or zip codes with no racial majority.

The results from our study revealed potential barriers to FBSEs for racial and ethnic minorities in LA County, which supports previous research on the impact of SES, race, and insurance on access to dermatologic care.2,3 Predominantly Hispanic zip codes have significantly lower income (P<.0001) and fewer dermatologists (P=.001) compared to zip codes that are predominantly non-Hispanic White, reflecting how lower SES correlates with worse health outcomes and higher melanoma mortality. Conversely, predominantly non-Hispanic White areas with higher income have better access to dermatologists, which may contribute to the improved melanoma survival rates among White patients. Additionally, most dermatologists accept only private insurance, further highlighting the disparity in FBSE access for non-White patients across LA County. While our study focused on FBSE access, our findings may point to a wider barrier to dermatologic care, especially in zip codes with fewer dermatologists. Further studies are needed to determine whether these areas also face barriers to accessing primary care.

Our study was limited by the exclusion of nonphysician providers (eg, nurse practitioners, physician assistants), a small sample size, and lack of available economic data for predominantly Black zip codes.4 Additionally, the exclusion of practices with exclusive insurance plans (eg, Kaiser Permanente) limited the generalizability of our findings, as our results did not account for the populations served by these practices. Furthermore, our analysis did not account for variations in practice size or the proportion of care provided to patients with different insurance types, which could impact overall accessibility. Additional studies are needed to explore the impact of these factors on access to general dermatologic care and not just FBSEs.

Racial/ethnic minorities and lower SES populations face major barriers to FBSE access in LA County, such as difficulty finding a dermatologist in their area or one who accepts Medi-Cal. Addressing these disparities is crucial for improving skin cancer outcomes. Further research is needed to develop strategies to eliminate these barriers to dermatologic care, such as increasing access to teledermatology, offering mobile dermatology clinics, and improving insurance coverage.

References
  1. Chiaravalloti AJ, Laduca JR. Melanoma screening by means of complete skin exams for all patients in a dermatology practice reduces the thickness of primary melanomas at diagnosis. J Clin Aesthet Dermatol. 2014;7:18-22.
  2. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
  3. Baranowski MLH, Yeung H, Chen SC, et al. Factors associated with time to surgery in melanoma: an analysis of the National Cancer Database. J Am Acad Dermatol. 2019;81:908-916.
  4. United States Census Bureau. Explore census data. Accessed March 17, 2025. https://data.census.gov/all?q=los+angeles+county
  5. Berkowitz SA, Traore CY, Singer DE, et al. Evaluating area-based socioeconomic status indicators for monitoring disparities within health care systems: results from a primary care network. Health Serv Res. 2015;50:398-417.
  6. Jacobs B, Ir P, Bigdeli M, et al. Addressing access barriers to health services: an analytical framework for selecting appropriate interventions in lowincome Asian countries. Health Policy Plan. 2012;27:288-300.
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Marine Minasyan, Marian Banh, Kyra Diehl, Elise Krippaehne, Dr. Kesler, Dr. Goulding, Michelle Booth, Marissa Tran, Kiana Hosseinian, Nejma Wais, Amal Shafi, Suha Godil, Monique Cantu, and Niyati Panchal are from the College of Osteopathic Medicine of the Pacific, Western University of Health Science, Pomona, California. Drs. Yumeen and Wisco are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Ganesh Tilve is from Mercer Healthcare Consulting, Irvine, California. Dr. Vance is from the Department of Exercise and Nutrition Sciences, State University of New York, Plattsburgh.

The authors have no relevant financial disclosures to report.

This study received approval from Western University of Health Sciences institutional review board (IRB X24044).

Correspondence: Marine Minasyan, BS ([email protected]).

Cutis. 2025 May;115(5):167-168. doi:10.12788/cutis.1210

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Marine Minasyan, Marian Banh, Kyra Diehl, Elise Krippaehne, Dr. Kesler, Dr. Goulding, Michelle Booth, Marissa Tran, Kiana Hosseinian, Nejma Wais, Amal Shafi, Suha Godil, Monique Cantu, and Niyati Panchal are from the College of Osteopathic Medicine of the Pacific, Western University of Health Science, Pomona, California. Drs. Yumeen and Wisco are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Ganesh Tilve is from Mercer Healthcare Consulting, Irvine, California. Dr. Vance is from the Department of Exercise and Nutrition Sciences, State University of New York, Plattsburgh.

The authors have no relevant financial disclosures to report.

This study received approval from Western University of Health Sciences institutional review board (IRB X24044).

Correspondence: Marine Minasyan, BS ([email protected]).

Cutis. 2025 May;115(5):167-168. doi:10.12788/cutis.1210

Author and Disclosure Information

Marine Minasyan, Marian Banh, Kyra Diehl, Elise Krippaehne, Dr. Kesler, Dr. Goulding, Michelle Booth, Marissa Tran, Kiana Hosseinian, Nejma Wais, Amal Shafi, Suha Godil, Monique Cantu, and Niyati Panchal are from the College of Osteopathic Medicine of the Pacific, Western University of Health Science, Pomona, California. Drs. Yumeen and Wisco are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Ganesh Tilve is from Mercer Healthcare Consulting, Irvine, California. Dr. Vance is from the Department of Exercise and Nutrition Sciences, State University of New York, Plattsburgh.

The authors have no relevant financial disclosures to report.

This study received approval from Western University of Health Sciences institutional review board (IRB X24044).

Correspondence: Marine Minasyan, BS ([email protected]).

Cutis. 2025 May;115(5):167-168. doi:10.12788/cutis.1210

Article PDF
Article PDF

To the Editor:

Early skin cancer detection improves patient outcomes1; however, socioeconomic and racial disparities may impact access to dermatologic care.2 Although non-Hispanic White individuals have a high incidence of skin cancer, they experience higher melanoma-specific survival rates than non-White patients, who often receive later-stage diagnoses and experience higher mortality.2 Furthermore, racial/ ethnic minorities often face longer surgery wait times after diagnosis and have lower socioeconomic status (SES) and less favorable health insurance coverage, contributing to poorer outcomes.2,3

To examine access to full-body skin examinations (FBSEs) by board-certified dermatologists in Los Angeles (LA) County, California, we analyzed the availability of FBSEs based on racial demographics, income, and insurance type (Medicaid [Medi-Cal] vs private [Blue Cross Blue Shield (BCBS)]). Demographic data by zip code were obtained from the US Census Bureau.4 This validated metric highlights socioeconomic disparities and minimizes data gaps5,6 and was used to assess health care access among different population subgroups. Dermatologists’ contact information was obtained from the Find a Dermatologist page on the American Academy of Dermatology website and the listed phone numbers of their practice were used to contact them. Practices with board-certified dermatologists accepting new patients were included in the study; practices were not included if they had exclusive insurance plans; were pediatric, cosmetic, or research only; or were nonresponsive to calls. From August 2022 to September 2022, each practice was called twice within a 36-hour period—once by a simulated patient with Medi-Cal and once by a simulated patient with BCBS—and were asked about availability for new patient FBSE appointments and accepted insurance types. Data were analyzed using SAS software (SAS Institute Inc.).

Los Angeles County comprises 269 zip codes, of which 82 (30.5%) have dermatology practices. Of 213 total dermatologists in LA County listed on the American Academy of Dermatology website, 193 (90.6%) met preliminary criteria, and 169 (79.3%) were successfully contacted. Almost all (94.6% [160/169]) accepted new patients for FBSEs; of those, 63.1% (101/160) accepted only private insurance, 16.9% (27/160) accepted both private insurance and Medi-Cal, and 16.2% (26/160) did not accept any insurance. Racial predominance for each dermatology practice was analyzed by zip code (Table). Dermatologists included in our study were significantly more concentrated in predominantly non- Hispanic White areas of LA County vs predominantly Hispanic areas (P<.0001). Notably, the average income in predominantly non-Hispanic White zip codes ($114,757.74) was significantly higher than in predominantly Hispanic areas ($58,278.54)(P=.001)(Table).4

CT115005167-Table

In LA County, 40.1% (108/269) of zip codes have no racial majority, 28.2% (76/269) are predominantly Hispanic, 27.5% (74/269) are predominantly non-Hispanic White, 2.2% (6/269) are predominantly Black, and 1.9% (5/269) are predominantly Asian.4 There are no dermatologists in predominantly Black zip codes, 2 in predominantly Asian zip codes, 14 in predominantly Hispanic zip codes, 38 in zip codes with no racial majority, and 106 in predominantly non-Hispanic White zip codes. There are significantly more dermatologists in predominantly non-Hispanic White zip codes compared to predominantly Hispanic zip codes (P<.0001). In LA County, the average income in predominantly Asian, non-Hispanic White, and Hispanic zip codes was $93,594, $114,757.84, and $58,278.54, respectively, in 2021.4 The average income in predominantly non-Hispanic White zip codes was significantly higher than in predominantly Hispanic zip codes (P=.001). There were no income data available for predominantly Black zip codes or zip codes with no racial majority.

The results from our study revealed potential barriers to FBSEs for racial and ethnic minorities in LA County, which supports previous research on the impact of SES, race, and insurance on access to dermatologic care.2,3 Predominantly Hispanic zip codes have significantly lower income (P<.0001) and fewer dermatologists (P=.001) compared to zip codes that are predominantly non-Hispanic White, reflecting how lower SES correlates with worse health outcomes and higher melanoma mortality. Conversely, predominantly non-Hispanic White areas with higher income have better access to dermatologists, which may contribute to the improved melanoma survival rates among White patients. Additionally, most dermatologists accept only private insurance, further highlighting the disparity in FBSE access for non-White patients across LA County. While our study focused on FBSE access, our findings may point to a wider barrier to dermatologic care, especially in zip codes with fewer dermatologists. Further studies are needed to determine whether these areas also face barriers to accessing primary care.

Our study was limited by the exclusion of nonphysician providers (eg, nurse practitioners, physician assistants), a small sample size, and lack of available economic data for predominantly Black zip codes.4 Additionally, the exclusion of practices with exclusive insurance plans (eg, Kaiser Permanente) limited the generalizability of our findings, as our results did not account for the populations served by these practices. Furthermore, our analysis did not account for variations in practice size or the proportion of care provided to patients with different insurance types, which could impact overall accessibility. Additional studies are needed to explore the impact of these factors on access to general dermatologic care and not just FBSEs.

Racial/ethnic minorities and lower SES populations face major barriers to FBSE access in LA County, such as difficulty finding a dermatologist in their area or one who accepts Medi-Cal. Addressing these disparities is crucial for improving skin cancer outcomes. Further research is needed to develop strategies to eliminate these barriers to dermatologic care, such as increasing access to teledermatology, offering mobile dermatology clinics, and improving insurance coverage.

To the Editor:

Early skin cancer detection improves patient outcomes1; however, socioeconomic and racial disparities may impact access to dermatologic care.2 Although non-Hispanic White individuals have a high incidence of skin cancer, they experience higher melanoma-specific survival rates than non-White patients, who often receive later-stage diagnoses and experience higher mortality.2 Furthermore, racial/ ethnic minorities often face longer surgery wait times after diagnosis and have lower socioeconomic status (SES) and less favorable health insurance coverage, contributing to poorer outcomes.2,3

To examine access to full-body skin examinations (FBSEs) by board-certified dermatologists in Los Angeles (LA) County, California, we analyzed the availability of FBSEs based on racial demographics, income, and insurance type (Medicaid [Medi-Cal] vs private [Blue Cross Blue Shield (BCBS)]). Demographic data by zip code were obtained from the US Census Bureau.4 This validated metric highlights socioeconomic disparities and minimizes data gaps5,6 and was used to assess health care access among different population subgroups. Dermatologists’ contact information was obtained from the Find a Dermatologist page on the American Academy of Dermatology website and the listed phone numbers of their practice were used to contact them. Practices with board-certified dermatologists accepting new patients were included in the study; practices were not included if they had exclusive insurance plans; were pediatric, cosmetic, or research only; or were nonresponsive to calls. From August 2022 to September 2022, each practice was called twice within a 36-hour period—once by a simulated patient with Medi-Cal and once by a simulated patient with BCBS—and were asked about availability for new patient FBSE appointments and accepted insurance types. Data were analyzed using SAS software (SAS Institute Inc.).

Los Angeles County comprises 269 zip codes, of which 82 (30.5%) have dermatology practices. Of 213 total dermatologists in LA County listed on the American Academy of Dermatology website, 193 (90.6%) met preliminary criteria, and 169 (79.3%) were successfully contacted. Almost all (94.6% [160/169]) accepted new patients for FBSEs; of those, 63.1% (101/160) accepted only private insurance, 16.9% (27/160) accepted both private insurance and Medi-Cal, and 16.2% (26/160) did not accept any insurance. Racial predominance for each dermatology practice was analyzed by zip code (Table). Dermatologists included in our study were significantly more concentrated in predominantly non- Hispanic White areas of LA County vs predominantly Hispanic areas (P<.0001). Notably, the average income in predominantly non-Hispanic White zip codes ($114,757.74) was significantly higher than in predominantly Hispanic areas ($58,278.54)(P=.001)(Table).4

CT115005167-Table

In LA County, 40.1% (108/269) of zip codes have no racial majority, 28.2% (76/269) are predominantly Hispanic, 27.5% (74/269) are predominantly non-Hispanic White, 2.2% (6/269) are predominantly Black, and 1.9% (5/269) are predominantly Asian.4 There are no dermatologists in predominantly Black zip codes, 2 in predominantly Asian zip codes, 14 in predominantly Hispanic zip codes, 38 in zip codes with no racial majority, and 106 in predominantly non-Hispanic White zip codes. There are significantly more dermatologists in predominantly non-Hispanic White zip codes compared to predominantly Hispanic zip codes (P<.0001). In LA County, the average income in predominantly Asian, non-Hispanic White, and Hispanic zip codes was $93,594, $114,757.84, and $58,278.54, respectively, in 2021.4 The average income in predominantly non-Hispanic White zip codes was significantly higher than in predominantly Hispanic zip codes (P=.001). There were no income data available for predominantly Black zip codes or zip codes with no racial majority.

The results from our study revealed potential barriers to FBSEs for racial and ethnic minorities in LA County, which supports previous research on the impact of SES, race, and insurance on access to dermatologic care.2,3 Predominantly Hispanic zip codes have significantly lower income (P<.0001) and fewer dermatologists (P=.001) compared to zip codes that are predominantly non-Hispanic White, reflecting how lower SES correlates with worse health outcomes and higher melanoma mortality. Conversely, predominantly non-Hispanic White areas with higher income have better access to dermatologists, which may contribute to the improved melanoma survival rates among White patients. Additionally, most dermatologists accept only private insurance, further highlighting the disparity in FBSE access for non-White patients across LA County. While our study focused on FBSE access, our findings may point to a wider barrier to dermatologic care, especially in zip codes with fewer dermatologists. Further studies are needed to determine whether these areas also face barriers to accessing primary care.

Our study was limited by the exclusion of nonphysician providers (eg, nurse practitioners, physician assistants), a small sample size, and lack of available economic data for predominantly Black zip codes.4 Additionally, the exclusion of practices with exclusive insurance plans (eg, Kaiser Permanente) limited the generalizability of our findings, as our results did not account for the populations served by these practices. Furthermore, our analysis did not account for variations in practice size or the proportion of care provided to patients with different insurance types, which could impact overall accessibility. Additional studies are needed to explore the impact of these factors on access to general dermatologic care and not just FBSEs.

Racial/ethnic minorities and lower SES populations face major barriers to FBSE access in LA County, such as difficulty finding a dermatologist in their area or one who accepts Medi-Cal. Addressing these disparities is crucial for improving skin cancer outcomes. Further research is needed to develop strategies to eliminate these barriers to dermatologic care, such as increasing access to teledermatology, offering mobile dermatology clinics, and improving insurance coverage.

References
  1. Chiaravalloti AJ, Laduca JR. Melanoma screening by means of complete skin exams for all patients in a dermatology practice reduces the thickness of primary melanomas at diagnosis. J Clin Aesthet Dermatol. 2014;7:18-22.
  2. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
  3. Baranowski MLH, Yeung H, Chen SC, et al. Factors associated with time to surgery in melanoma: an analysis of the National Cancer Database. J Am Acad Dermatol. 2019;81:908-916.
  4. United States Census Bureau. Explore census data. Accessed March 17, 2025. https://data.census.gov/all?q=los+angeles+county
  5. Berkowitz SA, Traore CY, Singer DE, et al. Evaluating area-based socioeconomic status indicators for monitoring disparities within health care systems: results from a primary care network. Health Serv Res. 2015;50:398-417.
  6. Jacobs B, Ir P, Bigdeli M, et al. Addressing access barriers to health services: an analytical framework for selecting appropriate interventions in lowincome Asian countries. Health Policy Plan. 2012;27:288-300.
References
  1. Chiaravalloti AJ, Laduca JR. Melanoma screening by means of complete skin exams for all patients in a dermatology practice reduces the thickness of primary melanomas at diagnosis. J Clin Aesthet Dermatol. 2014;7:18-22.
  2. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
  3. Baranowski MLH, Yeung H, Chen SC, et al. Factors associated with time to surgery in melanoma: an analysis of the National Cancer Database. J Am Acad Dermatol. 2019;81:908-916.
  4. United States Census Bureau. Explore census data. Accessed March 17, 2025. https://data.census.gov/all?q=los+angeles+county
  5. Berkowitz SA, Traore CY, Singer DE, et al. Evaluating area-based socioeconomic status indicators for monitoring disparities within health care systems: results from a primary care network. Health Serv Res. 2015;50:398-417.
  6. Jacobs B, Ir P, Bigdeli M, et al. Addressing access barriers to health services: an analytical framework for selecting appropriate interventions in lowincome Asian countries. Health Policy Plan. 2012;27:288-300.
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Evaluating Access to Full-Body Skin Examinations in Los Angeles County, California

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Evaluating Access to Full-Body Skin Examinations in Los Angeles County, California

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PRACTICE POINTS

  • Socioeconomic and racial disparities impact access to full-body skin examinations (FBSEs) in Los Angeles County.
  • Most dermatologists included in this study were accepting new patients for a FBSE.
  • There are significantly more dermatologists in predominantly non-Hispanic White zip codes than in predominantly Hispanic zip codes in Los Angeles County.
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Basal Cell Carcinoma Arising From an Infantile Hemangioma Treated With Gold Radon Seeds

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Basal Cell Carcinoma Arising From an Infantile Hemangioma Treated With Gold Radon Seeds

To the Editor:

Basal cell carcinoma (BCC), which is the most common type of skin cancer, typically arises on sun-damaged skin as a result of long-term exposure to UV radiation. Another known risk factor for BCC is exposure to ionizing radiation, though this is less commonly encountered.1 We present a unique case of a BCC arising at the site of an involuted infantile hemangioma that had been treated with implanted and retained gold radon seeds more than 7 decades prior. This case highlights the importance of obtaining a detailed history of radiation exposures to better counsel patients about skin cancer risk and manage disease in complex skin locations.

A 75-year-old woman presented to an outside dermatologist for evaluation of a pink papule on the right upper cutaneous lip that had enlarged over several months (Figure 1). The patient’s medical history was remarkable for an infantile hemangioma present since shortly after birth in the same location that had been treated with 10 implanted gold radon seeds when she was 6 years old. Over her lifetime, several seeds had self-extruded from the area, but some remained within the subcutaneous tissue as confirmed by dental radiographs. A shave biopsy of the papule demonstrated a superficial BCC, and the patient was referred to our institution for Mohs micrographic surgery.

CT115005160-Fig1_AB
FIGURE 1. A, A 75-year-old woman with a superficial basal cell carcinoma on the right upper cutaneous lip. B, The patient at 6 months of age with an infantile hemangioma that arose shortly after birth in the same location.

Intraoperative frozen sections revealed both superficial and nodular BCC, and the tumor was cleared in 3 stages. During surgery, a gold radon seed was visualized at the base of the excised BCC and was removed from the subcutaneous tissue (Figure 2). The primary defect on the upper lip was closed with a rotation flap. The patient returned for follow-up 2 months later and showed good healing and cosmetic outcome.

CT115005160-Fig2_AB
FIGURE 2. A and B, A gold radon seed was visible at the base of the excised basal cell carcinoma (white arrow) and subsequently was removed.

Although not commonly encountered, ionizing radiation is a known risk factor for BCC.1 Basal cell carcinoma arising from implanted gold radon seeds represents a minority of reported cases.2,3 Radium was first used to treat skin disease in the early 1900s.1 The radioactive decay of radium produced tissue destruction via alpha, beta, and gamma particles, which slowly released over weeks when radium was packaged into a capsule.4 Following implantation of the capsule, DNA damage occurred due to double-stranded breaks, chromosomal aberrations, and generation of reactive oxygen species. The downstream effect of these cellular insults resulted in cell-cycle shortening, apoptosis, and carcinogenesis.5

Gold radon seeds were used to treat infantile hemangiomas in the United States and Europe from the early 1940s to the 1960s; their use declined dramatically in the 1950s due to adverse effects and discovery of the potential for future malignancies as well as the development of safer and more effective treatments.1,3 Our patient received a substantial dose of ionizing radiation from the implantation of gold radon seeds at the site of the infantile hemangioma, which dramatically increased her risk for BCC in this location.

Infantile hemangiomas are the most common vascular tumors in children. Most infantile hemangiomas regress spontaneously and are stably involuted by about 5 or 6 years of age.6 Treatment is indicated for rapidly growing hemangiomas that are at risk for ulceration or are located by critical structures (eg, the eyes or airway). Hemangiomas located on or near the lips should be treated to avoid disfigurement and loss of function as a consequence of rapid growth and involution.7 The treatment of choice for large or high-risk infantile hemangiomas over the past 10 to 15 years has been beta blockers.6-8 Propranolol hydrochloride, a systemic beta blocker, was approved by the US Food and Drug Administration in 2014 for the treatment of infantile hemangiomas and has demonstrated safety and effectiveness in promoting involution in these lesions.8 Unlike radiation therapy from implanted gold radon seeds, propranolol does not increase the risk for BCC. Although other risk factors such as skin type and cumulative UV exposure contribute to the development of BCC, the exact location of the BCC overlying the residual gold radon seeds was highly suggestive of ionizing radiation playing a major role in the carcinogenesis of the tumor in our patient.

Our case highlights the importance of screening elderly patients for exposures that may increase the risk for skin carcinogenesis. Dermatologists are accustomed to asking about history of UV exposure, sunburns, and use of sun-protective measures; however, direct questioning about less common sources of radiation exposure also may help stratify a patient’s risk for developing BCC. Although the US Preventive Services Task Force 2023 guidelines determined there is insufficient evidence to recommend visual skin cancer screening examinations in asymptomatic adults,9 we advocate for verbal screening of radiation exposure in both primary care and dermatology office settings. At a time when access to care, particularly dermatology services, is challenging, determining the appropriate interval for follow-up based on the patient’s skin cancer risk is imperative.

References
  1. Fürst CJ, Lundell M, Holm LE. Radiation therapy of hemangiomas, 1909- 1959. a cohort based on 50 years of clinical practice at Radiumhemmet, Stockholm. Acta Oncol. 1987;26:33-36. doi:10.3109/02841868709092974
  2. Bräuner EV, Loft S, Sørensen M, et al. Residential radon exposure and skin cancer incidence in a prospective Danish cohort. PLoS ONE. 2015;10:E0135642. doi:10.1371/journal.pone.0135642
  3. Weiss E, Sukal SA, Zimbler MS, et al. Basal cell carcinoma arising 57 years after interstitial radiotherapy of a nasal hemangioma. Dermatol Surg. 2008;34:1137-1140. doi:10.1111/j.1524-4725.2008.34229.x
  4. Lavery MJ, Lorenzelli D, Crema J. A radon seed identified during skin surgery: an unusual finding. Clin Exp Dermatol. 2021;46:604-606. doi:10.1111/ced.14454
  5. Robertson A, Allen J, Laney R, et al. The cellular and molecular carcinogenic effects of radon exposure: a review. Int J Mol Sci. 2013;14:14024-14063. doi:10.3390/ijms140714024
  6. Rodríguez Bandera AI, Sebaratnam DF, et al. Infantile hemangioma. part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392. doi:10.1016 /j.jaad.2021.08.019
  7. Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475. doi:10.1542/peds.2018-3475
  8. Sebaratnam DF, Rodríguez Bandera AL, Wong LF, et al. Infantile hemangioma. part 2: management. J Am Acad Dermatol. 2021;85: 1395-1404. doi:10.1016/j.jaad.2021.08.020
  9. US Preventive Services Task Force, Mangione CM, Barry MJ, Nicholson WK, et al. Screening for skin cancer: US Preventive Services Task Force recommendation statement. JAMA. 2023;329:1290-1295. doi:10.1001/jama.2023.4342
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From the Department of Dermatology, Medical College of Wisconsin, Milwaukee and Froedtert Health System, Milwaukee.

The authors have no relevant financial disclosures to report.

Correspondence: Melanie A. Clark, MD, Department of Dermatology, Medical College of Wisconsin, 8701 W Watertown Plank Rd, Milwaukee, WI 53226 ([email protected]).

Cutis. 2025 May;115(5):160-161. doi:10.12788/cutis.1212

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From the Department of Dermatology, Medical College of Wisconsin, Milwaukee and Froedtert Health System, Milwaukee.

The authors have no relevant financial disclosures to report.

Correspondence: Melanie A. Clark, MD, Department of Dermatology, Medical College of Wisconsin, 8701 W Watertown Plank Rd, Milwaukee, WI 53226 ([email protected]).

Cutis. 2025 May;115(5):160-161. doi:10.12788/cutis.1212

Author and Disclosure Information

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The authors have no relevant financial disclosures to report.

Correspondence: Melanie A. Clark, MD, Department of Dermatology, Medical College of Wisconsin, 8701 W Watertown Plank Rd, Milwaukee, WI 53226 ([email protected]).

Cutis. 2025 May;115(5):160-161. doi:10.12788/cutis.1212

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To the Editor:

Basal cell carcinoma (BCC), which is the most common type of skin cancer, typically arises on sun-damaged skin as a result of long-term exposure to UV radiation. Another known risk factor for BCC is exposure to ionizing radiation, though this is less commonly encountered.1 We present a unique case of a BCC arising at the site of an involuted infantile hemangioma that had been treated with implanted and retained gold radon seeds more than 7 decades prior. This case highlights the importance of obtaining a detailed history of radiation exposures to better counsel patients about skin cancer risk and manage disease in complex skin locations.

A 75-year-old woman presented to an outside dermatologist for evaluation of a pink papule on the right upper cutaneous lip that had enlarged over several months (Figure 1). The patient’s medical history was remarkable for an infantile hemangioma present since shortly after birth in the same location that had been treated with 10 implanted gold radon seeds when she was 6 years old. Over her lifetime, several seeds had self-extruded from the area, but some remained within the subcutaneous tissue as confirmed by dental radiographs. A shave biopsy of the papule demonstrated a superficial BCC, and the patient was referred to our institution for Mohs micrographic surgery.

CT115005160-Fig1_AB
FIGURE 1. A, A 75-year-old woman with a superficial basal cell carcinoma on the right upper cutaneous lip. B, The patient at 6 months of age with an infantile hemangioma that arose shortly after birth in the same location.

Intraoperative frozen sections revealed both superficial and nodular BCC, and the tumor was cleared in 3 stages. During surgery, a gold radon seed was visualized at the base of the excised BCC and was removed from the subcutaneous tissue (Figure 2). The primary defect on the upper lip was closed with a rotation flap. The patient returned for follow-up 2 months later and showed good healing and cosmetic outcome.

CT115005160-Fig2_AB
FIGURE 2. A and B, A gold radon seed was visible at the base of the excised basal cell carcinoma (white arrow) and subsequently was removed.

Although not commonly encountered, ionizing radiation is a known risk factor for BCC.1 Basal cell carcinoma arising from implanted gold radon seeds represents a minority of reported cases.2,3 Radium was first used to treat skin disease in the early 1900s.1 The radioactive decay of radium produced tissue destruction via alpha, beta, and gamma particles, which slowly released over weeks when radium was packaged into a capsule.4 Following implantation of the capsule, DNA damage occurred due to double-stranded breaks, chromosomal aberrations, and generation of reactive oxygen species. The downstream effect of these cellular insults resulted in cell-cycle shortening, apoptosis, and carcinogenesis.5

Gold radon seeds were used to treat infantile hemangiomas in the United States and Europe from the early 1940s to the 1960s; their use declined dramatically in the 1950s due to adverse effects and discovery of the potential for future malignancies as well as the development of safer and more effective treatments.1,3 Our patient received a substantial dose of ionizing radiation from the implantation of gold radon seeds at the site of the infantile hemangioma, which dramatically increased her risk for BCC in this location.

Infantile hemangiomas are the most common vascular tumors in children. Most infantile hemangiomas regress spontaneously and are stably involuted by about 5 or 6 years of age.6 Treatment is indicated for rapidly growing hemangiomas that are at risk for ulceration or are located by critical structures (eg, the eyes or airway). Hemangiomas located on or near the lips should be treated to avoid disfigurement and loss of function as a consequence of rapid growth and involution.7 The treatment of choice for large or high-risk infantile hemangiomas over the past 10 to 15 years has been beta blockers.6-8 Propranolol hydrochloride, a systemic beta blocker, was approved by the US Food and Drug Administration in 2014 for the treatment of infantile hemangiomas and has demonstrated safety and effectiveness in promoting involution in these lesions.8 Unlike radiation therapy from implanted gold radon seeds, propranolol does not increase the risk for BCC. Although other risk factors such as skin type and cumulative UV exposure contribute to the development of BCC, the exact location of the BCC overlying the residual gold radon seeds was highly suggestive of ionizing radiation playing a major role in the carcinogenesis of the tumor in our patient.

Our case highlights the importance of screening elderly patients for exposures that may increase the risk for skin carcinogenesis. Dermatologists are accustomed to asking about history of UV exposure, sunburns, and use of sun-protective measures; however, direct questioning about less common sources of radiation exposure also may help stratify a patient’s risk for developing BCC. Although the US Preventive Services Task Force 2023 guidelines determined there is insufficient evidence to recommend visual skin cancer screening examinations in asymptomatic adults,9 we advocate for verbal screening of radiation exposure in both primary care and dermatology office settings. At a time when access to care, particularly dermatology services, is challenging, determining the appropriate interval for follow-up based on the patient’s skin cancer risk is imperative.

To the Editor:

Basal cell carcinoma (BCC), which is the most common type of skin cancer, typically arises on sun-damaged skin as a result of long-term exposure to UV radiation. Another known risk factor for BCC is exposure to ionizing radiation, though this is less commonly encountered.1 We present a unique case of a BCC arising at the site of an involuted infantile hemangioma that had been treated with implanted and retained gold radon seeds more than 7 decades prior. This case highlights the importance of obtaining a detailed history of radiation exposures to better counsel patients about skin cancer risk and manage disease in complex skin locations.

A 75-year-old woman presented to an outside dermatologist for evaluation of a pink papule on the right upper cutaneous lip that had enlarged over several months (Figure 1). The patient’s medical history was remarkable for an infantile hemangioma present since shortly after birth in the same location that had been treated with 10 implanted gold radon seeds when she was 6 years old. Over her lifetime, several seeds had self-extruded from the area, but some remained within the subcutaneous tissue as confirmed by dental radiographs. A shave biopsy of the papule demonstrated a superficial BCC, and the patient was referred to our institution for Mohs micrographic surgery.

CT115005160-Fig1_AB
FIGURE 1. A, A 75-year-old woman with a superficial basal cell carcinoma on the right upper cutaneous lip. B, The patient at 6 months of age with an infantile hemangioma that arose shortly after birth in the same location.

Intraoperative frozen sections revealed both superficial and nodular BCC, and the tumor was cleared in 3 stages. During surgery, a gold radon seed was visualized at the base of the excised BCC and was removed from the subcutaneous tissue (Figure 2). The primary defect on the upper lip was closed with a rotation flap. The patient returned for follow-up 2 months later and showed good healing and cosmetic outcome.

CT115005160-Fig2_AB
FIGURE 2. A and B, A gold radon seed was visible at the base of the excised basal cell carcinoma (white arrow) and subsequently was removed.

Although not commonly encountered, ionizing radiation is a known risk factor for BCC.1 Basal cell carcinoma arising from implanted gold radon seeds represents a minority of reported cases.2,3 Radium was first used to treat skin disease in the early 1900s.1 The radioactive decay of radium produced tissue destruction via alpha, beta, and gamma particles, which slowly released over weeks when radium was packaged into a capsule.4 Following implantation of the capsule, DNA damage occurred due to double-stranded breaks, chromosomal aberrations, and generation of reactive oxygen species. The downstream effect of these cellular insults resulted in cell-cycle shortening, apoptosis, and carcinogenesis.5

Gold radon seeds were used to treat infantile hemangiomas in the United States and Europe from the early 1940s to the 1960s; their use declined dramatically in the 1950s due to adverse effects and discovery of the potential for future malignancies as well as the development of safer and more effective treatments.1,3 Our patient received a substantial dose of ionizing radiation from the implantation of gold radon seeds at the site of the infantile hemangioma, which dramatically increased her risk for BCC in this location.

Infantile hemangiomas are the most common vascular tumors in children. Most infantile hemangiomas regress spontaneously and are stably involuted by about 5 or 6 years of age.6 Treatment is indicated for rapidly growing hemangiomas that are at risk for ulceration or are located by critical structures (eg, the eyes or airway). Hemangiomas located on or near the lips should be treated to avoid disfigurement and loss of function as a consequence of rapid growth and involution.7 The treatment of choice for large or high-risk infantile hemangiomas over the past 10 to 15 years has been beta blockers.6-8 Propranolol hydrochloride, a systemic beta blocker, was approved by the US Food and Drug Administration in 2014 for the treatment of infantile hemangiomas and has demonstrated safety and effectiveness in promoting involution in these lesions.8 Unlike radiation therapy from implanted gold radon seeds, propranolol does not increase the risk for BCC. Although other risk factors such as skin type and cumulative UV exposure contribute to the development of BCC, the exact location of the BCC overlying the residual gold radon seeds was highly suggestive of ionizing radiation playing a major role in the carcinogenesis of the tumor in our patient.

Our case highlights the importance of screening elderly patients for exposures that may increase the risk for skin carcinogenesis. Dermatologists are accustomed to asking about history of UV exposure, sunburns, and use of sun-protective measures; however, direct questioning about less common sources of radiation exposure also may help stratify a patient’s risk for developing BCC. Although the US Preventive Services Task Force 2023 guidelines determined there is insufficient evidence to recommend visual skin cancer screening examinations in asymptomatic adults,9 we advocate for verbal screening of radiation exposure in both primary care and dermatology office settings. At a time when access to care, particularly dermatology services, is challenging, determining the appropriate interval for follow-up based on the patient’s skin cancer risk is imperative.

References
  1. Fürst CJ, Lundell M, Holm LE. Radiation therapy of hemangiomas, 1909- 1959. a cohort based on 50 years of clinical practice at Radiumhemmet, Stockholm. Acta Oncol. 1987;26:33-36. doi:10.3109/02841868709092974
  2. Bräuner EV, Loft S, Sørensen M, et al. Residential radon exposure and skin cancer incidence in a prospective Danish cohort. PLoS ONE. 2015;10:E0135642. doi:10.1371/journal.pone.0135642
  3. Weiss E, Sukal SA, Zimbler MS, et al. Basal cell carcinoma arising 57 years after interstitial radiotherapy of a nasal hemangioma. Dermatol Surg. 2008;34:1137-1140. doi:10.1111/j.1524-4725.2008.34229.x
  4. Lavery MJ, Lorenzelli D, Crema J. A radon seed identified during skin surgery: an unusual finding. Clin Exp Dermatol. 2021;46:604-606. doi:10.1111/ced.14454
  5. Robertson A, Allen J, Laney R, et al. The cellular and molecular carcinogenic effects of radon exposure: a review. Int J Mol Sci. 2013;14:14024-14063. doi:10.3390/ijms140714024
  6. Rodríguez Bandera AI, Sebaratnam DF, et al. Infantile hemangioma. part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392. doi:10.1016 /j.jaad.2021.08.019
  7. Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475. doi:10.1542/peds.2018-3475
  8. Sebaratnam DF, Rodríguez Bandera AL, Wong LF, et al. Infantile hemangioma. part 2: management. J Am Acad Dermatol. 2021;85: 1395-1404. doi:10.1016/j.jaad.2021.08.020
  9. US Preventive Services Task Force, Mangione CM, Barry MJ, Nicholson WK, et al. Screening for skin cancer: US Preventive Services Task Force recommendation statement. JAMA. 2023;329:1290-1295. doi:10.1001/jama.2023.4342
References
  1. Fürst CJ, Lundell M, Holm LE. Radiation therapy of hemangiomas, 1909- 1959. a cohort based on 50 years of clinical practice at Radiumhemmet, Stockholm. Acta Oncol. 1987;26:33-36. doi:10.3109/02841868709092974
  2. Bräuner EV, Loft S, Sørensen M, et al. Residential radon exposure and skin cancer incidence in a prospective Danish cohort. PLoS ONE. 2015;10:E0135642. doi:10.1371/journal.pone.0135642
  3. Weiss E, Sukal SA, Zimbler MS, et al. Basal cell carcinoma arising 57 years after interstitial radiotherapy of a nasal hemangioma. Dermatol Surg. 2008;34:1137-1140. doi:10.1111/j.1524-4725.2008.34229.x
  4. Lavery MJ, Lorenzelli D, Crema J. A radon seed identified during skin surgery: an unusual finding. Clin Exp Dermatol. 2021;46:604-606. doi:10.1111/ced.14454
  5. Robertson A, Allen J, Laney R, et al. The cellular and molecular carcinogenic effects of radon exposure: a review. Int J Mol Sci. 2013;14:14024-14063. doi:10.3390/ijms140714024
  6. Rodríguez Bandera AI, Sebaratnam DF, et al. Infantile hemangioma. part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392. doi:10.1016 /j.jaad.2021.08.019
  7. Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475. doi:10.1542/peds.2018-3475
  8. Sebaratnam DF, Rodríguez Bandera AL, Wong LF, et al. Infantile hemangioma. part 2: management. J Am Acad Dermatol. 2021;85: 1395-1404. doi:10.1016/j.jaad.2021.08.020
  9. US Preventive Services Task Force, Mangione CM, Barry MJ, Nicholson WK, et al. Screening for skin cancer: US Preventive Services Task Force recommendation statement. JAMA. 2023;329:1290-1295. doi:10.1001/jama.2023.4342
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Basal Cell Carcinoma Arising From an Infantile Hemangioma Treated With Gold Radon Seeds

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PRACTICE POINTS

  • Historical use of ionizing radiation to treat skin disease is a risk factor for basal cell carcinoma (BCC).
  • Mohs micrographic surgery is the treatment of choice for BCC in high-risk areas such as the nose, eyelids, and lips, where tissue conservation and complete margin control are essential.
  • Elderly patients should be screened for less common sources of radiation exposure for better risk stratification and to determine appropriate intervals for follow-up with a dermatologist.
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Multiple Firm Papules on the Wrists and Forearms

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Multiple Firm Papules on the Wrists and Forearms

THE DIAGNOSIS: Acral Persistent Papular Mucinosis

Histopathologic analysis revealed conspicuous interstitial mucin deposition throughout the upper to mid reticular dermis in the absence of a cellular infiltrate or fibroplasia. Colloidal iron staining confirmed the presence of mucin. In correlation with the clinical presentation, a diagnosis of acral persistent papular mucinosis (APPM) was made. The patient was counseled on the benign disease course and lack of associated comorbidities, and additional treatment was not pursued.

Acral persistent papular mucinosis is a rare distinct subtype of cutaneous mucinosis that initially was described by Rongioletti et al1 in 1986. As a localized form of lichen myxedematosus, APPM is characterized by mucin deposition in the dermis with no systemic involvement. The precise pathogenesis remains unclear, although some investigators have suggested that cytokine-mediated stimulation of glycosaminoglycan production may contribute to increased mucin accumulation in the dermis.2 Acral persistent papular mucinosis predominantly affects middle-aged women with a 5:1 female-to-male predominance.3 Clinically, patients present with discrete, nonfollicular, waxy papules that typically measure 2 to 5 mm and are distributed symmetrically on the extensor surfaces of the wrists and forearms. While the lesions generally are asymptomatic, some patients may report mild pruritus. The condition is chronic, with lesions seldom resolving and often increasing in number over time.3

Histologically, APPM is characterized by focal deposits of mucin in the upper reticular dermis with no evidence of increased fibroblast proliferation or fibrosis.4 This feature is pivotal in differentiating APPM from other subtypes of localized lichen myxedematosus and similar dermatoses. Diagnosis of APPM requires exclusion of systemic involvement, including thyroid abnormalities and monoclonal gammopathy, aligning with its classification as a purely cutaneous condition.5 Management of APPM is unclear due to its rarity. Reassurance for patients of its benign nature as well as clinical observation are recommended, though some reports cite benefits of treatment with topical corticosteroids or calcineurin inhibitors.6,7 The long-term prognosis for patients with APPM is favorable, although the persistence of and potential increase in lesions over time can be a cosmetic concern.

The differential diagnoses for APPM include scleromyxedema, scleredema, and other cutaneous eruptions that manifest as smooth flesh-colored papules, such as granuloma annulare and lichen nitidus.3 Scleromyxedema is a systemic cutaneous mucinosis that is part of the same disease spectrum as lichen myxedematosus. The papular eruption of scleromyxedema is much more widespread, and coalescing of the lesions may lead to characteristic skin thickening, creating leonine facies and deep furrowing over the trunk.8 Extracutaneous manifestations are frequent in scleromyxedema, and up to 90% of patients exhibit evidence of an underlying plasma cell dyscrasia.2 Histopathologically, scleromyxedema shows extensive fibroblast proliferation and fibrosis, in contrast to the findings of APPM (Figure 1).

Hill-dermpath-1
FIGURE 1. Scleromyxedema shows mucin deposition and fibroblast proliferation in the upper dermis (H&E, original magnification ×100).

The histopathology of APPM is most similar to scleredema, a rare fibromucinous disorder of the skin associated with diabetes, infection (especially poststreptococcal), or monoclonal gammopathy.9 Biopsy evaluation of scleredema reveals a normal epidermis with mucin deposition between collagen bundles predominantly in the deep reticular dermis as well as absent fibroblast proliferation (Figure 2). Unlike APPM, scleredema manifests with diffuse woody induration with erythema and hyperpigmentation on the posterior neck and upper back.9 On physical examination, the distinct clinical features of scleredema distinguish this condition from APPM and scleromyxedema.

Hill-dermpath-2
FIGURE 2. Scleredema demonstrates mucin deposition between thickened collagen bundles in the deep dermis with absent fibrosis (H&E, original magnification ×50).

Papular granuloma annulare also was considered in our patient due to the presence of small flesh-colored papules. Histologically, granuloma annulare is characterized by palisading granulomas and mucin deposition in the dermis.10 However, the pattern of mucin deposition differs from that seen in APPM. In granuloma annulare, mucin is observed around foci of degenerated collagen (Figure 3), which was not observed in our patient.10 Additionally, the absence of an inflammatory infiltrate in our patient further ruled out this diagnosis.

Hill-dermpath-3
FIGURE 3. Histopathology of granuloma annulare shows focal collagen degeneration with mucin deposition and surrounding histiocytic infiltrate (H&E, original magnification ×50).

Lichen nitidus also could be considered in the differential diagnosis for ACCM. It typically manifests with minute, clustered, monomorphous papules with a predilection for the chest, abdomen, flexural forearms, and genitalia. The histology of lichen nitidus is distinct, showing a well-circumscribed lymphohistiocytic infiltrate in the papillary dermis bordered by epidermal ridges, resembling a ball and clutch appearance (Figure 4).11

Hill-dermpath-4
FIGURE 4. Lichen nitidus demonstrates a well-circumscribed dense lymphohistiocytic infiltrate in the upper dermis (H&E, original magnification ×20).

Although the clinical differential diagnosis in our patient was broad, histopathologic evaluation played a crucial role in confirming the diagnosis of APPM. This benign condition could be overlooked by patients and physicians; thorough clinical evaluation is necessary to rule out systemic mucinoses, which are associated with higher risks of morbidity and mortality.

References
  1. Rongioletti F, Rebora A. Acral persistent papular mucinosis: a new entity. Arch Dermatol. 1986;122:1237-1239. doi:10.1001 /archderm.1986.01660230027002
  2. Christman MP, Sukhdeo K, Kim RH, et al. Papular mucinosis, or localized lichen myxedematosus (LM)(discrete papular type). Dermatol Online J. 2017;23:13030/qt3xp109qd.
  3. Rongioletti F, Ferreli C, Atzori L. Acral persistent papular mucinosis. Clin Dermatol. 2021;39:211-214. doi:10.1016/j.clindermatol.2020.10.001
  4. Rongioletti F, Rebora A. Cutaneous mucinoses: microscopic criteria for diagnosis. Am J Dermatopathol. 2001;23:257-267. doi:10.1097/00000372- 200106000-00022
  5. Rongioletti F. Lichen myxedematosus (papular mucinosis): new concepts and perspectives for an old disease. Semin Cutan Med Surg. 2006;25:100-104. doi:10.1016/j.sder.2006.04.001
  6. Jun JY, Oh SH, Shim JH, et al. Acral persistent papular mucinosis with partial response to tacrolimus ointment. Ann Dermatol. 2016;28:517-519. doi:10.5021/ad.2016.28.4.517
  7. Rongioletti F, Zaccaria E, Cozzani E, et al. Treatment of localized lichen myxedematosus of discrete type with tacrolimus ointment. J Am Acad Dermatol. 2008;58:530-532. doi:10.1016/j.jaad.2006.10.021
  8. Rongioletti F, Merlo G, Cinotti E, et al. Scleromyxedema: a multicenter study of characteristics, comorbidities, course, and therapy in 30 patients. J Am Acad Dermatol. 2013;69:66-72. doi:10.1016 /j.jaad.2013.01.007
  9. Rongioletti F, Kaiser F, Cinotti E, et al. Scleredema. a multicentre study of characteristics, comorbidities, course and therapy in 44 patients. J Eur Acad Dermatol Venereol. 2015;29:2399-2404. doi:10.1111/jdv.13272
  10. Piette EW, Rosenbach M. Granuloma annulare: clinical and histologic variants, epidemiology, and genetics. J Am Acad Dermatol. 2016;75:457-465. doi:10.1016/j.jaad.2015.03.054
  11. Al-Mutairi N, Hassanein A, Nour-Eldin O, et al. Generalized lichen nitidus. Pediatr Dermatol. 2005;22:158-160. doi:10.1111 /j.1525-1470.2005.22215.x
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The authors have no relevant financial disclosures to report.

Correspondence: Michael A. Cardis, MD, MedStar Washington Hospital Center Department of Dermatology, 110 Irving Street NW, Washington, DC, 20010 ([email protected]).

Cutis. 2025 May;115(5):159, 165-166. doi:10.12788/cutis.1206

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Dr. Hill is from the Department of Dermatology, Georgetown University School of Medicine, Washington, DC. Drs. Russomanno and Cardis are from the Department of Dermatology, MedStar Washington Hospital Center, Washington, DC.

The authors have no relevant financial disclosures to report.

Correspondence: Michael A. Cardis, MD, MedStar Washington Hospital Center Department of Dermatology, 110 Irving Street NW, Washington, DC, 20010 ([email protected]).

Cutis. 2025 May;115(5):159, 165-166. doi:10.12788/cutis.1206

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Dr. Hill is from the Department of Dermatology, Georgetown University School of Medicine, Washington, DC. Drs. Russomanno and Cardis are from the Department of Dermatology, MedStar Washington Hospital Center, Washington, DC.

The authors have no relevant financial disclosures to report.

Correspondence: Michael A. Cardis, MD, MedStar Washington Hospital Center Department of Dermatology, 110 Irving Street NW, Washington, DC, 20010 ([email protected]).

Cutis. 2025 May;115(5):159, 165-166. doi:10.12788/cutis.1206

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THE DIAGNOSIS: Acral Persistent Papular Mucinosis

Histopathologic analysis revealed conspicuous interstitial mucin deposition throughout the upper to mid reticular dermis in the absence of a cellular infiltrate or fibroplasia. Colloidal iron staining confirmed the presence of mucin. In correlation with the clinical presentation, a diagnosis of acral persistent papular mucinosis (APPM) was made. The patient was counseled on the benign disease course and lack of associated comorbidities, and additional treatment was not pursued.

Acral persistent papular mucinosis is a rare distinct subtype of cutaneous mucinosis that initially was described by Rongioletti et al1 in 1986. As a localized form of lichen myxedematosus, APPM is characterized by mucin deposition in the dermis with no systemic involvement. The precise pathogenesis remains unclear, although some investigators have suggested that cytokine-mediated stimulation of glycosaminoglycan production may contribute to increased mucin accumulation in the dermis.2 Acral persistent papular mucinosis predominantly affects middle-aged women with a 5:1 female-to-male predominance.3 Clinically, patients present with discrete, nonfollicular, waxy papules that typically measure 2 to 5 mm and are distributed symmetrically on the extensor surfaces of the wrists and forearms. While the lesions generally are asymptomatic, some patients may report mild pruritus. The condition is chronic, with lesions seldom resolving and often increasing in number over time.3

Histologically, APPM is characterized by focal deposits of mucin in the upper reticular dermis with no evidence of increased fibroblast proliferation or fibrosis.4 This feature is pivotal in differentiating APPM from other subtypes of localized lichen myxedematosus and similar dermatoses. Diagnosis of APPM requires exclusion of systemic involvement, including thyroid abnormalities and monoclonal gammopathy, aligning with its classification as a purely cutaneous condition.5 Management of APPM is unclear due to its rarity. Reassurance for patients of its benign nature as well as clinical observation are recommended, though some reports cite benefits of treatment with topical corticosteroids or calcineurin inhibitors.6,7 The long-term prognosis for patients with APPM is favorable, although the persistence of and potential increase in lesions over time can be a cosmetic concern.

The differential diagnoses for APPM include scleromyxedema, scleredema, and other cutaneous eruptions that manifest as smooth flesh-colored papules, such as granuloma annulare and lichen nitidus.3 Scleromyxedema is a systemic cutaneous mucinosis that is part of the same disease spectrum as lichen myxedematosus. The papular eruption of scleromyxedema is much more widespread, and coalescing of the lesions may lead to characteristic skin thickening, creating leonine facies and deep furrowing over the trunk.8 Extracutaneous manifestations are frequent in scleromyxedema, and up to 90% of patients exhibit evidence of an underlying plasma cell dyscrasia.2 Histopathologically, scleromyxedema shows extensive fibroblast proliferation and fibrosis, in contrast to the findings of APPM (Figure 1).

Hill-dermpath-1
FIGURE 1. Scleromyxedema shows mucin deposition and fibroblast proliferation in the upper dermis (H&E, original magnification ×100).

The histopathology of APPM is most similar to scleredema, a rare fibromucinous disorder of the skin associated with diabetes, infection (especially poststreptococcal), or monoclonal gammopathy.9 Biopsy evaluation of scleredema reveals a normal epidermis with mucin deposition between collagen bundles predominantly in the deep reticular dermis as well as absent fibroblast proliferation (Figure 2). Unlike APPM, scleredema manifests with diffuse woody induration with erythema and hyperpigmentation on the posterior neck and upper back.9 On physical examination, the distinct clinical features of scleredema distinguish this condition from APPM and scleromyxedema.

Hill-dermpath-2
FIGURE 2. Scleredema demonstrates mucin deposition between thickened collagen bundles in the deep dermis with absent fibrosis (H&E, original magnification ×50).

Papular granuloma annulare also was considered in our patient due to the presence of small flesh-colored papules. Histologically, granuloma annulare is characterized by palisading granulomas and mucin deposition in the dermis.10 However, the pattern of mucin deposition differs from that seen in APPM. In granuloma annulare, mucin is observed around foci of degenerated collagen (Figure 3), which was not observed in our patient.10 Additionally, the absence of an inflammatory infiltrate in our patient further ruled out this diagnosis.

Hill-dermpath-3
FIGURE 3. Histopathology of granuloma annulare shows focal collagen degeneration with mucin deposition and surrounding histiocytic infiltrate (H&E, original magnification ×50).

Lichen nitidus also could be considered in the differential diagnosis for ACCM. It typically manifests with minute, clustered, monomorphous papules with a predilection for the chest, abdomen, flexural forearms, and genitalia. The histology of lichen nitidus is distinct, showing a well-circumscribed lymphohistiocytic infiltrate in the papillary dermis bordered by epidermal ridges, resembling a ball and clutch appearance (Figure 4).11

Hill-dermpath-4
FIGURE 4. Lichen nitidus demonstrates a well-circumscribed dense lymphohistiocytic infiltrate in the upper dermis (H&E, original magnification ×20).

Although the clinical differential diagnosis in our patient was broad, histopathologic evaluation played a crucial role in confirming the diagnosis of APPM. This benign condition could be overlooked by patients and physicians; thorough clinical evaluation is necessary to rule out systemic mucinoses, which are associated with higher risks of morbidity and mortality.

THE DIAGNOSIS: Acral Persistent Papular Mucinosis

Histopathologic analysis revealed conspicuous interstitial mucin deposition throughout the upper to mid reticular dermis in the absence of a cellular infiltrate or fibroplasia. Colloidal iron staining confirmed the presence of mucin. In correlation with the clinical presentation, a diagnosis of acral persistent papular mucinosis (APPM) was made. The patient was counseled on the benign disease course and lack of associated comorbidities, and additional treatment was not pursued.

Acral persistent papular mucinosis is a rare distinct subtype of cutaneous mucinosis that initially was described by Rongioletti et al1 in 1986. As a localized form of lichen myxedematosus, APPM is characterized by mucin deposition in the dermis with no systemic involvement. The precise pathogenesis remains unclear, although some investigators have suggested that cytokine-mediated stimulation of glycosaminoglycan production may contribute to increased mucin accumulation in the dermis.2 Acral persistent papular mucinosis predominantly affects middle-aged women with a 5:1 female-to-male predominance.3 Clinically, patients present with discrete, nonfollicular, waxy papules that typically measure 2 to 5 mm and are distributed symmetrically on the extensor surfaces of the wrists and forearms. While the lesions generally are asymptomatic, some patients may report mild pruritus. The condition is chronic, with lesions seldom resolving and often increasing in number over time.3

Histologically, APPM is characterized by focal deposits of mucin in the upper reticular dermis with no evidence of increased fibroblast proliferation or fibrosis.4 This feature is pivotal in differentiating APPM from other subtypes of localized lichen myxedematosus and similar dermatoses. Diagnosis of APPM requires exclusion of systemic involvement, including thyroid abnormalities and monoclonal gammopathy, aligning with its classification as a purely cutaneous condition.5 Management of APPM is unclear due to its rarity. Reassurance for patients of its benign nature as well as clinical observation are recommended, though some reports cite benefits of treatment with topical corticosteroids or calcineurin inhibitors.6,7 The long-term prognosis for patients with APPM is favorable, although the persistence of and potential increase in lesions over time can be a cosmetic concern.

The differential diagnoses for APPM include scleromyxedema, scleredema, and other cutaneous eruptions that manifest as smooth flesh-colored papules, such as granuloma annulare and lichen nitidus.3 Scleromyxedema is a systemic cutaneous mucinosis that is part of the same disease spectrum as lichen myxedematosus. The papular eruption of scleromyxedema is much more widespread, and coalescing of the lesions may lead to characteristic skin thickening, creating leonine facies and deep furrowing over the trunk.8 Extracutaneous manifestations are frequent in scleromyxedema, and up to 90% of patients exhibit evidence of an underlying plasma cell dyscrasia.2 Histopathologically, scleromyxedema shows extensive fibroblast proliferation and fibrosis, in contrast to the findings of APPM (Figure 1).

Hill-dermpath-1
FIGURE 1. Scleromyxedema shows mucin deposition and fibroblast proliferation in the upper dermis (H&E, original magnification ×100).

The histopathology of APPM is most similar to scleredema, a rare fibromucinous disorder of the skin associated with diabetes, infection (especially poststreptococcal), or monoclonal gammopathy.9 Biopsy evaluation of scleredema reveals a normal epidermis with mucin deposition between collagen bundles predominantly in the deep reticular dermis as well as absent fibroblast proliferation (Figure 2). Unlike APPM, scleredema manifests with diffuse woody induration with erythema and hyperpigmentation on the posterior neck and upper back.9 On physical examination, the distinct clinical features of scleredema distinguish this condition from APPM and scleromyxedema.

Hill-dermpath-2
FIGURE 2. Scleredema demonstrates mucin deposition between thickened collagen bundles in the deep dermis with absent fibrosis (H&E, original magnification ×50).

Papular granuloma annulare also was considered in our patient due to the presence of small flesh-colored papules. Histologically, granuloma annulare is characterized by palisading granulomas and mucin deposition in the dermis.10 However, the pattern of mucin deposition differs from that seen in APPM. In granuloma annulare, mucin is observed around foci of degenerated collagen (Figure 3), which was not observed in our patient.10 Additionally, the absence of an inflammatory infiltrate in our patient further ruled out this diagnosis.

Hill-dermpath-3
FIGURE 3. Histopathology of granuloma annulare shows focal collagen degeneration with mucin deposition and surrounding histiocytic infiltrate (H&E, original magnification ×50).

Lichen nitidus also could be considered in the differential diagnosis for ACCM. It typically manifests with minute, clustered, monomorphous papules with a predilection for the chest, abdomen, flexural forearms, and genitalia. The histology of lichen nitidus is distinct, showing a well-circumscribed lymphohistiocytic infiltrate in the papillary dermis bordered by epidermal ridges, resembling a ball and clutch appearance (Figure 4).11

Hill-dermpath-4
FIGURE 4. Lichen nitidus demonstrates a well-circumscribed dense lymphohistiocytic infiltrate in the upper dermis (H&E, original magnification ×20).

Although the clinical differential diagnosis in our patient was broad, histopathologic evaluation played a crucial role in confirming the diagnosis of APPM. This benign condition could be overlooked by patients and physicians; thorough clinical evaluation is necessary to rule out systemic mucinoses, which are associated with higher risks of morbidity and mortality.

References
  1. Rongioletti F, Rebora A. Acral persistent papular mucinosis: a new entity. Arch Dermatol. 1986;122:1237-1239. doi:10.1001 /archderm.1986.01660230027002
  2. Christman MP, Sukhdeo K, Kim RH, et al. Papular mucinosis, or localized lichen myxedematosus (LM)(discrete papular type). Dermatol Online J. 2017;23:13030/qt3xp109qd.
  3. Rongioletti F, Ferreli C, Atzori L. Acral persistent papular mucinosis. Clin Dermatol. 2021;39:211-214. doi:10.1016/j.clindermatol.2020.10.001
  4. Rongioletti F, Rebora A. Cutaneous mucinoses: microscopic criteria for diagnosis. Am J Dermatopathol. 2001;23:257-267. doi:10.1097/00000372- 200106000-00022
  5. Rongioletti F. Lichen myxedematosus (papular mucinosis): new concepts and perspectives for an old disease. Semin Cutan Med Surg. 2006;25:100-104. doi:10.1016/j.sder.2006.04.001
  6. Jun JY, Oh SH, Shim JH, et al. Acral persistent papular mucinosis with partial response to tacrolimus ointment. Ann Dermatol. 2016;28:517-519. doi:10.5021/ad.2016.28.4.517
  7. Rongioletti F, Zaccaria E, Cozzani E, et al. Treatment of localized lichen myxedematosus of discrete type with tacrolimus ointment. J Am Acad Dermatol. 2008;58:530-532. doi:10.1016/j.jaad.2006.10.021
  8. Rongioletti F, Merlo G, Cinotti E, et al. Scleromyxedema: a multicenter study of characteristics, comorbidities, course, and therapy in 30 patients. J Am Acad Dermatol. 2013;69:66-72. doi:10.1016 /j.jaad.2013.01.007
  9. Rongioletti F, Kaiser F, Cinotti E, et al. Scleredema. a multicentre study of characteristics, comorbidities, course and therapy in 44 patients. J Eur Acad Dermatol Venereol. 2015;29:2399-2404. doi:10.1111/jdv.13272
  10. Piette EW, Rosenbach M. Granuloma annulare: clinical and histologic variants, epidemiology, and genetics. J Am Acad Dermatol. 2016;75:457-465. doi:10.1016/j.jaad.2015.03.054
  11. Al-Mutairi N, Hassanein A, Nour-Eldin O, et al. Generalized lichen nitidus. Pediatr Dermatol. 2005;22:158-160. doi:10.1111 /j.1525-1470.2005.22215.x
References
  1. Rongioletti F, Rebora A. Acral persistent papular mucinosis: a new entity. Arch Dermatol. 1986;122:1237-1239. doi:10.1001 /archderm.1986.01660230027002
  2. Christman MP, Sukhdeo K, Kim RH, et al. Papular mucinosis, or localized lichen myxedematosus (LM)(discrete papular type). Dermatol Online J. 2017;23:13030/qt3xp109qd.
  3. Rongioletti F, Ferreli C, Atzori L. Acral persistent papular mucinosis. Clin Dermatol. 2021;39:211-214. doi:10.1016/j.clindermatol.2020.10.001
  4. Rongioletti F, Rebora A. Cutaneous mucinoses: microscopic criteria for diagnosis. Am J Dermatopathol. 2001;23:257-267. doi:10.1097/00000372- 200106000-00022
  5. Rongioletti F. Lichen myxedematosus (papular mucinosis): new concepts and perspectives for an old disease. Semin Cutan Med Surg. 2006;25:100-104. doi:10.1016/j.sder.2006.04.001
  6. Jun JY, Oh SH, Shim JH, et al. Acral persistent papular mucinosis with partial response to tacrolimus ointment. Ann Dermatol. 2016;28:517-519. doi:10.5021/ad.2016.28.4.517
  7. Rongioletti F, Zaccaria E, Cozzani E, et al. Treatment of localized lichen myxedematosus of discrete type with tacrolimus ointment. J Am Acad Dermatol. 2008;58:530-532. doi:10.1016/j.jaad.2006.10.021
  8. Rongioletti F, Merlo G, Cinotti E, et al. Scleromyxedema: a multicenter study of characteristics, comorbidities, course, and therapy in 30 patients. J Am Acad Dermatol. 2013;69:66-72. doi:10.1016 /j.jaad.2013.01.007
  9. Rongioletti F, Kaiser F, Cinotti E, et al. Scleredema. a multicentre study of characteristics, comorbidities, course and therapy in 44 patients. J Eur Acad Dermatol Venereol. 2015;29:2399-2404. doi:10.1111/jdv.13272
  10. Piette EW, Rosenbach M. Granuloma annulare: clinical and histologic variants, epidemiology, and genetics. J Am Acad Dermatol. 2016;75:457-465. doi:10.1016/j.jaad.2015.03.054
  11. Al-Mutairi N, Hassanein A, Nour-Eldin O, et al. Generalized lichen nitidus. Pediatr Dermatol. 2005;22:158-160. doi:10.1111 /j.1525-1470.2005.22215.x
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Multiple Firm Papules on the Wrists and Forearms

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A 69-year-old woman presented to the dermatology department with persistent asymptomatic skin lesions on the wrists and forearms of several months’ duration. The lesions had slowly grown in number over the past few months with no identifiable triggers. The patient reported no known history of injury or trauma to the affected sites and was not taking any prescription medications other than daily vitamins. She denied any family history of similar lesions and was otherwise healthy. Physical examination revealed multiple waxy, firm, hypopigmented, 3- to 5-mm papules located exclusively on the dorsal wrists and forearms. No extracutaneous involvement was observed. A 4-mm punch biopsy from the forearm was obtained.

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H&E, original magnification ×100 (inset: colloidal iron, original magnification ×100).
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Advances in Screening for Barrett’s Esophagus and Esophageal Adenocarcinoma

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Advances in Screening for Barrett’s Esophagus and Esophageal Adenocarcinoma

Click to view more from Gastroenterology Data Trends 2025.

References
  1. Vantanasiri K, Kamboj AK, Kisiel JB, Iyer PG. Advances in Screening for Barrett Esophagus and Esophageal Adenocarcinoma. Mayo Clin Proc. 2024;99(3):459-473. doi:10.1016/j.mayocp.2023.07.014
  2. Cancer Stat Facts: Esophageal Cancer. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 12, 2025. https://seer.cancer.gov/statfacts/html/esoph.html
  3. Seer*Explorer: Esophagus. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 4, 2025. https://seer.cancer.gov/statistics-network/explorer/application.html
  4. Kolb JM, Chen M, Tavakkoli A, et al. Understanding Compliance, Practice Patterns, and Barriers Among Gastroenterologists and Primary Care Providers Is Crucial for Developing Strategies to Improve Screening for Barrett’s Esophagus. Gastroenterology. 2022;162(6):1568-1573.e4. doi:10.1053/j.gastro.2022.02.003
  5. Kunzmann AT, Thrift AP, Cardwell CR, et al. Model for Identifying Individuals at Risk for Esophageal Adenocarcinoma. Clin Gastroenterol Hepatol. 2018;16(8):1229-1236.e4. doi:10.1016/j.cgh.2018.03.014
  6. Rubenstein JH, Evans RR, Burns JA, et al. Patients With Adenocarcinoma of the Esophagus or Esophagogastric Junction Frequently Have Potential Screening Opportunities. Gastroenterology. 2022;162(4):1349-1351.e5. doi:10.1053/j.gastro.2021.12.255
  7. Xie S-H, Ness-Jensen E, Medefelt N, Lagergren J. Assessing the feasibility of targeted screening for esophageal adenocarcinoma based on individual risk assessment in a population-based cohort study in Norway (The HUNT Study). Am J Gastroenterol. 2018;113(6):829-835. doi:10.1038/s41395-018-0069-9
  8. Rubenstein JH, Fontaine S, MacDonald PW, et al. Predicting Incident Adenocarcinoma of the Esophagus or Gastric Cardia Using Machine Learning of Electronic Health Records. Gastroenterology. 2023;165(6):1420-1429.e10. doi:10.1053/j.gastro.2023.08.011
  9. Fitzgerald RC, di Pietro M, O’Donovan M, et al. Cytosponge-trefoil factor 3 versus usual care to identify Barrett’s oesophagus in a primary care setting: a multicentre, pragmatic, randomised controlled trial. Lancet. 2020;396(10247):333-344. doi:10.1016/S0140-6736(20)31099-0
  10. Moinova HR, Verma S, Dumot J, et al. Multicenter, Prospective Trial of Nonendoscopic
    Biomarker-Driven Detection of Barrett’s Esophagus and Esophageal Adenocarcinoma. Am J Gastroenterol. 2024;119(11):2206-2214. doi:10.14309/ajg.0000000000002850
  11. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett’s Esophagus: An Updated ACG Guideline. Am J Gastroenterol. 2022;117(4):559-587. doi:10.14309/ajg.0000000000001680
  12. ASGE STANDARDS OF PRACTICE COMMITTEE; Qumseya B, Sultan S, Bain P, et al. ASGE guideline on screening and surveillance of Barrett’s esophagus. Gastrointest Endosc. 2019;90(3):335-359.e2. doi:10.1016/j.gie.2019.05.012
  13. Muthusamy VR, Wani S, Gyawali CP, Komanduri S. CGIT Barrett’s Esophagus Consensus Conference Participants. AGA Clinical Practice Update on New Technology and Innovation for Surveillance and Screening in Barrett’s Esophagus: Expert review. Clin Gastroenterol Hepatol. 2022;20(12):2696-2706. doi:10.1016/j.cgh.2022.06.003
  14. Xie SH, Lagergren J. A model for predicting individuals’ absolute risk of esophageal adenocarcinoma: Moving toward tailored screening and prevention. Int J Cancer. 2016;138(12):2813-2819. doi:10.1002/ijc.29988
  15. Rubenstein JH, McConnell D, Waljee AK, et al. Validation and Comparison of Tools for Selecting Individuals to Screen for Barrett’s Esophagus and Early Neoplasia. Gastroenterology. 2020;158(8):2082-2092. doi:10.1053/j.gastro.2020.02.037
  16. Iyer PG, Sachdeva K, Leggett CL, et al. Development of Electronic Health Record–Based Machine Learning Models to Predict Barrett’s Esophagus and Esophageal Adenocarcinoma Risk. Clin Transl Gastroenterol. 2023;14(10):e00637. doi:10.14309/ctg.0000000000000637
  17. Ross-Innes CS, Debiram-Beecham I, O’Donovan M, et al; BEST2 Study Group. Evaluation of a minimally invasive cell sampling device coupled with assessment of trefoil factor 3 expression for diagnosing Barrett’s esophagus: a multicenter case-control study. PLoS Med. 2015;12(1):e1001780. doi:10.1371/journal.pmed.1001780
Author and Disclosure Information

Joel Rubenstein, MD, MS
Professor, Department of Internal Medicine,
Division of Gastroenterology, University of
Michigan Medical School Director, Barrett's
Esophagus Program, Michigan Medicine,
Ann Arbor, Michigan
Disclosures: Received research grant from: Lucid Diagnostics

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Joel Rubenstein, MD, MS
Professor, Department of Internal Medicine,
Division of Gastroenterology, University of
Michigan Medical School Director, Barrett's
Esophagus Program, Michigan Medicine,
Ann Arbor, Michigan
Disclosures: Received research grant from: Lucid Diagnostics

Author and Disclosure Information

Joel Rubenstein, MD, MS
Professor, Department of Internal Medicine,
Division of Gastroenterology, University of
Michigan Medical School Director, Barrett's
Esophagus Program, Michigan Medicine,
Ann Arbor, Michigan
Disclosures: Received research grant from: Lucid Diagnostics

Click to view more from Gastroenterology Data Trends 2025.

Click to view more from Gastroenterology Data Trends 2025.

References
  1. Vantanasiri K, Kamboj AK, Kisiel JB, Iyer PG. Advances in Screening for Barrett Esophagus and Esophageal Adenocarcinoma. Mayo Clin Proc. 2024;99(3):459-473. doi:10.1016/j.mayocp.2023.07.014
  2. Cancer Stat Facts: Esophageal Cancer. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 12, 2025. https://seer.cancer.gov/statfacts/html/esoph.html
  3. Seer*Explorer: Esophagus. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 4, 2025. https://seer.cancer.gov/statistics-network/explorer/application.html
  4. Kolb JM, Chen M, Tavakkoli A, et al. Understanding Compliance, Practice Patterns, and Barriers Among Gastroenterologists and Primary Care Providers Is Crucial for Developing Strategies to Improve Screening for Barrett’s Esophagus. Gastroenterology. 2022;162(6):1568-1573.e4. doi:10.1053/j.gastro.2022.02.003
  5. Kunzmann AT, Thrift AP, Cardwell CR, et al. Model for Identifying Individuals at Risk for Esophageal Adenocarcinoma. Clin Gastroenterol Hepatol. 2018;16(8):1229-1236.e4. doi:10.1016/j.cgh.2018.03.014
  6. Rubenstein JH, Evans RR, Burns JA, et al. Patients With Adenocarcinoma of the Esophagus or Esophagogastric Junction Frequently Have Potential Screening Opportunities. Gastroenterology. 2022;162(4):1349-1351.e5. doi:10.1053/j.gastro.2021.12.255
  7. Xie S-H, Ness-Jensen E, Medefelt N, Lagergren J. Assessing the feasibility of targeted screening for esophageal adenocarcinoma based on individual risk assessment in a population-based cohort study in Norway (The HUNT Study). Am J Gastroenterol. 2018;113(6):829-835. doi:10.1038/s41395-018-0069-9
  8. Rubenstein JH, Fontaine S, MacDonald PW, et al. Predicting Incident Adenocarcinoma of the Esophagus or Gastric Cardia Using Machine Learning of Electronic Health Records. Gastroenterology. 2023;165(6):1420-1429.e10. doi:10.1053/j.gastro.2023.08.011
  9. Fitzgerald RC, di Pietro M, O’Donovan M, et al. Cytosponge-trefoil factor 3 versus usual care to identify Barrett’s oesophagus in a primary care setting: a multicentre, pragmatic, randomised controlled trial. Lancet. 2020;396(10247):333-344. doi:10.1016/S0140-6736(20)31099-0
  10. Moinova HR, Verma S, Dumot J, et al. Multicenter, Prospective Trial of Nonendoscopic
    Biomarker-Driven Detection of Barrett’s Esophagus and Esophageal Adenocarcinoma. Am J Gastroenterol. 2024;119(11):2206-2214. doi:10.14309/ajg.0000000000002850
  11. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett’s Esophagus: An Updated ACG Guideline. Am J Gastroenterol. 2022;117(4):559-587. doi:10.14309/ajg.0000000000001680
  12. ASGE STANDARDS OF PRACTICE COMMITTEE; Qumseya B, Sultan S, Bain P, et al. ASGE guideline on screening and surveillance of Barrett’s esophagus. Gastrointest Endosc. 2019;90(3):335-359.e2. doi:10.1016/j.gie.2019.05.012
  13. Muthusamy VR, Wani S, Gyawali CP, Komanduri S. CGIT Barrett’s Esophagus Consensus Conference Participants. AGA Clinical Practice Update on New Technology and Innovation for Surveillance and Screening in Barrett’s Esophagus: Expert review. Clin Gastroenterol Hepatol. 2022;20(12):2696-2706. doi:10.1016/j.cgh.2022.06.003
  14. Xie SH, Lagergren J. A model for predicting individuals’ absolute risk of esophageal adenocarcinoma: Moving toward tailored screening and prevention. Int J Cancer. 2016;138(12):2813-2819. doi:10.1002/ijc.29988
  15. Rubenstein JH, McConnell D, Waljee AK, et al. Validation and Comparison of Tools for Selecting Individuals to Screen for Barrett’s Esophagus and Early Neoplasia. Gastroenterology. 2020;158(8):2082-2092. doi:10.1053/j.gastro.2020.02.037
  16. Iyer PG, Sachdeva K, Leggett CL, et al. Development of Electronic Health Record–Based Machine Learning Models to Predict Barrett’s Esophagus and Esophageal Adenocarcinoma Risk. Clin Transl Gastroenterol. 2023;14(10):e00637. doi:10.14309/ctg.0000000000000637
  17. Ross-Innes CS, Debiram-Beecham I, O’Donovan M, et al; BEST2 Study Group. Evaluation of a minimally invasive cell sampling device coupled with assessment of trefoil factor 3 expression for diagnosing Barrett’s esophagus: a multicenter case-control study. PLoS Med. 2015;12(1):e1001780. doi:10.1371/journal.pmed.1001780
References
  1. Vantanasiri K, Kamboj AK, Kisiel JB, Iyer PG. Advances in Screening for Barrett Esophagus and Esophageal Adenocarcinoma. Mayo Clin Proc. 2024;99(3):459-473. doi:10.1016/j.mayocp.2023.07.014
  2. Cancer Stat Facts: Esophageal Cancer. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 12, 2025. https://seer.cancer.gov/statfacts/html/esoph.html
  3. Seer*Explorer: Esophagus. NIH National Cancer Institute: Survival, Epidemiology, and End Results Program web site. Accessed March 4, 2025. https://seer.cancer.gov/statistics-network/explorer/application.html
  4. Kolb JM, Chen M, Tavakkoli A, et al. Understanding Compliance, Practice Patterns, and Barriers Among Gastroenterologists and Primary Care Providers Is Crucial for Developing Strategies to Improve Screening for Barrett’s Esophagus. Gastroenterology. 2022;162(6):1568-1573.e4. doi:10.1053/j.gastro.2022.02.003
  5. Kunzmann AT, Thrift AP, Cardwell CR, et al. Model for Identifying Individuals at Risk for Esophageal Adenocarcinoma. Clin Gastroenterol Hepatol. 2018;16(8):1229-1236.e4. doi:10.1016/j.cgh.2018.03.014
  6. Rubenstein JH, Evans RR, Burns JA, et al. Patients With Adenocarcinoma of the Esophagus or Esophagogastric Junction Frequently Have Potential Screening Opportunities. Gastroenterology. 2022;162(4):1349-1351.e5. doi:10.1053/j.gastro.2021.12.255
  7. Xie S-H, Ness-Jensen E, Medefelt N, Lagergren J. Assessing the feasibility of targeted screening for esophageal adenocarcinoma based on individual risk assessment in a population-based cohort study in Norway (The HUNT Study). Am J Gastroenterol. 2018;113(6):829-835. doi:10.1038/s41395-018-0069-9
  8. Rubenstein JH, Fontaine S, MacDonald PW, et al. Predicting Incident Adenocarcinoma of the Esophagus or Gastric Cardia Using Machine Learning of Electronic Health Records. Gastroenterology. 2023;165(6):1420-1429.e10. doi:10.1053/j.gastro.2023.08.011
  9. Fitzgerald RC, di Pietro M, O’Donovan M, et al. Cytosponge-trefoil factor 3 versus usual care to identify Barrett’s oesophagus in a primary care setting: a multicentre, pragmatic, randomised controlled trial. Lancet. 2020;396(10247):333-344. doi:10.1016/S0140-6736(20)31099-0
  10. Moinova HR, Verma S, Dumot J, et al. Multicenter, Prospective Trial of Nonendoscopic
    Biomarker-Driven Detection of Barrett’s Esophagus and Esophageal Adenocarcinoma. Am J Gastroenterol. 2024;119(11):2206-2214. doi:10.14309/ajg.0000000000002850
  11. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett’s Esophagus: An Updated ACG Guideline. Am J Gastroenterol. 2022;117(4):559-587. doi:10.14309/ajg.0000000000001680
  12. ASGE STANDARDS OF PRACTICE COMMITTEE; Qumseya B, Sultan S, Bain P, et al. ASGE guideline on screening and surveillance of Barrett’s esophagus. Gastrointest Endosc. 2019;90(3):335-359.e2. doi:10.1016/j.gie.2019.05.012
  13. Muthusamy VR, Wani S, Gyawali CP, Komanduri S. CGIT Barrett’s Esophagus Consensus Conference Participants. AGA Clinical Practice Update on New Technology and Innovation for Surveillance and Screening in Barrett’s Esophagus: Expert review. Clin Gastroenterol Hepatol. 2022;20(12):2696-2706. doi:10.1016/j.cgh.2022.06.003
  14. Xie SH, Lagergren J. A model for predicting individuals’ absolute risk of esophageal adenocarcinoma: Moving toward tailored screening and prevention. Int J Cancer. 2016;138(12):2813-2819. doi:10.1002/ijc.29988
  15. Rubenstein JH, McConnell D, Waljee AK, et al. Validation and Comparison of Tools for Selecting Individuals to Screen for Barrett’s Esophagus and Early Neoplasia. Gastroenterology. 2020;158(8):2082-2092. doi:10.1053/j.gastro.2020.02.037
  16. Iyer PG, Sachdeva K, Leggett CL, et al. Development of Electronic Health Record–Based Machine Learning Models to Predict Barrett’s Esophagus and Esophageal Adenocarcinoma Risk. Clin Transl Gastroenterol. 2023;14(10):e00637. doi:10.14309/ctg.0000000000000637
  17. Ross-Innes CS, Debiram-Beecham I, O’Donovan M, et al; BEST2 Study Group. Evaluation of a minimally invasive cell sampling device coupled with assessment of trefoil factor 3 expression for diagnosing Barrett’s esophagus: a multicenter case-control study. PLoS Med. 2015;12(1):e1001780. doi:10.1371/journal.pmed.1001780
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Barrett’s esophagus (BE) is a metaplastic transformation of the esophageal lining and the sole known precursor to esophageal adenocarcinoma (EAC), a malignancy with a 20% 5-year survival rate and about 16,000 new cases per year.1-3 Despite a lack of high-quality evidence supporting screening, guidelines suggest screening and focus heavily on endoscopy for individuals with gastroesophageal reflux disease (GERD) and other risk factors.1 Barriers to screening include reliance on GERD symptoms (given only 50% of individuals with EAC report prior GERD symptoms), provider lack of knowledge about guidelines, and the invasive nature of endoscopy.4,5 Fewer than 20% of EAC cases are detected as part of screening and surveillance.6 As many as 85% of individuals with EAC also had at least 1 missed opportunity where screening endoscopy could have been offered earlier.6

Predictive algorithms incorporating factors like age, GERD, obesity, and smoking history (e.g., Nord-Trøndelag Health Study [HUNT], Kunzmann, Kettles Esophageal and Cardia Adenocarcinoma predictioN [K-ECAN] tools) have been developed to better identify at-risk populations who should undergo screening.5,7,8 New screening modalities are also being developed. Non-endoscopic tools, such as EsoCheck with EsoGuard and Cytosponge, offer minimally invasive alternatives for detecting BE.9,10 Future efforts should focus on enhancing risk stratification, improving the referral process to screen appropriate populations, and integrating new technologies to enable earlier diagnosis and intervention, potentially improving survival outcomes for EAC.

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References
  1. Jones JM. LGBTQ+ identification in U.S. rises to 9.3%. Gallup.com website. February 20, 2025. Accessed March 4, 2025. https://news.gallup.com/poll/656708/lgbtq-identification-rises.aspx.
  2. Newman KL, Vélez C, Paul S, Radix AE, Streed CG Jr, Targownik LE. Research Considerations in Digestive and Liver Disease in Transgender and Gender-Diverse Populations. Gastroenterology. 2023;165(3):523-528.e1. doi:10.1053/j.gastro.2023.07.011
  3. Vélez C, Newman KL, Paul S, Berli JU, Tangpricha V, Targownik LE. Approaching Digestive Health Care in Transgender and Gender-Diverse Communities. Clin Gastroenterol Hepatol. 2024;22(3):441-447.e2. doi:10.1016/j.cgh.2023.12.001
  4. Condray CD, Newman KL, Chedid VG. Consequences of bathroom restriction on transgender individuals with gastrointestinal conditions in the United States. Nat Rev Gastroenterol Hepatol. 2024;21(10):662-663. doi:10.1038/s41575-024-00975-4
  5. Tsai C, Abdelhalim S, Wong S-Y, Xie X, Agrawal M, Keefer LA. Trauma-Informed Care in Gastroenterology: A Survey of Provider Attitudes, Knowledge, and Skills. Clin Gastroenterol Hepatol. 2024 Oct 24:S1542-3565(24)00953-4. doi:10.1016/j.cgh.2024.09.015
  6. Newman KL, Chedid VG, Boden EK. A Systematic Review of Inflammatory Bowel Disease Epidemiology and Health Outcomes in Sexual and Gender Minority Individuals. Gastroenterology. 2023;164(6):866-871. doi:10.1053/j.gastro.2022.11.048
  7. Hassan B, Suchan A, Brown M, Kishan A, Liang F, Truta B. The Impact of Hormone Therapy on Inflammatory Bowel Disease in Transgender and Nonbinary Individuals. Inflamm Bowel Dis. 2024 Oct 16:izae236. doi:10.1093/ibd/izae236
  8. Elhence H, Dodge JL, Kahn JA, Lee BP. Characteristics and Outcomes Among US Commercially Insured Transgender Adults With Cirrhosis: A National Cohort Study. Am J Gastroenterol. 2024;119(12):2455-2461. doi:10.14309/ajg.0000000000002907
  9. Stier EA, Clarke MA, Deshmukh AA, et al. International Anal Neoplasia Society’s consensus guidelines for anal cancer screening. Int J Cancer. 2024;154(10):1694-1702. doi:10.1002/ijc.34850
  10. Nash R, Ward KC, Jemal A, Sandberg DE, Tangpricha V, Goodman M. Frequency and distribution of primary site among gender minority cancer patients: An analysis of U.S. national surveillance data. Cancer Epidemiol. 2018;54:1-6. doi:10.1016/j.canep.2018.02.008
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Disclosures: Received research grant from: Pfizer

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References
  1. Jones JM. LGBTQ+ identification in U.S. rises to 9.3%. Gallup.com website. February 20, 2025. Accessed March 4, 2025. https://news.gallup.com/poll/656708/lgbtq-identification-rises.aspx.
  2. Newman KL, Vélez C, Paul S, Radix AE, Streed CG Jr, Targownik LE. Research Considerations in Digestive and Liver Disease in Transgender and Gender-Diverse Populations. Gastroenterology. 2023;165(3):523-528.e1. doi:10.1053/j.gastro.2023.07.011
  3. Vélez C, Newman KL, Paul S, Berli JU, Tangpricha V, Targownik LE. Approaching Digestive Health Care in Transgender and Gender-Diverse Communities. Clin Gastroenterol Hepatol. 2024;22(3):441-447.e2. doi:10.1016/j.cgh.2023.12.001
  4. Condray CD, Newman KL, Chedid VG. Consequences of bathroom restriction on transgender individuals with gastrointestinal conditions in the United States. Nat Rev Gastroenterol Hepatol. 2024;21(10):662-663. doi:10.1038/s41575-024-00975-4
  5. Tsai C, Abdelhalim S, Wong S-Y, Xie X, Agrawal M, Keefer LA. Trauma-Informed Care in Gastroenterology: A Survey of Provider Attitudes, Knowledge, and Skills. Clin Gastroenterol Hepatol. 2024 Oct 24:S1542-3565(24)00953-4. doi:10.1016/j.cgh.2024.09.015
  6. Newman KL, Chedid VG, Boden EK. A Systematic Review of Inflammatory Bowel Disease Epidemiology and Health Outcomes in Sexual and Gender Minority Individuals. Gastroenterology. 2023;164(6):866-871. doi:10.1053/j.gastro.2022.11.048
  7. Hassan B, Suchan A, Brown M, Kishan A, Liang F, Truta B. The Impact of Hormone Therapy on Inflammatory Bowel Disease in Transgender and Nonbinary Individuals. Inflamm Bowel Dis. 2024 Oct 16:izae236. doi:10.1093/ibd/izae236
  8. Elhence H, Dodge JL, Kahn JA, Lee BP. Characteristics and Outcomes Among US Commercially Insured Transgender Adults With Cirrhosis: A National Cohort Study. Am J Gastroenterol. 2024;119(12):2455-2461. doi:10.14309/ajg.0000000000002907
  9. Stier EA, Clarke MA, Deshmukh AA, et al. International Anal Neoplasia Society’s consensus guidelines for anal cancer screening. Int J Cancer. 2024;154(10):1694-1702. doi:10.1002/ijc.34850
  10. Nash R, Ward KC, Jemal A, Sandberg DE, Tangpricha V, Goodman M. Frequency and distribution of primary site among gender minority cancer patients: An analysis of U.S. national surveillance data. Cancer Epidemiol. 2018;54:1-6. doi:10.1016/j.canep.2018.02.008
References
  1. Jones JM. LGBTQ+ identification in U.S. rises to 9.3%. Gallup.com website. February 20, 2025. Accessed March 4, 2025. https://news.gallup.com/poll/656708/lgbtq-identification-rises.aspx.
  2. Newman KL, Vélez C, Paul S, Radix AE, Streed CG Jr, Targownik LE. Research Considerations in Digestive and Liver Disease in Transgender and Gender-Diverse Populations. Gastroenterology. 2023;165(3):523-528.e1. doi:10.1053/j.gastro.2023.07.011
  3. Vélez C, Newman KL, Paul S, Berli JU, Tangpricha V, Targownik LE. Approaching Digestive Health Care in Transgender and Gender-Diverse Communities. Clin Gastroenterol Hepatol. 2024;22(3):441-447.e2. doi:10.1016/j.cgh.2023.12.001
  4. Condray CD, Newman KL, Chedid VG. Consequences of bathroom restriction on transgender individuals with gastrointestinal conditions in the United States. Nat Rev Gastroenterol Hepatol. 2024;21(10):662-663. doi:10.1038/s41575-024-00975-4
  5. Tsai C, Abdelhalim S, Wong S-Y, Xie X, Agrawal M, Keefer LA. Trauma-Informed Care in Gastroenterology: A Survey of Provider Attitudes, Knowledge, and Skills. Clin Gastroenterol Hepatol. 2024 Oct 24:S1542-3565(24)00953-4. doi:10.1016/j.cgh.2024.09.015
  6. Newman KL, Chedid VG, Boden EK. A Systematic Review of Inflammatory Bowel Disease Epidemiology and Health Outcomes in Sexual and Gender Minority Individuals. Gastroenterology. 2023;164(6):866-871. doi:10.1053/j.gastro.2022.11.048
  7. Hassan B, Suchan A, Brown M, Kishan A, Liang F, Truta B. The Impact of Hormone Therapy on Inflammatory Bowel Disease in Transgender and Nonbinary Individuals. Inflamm Bowel Dis. 2024 Oct 16:izae236. doi:10.1093/ibd/izae236
  8. Elhence H, Dodge JL, Kahn JA, Lee BP. Characteristics and Outcomes Among US Commercially Insured Transgender Adults With Cirrhosis: A National Cohort Study. Am J Gastroenterol. 2024;119(12):2455-2461. doi:10.14309/ajg.0000000000002907
  9. Stier EA, Clarke MA, Deshmukh AA, et al. International Anal Neoplasia Society’s consensus guidelines for anal cancer screening. Int J Cancer. 2024;154(10):1694-1702. doi:10.1002/ijc.34850
  10. Nash R, Ward KC, Jemal A, Sandberg DE, Tangpricha V, Goodman M. Frequency and distribution of primary site among gender minority cancer patients: An analysis of U.S. national surveillance data. Cancer Epidemiol. 2018;54:1-6. doi:10.1016/j.canep.2018.02.008
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Overall, 1.3% of US adults identify as transgender or gender-diverse (TGD), with a higher prevalence of TGD-identified people in younger generations.1,2 This finding suggests that all clinicians will provide care to TGD patients.1,2 TGD individuals are more likely to experience health care discrimination than cisgender individuals, resulting in reduced access to and utilization of care.2,3 It is important for health care providers, including gastroenterologists and hepatologists, to create a welcoming and gender-affirming environment—offering single-occupancy handicap-accessible bathrooms, displaying nondiscrimination policies, using inclusive intake forms, and providing training for clinicians to increase knowledge of TGD health needs and address biases.3,4 This type of environment can help reduce negative outcomes for TGD patients seeking care.3,4 Understanding the minority stress model and trauma-informed care approaches can also be useful for caring for TGD patients.2,5 A recent study found that up to 51% of gastrointestinal (GI) providers are not at all familiar with trauma-informed care, highlighting the need for further education.5

High-quality research on GI conditions in TGD populations is limited, and potential proposed biological effects of gender-affirming hormone therapy (GAHT) are still theoretical. Studies have shown that the prevalence of inflammatory bowel disease (IBD) is similar between TGD and cisgender individuals, and that GAHT does not affect flare-ups of IBD, although the sample sizes have been small.6,7 Hepatic conditions such as cirrhosis were shown to be more common in TGD communities, which may be largely due to preventable causes of cirrhosis (e.g., alcohol-associated or viral etiologies) and delayed diagnosis and treatment before progression.8 More research is needed in TGD patients with GI conditions, and best practices for their design and conduct, such as partnering with TGD people, designing studies with cultural humility in mind, using rigorous research methods, and checking for implicit biases in studies, must be followed.2

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References
  1. Lin K, Mehrotra A, Tsai TC. Metabolic Bariatric Surgery in the Era of GLP-1 Receptor Agonists for Obesity Management. JAMA Netw Open. 2024;7(10):e2441380. doi:10.1001/jamanetworkopen.2024.41380
  2. Camilleri M, El-Omar EM. Ten reasons gastroenterologists and hepatologists should be treating obesity. Gut. 2023;72(6):1033-1038. doi:10.1136/gutjnl-2023-329639
  3. Camilleri M. Definite benefits of GLP-1 receptor agonists: what is the risk of gastroparesis and lung aspiration? Gut. 2024. doi:10.1136/gutjnl-2024-333036
  4. Camilleri M, Carlson P, Dilmaghani S. Letter to the Editor. Prevalence and variations in gastric emptying delay in response to GLP-1 receptor agonist liraglutide. Obesity (Silver Spring). 2024;32(2):232-233. doi:10.1002/oby.23941
  5. Camilleri, M. Incretin impact on gastric function in obesity: physiology, and pharmacological, surgical and endoscopic treatments. J Physiol. 2024.doi:10.1113/JP287535
  6. Kindel TL, Wang AY, Wadhwa A, et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity;
    Society of American Gastrointestinal and Endoscopic Surgeons. Multisociety Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024:S1542-3565(24)00910-8. doi:10.1016/j.cgh.2024.10.003
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Disclosures: Serve(d) as a member of board for: Phenomix; Received
research grant from: VANDA

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References
  1. Lin K, Mehrotra A, Tsai TC. Metabolic Bariatric Surgery in the Era of GLP-1 Receptor Agonists for Obesity Management. JAMA Netw Open. 2024;7(10):e2441380. doi:10.1001/jamanetworkopen.2024.41380
  2. Camilleri M, El-Omar EM. Ten reasons gastroenterologists and hepatologists should be treating obesity. Gut. 2023;72(6):1033-1038. doi:10.1136/gutjnl-2023-329639
  3. Camilleri M. Definite benefits of GLP-1 receptor agonists: what is the risk of gastroparesis and lung aspiration? Gut. 2024. doi:10.1136/gutjnl-2024-333036
  4. Camilleri M, Carlson P, Dilmaghani S. Letter to the Editor. Prevalence and variations in gastric emptying delay in response to GLP-1 receptor agonist liraglutide. Obesity (Silver Spring). 2024;32(2):232-233. doi:10.1002/oby.23941
  5. Camilleri, M. Incretin impact on gastric function in obesity: physiology, and pharmacological, surgical and endoscopic treatments. J Physiol. 2024.doi:10.1113/JP287535
  6. Kindel TL, Wang AY, Wadhwa A, et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity;
    Society of American Gastrointestinal and Endoscopic Surgeons. Multisociety Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024:S1542-3565(24)00910-8. doi:10.1016/j.cgh.2024.10.003
References
  1. Lin K, Mehrotra A, Tsai TC. Metabolic Bariatric Surgery in the Era of GLP-1 Receptor Agonists for Obesity Management. JAMA Netw Open. 2024;7(10):e2441380. doi:10.1001/jamanetworkopen.2024.41380
  2. Camilleri M, El-Omar EM. Ten reasons gastroenterologists and hepatologists should be treating obesity. Gut. 2023;72(6):1033-1038. doi:10.1136/gutjnl-2023-329639
  3. Camilleri M. Definite benefits of GLP-1 receptor agonists: what is the risk of gastroparesis and lung aspiration? Gut. 2024. doi:10.1136/gutjnl-2024-333036
  4. Camilleri M, Carlson P, Dilmaghani S. Letter to the Editor. Prevalence and variations in gastric emptying delay in response to GLP-1 receptor agonist liraglutide. Obesity (Silver Spring). 2024;32(2):232-233. doi:10.1002/oby.23941
  5. Camilleri, M. Incretin impact on gastric function in obesity: physiology, and pharmacological, surgical and endoscopic treatments. J Physiol. 2024.doi:10.1113/JP287535
  6. Kindel TL, Wang AY, Wadhwa A, et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity;
    Society of American Gastrointestinal and Endoscopic Surgeons. Multisociety Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024:S1542-3565(24)00910-8. doi:10.1016/j.cgh.2024.10.003
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Since 2022, glucagon-like peptide 1 (GLP-1) receptor agonist (RA) use has increased by more than 100%, whereas other obesity interventions, such as bariatric surgery, have decreased.1 There is an ongoing debate on the gastroenterologist’s role in treating obesity.2 Obesity has a profound impact not only on diabetes and cardiovascular and neurologic disease, but also on gastrointestinal (GI) conditions and liver health.2 Thus, obesity is a significant risk factor for other diseases like metabolic dysfunction-associated steatotic liver disease, inflammatory bowel disease, and gastroesophageal reflux disease.

As GLP-1 RA use increases, questions about the risk-benefit profile have arisen, especially among gastroenterologists who assess some of the treatmentrelated GI side effects. GLP-1 RA benefits extend beyond weight loss and diabetes control, improving cardiovascular and neurological outcomes as well.3 However, challenges remain. GLP-1 RAs are associated with delayed gastric emptying, which, though generally manageable, raises concerns about rare complications such as aspiration during procedures.3,4 Despite these concerns, a 2024 study indicates that delayed gastric emptying may normalize in patients over time and rarely, if ever, interferes with clinical practice.3,4 Moreover, for patients with other GI side effects, such as nausea and vomiting, titration adjustments and slower escalation can be helpful.5 According to a review of published data, even though there may be some food retained in the stomach at the time of gastroscopy, the risk for aspiration is extremely low and the examination can usually be completed satisfactorily without having to repeat the endoscopy.3

New multisociety guidelines were released in 2024 on the risk for aspiration in patients on GLP-1 RAs during the periprocedural period, emphasizing balancing benefits of obesity treatment with risks for delayed gastric emptying.6 Although there are many benefits with GLP-1 RAs, questions remain about long-term safety, such as potential impacts on muscle mass and heart health, underlining the need for further research.

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IBS: Mental Health Factors and Comorbidities

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References
  1. Staudacher HM, Black CJ, Teasdale SB, Mikocka-Walus A, Keefer L. Irritable bowel syndrome and mental health comorbidity - approach to multidisciplinary management. Nat Rev Gastroenterol Hepatol. 2023;20(9):582-596. doi:10.1038/s41575-023-00794-z
  2. Ballou S, Vasant DH, Guadagnoli L, et al. A primer for the gastroenterology provider on psychosocial assessment of patients with disorders of gut-brain interaction. Neurogastroenterol Motil. 2024;36(12):e14894. doi:10.1111/nmo.14894
  3. Keefer L, Ballou SK, Drossman DA, Ringstrom G, Elsenbruch S, Ljótsson B. A Rome Working Team Report on Brain-Gut Behavior Therapies for Disorders of Gut-Brain Interaction. Gastroenterology. 2022;162(1):300-315. doi:10.1053/j.gastro.2021.09.015
  4. Goodoory VC, Khasawneh M, Thakur ER, et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024;167(5):934-943.e5. doi:10.1053/j.gastro.2024.05.010
  5. Chang L, Sultan S, Lembo A, Verne GN, Smalley W, Heidelbaugh JJ. AGA Clinical Practice Guideline on the Pharmacological Management of Irritable Bowel Syndrome With Constipation. Gastroenterology. 2022;163(1):118-136. doi:10.1053/j.gastro.2022.04.016
  6. Drossman DA, Tack J, Ford AC, Szigethy E, Törnblom H, Van Oudenhove L. Neuromodulators for Functional Gastrointestinal Disorders (Disorders of Gut-Brain Interaction): A Rome Foundation Working Team Report. Gastroenterology. 2018;154(4):1140-1171.e1. doi:10.1053/j.gastro.2017.11.279
  7. Hasan SS, Ballou S, Keefer L, Vasant DH. Improving access to gut-directed hypnotherapy for irritable bowel syndrome in the digital therapeutics’ era: Are mobile applications a “smart” solution? Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  8. Tarar ZI, Farooq U, Zafar Y, et al. Burden of anxiety and depression among hospitalized patients with irritable bowel syndrome: a nationwide analysis. Ir J Med Sci. 2023;192(5):2159-2166. doi:10.1007/s11845-022-03258-6
  9. Barbara G, Aziz I, Ballou S, et al. Rome Foundation Working Team Report on overlap in disorders of gut-brain interaction. Nat Rev Gastroenterol Hepatol. doi:10.1038/s41575-024-01033-9
  10. Thakur ER, Kunik M, Jarbrink-Sehgal ME, Lackner J, Dindo L, El-Serag H. Behavior Medicine Management of Irritable Bowel Syndrome: A Referral Toolkit for Gastroenterology Providers. 2018. Accessed February 19, 2025. https://www.mirecc.va.gov/VISN16/docs/ibs-referral-toolkit.pdf
  11. Irritable bowel syndrome (IBS). Johns Hopkins Medicine website. Accessed February 19, 2025. https://www.hopkinsmedicine.org/health/conditionsanddiseases/irritable-bowel-syndrome-ibs
  12. Burton-Murray H, Guadagnoli L, Kamp K, et al. Rome Foundation Working Team Report: Consensus Statement on the Design and Conduct of Behavioural Clinical Trials for Disorders of Gut-Brain Interaction. Aliment Pharmacol Ther. 2025;61(5):787-802. doi:10.1111/apt.18482
  13. Rome GastroPsych. Rome Foundation website. Accessed February 19, 2025. https://romegipsych.org/
  14. Scarlata K, Riehl M. Mind Your Gut: The Science-based, Whole-body Guide to Living Well with IBS. Hachette Book Group, 2025.
  15. IFFGD International Foundation for Gastrointestinal Disorders. IFFGD website. January 10, 2025. Accessed February 19, 2025. https://iffgd.org/
  16. GI Psychology: Mind Your Gut website. April 2, 2024. Accessed February 19, 2025. https://www.gipsychology.com/
  17. Drossman DA, Ruddy J. Gut Feelings: Disorders of the Gut-Brain Interaction (DGBI) and the Patient-Doctor Relationship. DrossmanCare Chapel Hill, 2020.
  18. Tuesday Night IBS website. Accessed February 19, 2025. https://www.tuesdaynightibs.com/
Author and Disclosure Information

Lin Chang, MD
Professor, David Geffen School of Medicine,
UCLA; Vice-Chief, Vatche and Tamar
Manoukian, Division of Digestive Diseases,
UCLA Digestive Diseases Center,
Los Angeles, California

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: Ardelyx; Alfasigma; Atmo; GLaxoSmithKline;
Food Marble; Vibrant; Nerva; Received research grant from: AnX Robotica;
Ironwood; Received income in an amount equal to or greater than $250
from: Alfasigma; Atmo; GLaxoSmithKline; Food Marble; Have stock options
in: Trellus Health; Food Marble; ModifyHealth

Laurie A. Keefer, PhD
Professor, Department of Medicine and
Psychiatry, Division of Gastroenterology, Icahn
School of Medicine at Mount Sinai; Gastro
Psychologist, Inflammatory Bowel Disease Center,
Mount Sinai Hospital, New York, New York

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: AbbVie; Pfizer; Eli Lilly; Reckitt Health; Johnson
and Johnson; Rome Foundation; Received research grant from: Ardelyx
Have a 5% or greater equity interest in: Trellus Health

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Author and Disclosure Information

Lin Chang, MD
Professor, David Geffen School of Medicine,
UCLA; Vice-Chief, Vatche and Tamar
Manoukian, Division of Digestive Diseases,
UCLA Digestive Diseases Center,
Los Angeles, California

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: Ardelyx; Alfasigma; Atmo; GLaxoSmithKline;
Food Marble; Vibrant; Nerva; Received research grant from: AnX Robotica;
Ironwood; Received income in an amount equal to or greater than $250
from: Alfasigma; Atmo; GLaxoSmithKline; Food Marble; Have stock options
in: Trellus Health; Food Marble; ModifyHealth

Laurie A. Keefer, PhD
Professor, Department of Medicine and
Psychiatry, Division of Gastroenterology, Icahn
School of Medicine at Mount Sinai; Gastro
Psychologist, Inflammatory Bowel Disease Center,
Mount Sinai Hospital, New York, New York

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: AbbVie; Pfizer; Eli Lilly; Reckitt Health; Johnson
and Johnson; Rome Foundation; Received research grant from: Ardelyx
Have a 5% or greater equity interest in: Trellus Health

Author and Disclosure Information

Lin Chang, MD
Professor, David Geffen School of Medicine,
UCLA; Vice-Chief, Vatche and Tamar
Manoukian, Division of Digestive Diseases,
UCLA Digestive Diseases Center,
Los Angeles, California

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: Ardelyx; Alfasigma; Atmo; GLaxoSmithKline;
Food Marble; Vibrant; Nerva; Received research grant from: AnX Robotica;
Ironwood; Received income in an amount equal to or greater than $250
from: Alfasigma; Atmo; GLaxoSmithKline; Food Marble; Have stock options
in: Trellus Health; Food Marble; ModifyHealth

Laurie A. Keefer, PhD
Professor, Department of Medicine and
Psychiatry, Division of Gastroenterology, Icahn
School of Medicine at Mount Sinai; Gastro
Psychologist, Inflammatory Bowel Disease Center,
Mount Sinai Hospital, New York, New York

Disclosures: Serve(d) as a director, officer, partner, employee, advisor,
consultant, or trustee for: AbbVie; Pfizer; Eli Lilly; Reckitt Health; Johnson
and Johnson; Rome Foundation; Received research grant from: Ardelyx
Have a 5% or greater equity interest in: Trellus Health

Click to view more from Gastroenterology Data Trends 2025. 

Click to view more from Gastroenterology Data Trends 2025. 

References
  1. Staudacher HM, Black CJ, Teasdale SB, Mikocka-Walus A, Keefer L. Irritable bowel syndrome and mental health comorbidity - approach to multidisciplinary management. Nat Rev Gastroenterol Hepatol. 2023;20(9):582-596. doi:10.1038/s41575-023-00794-z
  2. Ballou S, Vasant DH, Guadagnoli L, et al. A primer for the gastroenterology provider on psychosocial assessment of patients with disorders of gut-brain interaction. Neurogastroenterol Motil. 2024;36(12):e14894. doi:10.1111/nmo.14894
  3. Keefer L, Ballou SK, Drossman DA, Ringstrom G, Elsenbruch S, Ljótsson B. A Rome Working Team Report on Brain-Gut Behavior Therapies for Disorders of Gut-Brain Interaction. Gastroenterology. 2022;162(1):300-315. doi:10.1053/j.gastro.2021.09.015
  4. Goodoory VC, Khasawneh M, Thakur ER, et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024;167(5):934-943.e5. doi:10.1053/j.gastro.2024.05.010
  5. Chang L, Sultan S, Lembo A, Verne GN, Smalley W, Heidelbaugh JJ. AGA Clinical Practice Guideline on the Pharmacological Management of Irritable Bowel Syndrome With Constipation. Gastroenterology. 2022;163(1):118-136. doi:10.1053/j.gastro.2022.04.016
  6. Drossman DA, Tack J, Ford AC, Szigethy E, Törnblom H, Van Oudenhove L. Neuromodulators for Functional Gastrointestinal Disorders (Disorders of Gut-Brain Interaction): A Rome Foundation Working Team Report. Gastroenterology. 2018;154(4):1140-1171.e1. doi:10.1053/j.gastro.2017.11.279
  7. Hasan SS, Ballou S, Keefer L, Vasant DH. Improving access to gut-directed hypnotherapy for irritable bowel syndrome in the digital therapeutics’ era: Are mobile applications a “smart” solution? Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  8. Tarar ZI, Farooq U, Zafar Y, et al. Burden of anxiety and depression among hospitalized patients with irritable bowel syndrome: a nationwide analysis. Ir J Med Sci. 2023;192(5):2159-2166. doi:10.1007/s11845-022-03258-6
  9. Barbara G, Aziz I, Ballou S, et al. Rome Foundation Working Team Report on overlap in disorders of gut-brain interaction. Nat Rev Gastroenterol Hepatol. doi:10.1038/s41575-024-01033-9
  10. Thakur ER, Kunik M, Jarbrink-Sehgal ME, Lackner J, Dindo L, El-Serag H. Behavior Medicine Management of Irritable Bowel Syndrome: A Referral Toolkit for Gastroenterology Providers. 2018. Accessed February 19, 2025. https://www.mirecc.va.gov/VISN16/docs/ibs-referral-toolkit.pdf
  11. Irritable bowel syndrome (IBS). Johns Hopkins Medicine website. Accessed February 19, 2025. https://www.hopkinsmedicine.org/health/conditionsanddiseases/irritable-bowel-syndrome-ibs
  12. Burton-Murray H, Guadagnoli L, Kamp K, et al. Rome Foundation Working Team Report: Consensus Statement on the Design and Conduct of Behavioural Clinical Trials for Disorders of Gut-Brain Interaction. Aliment Pharmacol Ther. 2025;61(5):787-802. doi:10.1111/apt.18482
  13. Rome GastroPsych. Rome Foundation website. Accessed February 19, 2025. https://romegipsych.org/
  14. Scarlata K, Riehl M. Mind Your Gut: The Science-based, Whole-body Guide to Living Well with IBS. Hachette Book Group, 2025.
  15. IFFGD International Foundation for Gastrointestinal Disorders. IFFGD website. January 10, 2025. Accessed February 19, 2025. https://iffgd.org/
  16. GI Psychology: Mind Your Gut website. April 2, 2024. Accessed February 19, 2025. https://www.gipsychology.com/
  17. Drossman DA, Ruddy J. Gut Feelings: Disorders of the Gut-Brain Interaction (DGBI) and the Patient-Doctor Relationship. DrossmanCare Chapel Hill, 2020.
  18. Tuesday Night IBS website. Accessed February 19, 2025. https://www.tuesdaynightibs.com/
References
  1. Staudacher HM, Black CJ, Teasdale SB, Mikocka-Walus A, Keefer L. Irritable bowel syndrome and mental health comorbidity - approach to multidisciplinary management. Nat Rev Gastroenterol Hepatol. 2023;20(9):582-596. doi:10.1038/s41575-023-00794-z
  2. Ballou S, Vasant DH, Guadagnoli L, et al. A primer for the gastroenterology provider on psychosocial assessment of patients with disorders of gut-brain interaction. Neurogastroenterol Motil. 2024;36(12):e14894. doi:10.1111/nmo.14894
  3. Keefer L, Ballou SK, Drossman DA, Ringstrom G, Elsenbruch S, Ljótsson B. A Rome Working Team Report on Brain-Gut Behavior Therapies for Disorders of Gut-Brain Interaction. Gastroenterology. 2022;162(1):300-315. doi:10.1053/j.gastro.2021.09.015
  4. Goodoory VC, Khasawneh M, Thakur ER, et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024;167(5):934-943.e5. doi:10.1053/j.gastro.2024.05.010
  5. Chang L, Sultan S, Lembo A, Verne GN, Smalley W, Heidelbaugh JJ. AGA Clinical Practice Guideline on the Pharmacological Management of Irritable Bowel Syndrome With Constipation. Gastroenterology. 2022;163(1):118-136. doi:10.1053/j.gastro.2022.04.016
  6. Drossman DA, Tack J, Ford AC, Szigethy E, Törnblom H, Van Oudenhove L. Neuromodulators for Functional Gastrointestinal Disorders (Disorders of Gut-Brain Interaction): A Rome Foundation Working Team Report. Gastroenterology. 2018;154(4):1140-1171.e1. doi:10.1053/j.gastro.2017.11.279
  7. Hasan SS, Ballou S, Keefer L, Vasant DH. Improving access to gut-directed hypnotherapy for irritable bowel syndrome in the digital therapeutics’ era: Are mobile applications a “smart” solution? Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  8. Tarar ZI, Farooq U, Zafar Y, et al. Burden of anxiety and depression among hospitalized patients with irritable bowel syndrome: a nationwide analysis. Ir J Med Sci. 2023;192(5):2159-2166. doi:10.1007/s11845-022-03258-6
  9. Barbara G, Aziz I, Ballou S, et al. Rome Foundation Working Team Report on overlap in disorders of gut-brain interaction. Nat Rev Gastroenterol Hepatol. doi:10.1038/s41575-024-01033-9
  10. Thakur ER, Kunik M, Jarbrink-Sehgal ME, Lackner J, Dindo L, El-Serag H. Behavior Medicine Management of Irritable Bowel Syndrome: A Referral Toolkit for Gastroenterology Providers. 2018. Accessed February 19, 2025. https://www.mirecc.va.gov/VISN16/docs/ibs-referral-toolkit.pdf
  11. Irritable bowel syndrome (IBS). Johns Hopkins Medicine website. Accessed February 19, 2025. https://www.hopkinsmedicine.org/health/conditionsanddiseases/irritable-bowel-syndrome-ibs
  12. Burton-Murray H, Guadagnoli L, Kamp K, et al. Rome Foundation Working Team Report: Consensus Statement on the Design and Conduct of Behavioural Clinical Trials for Disorders of Gut-Brain Interaction. Aliment Pharmacol Ther. 2025;61(5):787-802. doi:10.1111/apt.18482
  13. Rome GastroPsych. Rome Foundation website. Accessed February 19, 2025. https://romegipsych.org/
  14. Scarlata K, Riehl M. Mind Your Gut: The Science-based, Whole-body Guide to Living Well with IBS. Hachette Book Group, 2025.
  15. IFFGD International Foundation for Gastrointestinal Disorders. IFFGD website. January 10, 2025. Accessed February 19, 2025. https://iffgd.org/
  16. GI Psychology: Mind Your Gut website. April 2, 2024. Accessed February 19, 2025. https://www.gipsychology.com/
  17. Drossman DA, Ruddy J. Gut Feelings: Disorders of the Gut-Brain Interaction (DGBI) and the Patient-Doctor Relationship. DrossmanCare Chapel Hill, 2020.
  18. Tuesday Night IBS website. Accessed February 19, 2025. https://www.tuesdaynightibs.com/
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Irritable bowel syndrome (IBS), a disorder of gut-brain interaction, affects up to 10% of the global population.1 Psychological symptoms often are associated with IBS, increasing its burden and affecting quality of life.1-3 About one third of patients with IBS experience anxiety or depression.1 Multidisciplinary care, involving gastroenterologists, psychologists, and dietitians, is crucial to address both physical and emotional symptoms in patients with IBS.1

Effective clinical pathways vary by patient profile. Some patients may have maladaptive cognitive processes that affect coping with IBS (e.g., avoidance behaviors and symptom-related anxiety) but do not meet criteria for a psychiatric disorder.2 For these patients, referral to brain-gut behavior therapy (BGBT) is advised.2 BGBTs can include cognitive behavioral therapy (CBT), gut-directed hypnotherapy, and mindfulness-based interventions, among others.3 These approaches can improve not only mental health symptoms and symptom-related stress but also gastrointestinal (GI) symptoms.4 For patients with psychiatric illnesses, referrals to psychiatrists or psychologists specialized in the patient’s specific comorbid condition are recommended.2 It is also helpful for GI professionals to familiarize themselves with a few antidepressant medications for symptom-specific anxiety or mood symptoms when a psychiatrist is unavailable.5,6 Some antidepressants, called central neuromodulators, also improve IBS symptoms.5,6

Access to integrated IBS care remains a challenge. The number of GI psychologists is limited. Most digital applications aiming to bridge this gap have limitations, such as nonpersonalized approaches and problems with engagement.7 Other options to provide care for patients with IBS and psychological symptoms include support groups or nurse-led self-management programs, education, patient advocacy organizations, and placement of educational material in clinic waiting areas.3

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AGA Data Trends 2025: MASLD

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New and Emerging Treatments for MASLD/MASH

References
  1. Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
  2. Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
  3. Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
  4. Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
  5. Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
  6. Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
  7. Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
  8. Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
  9. Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
  10. Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
  11. Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493                                    
  12. Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025.  https://www.natap.org/2024/EASL/EASL_41.htm 
  13. Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
  14. Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
  15. Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
  16. Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html 
  17. Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/ 
  18. 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/ 
  19. 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/                                                                                                                                                                          
  20. Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash 
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Arizona Liver Health
Phoenix, Arizona 

Naim Alkhouri, MD, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; AstraZeneca; Echosens; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; Perspectum Served as a speaker or a member of a speaker’s bureau for: 89bio; Akero; Boehringer Ingelheim; Echosens; Fibronostics; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; NorthSea Therapeutics; Novo Nordisk; Perspectum; Pfizer; Regeneron Received research grant from: 89bio; Akero; Arbutus; AstraZeneca; BioAge; Boehringer Ingelheim; Bristol Myers Squibb; Corcept Therapeutics; CymaBay Therapeutics; DSM; Galectin Therapeutics; Genentech; Genfit; Gilead; Healio; Hepagene; Intercept; Inventiva; Ionis Pharmaceuticals; Ipsen; Lilly; Madrigal Pharmaceuticals; Merck; NGM; Novo Nordisk; Perspectum; Pfizer; PharmaIN; Poxel; Viking Therapeutics; Zydus

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Naim Alkhouri, MD
Chief Medical Officer, Department of Hepatology
Arizona Liver Health
Phoenix, Arizona 

Naim Alkhouri, MD, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; AstraZeneca; Echosens; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; Perspectum Served as a speaker or a member of a speaker’s bureau for: 89bio; Akero; Boehringer Ingelheim; Echosens; Fibronostics; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; NorthSea Therapeutics; Novo Nordisk; Perspectum; Pfizer; Regeneron Received research grant from: 89bio; Akero; Arbutus; AstraZeneca; BioAge; Boehringer Ingelheim; Bristol Myers Squibb; Corcept Therapeutics; CymaBay Therapeutics; DSM; Galectin Therapeutics; Genentech; Genfit; Gilead; Healio; Hepagene; Intercept; Inventiva; Ionis Pharmaceuticals; Ipsen; Lilly; Madrigal Pharmaceuticals; Merck; NGM; Novo Nordisk; Perspectum; Pfizer; PharmaIN; Poxel; Viking Therapeutics; Zydus

Author and Disclosure Information

Naim Alkhouri, MD
Chief Medical Officer, Department of Hepatology
Arizona Liver Health
Phoenix, Arizona 

Naim Alkhouri, MD, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; AstraZeneca; Echosens; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; Perspectum Served as a speaker or a member of a speaker’s bureau for: 89bio; Akero; Boehringer Ingelheim; Echosens; Fibronostics; Gilead Sciences; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; NorthSea Therapeutics; Novo Nordisk; Perspectum; Pfizer; Regeneron Received research grant from: 89bio; Akero; Arbutus; AstraZeneca; BioAge; Boehringer Ingelheim; Bristol Myers Squibb; Corcept Therapeutics; CymaBay Therapeutics; DSM; Galectin Therapeutics; Genentech; Genfit; Gilead; Healio; Hepagene; Intercept; Inventiva; Ionis Pharmaceuticals; Ipsen; Lilly; Madrigal Pharmaceuticals; Merck; NGM; Novo Nordisk; Perspectum; Pfizer; PharmaIN; Poxel; Viking Therapeutics; Zydus

References
  1. Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
  2. Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
  3. Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
  4. Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
  5. Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
  6. Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
  7. Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
  8. Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
  9. Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
  10. Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
  11. Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493                                    
  12. Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025.  https://www.natap.org/2024/EASL/EASL_41.htm 
  13. Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
  14. Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
  15. Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
  16. Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html 
  17. Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/ 
  18. 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/ 
  19. 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/                                                                                                                                                                          
  20. Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash 
References
  1. Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
  2. Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
  3. Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
  4. Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
  5. Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
  6. Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
  7. Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
  8. Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
  9. Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
  10. Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
  11. Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493                                    
  12. Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025.  https://www.natap.org/2024/EASL/EASL_41.htm 
  13. Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
  14. Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
  15. Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
  16. Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html 
  17. Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/ 
  18. 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/ 
  19. 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/                                                                                                                                                                          
  20. Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash 
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New and Emerging Treatments for MASLD/MASH

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With the global rise in metabolic dysfunction-associated steatotic liver disease (MASLD), the lack of approved medications is striking.1,2 Fortunately, during the past year, significant advancements have been made in the US treatment landscape for MASLD. Recent insights into the heterogeneous nature of MASLD have spurred the discovery of novel therapeutic agents and the repurposing of drugs (e.g., semaglutide) available for type 2 diabetes and obesity.1,3

Although lifestyle modifications like diet and exercise remain the cornerstones of treatment,1,2,4 effective pharmacologic options have been elusive. Numerous phase 3 trials are underway, and more promising therapies will likely become available within the next few years. In 2024, the FDA conditionally approved resmetirom, a thyroid hormone receptor-β selective drug, for treating non-cirrhotic metabolic dysfunction-associated steatohepatitis (MASH) with moderate to advanced fibrosis.4 Although this condition is highly underdiagnosed,5 combination therapy may improve outcomes,1,3,6 with greater efficacy for metabolic treatments initiated in the early stages and for liver-targeting drugs initiated in the advanced stages.3

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New Therapeutic Frontiers in the Treatment of Eosinophilic Esophagitis

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New Therapeutic Frontiers in the Treatment of Eosinophilic Esophagitis

References
  1. Rossi CM, Santacroce G, Lenti MV, di Sabatino A. Eosinophilic esophagitis in the era of biologics. Expert Rev Gastroenterol Hepatol. 2024;18(6):271-281. doi:10.1080/17474124.2024.2374471

  2. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology. 2018;155(4):1022-1033.e10. doi:10.1053/j.gastro.2018.07.009

  3. Geow R, Arena G, Siah C, Picardo S. A retrospective real-world study on the safety and efficacy of budesonide orodispersible tablets for the induction therapy of eosinophilic oesophagitis. Therap Adv Gastroenterol. 2024;17:17562848241290346. doi:10.1177/17562848241290346

  4. Sato H, Dellon ES, Aceves SS, et al. Clinical and molecular correlates of the Index of Severity for Eosinophilic Esophagitis. J Allergy Clin Immunol. 2024;154(2):375-386.e4. doi:10.1016/j.jaci.2024.04.025

  5. Dellon ES, Khoury P, Muir AB, et al. A Clinical Severity Index for Eosinophilic Esophagitis: Development, Consensus, and Future Directions. Gastroenterology. 2022;163(1):59-76. doi:10.1053/j.gastro.2022.03.025   

  6. Thel HL, Anderson C, Xue AZ, Jensen ET, Dellon ES. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025;23(2)272-280. doi:10.1016/j.cgh.2024.09.031

  7. Yang E-J, Jung KW. Role of endoscopy in eosinophilic esophagitis. Clin Endosc2025;58(1):1-9. doi.org/10.5946/ce.2024.023 

  8. Chehade M, Dellon ES, Spergel JM, et al. Dupilumab for Eosinophilic Esophagitis in Patients 1 to 11 Years of Age. N Engl J Med. 2024;390(24):2239-2251. doi:10.1056/NEJMoa2312282

  9. Hirano I, Collins MH, Katzka DA, et al; ORBIT1/SHP621-301 Investigators. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022;20(3):525-534.e10. doi:10.1016/j.cgh.2021.04.022 

  10. Dellon ES, Katzka DA, Collins MH, et al; MP-101-06 Investigators. Budesonide Oral Suspension Improves Symptomatic, Endoscopic, and Histologic Parameters Compared With Placebo in Patients With Eosinophilic Esophagitis. Gastroenterology. 2017;152(4):776-786.e5. doi:10.1053/j.gastro.2016.11.021

  11. Dellon ES, Charriez CM, Zhang S, et al. Cendakimab efficacy and safety in adult and adolescent patients with eosinophilic esophagitis 48-week results from the randomized, placebo-controlled, phase 3 study (late-breaking abstract). Paper presented at: ACG 2024 Annual Scientific Meeting. Philadelphia, Pennsylvania. October 25-30, 2024.

  12. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. Efficacy and Safety of Tezepelumab in Patients With Eosinophilic Esophagitis (CROSSING). ClinicalTrials.gov ID NCT05583227. Published December 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05583227 

  13. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study to Investigate the Efficacy and Safety of NSI-8226 in Adults with Eosinophilic Esophagitis. ClinicalTrials.gov ID NCT06598462. Published November 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT06598462 

  14. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study of CDX-0519 in Patients With Eosinophilic Esophagitis (EvolvE). ClinicalTrials.gov ID NCT05774184. Published June 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05774184

Author and Disclosure Information

Evan S. Dellon, MD, MPH
Professor Medicine; 
Director of the Center for Esophageal Diseases and Swallowing,
Department of Medicine, Division of Gastroenterology
University of North Carolina School of Medicine
Chapel Hill, North Carolina 

Evan S. Dellon, MD, MPH, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Abbvie; Adare/Ellodi; Akesobio; Alfasigma; ALK; Allakos; Amgen; Apollo; Aqilion; Arena/Pfizer; Aslan; AstraZeneca; Avir; Biocryst; Bryn; Calypso; Celgene/Receptos/BMS; Celldex; EsoCap; Eupraxia; Dr. Falk Pharma; Ferring; GI Reviewers; GSK; Holoclara; Invea; Knightpoint; LucidDx; Morphic; Nexstone Immunology/Uniquity; Nutricia; Parexel/Calyx; Phathom; Regeneron; Revolo; Robarts/Alimentiv; Sanofi; Shire/Takeda; Target RWE; Upstream Bio Received research grant from: Adare/Ellodi; Allakos; Arena/Pfizer; AstraZeneca; Celldex; Eupraxia; Ferring; GSK; Meritage; Miraca; Nutricia; Celgene/Receptos/BMS; Regeneron; Revolo; Sanofi; Shire/Takeda Received educational grant from: Allakos; Aqilion; Holoclara; Invea

Publications
Author and Disclosure Information

Evan S. Dellon, MD, MPH
Professor Medicine; 
Director of the Center for Esophageal Diseases and Swallowing,
Department of Medicine, Division of Gastroenterology
University of North Carolina School of Medicine
Chapel Hill, North Carolina 

Evan S. Dellon, MD, MPH, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Abbvie; Adare/Ellodi; Akesobio; Alfasigma; ALK; Allakos; Amgen; Apollo; Aqilion; Arena/Pfizer; Aslan; AstraZeneca; Avir; Biocryst; Bryn; Calypso; Celgene/Receptos/BMS; Celldex; EsoCap; Eupraxia; Dr. Falk Pharma; Ferring; GI Reviewers; GSK; Holoclara; Invea; Knightpoint; LucidDx; Morphic; Nexstone Immunology/Uniquity; Nutricia; Parexel/Calyx; Phathom; Regeneron; Revolo; Robarts/Alimentiv; Sanofi; Shire/Takeda; Target RWE; Upstream Bio Received research grant from: Adare/Ellodi; Allakos; Arena/Pfizer; AstraZeneca; Celldex; Eupraxia; Ferring; GSK; Meritage; Miraca; Nutricia; Celgene/Receptos/BMS; Regeneron; Revolo; Sanofi; Shire/Takeda Received educational grant from: Allakos; Aqilion; Holoclara; Invea

Author and Disclosure Information

Evan S. Dellon, MD, MPH
Professor Medicine; 
Director of the Center for Esophageal Diseases and Swallowing,
Department of Medicine, Division of Gastroenterology
University of North Carolina School of Medicine
Chapel Hill, North Carolina 

Evan S. Dellon, MD, MPH, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Abbvie; Adare/Ellodi; Akesobio; Alfasigma; ALK; Allakos; Amgen; Apollo; Aqilion; Arena/Pfizer; Aslan; AstraZeneca; Avir; Biocryst; Bryn; Calypso; Celgene/Receptos/BMS; Celldex; EsoCap; Eupraxia; Dr. Falk Pharma; Ferring; GI Reviewers; GSK; Holoclara; Invea; Knightpoint; LucidDx; Morphic; Nexstone Immunology/Uniquity; Nutricia; Parexel/Calyx; Phathom; Regeneron; Revolo; Robarts/Alimentiv; Sanofi; Shire/Takeda; Target RWE; Upstream Bio Received research grant from: Adare/Ellodi; Allakos; Arena/Pfizer; AstraZeneca; Celldex; Eupraxia; Ferring; GSK; Meritage; Miraca; Nutricia; Celgene/Receptos/BMS; Regeneron; Revolo; Sanofi; Shire/Takeda Received educational grant from: Allakos; Aqilion; Holoclara; Invea

References
  1. Rossi CM, Santacroce G, Lenti MV, di Sabatino A. Eosinophilic esophagitis in the era of biologics. Expert Rev Gastroenterol Hepatol. 2024;18(6):271-281. doi:10.1080/17474124.2024.2374471

  2. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology. 2018;155(4):1022-1033.e10. doi:10.1053/j.gastro.2018.07.009

  3. Geow R, Arena G, Siah C, Picardo S. A retrospective real-world study on the safety and efficacy of budesonide orodispersible tablets for the induction therapy of eosinophilic oesophagitis. Therap Adv Gastroenterol. 2024;17:17562848241290346. doi:10.1177/17562848241290346

  4. Sato H, Dellon ES, Aceves SS, et al. Clinical and molecular correlates of the Index of Severity for Eosinophilic Esophagitis. J Allergy Clin Immunol. 2024;154(2):375-386.e4. doi:10.1016/j.jaci.2024.04.025

  5. Dellon ES, Khoury P, Muir AB, et al. A Clinical Severity Index for Eosinophilic Esophagitis: Development, Consensus, and Future Directions. Gastroenterology. 2022;163(1):59-76. doi:10.1053/j.gastro.2022.03.025   

  6. Thel HL, Anderson C, Xue AZ, Jensen ET, Dellon ES. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025;23(2)272-280. doi:10.1016/j.cgh.2024.09.031

  7. Yang E-J, Jung KW. Role of endoscopy in eosinophilic esophagitis. Clin Endosc2025;58(1):1-9. doi.org/10.5946/ce.2024.023 

  8. Chehade M, Dellon ES, Spergel JM, et al. Dupilumab for Eosinophilic Esophagitis in Patients 1 to 11 Years of Age. N Engl J Med. 2024;390(24):2239-2251. doi:10.1056/NEJMoa2312282

  9. Hirano I, Collins MH, Katzka DA, et al; ORBIT1/SHP621-301 Investigators. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022;20(3):525-534.e10. doi:10.1016/j.cgh.2021.04.022 

  10. Dellon ES, Katzka DA, Collins MH, et al; MP-101-06 Investigators. Budesonide Oral Suspension Improves Symptomatic, Endoscopic, and Histologic Parameters Compared With Placebo in Patients With Eosinophilic Esophagitis. Gastroenterology. 2017;152(4):776-786.e5. doi:10.1053/j.gastro.2016.11.021

  11. Dellon ES, Charriez CM, Zhang S, et al. Cendakimab efficacy and safety in adult and adolescent patients with eosinophilic esophagitis 48-week results from the randomized, placebo-controlled, phase 3 study (late-breaking abstract). Paper presented at: ACG 2024 Annual Scientific Meeting. Philadelphia, Pennsylvania. October 25-30, 2024.

  12. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. Efficacy and Safety of Tezepelumab in Patients With Eosinophilic Esophagitis (CROSSING). ClinicalTrials.gov ID NCT05583227. Published December 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05583227 

  13. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study to Investigate the Efficacy and Safety of NSI-8226 in Adults with Eosinophilic Esophagitis. ClinicalTrials.gov ID NCT06598462. Published November 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT06598462 

  14. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study of CDX-0519 in Patients With Eosinophilic Esophagitis (EvolvE). ClinicalTrials.gov ID NCT05774184. Published June 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05774184

References
  1. Rossi CM, Santacroce G, Lenti MV, di Sabatino A. Eosinophilic esophagitis in the era of biologics. Expert Rev Gastroenterol Hepatol. 2024;18(6):271-281. doi:10.1080/17474124.2024.2374471

  2. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology. 2018;155(4):1022-1033.e10. doi:10.1053/j.gastro.2018.07.009

  3. Geow R, Arena G, Siah C, Picardo S. A retrospective real-world study on the safety and efficacy of budesonide orodispersible tablets for the induction therapy of eosinophilic oesophagitis. Therap Adv Gastroenterol. 2024;17:17562848241290346. doi:10.1177/17562848241290346

  4. Sato H, Dellon ES, Aceves SS, et al. Clinical and molecular correlates of the Index of Severity for Eosinophilic Esophagitis. J Allergy Clin Immunol. 2024;154(2):375-386.e4. doi:10.1016/j.jaci.2024.04.025

  5. Dellon ES, Khoury P, Muir AB, et al. A Clinical Severity Index for Eosinophilic Esophagitis: Development, Consensus, and Future Directions. Gastroenterology. 2022;163(1):59-76. doi:10.1053/j.gastro.2022.03.025   

  6. Thel HL, Anderson C, Xue AZ, Jensen ET, Dellon ES. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025;23(2)272-280. doi:10.1016/j.cgh.2024.09.031

  7. Yang E-J, Jung KW. Role of endoscopy in eosinophilic esophagitis. Clin Endosc2025;58(1):1-9. doi.org/10.5946/ce.2024.023 

  8. Chehade M, Dellon ES, Spergel JM, et al. Dupilumab for Eosinophilic Esophagitis in Patients 1 to 11 Years of Age. N Engl J Med. 2024;390(24):2239-2251. doi:10.1056/NEJMoa2312282

  9. Hirano I, Collins MH, Katzka DA, et al; ORBIT1/SHP621-301 Investigators. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022;20(3):525-534.e10. doi:10.1016/j.cgh.2021.04.022 

  10. Dellon ES, Katzka DA, Collins MH, et al; MP-101-06 Investigators. Budesonide Oral Suspension Improves Symptomatic, Endoscopic, and Histologic Parameters Compared With Placebo in Patients With Eosinophilic Esophagitis. Gastroenterology. 2017;152(4):776-786.e5. doi:10.1053/j.gastro.2016.11.021

  11. Dellon ES, Charriez CM, Zhang S, et al. Cendakimab efficacy and safety in adult and adolescent patients with eosinophilic esophagitis 48-week results from the randomized, placebo-controlled, phase 3 study (late-breaking abstract). Paper presented at: ACG 2024 Annual Scientific Meeting. Philadelphia, Pennsylvania. October 25-30, 2024.

  12. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. Efficacy and Safety of Tezepelumab in Patients With Eosinophilic Esophagitis (CROSSING). ClinicalTrials.gov ID NCT05583227. Published December 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05583227 

  13. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study to Investigate the Efficacy and Safety of NSI-8226 in Adults with Eosinophilic Esophagitis. ClinicalTrials.gov ID NCT06598462. Published November 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT06598462 

  14. National Institutes of Health, National Library of Medicine, Cinicaltrials.gov website. A Study of CDX-0519 in Patients With Eosinophilic Esophagitis (EvolvE). ClinicalTrials.gov ID NCT05774184. Published June 2024. Accessed February 3, 2025. https://clinicaltrials.gov/study/NCT05774184

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New Therapeutic Frontiers in the Treatment of Eosinophilic Esophagitis

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New Therapeutic Frontiers in the Treatment of Eosinophilic Esophagitis

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Eosinophilic esophagitis (EoE) is a chronic, immune-mediated disease characterized by symptoms of esophageal dysfunction and dense eosinophilic infiltration. The prevalence of EoE continues to increase in the United States, with genetic, environmental, and microbiome factors contributing to its rise.1 This condition manifests as dysphagia for solid food in adults and adolescents and can lead to esophageal remodeling if untreated; symptoms are non-specific in children. Diagnosis of EoE is per International Consensus Criteria.2 Management options include proton pump inhibitors, elimination diets, topical steroids, and biologics.1

Recent advances in treatment include the US FDA approval of the swallowed topical steroid budesonide oral suspension and of a monoclonal antibody targeting interleukins (IL)-4/IL-13 (dupilumab).3 The positioning of biologics continues to evolve but, as for other atopic conditions, they are mostly used as “step-up” treatment for more difficult-to-treat patients with EoE. The Index of Severity of Eosinophilic Esophagitis (I-SEE), developed in 2022, has been shown to be a promising clinical tool for assessing and following EoE severity that may ultimately help to better manage treatment modalities.4,5 After prescribing treatment, careful assessment of symptomatic, endoscopic, and histologic outcomes is needed to determine response.3 In addition, understanding of various inflammatory mechanisms has led to the ongoing development and evaluation of new biological drugs targeting the Th2 axis and fibrosis.1,3 More studies are needed to determine the effects of these emerging therapies as well as the long-term outcomes of existing treatments for patients with EoE.

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