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Diabetic dyslipidemia with eruptive xanthoma
A workup for secondary causes of hypertriglyceridemia was negative for hypothyroidism and nephrotic syndrome. She was currently taking no medications. She had no family history of dyslipidemia, and she denied alcohol consumption.
Based on the patient’s presentation, history, and the results of laboratory testing and skin biopsy, the diagnosis was eruptive xanthoma.
A RESULT OF ELEVATED TRIGLYCERIDES
Eruptive xanthoma is associated with elevation of chylomicrons and triglycerides.1 Hyperlipidemia that causes eruptive xanthoma may be familial (ie, due to a primary genetic defect) or secondary to another disease, or both.
Types of primary hypertriglyceridemia include elevated chylomicrons (Frederickson classification type I), elevated very-low-density lipoprotein (VLDL) (Frederickson type IV), and elevation of both chylomicrons and VLDL (Frederickson type V).2,3 Hypertriglyceridemia may also be secondary to obesity, diabetes mellitus, hypothyroidism, nephrotic syndrome, liver cirrhosis, excess ethanol ingestion, and medicines such as retinoids and estrogens.2,3
Lesions of eruptive xanthoma are yellowish papules 2 to 5 mm in diameter surrounded by an erythematous border. They are formed by clusters of foamy cells caused by phagocytosis of macrophages as a consequence of increased accumulations of intracellular lipids. The most common sites are the buttocks, extensor surfaces of the arms, and the back.4
Eruptive xanthoma occurs with markedly elevated triglyceride levels (ie, > 1,000 mg/dL),5 with an estimated prevalence of 18 cases per 100,000 people (< 0.02%).6 Diagnosis is usually established through the clinical history, physical examination, and prompt laboratory confirmation of hypertriglyceridemia. Skin biopsy is rarely if ever needed.
RECOGNIZE AND TREAT PROMPTLY TO AVOID FURTHER COMPLICATIONS
Severe hypertriglyceridemia poses an increased risk of acute pancreatitis. Early recognition and medical treatment in our patient prevented serious complications.
Treatment of eruptive xanthoma includes identifying the underlying cause of hypertriglyceridemia and commencing lifestyle modifications that include weight reduction, aerobic exercise, a strict low-fat diet with avoidance of simple carbohydrates and alcohol,7 and drug therapy.
The patient’s treatment plan
Although HMG-CoA reductase inhibitors (statins) have a modest triglyceride-lowering effect and are useful to modify cardiovascular risk, fibric acid derivatives (eg, gemfibrozil, fenofibrate) are the first-line therapy.8 Omega-3 fatty acids, statins, or niacin may be added if necessary.8
Our patient’s uncontrolled glycemia caused marked hypertriglyceridemia, perhaps from a decrease in lipoprotein lipase activity in adipose tissue and muscle. Lifestyle modifications, glucose-lowering agents (metformin, glimepiride), and fenofibrate were prescribed. She was also advised to seek medical attention if she developed upper-abdominal pain, which could be a symptom of pancreatitis.
- Flynn PD, Burns T, Breathnach S, Cox N, Griffiths C. Xanthomas and abnormalities of lipid metabolism and storage. In: Rook’s Textbook of Dermatology. 8th ed. Oxford: Blackwell Science; 2010.
- Breckenridge WC, Alaupovic P, Cox DW, Little JA. Apolipoprotein and lipoprotein concentrations in familial apolipoprotein C-II deficiency. Atherosclerosis 1982; 44(2):223–235. pmid:7138621
- Santamarina-Fojo S. The familial chylomicronemia syndrome. Endocrinol Metab Clin North Am 1998; 27(3):551–567. pmid:9785052
- Melmed S, Polonsky KS, Larsen PR, Kronenberg H. Williams Textbook of Endocrinology. 13th ed. Philadelphia: Elsevier; 2016.
- Zak A, Zeman M, Slaby A, Vecka M. Xanthomas: clinical and pathophysiological relations. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014; 158(2):181–188. doi:10.5507/bp.2014.016
- Leaf DA. Chylomicronemia and the chylomicronemia syndrome: a practical approach to management. Am J Med 2008; 121(1):10–12. doi:10.1016/j.amjmed.2007.10.004
- Hegele RA, Ginsberg HN, Chapman MJ, et al; European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management. Lancet Diabetes Endocrinol 2014; 2(8):655–666. doi:10.1016/S2213-8587(13)70191-8
- Berglund L, Brunzell JD, Goldberg AC, et al; Endocrine Society. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2012; 97(9):2969–2989. doi:10.1210/jc.2011-3213
A workup for secondary causes of hypertriglyceridemia was negative for hypothyroidism and nephrotic syndrome. She was currently taking no medications. She had no family history of dyslipidemia, and she denied alcohol consumption.
Based on the patient’s presentation, history, and the results of laboratory testing and skin biopsy, the diagnosis was eruptive xanthoma.
A RESULT OF ELEVATED TRIGLYCERIDES
Eruptive xanthoma is associated with elevation of chylomicrons and triglycerides.1 Hyperlipidemia that causes eruptive xanthoma may be familial (ie, due to a primary genetic defect) or secondary to another disease, or both.
Types of primary hypertriglyceridemia include elevated chylomicrons (Frederickson classification type I), elevated very-low-density lipoprotein (VLDL) (Frederickson type IV), and elevation of both chylomicrons and VLDL (Frederickson type V).2,3 Hypertriglyceridemia may also be secondary to obesity, diabetes mellitus, hypothyroidism, nephrotic syndrome, liver cirrhosis, excess ethanol ingestion, and medicines such as retinoids and estrogens.2,3
Lesions of eruptive xanthoma are yellowish papules 2 to 5 mm in diameter surrounded by an erythematous border. They are formed by clusters of foamy cells caused by phagocytosis of macrophages as a consequence of increased accumulations of intracellular lipids. The most common sites are the buttocks, extensor surfaces of the arms, and the back.4
Eruptive xanthoma occurs with markedly elevated triglyceride levels (ie, > 1,000 mg/dL),5 with an estimated prevalence of 18 cases per 100,000 people (< 0.02%).6 Diagnosis is usually established through the clinical history, physical examination, and prompt laboratory confirmation of hypertriglyceridemia. Skin biopsy is rarely if ever needed.
RECOGNIZE AND TREAT PROMPTLY TO AVOID FURTHER COMPLICATIONS
Severe hypertriglyceridemia poses an increased risk of acute pancreatitis. Early recognition and medical treatment in our patient prevented serious complications.
Treatment of eruptive xanthoma includes identifying the underlying cause of hypertriglyceridemia and commencing lifestyle modifications that include weight reduction, aerobic exercise, a strict low-fat diet with avoidance of simple carbohydrates and alcohol,7 and drug therapy.
The patient’s treatment plan
Although HMG-CoA reductase inhibitors (statins) have a modest triglyceride-lowering effect and are useful to modify cardiovascular risk, fibric acid derivatives (eg, gemfibrozil, fenofibrate) are the first-line therapy.8 Omega-3 fatty acids, statins, or niacin may be added if necessary.8
Our patient’s uncontrolled glycemia caused marked hypertriglyceridemia, perhaps from a decrease in lipoprotein lipase activity in adipose tissue and muscle. Lifestyle modifications, glucose-lowering agents (metformin, glimepiride), and fenofibrate were prescribed. She was also advised to seek medical attention if she developed upper-abdominal pain, which could be a symptom of pancreatitis.
A workup for secondary causes of hypertriglyceridemia was negative for hypothyroidism and nephrotic syndrome. She was currently taking no medications. She had no family history of dyslipidemia, and she denied alcohol consumption.
Based on the patient’s presentation, history, and the results of laboratory testing and skin biopsy, the diagnosis was eruptive xanthoma.
A RESULT OF ELEVATED TRIGLYCERIDES
Eruptive xanthoma is associated with elevation of chylomicrons and triglycerides.1 Hyperlipidemia that causes eruptive xanthoma may be familial (ie, due to a primary genetic defect) or secondary to another disease, or both.
Types of primary hypertriglyceridemia include elevated chylomicrons (Frederickson classification type I), elevated very-low-density lipoprotein (VLDL) (Frederickson type IV), and elevation of both chylomicrons and VLDL (Frederickson type V).2,3 Hypertriglyceridemia may also be secondary to obesity, diabetes mellitus, hypothyroidism, nephrotic syndrome, liver cirrhosis, excess ethanol ingestion, and medicines such as retinoids and estrogens.2,3
Lesions of eruptive xanthoma are yellowish papules 2 to 5 mm in diameter surrounded by an erythematous border. They are formed by clusters of foamy cells caused by phagocytosis of macrophages as a consequence of increased accumulations of intracellular lipids. The most common sites are the buttocks, extensor surfaces of the arms, and the back.4
Eruptive xanthoma occurs with markedly elevated triglyceride levels (ie, > 1,000 mg/dL),5 with an estimated prevalence of 18 cases per 100,000 people (< 0.02%).6 Diagnosis is usually established through the clinical history, physical examination, and prompt laboratory confirmation of hypertriglyceridemia. Skin biopsy is rarely if ever needed.
RECOGNIZE AND TREAT PROMPTLY TO AVOID FURTHER COMPLICATIONS
Severe hypertriglyceridemia poses an increased risk of acute pancreatitis. Early recognition and medical treatment in our patient prevented serious complications.
Treatment of eruptive xanthoma includes identifying the underlying cause of hypertriglyceridemia and commencing lifestyle modifications that include weight reduction, aerobic exercise, a strict low-fat diet with avoidance of simple carbohydrates and alcohol,7 and drug therapy.
The patient’s treatment plan
Although HMG-CoA reductase inhibitors (statins) have a modest triglyceride-lowering effect and are useful to modify cardiovascular risk, fibric acid derivatives (eg, gemfibrozil, fenofibrate) are the first-line therapy.8 Omega-3 fatty acids, statins, or niacin may be added if necessary.8
Our patient’s uncontrolled glycemia caused marked hypertriglyceridemia, perhaps from a decrease in lipoprotein lipase activity in adipose tissue and muscle. Lifestyle modifications, glucose-lowering agents (metformin, glimepiride), and fenofibrate were prescribed. She was also advised to seek medical attention if she developed upper-abdominal pain, which could be a symptom of pancreatitis.
- Flynn PD, Burns T, Breathnach S, Cox N, Griffiths C. Xanthomas and abnormalities of lipid metabolism and storage. In: Rook’s Textbook of Dermatology. 8th ed. Oxford: Blackwell Science; 2010.
- Breckenridge WC, Alaupovic P, Cox DW, Little JA. Apolipoprotein and lipoprotein concentrations in familial apolipoprotein C-II deficiency. Atherosclerosis 1982; 44(2):223–235. pmid:7138621
- Santamarina-Fojo S. The familial chylomicronemia syndrome. Endocrinol Metab Clin North Am 1998; 27(3):551–567. pmid:9785052
- Melmed S, Polonsky KS, Larsen PR, Kronenberg H. Williams Textbook of Endocrinology. 13th ed. Philadelphia: Elsevier; 2016.
- Zak A, Zeman M, Slaby A, Vecka M. Xanthomas: clinical and pathophysiological relations. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014; 158(2):181–188. doi:10.5507/bp.2014.016
- Leaf DA. Chylomicronemia and the chylomicronemia syndrome: a practical approach to management. Am J Med 2008; 121(1):10–12. doi:10.1016/j.amjmed.2007.10.004
- Hegele RA, Ginsberg HN, Chapman MJ, et al; European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management. Lancet Diabetes Endocrinol 2014; 2(8):655–666. doi:10.1016/S2213-8587(13)70191-8
- Berglund L, Brunzell JD, Goldberg AC, et al; Endocrine Society. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2012; 97(9):2969–2989. doi:10.1210/jc.2011-3213
- Flynn PD, Burns T, Breathnach S, Cox N, Griffiths C. Xanthomas and abnormalities of lipid metabolism and storage. In: Rook’s Textbook of Dermatology. 8th ed. Oxford: Blackwell Science; 2010.
- Breckenridge WC, Alaupovic P, Cox DW, Little JA. Apolipoprotein and lipoprotein concentrations in familial apolipoprotein C-II deficiency. Atherosclerosis 1982; 44(2):223–235. pmid:7138621
- Santamarina-Fojo S. The familial chylomicronemia syndrome. Endocrinol Metab Clin North Am 1998; 27(3):551–567. pmid:9785052
- Melmed S, Polonsky KS, Larsen PR, Kronenberg H. Williams Textbook of Endocrinology. 13th ed. Philadelphia: Elsevier; 2016.
- Zak A, Zeman M, Slaby A, Vecka M. Xanthomas: clinical and pathophysiological relations. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014; 158(2):181–188. doi:10.5507/bp.2014.016
- Leaf DA. Chylomicronemia and the chylomicronemia syndrome: a practical approach to management. Am J Med 2008; 121(1):10–12. doi:10.1016/j.amjmed.2007.10.004
- Hegele RA, Ginsberg HN, Chapman MJ, et al; European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management. Lancet Diabetes Endocrinol 2014; 2(8):655–666. doi:10.1016/S2213-8587(13)70191-8
- Berglund L, Brunzell JD, Goldberg AC, et al; Endocrine Society. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2012; 97(9):2969–2989. doi:10.1210/jc.2011-3213
Cephalosporins remain empiric therapy for skin infections in pediatric AD
“Clindamycin, tetracyclines, or TMP‐SMX can be considered in patients suspected to have, or with a history of, MRSA [methicillin‐resistant S. aureus] infection,” wrote Cristopher C. Briscoe, MD, of the Washington University School of Medicine in St. Louis, Missouri, and his coauthors. The study was published in Pediatric Dermatology.
To determine the optimal empiric antibiotic for pediatric AD patients with skin infections, the researchers analyzed skin cultures from 106 patients seen at Saint Louis Children’s Hospital (SLCH). The results were also compared to cultures from pediatric patients who presented at the SLCH emergency department (ED) with S. aureus skin abscesses.
Of the 170 cultures that grew S. aureus, 130 (77.8%) grew MSSA, and 37 (22.2%) grew MRSA. Three of the cultures grew both. The prevalence of MRSA in the cohort differed from the prevalence in the ED patients (44%). The prevalence of either infection did not differ significantly by age, sex or race, though the average number of cultures in African American patients topped the average for Caucasian patients (1.8 vs. 1.2, P less than .003).
All patients with MSSA – in both the cohort and the ED – proved 100% susceptible to cefazolin. Cohort patients with MSSA saw lower susceptibility to doxycycline compared to the ED patients (89.4% vs. 97%), as did MRSA cohort patients to trimethoprim‐sulfamethoxazole (92% vs. 98%).
“When a patient with AD walks into your office and looks like they have an infection of their eczema, your go-to antibiotic is going to be one that targets MSSA,” said coauthor Carrie Coughlin, MD, of the Washington University School of Medicine in an interview. “You’ll still do a culture to prove or disprove that assumption, but it gives you a guide to help make that patient better in the short term while you work things up.”
“Also, remember that MSSA is not ‘better’ to have than MRSA,” she added. “You can now see some of the virulence factors from MRSA strains in MSSA strains, so treating both of them is important.”
The authors acknowledged their study’s limitations, including the limited generalizability of a single-center design and a lack of information as to the body sites from which the cultures were obtained. They were also unable to reliably determine prior antibiotic exposure, noting that “future work could examine whether prior exposure differed significantly in the MRSA and MSSA groups.”
The study was funded by grants from the Agency for Healthcare Research and Quality. The authors reported no conflicts of interest.
SOURCE: Briscoe CC et al. Pediatr Dermatol. 2019 May 24. doi: 10.1111/pde.13867.
“Clindamycin, tetracyclines, or TMP‐SMX can be considered in patients suspected to have, or with a history of, MRSA [methicillin‐resistant S. aureus] infection,” wrote Cristopher C. Briscoe, MD, of the Washington University School of Medicine in St. Louis, Missouri, and his coauthors. The study was published in Pediatric Dermatology.
To determine the optimal empiric antibiotic for pediatric AD patients with skin infections, the researchers analyzed skin cultures from 106 patients seen at Saint Louis Children’s Hospital (SLCH). The results were also compared to cultures from pediatric patients who presented at the SLCH emergency department (ED) with S. aureus skin abscesses.
Of the 170 cultures that grew S. aureus, 130 (77.8%) grew MSSA, and 37 (22.2%) grew MRSA. Three of the cultures grew both. The prevalence of MRSA in the cohort differed from the prevalence in the ED patients (44%). The prevalence of either infection did not differ significantly by age, sex or race, though the average number of cultures in African American patients topped the average for Caucasian patients (1.8 vs. 1.2, P less than .003).
All patients with MSSA – in both the cohort and the ED – proved 100% susceptible to cefazolin. Cohort patients with MSSA saw lower susceptibility to doxycycline compared to the ED patients (89.4% vs. 97%), as did MRSA cohort patients to trimethoprim‐sulfamethoxazole (92% vs. 98%).
“When a patient with AD walks into your office and looks like they have an infection of their eczema, your go-to antibiotic is going to be one that targets MSSA,” said coauthor Carrie Coughlin, MD, of the Washington University School of Medicine in an interview. “You’ll still do a culture to prove or disprove that assumption, but it gives you a guide to help make that patient better in the short term while you work things up.”
“Also, remember that MSSA is not ‘better’ to have than MRSA,” she added. “You can now see some of the virulence factors from MRSA strains in MSSA strains, so treating both of them is important.”
The authors acknowledged their study’s limitations, including the limited generalizability of a single-center design and a lack of information as to the body sites from which the cultures were obtained. They were also unable to reliably determine prior antibiotic exposure, noting that “future work could examine whether prior exposure differed significantly in the MRSA and MSSA groups.”
The study was funded by grants from the Agency for Healthcare Research and Quality. The authors reported no conflicts of interest.
SOURCE: Briscoe CC et al. Pediatr Dermatol. 2019 May 24. doi: 10.1111/pde.13867.
“Clindamycin, tetracyclines, or TMP‐SMX can be considered in patients suspected to have, or with a history of, MRSA [methicillin‐resistant S. aureus] infection,” wrote Cristopher C. Briscoe, MD, of the Washington University School of Medicine in St. Louis, Missouri, and his coauthors. The study was published in Pediatric Dermatology.
To determine the optimal empiric antibiotic for pediatric AD patients with skin infections, the researchers analyzed skin cultures from 106 patients seen at Saint Louis Children’s Hospital (SLCH). The results were also compared to cultures from pediatric patients who presented at the SLCH emergency department (ED) with S. aureus skin abscesses.
Of the 170 cultures that grew S. aureus, 130 (77.8%) grew MSSA, and 37 (22.2%) grew MRSA. Three of the cultures grew both. The prevalence of MRSA in the cohort differed from the prevalence in the ED patients (44%). The prevalence of either infection did not differ significantly by age, sex or race, though the average number of cultures in African American patients topped the average for Caucasian patients (1.8 vs. 1.2, P less than .003).
All patients with MSSA – in both the cohort and the ED – proved 100% susceptible to cefazolin. Cohort patients with MSSA saw lower susceptibility to doxycycline compared to the ED patients (89.4% vs. 97%), as did MRSA cohort patients to trimethoprim‐sulfamethoxazole (92% vs. 98%).
“When a patient with AD walks into your office and looks like they have an infection of their eczema, your go-to antibiotic is going to be one that targets MSSA,” said coauthor Carrie Coughlin, MD, of the Washington University School of Medicine in an interview. “You’ll still do a culture to prove or disprove that assumption, but it gives you a guide to help make that patient better in the short term while you work things up.”
“Also, remember that MSSA is not ‘better’ to have than MRSA,” she added. “You can now see some of the virulence factors from MRSA strains in MSSA strains, so treating both of them is important.”
The authors acknowledged their study’s limitations, including the limited generalizability of a single-center design and a lack of information as to the body sites from which the cultures were obtained. They were also unable to reliably determine prior antibiotic exposure, noting that “future work could examine whether prior exposure differed significantly in the MRSA and MSSA groups.”
The study was funded by grants from the Agency for Healthcare Research and Quality. The authors reported no conflicts of interest.
SOURCE: Briscoe CC et al. Pediatr Dermatol. 2019 May 24. doi: 10.1111/pde.13867.
FROM PEDIATRIC DERMATOLOGY
Tender nodules after leprosy Tx
The treating physicians believed that the patient had developed erythema nodosum leprosum (ENL), based on the tender nodules that are characteristic of this treatment reaction. The CDC was again consulted and representatives there agreed.
ENL is a known as a Type 2 reaction to the treatment for leprosy. Management involves the use of oral prednisone, which may be needed for a prolonged time. The antibiotics used to treat leprosy should not be stopped, as ENL is not an allergic reaction. It is due to the destruction of bacilli and the immune response to the release of bacterial antigens.
The patient was transferred to a leprosy hospital in Baton Rouge, Louisiana for further management. The prednisone was not sufficient, and he required further treatment with thalidomide. After 2 years of treatment, he appeared to be free of leprosy and no longer had the ENL.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the third edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The treating physicians believed that the patient had developed erythema nodosum leprosum (ENL), based on the tender nodules that are characteristic of this treatment reaction. The CDC was again consulted and representatives there agreed.
ENL is a known as a Type 2 reaction to the treatment for leprosy. Management involves the use of oral prednisone, which may be needed for a prolonged time. The antibiotics used to treat leprosy should not be stopped, as ENL is not an allergic reaction. It is due to the destruction of bacilli and the immune response to the release of bacterial antigens.
The patient was transferred to a leprosy hospital in Baton Rouge, Louisiana for further management. The prednisone was not sufficient, and he required further treatment with thalidomide. After 2 years of treatment, he appeared to be free of leprosy and no longer had the ENL.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the third edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The treating physicians believed that the patient had developed erythema nodosum leprosum (ENL), based on the tender nodules that are characteristic of this treatment reaction. The CDC was again consulted and representatives there agreed.
ENL is a known as a Type 2 reaction to the treatment for leprosy. Management involves the use of oral prednisone, which may be needed for a prolonged time. The antibiotics used to treat leprosy should not be stopped, as ENL is not an allergic reaction. It is due to the destruction of bacilli and the immune response to the release of bacterial antigens.
The patient was transferred to a leprosy hospital in Baton Rouge, Louisiana for further management. The prednisone was not sufficient, and he required further treatment with thalidomide. After 2 years of treatment, he appeared to be free of leprosy and no longer had the ENL.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the third edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
An Atypical Problem for Atopical People
At age 1, a girl developed a blistery rash on the left side of her face. It was soon followed by a low-grade fever and modest malaise. All symptoms cleared within 2 weeks. Now, at age 4, she continues to experience similar, periodic outbreaks in the same location.
She has already been seen by various providers, including a dermatologist, and received several different diagnoses. The dermatologist scraped the rash and determined it to be a fungal infection. However, the recommended topical antifungal cream had no effect. At least 3 other providers (all nondermatology) called it cellulitis and treated with oral antibiotics, but these attempts also failed.
EXAMINATION
There are no active lesions at the time of this initial examination and no palpable adenopathy in the region. There is a large area of erythema in a macular pattern over the right cheek. No scarring is visible.
The patient later returns when a new outbreak occurs. This time, there are distinct blisters and reactive adenopathy in the adjacent nodal areas.
What’s the diagnosis?
DISCUSSION
Results of a viral culture indicate herpes simplex.
The recurrence of persistent, vesicular rashes in the same location signifies a herpetic nature. Herpes simplex virus (HSV) is easier to diagnose in an adult patient, due to the ability to elicit a reliable history of premonitory symptoms. Small children have difficulty verbalizing the distinction between a tingle, an itch, and mild pain, which herald the onset of an HSV outbreak.
An episode of HSV can be triggered by anything that raises the body temperature (eg, stress, sickness, or sun exposure). Also important to note, these kinds of outbreaks can occur almost anywhere on the body, including ears, fingers, nipples, noses, and eyelids.
In my experience, most patients with longstanding herpes outbreaks are atopic (ie, allergy prone) or come from families in which atopy is common. Atopic patients are well known to be susceptible to all manner of skin infections, but most especially to herpes. It’s as if their immune systems overreact to pollen, mold, dust, and other allergens, while viral, fungal, and bacterial antigens fly under their immune radar.
In this case, the child was treated with valacyclovir on a chronic, as opposed to episodic, basis. With a bit of luck, this treatment will help to diminish HSV attacks as she matures.
TAKE-HOME LEARNING POINTS
- Anything that raises body temperature (sun, colds, or even stress) can trigger an episode of herpes simplex virus (HSV).
- Vesicular rashes that recur in the same location should be presumed herpetic, until proven otherwise. Usually, viral cultures aren’t necessary since the differential is so narrow.
- Atopy can predispose one to all manner of skin infections, including viral, fungal, and bacterial.
- Treatment of chronic HSV can be episodic or preventive, depending on the frequency and severity of attacks.
At age 1, a girl developed a blistery rash on the left side of her face. It was soon followed by a low-grade fever and modest malaise. All symptoms cleared within 2 weeks. Now, at age 4, she continues to experience similar, periodic outbreaks in the same location.
She has already been seen by various providers, including a dermatologist, and received several different diagnoses. The dermatologist scraped the rash and determined it to be a fungal infection. However, the recommended topical antifungal cream had no effect. At least 3 other providers (all nondermatology) called it cellulitis and treated with oral antibiotics, but these attempts also failed.
EXAMINATION
There are no active lesions at the time of this initial examination and no palpable adenopathy in the region. There is a large area of erythema in a macular pattern over the right cheek. No scarring is visible.
The patient later returns when a new outbreak occurs. This time, there are distinct blisters and reactive adenopathy in the adjacent nodal areas.
What’s the diagnosis?
DISCUSSION
Results of a viral culture indicate herpes simplex.
The recurrence of persistent, vesicular rashes in the same location signifies a herpetic nature. Herpes simplex virus (HSV) is easier to diagnose in an adult patient, due to the ability to elicit a reliable history of premonitory symptoms. Small children have difficulty verbalizing the distinction between a tingle, an itch, and mild pain, which herald the onset of an HSV outbreak.
An episode of HSV can be triggered by anything that raises the body temperature (eg, stress, sickness, or sun exposure). Also important to note, these kinds of outbreaks can occur almost anywhere on the body, including ears, fingers, nipples, noses, and eyelids.
In my experience, most patients with longstanding herpes outbreaks are atopic (ie, allergy prone) or come from families in which atopy is common. Atopic patients are well known to be susceptible to all manner of skin infections, but most especially to herpes. It’s as if their immune systems overreact to pollen, mold, dust, and other allergens, while viral, fungal, and bacterial antigens fly under their immune radar.
In this case, the child was treated with valacyclovir on a chronic, as opposed to episodic, basis. With a bit of luck, this treatment will help to diminish HSV attacks as she matures.
TAKE-HOME LEARNING POINTS
- Anything that raises body temperature (sun, colds, or even stress) can trigger an episode of herpes simplex virus (HSV).
- Vesicular rashes that recur in the same location should be presumed herpetic, until proven otherwise. Usually, viral cultures aren’t necessary since the differential is so narrow.
- Atopy can predispose one to all manner of skin infections, including viral, fungal, and bacterial.
- Treatment of chronic HSV can be episodic or preventive, depending on the frequency and severity of attacks.
At age 1, a girl developed a blistery rash on the left side of her face. It was soon followed by a low-grade fever and modest malaise. All symptoms cleared within 2 weeks. Now, at age 4, she continues to experience similar, periodic outbreaks in the same location.
She has already been seen by various providers, including a dermatologist, and received several different diagnoses. The dermatologist scraped the rash and determined it to be a fungal infection. However, the recommended topical antifungal cream had no effect. At least 3 other providers (all nondermatology) called it cellulitis and treated with oral antibiotics, but these attempts also failed.
EXAMINATION
There are no active lesions at the time of this initial examination and no palpable adenopathy in the region. There is a large area of erythema in a macular pattern over the right cheek. No scarring is visible.
The patient later returns when a new outbreak occurs. This time, there are distinct blisters and reactive adenopathy in the adjacent nodal areas.
What’s the diagnosis?
DISCUSSION
Results of a viral culture indicate herpes simplex.
The recurrence of persistent, vesicular rashes in the same location signifies a herpetic nature. Herpes simplex virus (HSV) is easier to diagnose in an adult patient, due to the ability to elicit a reliable history of premonitory symptoms. Small children have difficulty verbalizing the distinction between a tingle, an itch, and mild pain, which herald the onset of an HSV outbreak.
An episode of HSV can be triggered by anything that raises the body temperature (eg, stress, sickness, or sun exposure). Also important to note, these kinds of outbreaks can occur almost anywhere on the body, including ears, fingers, nipples, noses, and eyelids.
In my experience, most patients with longstanding herpes outbreaks are atopic (ie, allergy prone) or come from families in which atopy is common. Atopic patients are well known to be susceptible to all manner of skin infections, but most especially to herpes. It’s as if their immune systems overreact to pollen, mold, dust, and other allergens, while viral, fungal, and bacterial antigens fly under their immune radar.
In this case, the child was treated with valacyclovir on a chronic, as opposed to episodic, basis. With a bit of luck, this treatment will help to diminish HSV attacks as she matures.
TAKE-HOME LEARNING POINTS
- Anything that raises body temperature (sun, colds, or even stress) can trigger an episode of herpes simplex virus (HSV).
- Vesicular rashes that recur in the same location should be presumed herpetic, until proven otherwise. Usually, viral cultures aren’t necessary since the differential is so narrow.
- Atopy can predispose one to all manner of skin infections, including viral, fungal, and bacterial.
- Treatment of chronic HSV can be episodic or preventive, depending on the frequency and severity of attacks.
FDA approves Taltz for treatment of ankylosing spondylitis
press release from Eli Lilly.
(AS), according to aAS is the third indication for ixekizumab, along with moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and active psoriatic arthritis in adults.
Approval of the humanized interleukin-17A antagonist was based on results from a pair of randomized, double-blind, placebo-controlled, phase 3 studies involving 657 adult patients with active AS: the COAST-V trial in those naive to biologic disease-modifying antirheumatic drugs (bDMARDs) and the COAST-W trial in those who were intolerant or had inadequate response to tumor necrosis factor (TNF) inhibitors. The primary endpoint in both trials was achievement of 40% improvement in Assessment of Spondyloarthritis International Society criteria (ASAS40) at 16 weeks, compared with placebo.
In COAST-V, 48% of patients who received ixekizumab achieved ASAS40, compared with 18% of controls (P less than .0001). In COAST-W, 25% of patients who received ixekizumab achieved ASAS40 versus 13% of controls (P less than .05). The adverse events reported during both trials were consistent with the safety profile in patients who receive ixekizumab for the treatment of plaque psoriasis, including injection-site reactions, upper respiratory tract infections, nausea, and tinea infections.
“Results from the phase 3 clinical trial program in ankylosing spondylitis show that Taltz helped reduce pain and inflammation and improve function in patients who had never been treated with a bDMARD as well as those who previously failed TNF inhibitors. This approval is an important milestone for patients and physicians who are looking for a much-needed alternative to address symptoms of AS,” said Philip Mease, MD, of Providence St. Joseph Health and the University of Washington, both in Seattle.
press release from Eli Lilly.
(AS), according to aAS is the third indication for ixekizumab, along with moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and active psoriatic arthritis in adults.
Approval of the humanized interleukin-17A antagonist was based on results from a pair of randomized, double-blind, placebo-controlled, phase 3 studies involving 657 adult patients with active AS: the COAST-V trial in those naive to biologic disease-modifying antirheumatic drugs (bDMARDs) and the COAST-W trial in those who were intolerant or had inadequate response to tumor necrosis factor (TNF) inhibitors. The primary endpoint in both trials was achievement of 40% improvement in Assessment of Spondyloarthritis International Society criteria (ASAS40) at 16 weeks, compared with placebo.
In COAST-V, 48% of patients who received ixekizumab achieved ASAS40, compared with 18% of controls (P less than .0001). In COAST-W, 25% of patients who received ixekizumab achieved ASAS40 versus 13% of controls (P less than .05). The adverse events reported during both trials were consistent with the safety profile in patients who receive ixekizumab for the treatment of plaque psoriasis, including injection-site reactions, upper respiratory tract infections, nausea, and tinea infections.
“Results from the phase 3 clinical trial program in ankylosing spondylitis show that Taltz helped reduce pain and inflammation and improve function in patients who had never been treated with a bDMARD as well as those who previously failed TNF inhibitors. This approval is an important milestone for patients and physicians who are looking for a much-needed alternative to address symptoms of AS,” said Philip Mease, MD, of Providence St. Joseph Health and the University of Washington, both in Seattle.
press release from Eli Lilly.
(AS), according to aAS is the third indication for ixekizumab, along with moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and active psoriatic arthritis in adults.
Approval of the humanized interleukin-17A antagonist was based on results from a pair of randomized, double-blind, placebo-controlled, phase 3 studies involving 657 adult patients with active AS: the COAST-V trial in those naive to biologic disease-modifying antirheumatic drugs (bDMARDs) and the COAST-W trial in those who were intolerant or had inadequate response to tumor necrosis factor (TNF) inhibitors. The primary endpoint in both trials was achievement of 40% improvement in Assessment of Spondyloarthritis International Society criteria (ASAS40) at 16 weeks, compared with placebo.
In COAST-V, 48% of patients who received ixekizumab achieved ASAS40, compared with 18% of controls (P less than .0001). In COAST-W, 25% of patients who received ixekizumab achieved ASAS40 versus 13% of controls (P less than .05). The adverse events reported during both trials were consistent with the safety profile in patients who receive ixekizumab for the treatment of plaque psoriasis, including injection-site reactions, upper respiratory tract infections, nausea, and tinea infections.
“Results from the phase 3 clinical trial program in ankylosing spondylitis show that Taltz helped reduce pain and inflammation and improve function in patients who had never been treated with a bDMARD as well as those who previously failed TNF inhibitors. This approval is an important milestone for patients and physicians who are looking for a much-needed alternative to address symptoms of AS,” said Philip Mease, MD, of Providence St. Joseph Health and the University of Washington, both in Seattle.
Hidradenitis suppurativa linked to higher NAFLD risk
independent of other metabolic risk factors, a study has found.
The results of the case-control study of 70 individuals with hidradenitis suppurativa (HS) and 150 age- and gender-matched controls were published in the Journal of the European Academy of Dermatology and Venereology. Using hepatic ultrasonography and transient elastography, the investigators found that 51 (72.9%) the participants with HS also had nonalcoholic fatty liver disease (NAFLD), compared with 37 (24.7%) of the controls (P less than .001).
Those with HS and NAFLD were more likely to be obese, have more central adiposity, and meet more of the criteria for metabolic syndrome than those with HS but without NAFLD. They also showed higher serum ALT levels, higher triglycerides, and higher controlled attenuation parameter scores, which is a surrogate marker of liver steatosis.
However, the HS plus NAFLD group had similar rates of active smoking, diabetes, dyslipidemia, hypertension, and cardiovascular events, compared with those who had HS only. They also showed no differences in hemoglobin A1c, serum insulin, insulin resistance, or liver stiffness, compared with the HS-only group.
When researchers compared the participants with HS plus NAFLD with controls with NAFLD, they found the HS group had significantly higher levels of liver stiffness measurement, which is a surrogate marker of liver fibrosis and severity, but there were no differences in the degree of hepatic steatosis.
The individuals with HS plus NAFLD had significantly lower serum albumin, but significantly higher serum gamma–glutamyl transpeptidase and ferritin, compared with controls who had NAFLD. They were also more likely to have metabolic risk factors such as hypertension, dyslipidemia, and metabolic syndrome.
The multivariate analysis also showed that male sex was a protective factor, because the prevalence of obesity was higher in women.
After adjusting for classic cardiovascular and steatosis risk factors, the researchers calculated that HS was a significant and independent risk factor for NAFLD, with an odds ratio of 7.75 (P less than .001). The results provide “the first evidence that patients with HS have a significant high prevalence of NAFLD, which is independent of classic metabolic risk factors and, according to our results, probably not related to the severity of the disease,” wrote Carlos Durán-Vian, MD, from the department of dermatology at the University of Cantabria, Santander, Spain, and coauthors.
“We think that our findings might have potential clinical implications, and physicians involved in the care of patients with HS should be aware of the link between this entity and NAFLD, in order to improve the overall management of these patients,” they wrote, noting that HS is often associated with the same metabolic disorders that can promote fatty liver disease, such as obesity and metabolic syndrome. But the discovery that it is an independent risk factor demands other hypotheses to explain the association between the two conditions.
“In this sense, a possible explanation to deeper understanding the link between HS and NAFLD could be the presence of chronic inflammation due to persistent and abnormal secretion of adipokines (i.e. adiponectin, leptin, resistin) and several proinflammatory cytokines,” the authors wrote, pointing out that NAFLD is also common among people with immune-mediated inflammatory disorders.
The study had the limitation of being an observational, cross-sectional design, and the authors acknowledged that the cohort was relatively small. They also were unable to use liver biopsies to confirm the NAFLD diagnosis.
No funding or conflicts of interest were reported.
SOURCE: Durán-Vian C et al. J Eur Acad Dermatol Venereol. 2019 Jul 1. doi: 10.1111/jdv.15764.
independent of other metabolic risk factors, a study has found.
The results of the case-control study of 70 individuals with hidradenitis suppurativa (HS) and 150 age- and gender-matched controls were published in the Journal of the European Academy of Dermatology and Venereology. Using hepatic ultrasonography and transient elastography, the investigators found that 51 (72.9%) the participants with HS also had nonalcoholic fatty liver disease (NAFLD), compared with 37 (24.7%) of the controls (P less than .001).
Those with HS and NAFLD were more likely to be obese, have more central adiposity, and meet more of the criteria for metabolic syndrome than those with HS but without NAFLD. They also showed higher serum ALT levels, higher triglycerides, and higher controlled attenuation parameter scores, which is a surrogate marker of liver steatosis.
However, the HS plus NAFLD group had similar rates of active smoking, diabetes, dyslipidemia, hypertension, and cardiovascular events, compared with those who had HS only. They also showed no differences in hemoglobin A1c, serum insulin, insulin resistance, or liver stiffness, compared with the HS-only group.
When researchers compared the participants with HS plus NAFLD with controls with NAFLD, they found the HS group had significantly higher levels of liver stiffness measurement, which is a surrogate marker of liver fibrosis and severity, but there were no differences in the degree of hepatic steatosis.
The individuals with HS plus NAFLD had significantly lower serum albumin, but significantly higher serum gamma–glutamyl transpeptidase and ferritin, compared with controls who had NAFLD. They were also more likely to have metabolic risk factors such as hypertension, dyslipidemia, and metabolic syndrome.
The multivariate analysis also showed that male sex was a protective factor, because the prevalence of obesity was higher in women.
After adjusting for classic cardiovascular and steatosis risk factors, the researchers calculated that HS was a significant and independent risk factor for NAFLD, with an odds ratio of 7.75 (P less than .001). The results provide “the first evidence that patients with HS have a significant high prevalence of NAFLD, which is independent of classic metabolic risk factors and, according to our results, probably not related to the severity of the disease,” wrote Carlos Durán-Vian, MD, from the department of dermatology at the University of Cantabria, Santander, Spain, and coauthors.
“We think that our findings might have potential clinical implications, and physicians involved in the care of patients with HS should be aware of the link between this entity and NAFLD, in order to improve the overall management of these patients,” they wrote, noting that HS is often associated with the same metabolic disorders that can promote fatty liver disease, such as obesity and metabolic syndrome. But the discovery that it is an independent risk factor demands other hypotheses to explain the association between the two conditions.
“In this sense, a possible explanation to deeper understanding the link between HS and NAFLD could be the presence of chronic inflammation due to persistent and abnormal secretion of adipokines (i.e. adiponectin, leptin, resistin) and several proinflammatory cytokines,” the authors wrote, pointing out that NAFLD is also common among people with immune-mediated inflammatory disorders.
The study had the limitation of being an observational, cross-sectional design, and the authors acknowledged that the cohort was relatively small. They also were unable to use liver biopsies to confirm the NAFLD diagnosis.
No funding or conflicts of interest were reported.
SOURCE: Durán-Vian C et al. J Eur Acad Dermatol Venereol. 2019 Jul 1. doi: 10.1111/jdv.15764.
independent of other metabolic risk factors, a study has found.
The results of the case-control study of 70 individuals with hidradenitis suppurativa (HS) and 150 age- and gender-matched controls were published in the Journal of the European Academy of Dermatology and Venereology. Using hepatic ultrasonography and transient elastography, the investigators found that 51 (72.9%) the participants with HS also had nonalcoholic fatty liver disease (NAFLD), compared with 37 (24.7%) of the controls (P less than .001).
Those with HS and NAFLD were more likely to be obese, have more central adiposity, and meet more of the criteria for metabolic syndrome than those with HS but without NAFLD. They also showed higher serum ALT levels, higher triglycerides, and higher controlled attenuation parameter scores, which is a surrogate marker of liver steatosis.
However, the HS plus NAFLD group had similar rates of active smoking, diabetes, dyslipidemia, hypertension, and cardiovascular events, compared with those who had HS only. They also showed no differences in hemoglobin A1c, serum insulin, insulin resistance, or liver stiffness, compared with the HS-only group.
When researchers compared the participants with HS plus NAFLD with controls with NAFLD, they found the HS group had significantly higher levels of liver stiffness measurement, which is a surrogate marker of liver fibrosis and severity, but there were no differences in the degree of hepatic steatosis.
The individuals with HS plus NAFLD had significantly lower serum albumin, but significantly higher serum gamma–glutamyl transpeptidase and ferritin, compared with controls who had NAFLD. They were also more likely to have metabolic risk factors such as hypertension, dyslipidemia, and metabolic syndrome.
The multivariate analysis also showed that male sex was a protective factor, because the prevalence of obesity was higher in women.
After adjusting for classic cardiovascular and steatosis risk factors, the researchers calculated that HS was a significant and independent risk factor for NAFLD, with an odds ratio of 7.75 (P less than .001). The results provide “the first evidence that patients with HS have a significant high prevalence of NAFLD, which is independent of classic metabolic risk factors and, according to our results, probably not related to the severity of the disease,” wrote Carlos Durán-Vian, MD, from the department of dermatology at the University of Cantabria, Santander, Spain, and coauthors.
“We think that our findings might have potential clinical implications, and physicians involved in the care of patients with HS should be aware of the link between this entity and NAFLD, in order to improve the overall management of these patients,” they wrote, noting that HS is often associated with the same metabolic disorders that can promote fatty liver disease, such as obesity and metabolic syndrome. But the discovery that it is an independent risk factor demands other hypotheses to explain the association between the two conditions.
“In this sense, a possible explanation to deeper understanding the link between HS and NAFLD could be the presence of chronic inflammation due to persistent and abnormal secretion of adipokines (i.e. adiponectin, leptin, resistin) and several proinflammatory cytokines,” the authors wrote, pointing out that NAFLD is also common among people with immune-mediated inflammatory disorders.
The study had the limitation of being an observational, cross-sectional design, and the authors acknowledged that the cohort was relatively small. They also were unable to use liver biopsies to confirm the NAFLD diagnosis.
No funding or conflicts of interest were reported.
SOURCE: Durán-Vian C et al. J Eur Acad Dermatol Venereol. 2019 Jul 1. doi: 10.1111/jdv.15764.
FROM THE JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY
Nebraska issues SUNucate-based guidance for schools
Nebraska’s Department of Education recommended in a guidance that children be allowed to possess and use sunscreen products in school and at school-sponsored events, according to an Aug. 2 release from the American Society for Dermatologic Surgery.
The department’s guidance is based on model legislation developed by the SUNucate Coalition, which was created by the American Society for Dermatologic Surgery Association and “works to address barriers to sunscreen use in school and camps and promote sun-safe behavior.” The coalition was created in 2016 because of reports that some U.S. schools had banned sunscreen products as part of broader medication bans because of these products’ classification as an over-the-counter medication.
Twenty-three other states have moved to lift such bans; these states were joined by Arkansas, Connecticut, Illinois, Maine, Minnesota, Nevada, and now Nebraska in 2019 alone. The District of Columbia, Massachusetts, New Jersey, and Rhode Island are expected to follow suit.
Nebraska’s Department of Education recommended in a guidance that children be allowed to possess and use sunscreen products in school and at school-sponsored events, according to an Aug. 2 release from the American Society for Dermatologic Surgery.
The department’s guidance is based on model legislation developed by the SUNucate Coalition, which was created by the American Society for Dermatologic Surgery Association and “works to address barriers to sunscreen use in school and camps and promote sun-safe behavior.” The coalition was created in 2016 because of reports that some U.S. schools had banned sunscreen products as part of broader medication bans because of these products’ classification as an over-the-counter medication.
Twenty-three other states have moved to lift such bans; these states were joined by Arkansas, Connecticut, Illinois, Maine, Minnesota, Nevada, and now Nebraska in 2019 alone. The District of Columbia, Massachusetts, New Jersey, and Rhode Island are expected to follow suit.
Nebraska’s Department of Education recommended in a guidance that children be allowed to possess and use sunscreen products in school and at school-sponsored events, according to an Aug. 2 release from the American Society for Dermatologic Surgery.
The department’s guidance is based on model legislation developed by the SUNucate Coalition, which was created by the American Society for Dermatologic Surgery Association and “works to address barriers to sunscreen use in school and camps and promote sun-safe behavior.” The coalition was created in 2016 because of reports that some U.S. schools had banned sunscreen products as part of broader medication bans because of these products’ classification as an over-the-counter medication.
Twenty-three other states have moved to lift such bans; these states were joined by Arkansas, Connecticut, Illinois, Maine, Minnesota, Nevada, and now Nebraska in 2019 alone. The District of Columbia, Massachusetts, New Jersey, and Rhode Island are expected to follow suit.
A 2-month-old infant with a scalp rash that appeared after birth
With the perinatal history of prolonged labor and prolonged rupture of membranes, the diagnosis of halo scalp ring was made. This occurs secondary to prolonged pressure of the baby’s scalp with the mother’s pelvic bones, uterus, or cervical area, which causes decreased blood flow to the area, secondary ischemic damage, and in some cases scarring and hair loss.1
The degree of involvement is variable as some babies have mild alopecia and others have severe full-thickness necrosis and scarring. These lesions also can present with associated caput succedaneum and scalp molding, but these were not seen in our patient. Predisposing factors for halo scalp ring include caput succedaneum, prolonged or difficult labor, premature or prolonged rupture of membranes, vaginal delivery, vertex presentation, first delivery, as well as prematurity.2 On physical examination, a semicircular patch of alopecia with associated scarring, crusting, or erythema can be seen in some more severe cases.
The differential diagnosis includes aplasia cutis. In aplasia cutis, there is congenital loss of skin on the affected areas. The scalp usually is affected, but these lesions can occur in any other part of the body. Most patients with aplasia cutis have no other findings, but there are cases that can be associated with other cardiovascular, gastrointestinal, or central nervous system abnormalities. Neonatal lupus also can present with scarring lesions on the scalp, but they usually present a little after birth, mainly affecting the face. The mothers of this children usually have a diagnosis of connective tissue disease and may have positive antibodies to Sjögren’s syndrome antibody A, Sjögren’s syndrome antibody B, or antiribonucleoprotein antibody. Seborrheic dermatitis does not cause scarring alopecia. The lesions present as waxy scaly plaques on the scalp, erythematous waxy plaques behind the ears, face, and folds. Some patients can have hair loss secondary to the inflammation, but the hair grows back once the inflammation is controlled. Dissecting cellulitis is a type of scarring alopecia seen in pubescent and adult individuals. No cases of neonatal dissecting cellulitis have been described.
Halo scalp ring is not associated with any other systemic symptoms or syndromes. Extensive imaging and systemic work-up are not required unless the baby presents with other neurologic symptoms. The areas can be treated with petrolatum and observation as most lesions resolve.
In cases of extensive areas of scarring alopecia, referral to a plastic surgeon can be made to consider tissue expanders or scar revision prior to the child starting school if the lesions are causing psychological stressors.
The true prevalence of this condition is unknown. We believe halo ring alopecia is sometimes not diagnosed, and as lesions tend to resolve, most cases go unreported.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].
References
1. Arch Pediatr Adolesc Med. 2010;164(7):673.
2. Pediatr Dermatol. 2009 Nov-Dec;26(6):706-8.
3. Dermatol Online J. 2016 Nov 15;22(11).pii:13030/qt7rt592tz.
With the perinatal history of prolonged labor and prolonged rupture of membranes, the diagnosis of halo scalp ring was made. This occurs secondary to prolonged pressure of the baby’s scalp with the mother’s pelvic bones, uterus, or cervical area, which causes decreased blood flow to the area, secondary ischemic damage, and in some cases scarring and hair loss.1
The degree of involvement is variable as some babies have mild alopecia and others have severe full-thickness necrosis and scarring. These lesions also can present with associated caput succedaneum and scalp molding, but these were not seen in our patient. Predisposing factors for halo scalp ring include caput succedaneum, prolonged or difficult labor, premature or prolonged rupture of membranes, vaginal delivery, vertex presentation, first delivery, as well as prematurity.2 On physical examination, a semicircular patch of alopecia with associated scarring, crusting, or erythema can be seen in some more severe cases.
The differential diagnosis includes aplasia cutis. In aplasia cutis, there is congenital loss of skin on the affected areas. The scalp usually is affected, but these lesions can occur in any other part of the body. Most patients with aplasia cutis have no other findings, but there are cases that can be associated with other cardiovascular, gastrointestinal, or central nervous system abnormalities. Neonatal lupus also can present with scarring lesions on the scalp, but they usually present a little after birth, mainly affecting the face. The mothers of this children usually have a diagnosis of connective tissue disease and may have positive antibodies to Sjögren’s syndrome antibody A, Sjögren’s syndrome antibody B, or antiribonucleoprotein antibody. Seborrheic dermatitis does not cause scarring alopecia. The lesions present as waxy scaly plaques on the scalp, erythematous waxy plaques behind the ears, face, and folds. Some patients can have hair loss secondary to the inflammation, but the hair grows back once the inflammation is controlled. Dissecting cellulitis is a type of scarring alopecia seen in pubescent and adult individuals. No cases of neonatal dissecting cellulitis have been described.
Halo scalp ring is not associated with any other systemic symptoms or syndromes. Extensive imaging and systemic work-up are not required unless the baby presents with other neurologic symptoms. The areas can be treated with petrolatum and observation as most lesions resolve.
In cases of extensive areas of scarring alopecia, referral to a plastic surgeon can be made to consider tissue expanders or scar revision prior to the child starting school if the lesions are causing psychological stressors.
The true prevalence of this condition is unknown. We believe halo ring alopecia is sometimes not diagnosed, and as lesions tend to resolve, most cases go unreported.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].
References
1. Arch Pediatr Adolesc Med. 2010;164(7):673.
2. Pediatr Dermatol. 2009 Nov-Dec;26(6):706-8.
3. Dermatol Online J. 2016 Nov 15;22(11).pii:13030/qt7rt592tz.
With the perinatal history of prolonged labor and prolonged rupture of membranes, the diagnosis of halo scalp ring was made. This occurs secondary to prolonged pressure of the baby’s scalp with the mother’s pelvic bones, uterus, or cervical area, which causes decreased blood flow to the area, secondary ischemic damage, and in some cases scarring and hair loss.1
The degree of involvement is variable as some babies have mild alopecia and others have severe full-thickness necrosis and scarring. These lesions also can present with associated caput succedaneum and scalp molding, but these were not seen in our patient. Predisposing factors for halo scalp ring include caput succedaneum, prolonged or difficult labor, premature or prolonged rupture of membranes, vaginal delivery, vertex presentation, first delivery, as well as prematurity.2 On physical examination, a semicircular patch of alopecia with associated scarring, crusting, or erythema can be seen in some more severe cases.
The differential diagnosis includes aplasia cutis. In aplasia cutis, there is congenital loss of skin on the affected areas. The scalp usually is affected, but these lesions can occur in any other part of the body. Most patients with aplasia cutis have no other findings, but there are cases that can be associated with other cardiovascular, gastrointestinal, or central nervous system abnormalities. Neonatal lupus also can present with scarring lesions on the scalp, but they usually present a little after birth, mainly affecting the face. The mothers of this children usually have a diagnosis of connective tissue disease and may have positive antibodies to Sjögren’s syndrome antibody A, Sjögren’s syndrome antibody B, or antiribonucleoprotein antibody. Seborrheic dermatitis does not cause scarring alopecia. The lesions present as waxy scaly plaques on the scalp, erythematous waxy plaques behind the ears, face, and folds. Some patients can have hair loss secondary to the inflammation, but the hair grows back once the inflammation is controlled. Dissecting cellulitis is a type of scarring alopecia seen in pubescent and adult individuals. No cases of neonatal dissecting cellulitis have been described.
Halo scalp ring is not associated with any other systemic symptoms or syndromes. Extensive imaging and systemic work-up are not required unless the baby presents with other neurologic symptoms. The areas can be treated with petrolatum and observation as most lesions resolve.
In cases of extensive areas of scarring alopecia, referral to a plastic surgeon can be made to consider tissue expanders or scar revision prior to the child starting school if the lesions are causing psychological stressors.
The true prevalence of this condition is unknown. We believe halo ring alopecia is sometimes not diagnosed, and as lesions tend to resolve, most cases go unreported.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].
References
1. Arch Pediatr Adolesc Med. 2010;164(7):673.
2. Pediatr Dermatol. 2009 Nov-Dec;26(6):706-8.
3. Dermatol Online J. 2016 Nov 15;22(11).pii:13030/qt7rt592tz.
A 2-month-old male is referred to our pediatric dermatology clinic for evaluation of persistent seborrheic dermatitis. The mother reports that he presented with a rash on his scalp a few days after birth. She has been treating the crusted areas with clotrimazole and hydrocortisone and has noted improvement on the crusting, but now is worried that there is some scarring. The affected areas are not bleeding or tender. There are no other rashes elsewhere in the body.
He was born at 36 weeks from a 35-year-old gravida 1 para 0 woman with adequate prenatal care. The mother was diagnosed with preeclampsia and was induced. She had a prolonged labor and had premature rupture of membranes. The baby was delivered via cesarean section because of failure to progress and fetal distress; forceps, vacuum, and a scalp probe were not used during delivery. He was admitted to the neonatal unit for 5 days for sepsis work-up and respiratory distress. No intubation was needed.
Besides the preeclampsia, the mother denied any other medical conditions and was not taking any medications. He has met all developmental milestones for his age. He has no history of seizures.
On physical exam, there are semicircular patches of alopecia on the scalp. Some areas have pink, rubbery plaques with loss of hair follicles. On the frontal scalp, there are waxy plaques.
There is a blanchable violaceous patch on the occiput and there are some erythematous papules on the cheeks.
Boiling Points
This 37-year-old woman began developing “boils” under both arms at age 12. Over the years, the lesions have become more numerous and bothersome. They are often painful and large and are capable of bursting on their own, releasing purulent material. Occasionally, similar lesions appear under her breasts and in the groin. The problem seems to wax and wane with her menstrual cycle. Family history reveals that both her mother and one of her sisters have had the same problem, again starting around the time of menarche.
Whenever the patient seeks medical care, usually at the emergency department, the diagnosis is always the same: boils. Normally, the prescribed treatment includes incision, drainage, and packing of the largest lesions, followed by 2 weeks of oral antibiotics. While the problem generally improves after treatment, it invariably returns.
Her health is decent overall. However, she has been overweight for years and has been smoking since she was 14.
EXAMINATION
The patient’s left axilla shows ropy, hypertrophic scars, many comedones, and several fluctuant cystic subcutaneous masses. There is no frank erythema, although the patient indicates there often is.
No such changes are seen on examination of her right axilla. Instead, there is a slender 12-cm linear scar running across the axillary fold. Upon questioning, the patient reports that several years ago, a surgeon removed three-fourths of the skin and subcutaneous tissue from this area. This procedure cured the “boils” on her right arm, but it also left her with chronic lymphedema in that extremity.
Other intertriginous areas are free of significant changes.
What’s the diagnosis?
DISCUSSION
In the US, hidradenitis suppurativa (HS) affects 1% to 4% of the population and about 4 times as many females as males. But as this case demonstrates, it is consistently misidentified as “boils” or “staph infection” by providers unfamiliar with the correct diagnosis.
HS involves hair follicles in intertriginous areas of the body that are rich with apocrine glands (eg, armpit, groin). The condition, initially known as acne inversa, was first described in 1833 by Dr. Alfred Velpeau, a French surgeon. Despite some minor similarities, HS is not actually a form of acne, nor is it an infection. About one-third of HS patients inherit the condition, and generally, onset occurs post puberty, suggesting a hormonal component.
With HS, the hair follicle and associated apocrine gland fail to function normally. As sweat accumulates in subcutaneous tissue, it creates a chronic inflammatory reaction manifesting with large comedones, cysts, and abscesses. Eventually, it can result in ropy, hypertrophic scars on the surface and deep tracts connecting multiple lesions. HS is classified as mild (stage 1), moderate (stage 2), or severe (stage 3) using the Hurley staging system.
HS is notoriously difficult to cure, but the anti-inflammatory effects of some antibiotics (eg, minocycline, doxycycline) can offer some relief, as can anti-androgens (eg, spironolactone). The use of isotretinoin has yielded disappointing results. For small lesions, intralesional injection of glucocorticoids can be useful for short-term relief of pain and swelling.
The most encouraging recent development in HS treatment is the approval for the use of adalimumab (Humira) in severe cases that have failed to respond to other modalities. Even with use of this biologic, decent control is probably the best outcome—and that’s at an annual cost of $50,000, plus the patient’s exposure to potentially serious adverse effects due to immunosuppression.
Another approach is surgical, with all its attendant risks, as this patient experienced in her right axilla. Simple incision and drainage offer little beyond temporary relief of pain.
Environmental factors should not be overlooked; obesity and smoking have both been linked to HS in multiple studies.
TAKE-HOME LEARNING POINTS
- Hidradenitis suppurativa, also known as acne inversa, results from malfunction of the hair follicle and associated apocrine glands in intertriginous areas.
- HS can range from mild (with minor pustules and sparse comedones) to and severe (diffuse disease, affecting multiple areas with heavy ropy scarring, large painful abscesses, and connecting tracts).
- HS affects approximately 4 times as many females as males, almost all with post-pubertal onset—strongly suggestive of a hormonal component.
- Treatment is problematic, although the recent approval of adalimumab for use in HS is proving to be helpful, if not curative. Some oral antibiotics and anti-androgens have shown mixed results.
This 37-year-old woman began developing “boils” under both arms at age 12. Over the years, the lesions have become more numerous and bothersome. They are often painful and large and are capable of bursting on their own, releasing purulent material. Occasionally, similar lesions appear under her breasts and in the groin. The problem seems to wax and wane with her menstrual cycle. Family history reveals that both her mother and one of her sisters have had the same problem, again starting around the time of menarche.
Whenever the patient seeks medical care, usually at the emergency department, the diagnosis is always the same: boils. Normally, the prescribed treatment includes incision, drainage, and packing of the largest lesions, followed by 2 weeks of oral antibiotics. While the problem generally improves after treatment, it invariably returns.
Her health is decent overall. However, she has been overweight for years and has been smoking since she was 14.
EXAMINATION
The patient’s left axilla shows ropy, hypertrophic scars, many comedones, and several fluctuant cystic subcutaneous masses. There is no frank erythema, although the patient indicates there often is.
No such changes are seen on examination of her right axilla. Instead, there is a slender 12-cm linear scar running across the axillary fold. Upon questioning, the patient reports that several years ago, a surgeon removed three-fourths of the skin and subcutaneous tissue from this area. This procedure cured the “boils” on her right arm, but it also left her with chronic lymphedema in that extremity.
Other intertriginous areas are free of significant changes.
What’s the diagnosis?
DISCUSSION
In the US, hidradenitis suppurativa (HS) affects 1% to 4% of the population and about 4 times as many females as males. But as this case demonstrates, it is consistently misidentified as “boils” or “staph infection” by providers unfamiliar with the correct diagnosis.
HS involves hair follicles in intertriginous areas of the body that are rich with apocrine glands (eg, armpit, groin). The condition, initially known as acne inversa, was first described in 1833 by Dr. Alfred Velpeau, a French surgeon. Despite some minor similarities, HS is not actually a form of acne, nor is it an infection. About one-third of HS patients inherit the condition, and generally, onset occurs post puberty, suggesting a hormonal component.
With HS, the hair follicle and associated apocrine gland fail to function normally. As sweat accumulates in subcutaneous tissue, it creates a chronic inflammatory reaction manifesting with large comedones, cysts, and abscesses. Eventually, it can result in ropy, hypertrophic scars on the surface and deep tracts connecting multiple lesions. HS is classified as mild (stage 1), moderate (stage 2), or severe (stage 3) using the Hurley staging system.
HS is notoriously difficult to cure, but the anti-inflammatory effects of some antibiotics (eg, minocycline, doxycycline) can offer some relief, as can anti-androgens (eg, spironolactone). The use of isotretinoin has yielded disappointing results. For small lesions, intralesional injection of glucocorticoids can be useful for short-term relief of pain and swelling.
The most encouraging recent development in HS treatment is the approval for the use of adalimumab (Humira) in severe cases that have failed to respond to other modalities. Even with use of this biologic, decent control is probably the best outcome—and that’s at an annual cost of $50,000, plus the patient’s exposure to potentially serious adverse effects due to immunosuppression.
Another approach is surgical, with all its attendant risks, as this patient experienced in her right axilla. Simple incision and drainage offer little beyond temporary relief of pain.
Environmental factors should not be overlooked; obesity and smoking have both been linked to HS in multiple studies.
TAKE-HOME LEARNING POINTS
- Hidradenitis suppurativa, also known as acne inversa, results from malfunction of the hair follicle and associated apocrine glands in intertriginous areas.
- HS can range from mild (with minor pustules and sparse comedones) to and severe (diffuse disease, affecting multiple areas with heavy ropy scarring, large painful abscesses, and connecting tracts).
- HS affects approximately 4 times as many females as males, almost all with post-pubertal onset—strongly suggestive of a hormonal component.
- Treatment is problematic, although the recent approval of adalimumab for use in HS is proving to be helpful, if not curative. Some oral antibiotics and anti-androgens have shown mixed results.
This 37-year-old woman began developing “boils” under both arms at age 12. Over the years, the lesions have become more numerous and bothersome. They are often painful and large and are capable of bursting on their own, releasing purulent material. Occasionally, similar lesions appear under her breasts and in the groin. The problem seems to wax and wane with her menstrual cycle. Family history reveals that both her mother and one of her sisters have had the same problem, again starting around the time of menarche.
Whenever the patient seeks medical care, usually at the emergency department, the diagnosis is always the same: boils. Normally, the prescribed treatment includes incision, drainage, and packing of the largest lesions, followed by 2 weeks of oral antibiotics. While the problem generally improves after treatment, it invariably returns.
Her health is decent overall. However, she has been overweight for years and has been smoking since she was 14.
EXAMINATION
The patient’s left axilla shows ropy, hypertrophic scars, many comedones, and several fluctuant cystic subcutaneous masses. There is no frank erythema, although the patient indicates there often is.
No such changes are seen on examination of her right axilla. Instead, there is a slender 12-cm linear scar running across the axillary fold. Upon questioning, the patient reports that several years ago, a surgeon removed three-fourths of the skin and subcutaneous tissue from this area. This procedure cured the “boils” on her right arm, but it also left her with chronic lymphedema in that extremity.
Other intertriginous areas are free of significant changes.
What’s the diagnosis?
DISCUSSION
In the US, hidradenitis suppurativa (HS) affects 1% to 4% of the population and about 4 times as many females as males. But as this case demonstrates, it is consistently misidentified as “boils” or “staph infection” by providers unfamiliar with the correct diagnosis.
HS involves hair follicles in intertriginous areas of the body that are rich with apocrine glands (eg, armpit, groin). The condition, initially known as acne inversa, was first described in 1833 by Dr. Alfred Velpeau, a French surgeon. Despite some minor similarities, HS is not actually a form of acne, nor is it an infection. About one-third of HS patients inherit the condition, and generally, onset occurs post puberty, suggesting a hormonal component.
With HS, the hair follicle and associated apocrine gland fail to function normally. As sweat accumulates in subcutaneous tissue, it creates a chronic inflammatory reaction manifesting with large comedones, cysts, and abscesses. Eventually, it can result in ropy, hypertrophic scars on the surface and deep tracts connecting multiple lesions. HS is classified as mild (stage 1), moderate (stage 2), or severe (stage 3) using the Hurley staging system.
HS is notoriously difficult to cure, but the anti-inflammatory effects of some antibiotics (eg, minocycline, doxycycline) can offer some relief, as can anti-androgens (eg, spironolactone). The use of isotretinoin has yielded disappointing results. For small lesions, intralesional injection of glucocorticoids can be useful for short-term relief of pain and swelling.
The most encouraging recent development in HS treatment is the approval for the use of adalimumab (Humira) in severe cases that have failed to respond to other modalities. Even with use of this biologic, decent control is probably the best outcome—and that’s at an annual cost of $50,000, plus the patient’s exposure to potentially serious adverse effects due to immunosuppression.
Another approach is surgical, with all its attendant risks, as this patient experienced in her right axilla. Simple incision and drainage offer little beyond temporary relief of pain.
Environmental factors should not be overlooked; obesity and smoking have both been linked to HS in multiple studies.
TAKE-HOME LEARNING POINTS
- Hidradenitis suppurativa, also known as acne inversa, results from malfunction of the hair follicle and associated apocrine glands in intertriginous areas.
- HS can range from mild (with minor pustules and sparse comedones) to and severe (diffuse disease, affecting multiple areas with heavy ropy scarring, large painful abscesses, and connecting tracts).
- HS affects approximately 4 times as many females as males, almost all with post-pubertal onset—strongly suggestive of a hormonal component.
- Treatment is problematic, although the recent approval of adalimumab for use in HS is proving to be helpful, if not curative. Some oral antibiotics and anti-androgens have shown mixed results.
Tender swellings on legs
Based on the physical exam findings, the FP diagnosed erythema nodosum (EN) in this patient. He considered doing a punch biopsy down to the fat to prove that this was a panniculus, but realized that this was a classic presentation of EN. The lesions of EN are deep-seated nodules that may be more easily palpated than visualized. These lesions are initially firm, round or oval, and poorly demarcated. As seen in this case, the lesions may be bright red, warm, and painful.
The FP sought to consider the cause, and questioned the patient further about medications and other symptoms; however, he was unable to uncover any likely “suspects.” He then drew labs for a complete blood count, comprehensive metabolic panel, and uric acid and QuantiFERON TB gold tests. He started the patient on ibuprofen 400 mg tid with meals for the pain and inflammation.
On a follow-up visit 2 weeks later, all of the lab results were normal and the patient was about 50% improved. At this time, the FP obtained a chest x-ray to look for any evidence of sarcoidosis. The x-ray was also normal. (About half of all cases of EN are idiopathic, so the normal results were not surprising.) By the third visit the patient was 90% better and was happy to keep taking the ibuprofen to see if this would resolve completely.
After 6 weeks of treatment, there were no more tender erythematous nodules. All that remained was some postinflammatory hyperpigmentation. The patient was happy with these results and understood that she should return if the EN came back.
Photo courtesy of Hanuš Rozsypal, MD, and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
Based on the physical exam findings, the FP diagnosed erythema nodosum (EN) in this patient. He considered doing a punch biopsy down to the fat to prove that this was a panniculus, but realized that this was a classic presentation of EN. The lesions of EN are deep-seated nodules that may be more easily palpated than visualized. These lesions are initially firm, round or oval, and poorly demarcated. As seen in this case, the lesions may be bright red, warm, and painful.
The FP sought to consider the cause, and questioned the patient further about medications and other symptoms; however, he was unable to uncover any likely “suspects.” He then drew labs for a complete blood count, comprehensive metabolic panel, and uric acid and QuantiFERON TB gold tests. He started the patient on ibuprofen 400 mg tid with meals for the pain and inflammation.
On a follow-up visit 2 weeks later, all of the lab results were normal and the patient was about 50% improved. At this time, the FP obtained a chest x-ray to look for any evidence of sarcoidosis. The x-ray was also normal. (About half of all cases of EN are idiopathic, so the normal results were not surprising.) By the third visit the patient was 90% better and was happy to keep taking the ibuprofen to see if this would resolve completely.
After 6 weeks of treatment, there were no more tender erythematous nodules. All that remained was some postinflammatory hyperpigmentation. The patient was happy with these results and understood that she should return if the EN came back.
Photo courtesy of Hanuš Rozsypal, MD, and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
Based on the physical exam findings, the FP diagnosed erythema nodosum (EN) in this patient. He considered doing a punch biopsy down to the fat to prove that this was a panniculus, but realized that this was a classic presentation of EN. The lesions of EN are deep-seated nodules that may be more easily palpated than visualized. These lesions are initially firm, round or oval, and poorly demarcated. As seen in this case, the lesions may be bright red, warm, and painful.
The FP sought to consider the cause, and questioned the patient further about medications and other symptoms; however, he was unable to uncover any likely “suspects.” He then drew labs for a complete blood count, comprehensive metabolic panel, and uric acid and QuantiFERON TB gold tests. He started the patient on ibuprofen 400 mg tid with meals for the pain and inflammation.
On a follow-up visit 2 weeks later, all of the lab results were normal and the patient was about 50% improved. At this time, the FP obtained a chest x-ray to look for any evidence of sarcoidosis. The x-ray was also normal. (About half of all cases of EN are idiopathic, so the normal results were not surprising.) By the third visit the patient was 90% better and was happy to keep taking the ibuprofen to see if this would resolve completely.
After 6 weeks of treatment, there were no more tender erythematous nodules. All that remained was some postinflammatory hyperpigmentation. The patient was happy with these results and understood that she should return if the EN came back.
Photo courtesy of Hanuš Rozsypal, MD, and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ, Diaz L, Paulis R. Erythema nodosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1169-1173.
To learn more about the 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com