MDedge Dermatology

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×10⁹/L [reference range, 1.9–7.9×10⁹/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).^1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.^2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.² The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.⁴ Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.⁵ Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.^4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.^8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.⁴ Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.^10,11

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.⁵ The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.¹²

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.³ Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al¹³ identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.¹³ Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.^4,9,14,15 Thadepalli and Francis⁷ investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.⁷

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.¹ Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×10⁹/L [reference range, 1.9–7.9×10⁹/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).^1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.^2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.² The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.⁴ Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.⁵ Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.^4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.^8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.⁴ Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.^10,11

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.⁵ The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.¹²

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.³ Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al¹³ identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.¹³ Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.^4,9,14,15 Thadepalli and Francis⁷ investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.⁷

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.¹ Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×10⁹/L [reference range, 1.9–7.9×10⁹/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).^1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.^2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.² The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.⁴ Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.⁵ Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.^4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.^8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.⁴ Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.^10,11

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.⁵ The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.¹²

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.³ Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al¹³ identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.¹³ Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.^4,9,14,15 Thadepalli and Francis⁷ investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.⁷

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.¹ Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

A version of this article first appeared on Medscape.com.

A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

A version of this article first appeared on Medscape.com.

A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

A version of this article first appeared on Medscape.com.

At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

A version of this article first appeared on Medscape.com.

At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

A version of this article first appeared on Medscape.com.

At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

A version of this article first appeared on Medscape.com.

The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

A version of this article first appeared on WebMD.com.

The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

A version of this article first appeared on WebMD.com.

The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

A version of this article first appeared on WebMD.com.

To the Editor:

Generalized pustular psoriasis (GPP) is a rare but severe subtype of psoriasis that can present with systemic symptoms and organ failure, sometimes leading to hospitalization and even death.^1,2 Due to the rarity of this subtype and GPP being excluded from clinical trials for plaque psoriasis, there is limited information on the optimal treatment of this disease.

More than 20 systemic medications have been described in the literature for treating GPP, including systemic steroids, traditional immunosuppressants, retinoids, and biologics, which often are used in combination; none have been consistently effective.³ Among biologic therapies, the use of tumor necrosis factor α as well as IL-12/23 and IL-17 inhibitors has been reported, with the least amount of experience with IL-17 inhibitors.⁴

A 53-year-old Korean woman presented to the dermatology clinic for evaluation of a widespread painful rash involving the face, neck, torso, arms, and legs that had been treated intermittently with systemic steroids by her primary care physician for several months before presentation. She had no relevant medical or dermatologic history. She denied taking prescription or over-the-counter medications.

Physical examination revealed the patient was afebrile, but she reported general malaise and chills. She had widespread erythematous, annular, scaly plaques that coalesced into polycyclic plaques studded with nonfollicular-based pustules on the forehead, frontal hairline, neck, chest, abdomen, back, arms, and legs (Figure 1).

Two 4-mm punch biopsies were performed for hematoxylin and eosin staining and direct immunofluorescence. Histopathologic analysis showed prominent subcorneal neutrophilic pustules and spongiform collections of neutrophils in the spinous layer without notable eosinophils (Figure 2). Direct immunofluorescence was negative.

Based on the clinical history, physical examination, histopathology, and unremarkable drug history, a diagnosis of GPP was made. Initially, acitretin 25 mg/d was prescribed, but the patient was unable to start treatment because the cost of the drug was prohibitive. Her condition worsened, and she returned to the clinic 2 days later. Based on knowledge of an ongoing phase 3, open-label study for risankizumab in GPP, a sample of risankizumab 150 mg was administered subcutaneously in this patient. Three days later, most of the pustules on the upper half of the patient’s body had dried up and she began to desquamate from head to toe (Figure 3).The patient developed notable edema of the lower extremities, which required furosemide 20 mg/d andibuprofen 600 mg every 6 hours for symptom relief.

Ten days after the initial dose of risankizumab, the patient continued to steadily improve. All the pustules had dried up and she was already showing signs of re-epithelialization. Edema and pain also had notably improved. She received 2 additional samples of risankizumab 150 mg at weeks 4 and 16, at which point she was able to receive compassionate care through the drug manufacturer’s program. At follow-up 151 days after the initial dose of risankizumab, the patient’s skin was completely clear.

Generalized pustular psoriasis remains a difficult disease to study, given its rarity and unpredictable course. Spesolimab, a humanized anti–IL-36 receptor monoclonal antibody, was recently approved by the US Food and Drug Administration (FDA) for the treatment of GPP.⁵ In the pivotal trial (ClinicalTrials.gov Identifier NCT03782792),⁵ an astonishingly high 54% of patients (19/35) given a single dose of intravenous spesolimab reached the primary end point of no pustules at day 7. However, safety concerns, such as serious infections and severe cutaneous adverse reactions, as well as logistical challenges that come with intravenous administration for an acute disease, may prevent widespread adoption by community dermatologists.

Tumor necrosis factor α, IL-17, and IL-23 inhibitors currently are approved for the treatment of GPP in Japan, Thailand, and Taiwan based on small, nonrandomized, open-label studies.^6-10 More recently, results from a phase 3, randomized, open-label study to assess the efficacy and safety of 2 different dosing regimens of risankizumab with 8 Japanese patients with GPP were published.¹¹ However, there currently is only a single approved medication for GPP in Europe and the United States. Therefore, additional therapies, particularly those that have already been established in dermatology, would be welcome in treating this disease.

A number of questions still need to be answered regarding treating GPP with risankizumab:

• What is the optimal dose and schedule of this drug? Our patient received the standard 150-mg dose that is FDA approved for moderate to severe plaque psoriasis; would a higher dose, such as the FDA-approved 600-mg dosing used to treat Crohn disease, have led to a more rapid and durable response?¹²

• For how long should these patients be treated? Will their disease follow the same course as psoriasis vulgaris, requiring long-term, continuous treatment?

• An ongoing 5-year, open-label extension study of spesolimab might eventually answer that question and currently is recruiting participants (NCT03886246).

• Is there a way to predict a priori which patients will be responders? Biomarkers—especially through the use of tape stripping—are promising, but validation studies are still needed.¹³

• Because 69% (24/35) of enrolled patients in the treatment group of the spesolimab trial did not harbor a mutation of the IL36RN gene, how reliable is mutation status in predicting treatment response?⁵

Of note, some of these questions also apply to guttate psoriasis, a far more common subtype of psoriasis that also is worth exploring.

Nevertheless, these are exciting times for patients with GPP. What was once considered an obscure orphan disease is the focus of major recent publications³ and phase 3, randomized, placebo-controlled studies.⁵ We can be cautiously optimistic that in the next few years we will be in a better position to care for patients with GPP.

To the Editor:

Generalized pustular psoriasis (GPP) is a rare but severe subtype of psoriasis that can present with systemic symptoms and organ failure, sometimes leading to hospitalization and even death.^1,2 Due to the rarity of this subtype and GPP being excluded from clinical trials for plaque psoriasis, there is limited information on the optimal treatment of this disease.

More than 20 systemic medications have been described in the literature for treating GPP, including systemic steroids, traditional immunosuppressants, retinoids, and biologics, which often are used in combination; none have been consistently effective.³ Among biologic therapies, the use of tumor necrosis factor α as well as IL-12/23 and IL-17 inhibitors has been reported, with the least amount of experience with IL-17 inhibitors.⁴

A 53-year-old Korean woman presented to the dermatology clinic for evaluation of a widespread painful rash involving the face, neck, torso, arms, and legs that had been treated intermittently with systemic steroids by her primary care physician for several months before presentation. She had no relevant medical or dermatologic history. She denied taking prescription or over-the-counter medications.

Physical examination revealed the patient was afebrile, but she reported general malaise and chills. She had widespread erythematous, annular, scaly plaques that coalesced into polycyclic plaques studded with nonfollicular-based pustules on the forehead, frontal hairline, neck, chest, abdomen, back, arms, and legs (Figure 1).

Two 4-mm punch biopsies were performed for hematoxylin and eosin staining and direct immunofluorescence. Histopathologic analysis showed prominent subcorneal neutrophilic pustules and spongiform collections of neutrophils in the spinous layer without notable eosinophils (Figure 2). Direct immunofluorescence was negative.

Based on the clinical history, physical examination, histopathology, and unremarkable drug history, a diagnosis of GPP was made. Initially, acitretin 25 mg/d was prescribed, but the patient was unable to start treatment because the cost of the drug was prohibitive. Her condition worsened, and she returned to the clinic 2 days later. Based on knowledge of an ongoing phase 3, open-label study for risankizumab in GPP, a sample of risankizumab 150 mg was administered subcutaneously in this patient. Three days later, most of the pustules on the upper half of the patient’s body had dried up and she began to desquamate from head to toe (Figure 3).The patient developed notable edema of the lower extremities, which required furosemide 20 mg/d andibuprofen 600 mg every 6 hours for symptom relief.

Ten days after the initial dose of risankizumab, the patient continued to steadily improve. All the pustules had dried up and she was already showing signs of re-epithelialization. Edema and pain also had notably improved. She received 2 additional samples of risankizumab 150 mg at weeks 4 and 16, at which point she was able to receive compassionate care through the drug manufacturer’s program. At follow-up 151 days after the initial dose of risankizumab, the patient’s skin was completely clear.

Generalized pustular psoriasis remains a difficult disease to study, given its rarity and unpredictable course. Spesolimab, a humanized anti–IL-36 receptor monoclonal antibody, was recently approved by the US Food and Drug Administration (FDA) for the treatment of GPP.⁵ In the pivotal trial (ClinicalTrials.gov Identifier NCT03782792),⁵ an astonishingly high 54% of patients (19/35) given a single dose of intravenous spesolimab reached the primary end point of no pustules at day 7. However, safety concerns, such as serious infections and severe cutaneous adverse reactions, as well as logistical challenges that come with intravenous administration for an acute disease, may prevent widespread adoption by community dermatologists.

Tumor necrosis factor α, IL-17, and IL-23 inhibitors currently are approved for the treatment of GPP in Japan, Thailand, and Taiwan based on small, nonrandomized, open-label studies.^6-10 More recently, results from a phase 3, randomized, open-label study to assess the efficacy and safety of 2 different dosing regimens of risankizumab with 8 Japanese patients with GPP were published.¹¹ However, there currently is only a single approved medication for GPP in Europe and the United States. Therefore, additional therapies, particularly those that have already been established in dermatology, would be welcome in treating this disease.

A number of questions still need to be answered regarding treating GPP with risankizumab:

• What is the optimal dose and schedule of this drug? Our patient received the standard 150-mg dose that is FDA approved for moderate to severe plaque psoriasis; would a higher dose, such as the FDA-approved 600-mg dosing used to treat Crohn disease, have led to a more rapid and durable response?¹²

• For how long should these patients be treated? Will their disease follow the same course as psoriasis vulgaris, requiring long-term, continuous treatment?

• An ongoing 5-year, open-label extension study of spesolimab might eventually answer that question and currently is recruiting participants (NCT03886246).

• Is there a way to predict a priori which patients will be responders? Biomarkers—especially through the use of tape stripping—are promising, but validation studies are still needed.¹³

• Because 69% (24/35) of enrolled patients in the treatment group of the spesolimab trial did not harbor a mutation of the IL36RN gene, how reliable is mutation status in predicting treatment response?⁵

Of note, some of these questions also apply to guttate psoriasis, a far more common subtype of psoriasis that also is worth exploring.

Nevertheless, these are exciting times for patients with GPP. What was once considered an obscure orphan disease is the focus of major recent publications³ and phase 3, randomized, placebo-controlled studies.⁵ We can be cautiously optimistic that in the next few years we will be in a better position to care for patients with GPP.

To the Editor:

Generalized pustular psoriasis (GPP) is a rare but severe subtype of psoriasis that can present with systemic symptoms and organ failure, sometimes leading to hospitalization and even death.^1,2 Due to the rarity of this subtype and GPP being excluded from clinical trials for plaque psoriasis, there is limited information on the optimal treatment of this disease.

More than 20 systemic medications have been described in the literature for treating GPP, including systemic steroids, traditional immunosuppressants, retinoids, and biologics, which often are used in combination; none have been consistently effective.³ Among biologic therapies, the use of tumor necrosis factor α as well as IL-12/23 and IL-17 inhibitors has been reported, with the least amount of experience with IL-17 inhibitors.⁴

A 53-year-old Korean woman presented to the dermatology clinic for evaluation of a widespread painful rash involving the face, neck, torso, arms, and legs that had been treated intermittently with systemic steroids by her primary care physician for several months before presentation. She had no relevant medical or dermatologic history. She denied taking prescription or over-the-counter medications.

Physical examination revealed the patient was afebrile, but she reported general malaise and chills. She had widespread erythematous, annular, scaly plaques that coalesced into polycyclic plaques studded with nonfollicular-based pustules on the forehead, frontal hairline, neck, chest, abdomen, back, arms, and legs (Figure 1).

Two 4-mm punch biopsies were performed for hematoxylin and eosin staining and direct immunofluorescence. Histopathologic analysis showed prominent subcorneal neutrophilic pustules and spongiform collections of neutrophils in the spinous layer without notable eosinophils (Figure 2). Direct immunofluorescence was negative.

Based on the clinical history, physical examination, histopathology, and unremarkable drug history, a diagnosis of GPP was made. Initially, acitretin 25 mg/d was prescribed, but the patient was unable to start treatment because the cost of the drug was prohibitive. Her condition worsened, and she returned to the clinic 2 days later. Based on knowledge of an ongoing phase 3, open-label study for risankizumab in GPP, a sample of risankizumab 150 mg was administered subcutaneously in this patient. Three days later, most of the pustules on the upper half of the patient’s body had dried up and she began to desquamate from head to toe (Figure 3).The patient developed notable edema of the lower extremities, which required furosemide 20 mg/d andibuprofen 600 mg every 6 hours for symptom relief.

Ten days after the initial dose of risankizumab, the patient continued to steadily improve. All the pustules had dried up and she was already showing signs of re-epithelialization. Edema and pain also had notably improved. She received 2 additional samples of risankizumab 150 mg at weeks 4 and 16, at which point she was able to receive compassionate care through the drug manufacturer’s program. At follow-up 151 days after the initial dose of risankizumab, the patient’s skin was completely clear.

Generalized pustular psoriasis remains a difficult disease to study, given its rarity and unpredictable course. Spesolimab, a humanized anti–IL-36 receptor monoclonal antibody, was recently approved by the US Food and Drug Administration (FDA) for the treatment of GPP.⁵ In the pivotal trial (ClinicalTrials.gov Identifier NCT03782792),⁵ an astonishingly high 54% of patients (19/35) given a single dose of intravenous spesolimab reached the primary end point of no pustules at day 7. However, safety concerns, such as serious infections and severe cutaneous adverse reactions, as well as logistical challenges that come with intravenous administration for an acute disease, may prevent widespread adoption by community dermatologists.

Tumor necrosis factor α, IL-17, and IL-23 inhibitors currently are approved for the treatment of GPP in Japan, Thailand, and Taiwan based on small, nonrandomized, open-label studies.^6-10 More recently, results from a phase 3, randomized, open-label study to assess the efficacy and safety of 2 different dosing regimens of risankizumab with 8 Japanese patients with GPP were published.¹¹ However, there currently is only a single approved medication for GPP in Europe and the United States. Therefore, additional therapies, particularly those that have already been established in dermatology, would be welcome in treating this disease.

A number of questions still need to be answered regarding treating GPP with risankizumab:

• What is the optimal dose and schedule of this drug? Our patient received the standard 150-mg dose that is FDA approved for moderate to severe plaque psoriasis; would a higher dose, such as the FDA-approved 600-mg dosing used to treat Crohn disease, have led to a more rapid and durable response?¹²

• For how long should these patients be treated? Will their disease follow the same course as psoriasis vulgaris, requiring long-term, continuous treatment?

• An ongoing 5-year, open-label extension study of spesolimab might eventually answer that question and currently is recruiting participants (NCT03886246).

• Is there a way to predict a priori which patients will be responders? Biomarkers—especially through the use of tape stripping—are promising, but validation studies are still needed.¹³

• Because 69% (24/35) of enrolled patients in the treatment group of the spesolimab trial did not harbor a mutation of the IL36RN gene, how reliable is mutation status in predicting treatment response?⁵

Of note, some of these questions also apply to guttate psoriasis, a far more common subtype of psoriasis that also is worth exploring.

Nevertheless, these are exciting times for patients with GPP. What was once considered an obscure orphan disease is the focus of major recent publications³ and phase 3, randomized, placebo-controlled studies.⁵ We can be cautiously optimistic that in the next few years we will be in a better position to care for patients with GPP.

To the Editor:

Because the SARS-CoV-2 virus is constantly changing, routine vaccination to prevent COVID-19 infection is recommended. The messenger RNA (mRNA) vaccines from Pfizer-BioNTech and Moderna as well as the Ad26.COV2.S (Johnson & Johnson) and NVX-CoV2373 (Novavax) vaccines are the most commonly used COVID-19 vaccines in the United States. Adverse effects following vaccination against SARS-CoV-2 are well documented; recent studies report a small incidence of adverse effects in the general population, with most being minor (eg, headache, fever, muscle pain).^1,2 Interestingly, reports of exacerbation of psoriasis and new-onset psoriasis following COVID-19 vaccination suggest a potential association.^3,4 However, the literature investigating the vaccine adverse effect profile in this demographic is scarce. We examined the incidence of adverse effects from SARS-CoV-2 vaccines in patients with psoriasis.

This retrospective cohort study used the COVID-19 Research Database (https://covid19researchdatabase.org/) to examine the adverse effects following the first and second doses of the mRNA vaccines in patients with and without psoriasis. The sample size for the Ad26.COV2.S vaccine was too small to analyze.

Claims were evaluated from August to October 2021 for 2 diagnoses of psoriasis prior to January 1, 2020, using the International Classification of Diseases, Tenth Revision (ICD-10) code L40.9 to increase the positive predictive value and ensure that the diagnosis preceded the COVID-19 pandemic. Patients younger than 18 years and those who did not receive 2 doses of a SARS-CoV-2 vaccine were excluded. Controls who did not have a diagnosis of psoriasis were matched for age, sex, and hypertension at a 4:1 ratio. Hypertension represented the most common comorbidity that could feasibly be controlled for in this study population. Other comorbidities recorded included obesity, type 2 diabetes mellitus, congestive heart failure, asthma, chronic obstructive pulmonary disease, chronic ischemic heart disease, rhinitis, and chronic kidney disease.

Common adverse effects as long as 30 days after vaccination were identified using ICD-10 codes. Adverse effects of interest were anaphylactic reaction, initial encounter of adverse effect of viral vaccines, fever, allergic urticaria, weakness, altered mental status, malaise, allergic reaction, chest pain, symptoms involving circulatory or respiratory systems, localized rash, axillary lymphadenopathy, infection, and myocarditis.⁵ Poisson regression was performed using Stata 17 analytical software.

We identified 4273 patients with psoriasis and 17,092 controls who received mRNA COVID-19 vaccines (Table). Adjusted odds ratios (aORs) for doses 1 and 2 were calculated for each vaccine (eTable). Adverse effects with sufficient data to generate an aOR included weakness, altered mental status, malaise, chest pain, and symptoms involving the circulatory or respiratory system. The aORs for allergic urticaria and initial encounter of adverse effect of viral vaccines were only calculated for the Moderna mRNA vaccine due to low sample size.

This study demonstrated that patients with psoriasis do not appear to have a significantly increased risk of adverse effects from mRNA SARS-CoV-2 vaccines. Although the ORs in this study were not significant, most recorded adverse effects demonstrated an aOR less than 1, suggesting that there might be a lower risk of certain adverse effects in psoriasis patients. This could be explained by the immunomodulatory effects of certain systemic psoriasis treatments that might influence the adverse effect presentation.

The study is limited by the lack of treatment data, small sample size, and the fact that it did not assess flares or worsening of psoriasis with the vaccines. Underreporting of adverse effects by patients and underdiagnosis of adverse effects secondary to SARS-CoV-2 vaccines due to its novel nature, incompletely understood consequences, and limited ICD-10 codes associated with adverse effects all contributed to the small sample size.

Our findings suggest that the risk for immediate adverse effects from the mRNA SARS-CoV-2 vaccines is not increased among psoriasis patients. However, the impact of immunomodulatory agents on vaccine efficacy and expected adverse effects should be investigated. As more individuals receive the COVID-19 vaccine, the adverse effect profile in patients with psoriasis is an important area of investigation.

To the Editor:

Because the SARS-CoV-2 virus is constantly changing, routine vaccination to prevent COVID-19 infection is recommended. The messenger RNA (mRNA) vaccines from Pfizer-BioNTech and Moderna as well as the Ad26.COV2.S (Johnson & Johnson) and NVX-CoV2373 (Novavax) vaccines are the most commonly used COVID-19 vaccines in the United States. Adverse effects following vaccination against SARS-CoV-2 are well documented; recent studies report a small incidence of adverse effects in the general population, with most being minor (eg, headache, fever, muscle pain).^1,2 Interestingly, reports of exacerbation of psoriasis and new-onset psoriasis following COVID-19 vaccination suggest a potential association.^3,4 However, the literature investigating the vaccine adverse effect profile in this demographic is scarce. We examined the incidence of adverse effects from SARS-CoV-2 vaccines in patients with psoriasis.

This retrospective cohort study used the COVID-19 Research Database (https://covid19researchdatabase.org/) to examine the adverse effects following the first and second doses of the mRNA vaccines in patients with and without psoriasis. The sample size for the Ad26.COV2.S vaccine was too small to analyze.

Claims were evaluated from August to October 2021 for 2 diagnoses of psoriasis prior to January 1, 2020, using the International Classification of Diseases, Tenth Revision (ICD-10) code L40.9 to increase the positive predictive value and ensure that the diagnosis preceded the COVID-19 pandemic. Patients younger than 18 years and those who did not receive 2 doses of a SARS-CoV-2 vaccine were excluded. Controls who did not have a diagnosis of psoriasis were matched for age, sex, and hypertension at a 4:1 ratio. Hypertension represented the most common comorbidity that could feasibly be controlled for in this study population. Other comorbidities recorded included obesity, type 2 diabetes mellitus, congestive heart failure, asthma, chronic obstructive pulmonary disease, chronic ischemic heart disease, rhinitis, and chronic kidney disease.

Common adverse effects as long as 30 days after vaccination were identified using ICD-10 codes. Adverse effects of interest were anaphylactic reaction, initial encounter of adverse effect of viral vaccines, fever, allergic urticaria, weakness, altered mental status, malaise, allergic reaction, chest pain, symptoms involving circulatory or respiratory systems, localized rash, axillary lymphadenopathy, infection, and myocarditis.⁵ Poisson regression was performed using Stata 17 analytical software.

We identified 4273 patients with psoriasis and 17,092 controls who received mRNA COVID-19 vaccines (Table). Adjusted odds ratios (aORs) for doses 1 and 2 were calculated for each vaccine (eTable). Adverse effects with sufficient data to generate an aOR included weakness, altered mental status, malaise, chest pain, and symptoms involving the circulatory or respiratory system. The aORs for allergic urticaria and initial encounter of adverse effect of viral vaccines were only calculated for the Moderna mRNA vaccine due to low sample size.

This study demonstrated that patients with psoriasis do not appear to have a significantly increased risk of adverse effects from mRNA SARS-CoV-2 vaccines. Although the ORs in this study were not significant, most recorded adverse effects demonstrated an aOR less than 1, suggesting that there might be a lower risk of certain adverse effects in psoriasis patients. This could be explained by the immunomodulatory effects of certain systemic psoriasis treatments that might influence the adverse effect presentation.

The study is limited by the lack of treatment data, small sample size, and the fact that it did not assess flares or worsening of psoriasis with the vaccines. Underreporting of adverse effects by patients and underdiagnosis of adverse effects secondary to SARS-CoV-2 vaccines due to its novel nature, incompletely understood consequences, and limited ICD-10 codes associated with adverse effects all contributed to the small sample size.

Our findings suggest that the risk for immediate adverse effects from the mRNA SARS-CoV-2 vaccines is not increased among psoriasis patients. However, the impact of immunomodulatory agents on vaccine efficacy and expected adverse effects should be investigated. As more individuals receive the COVID-19 vaccine, the adverse effect profile in patients with psoriasis is an important area of investigation.

To the Editor:

Because the SARS-CoV-2 virus is constantly changing, routine vaccination to prevent COVID-19 infection is recommended. The messenger RNA (mRNA) vaccines from Pfizer-BioNTech and Moderna as well as the Ad26.COV2.S (Johnson & Johnson) and NVX-CoV2373 (Novavax) vaccines are the most commonly used COVID-19 vaccines in the United States. Adverse effects following vaccination against SARS-CoV-2 are well documented; recent studies report a small incidence of adverse effects in the general population, with most being minor (eg, headache, fever, muscle pain).^1,2 Interestingly, reports of exacerbation of psoriasis and new-onset psoriasis following COVID-19 vaccination suggest a potential association.^3,4 However, the literature investigating the vaccine adverse effect profile in this demographic is scarce. We examined the incidence of adverse effects from SARS-CoV-2 vaccines in patients with psoriasis.

This retrospective cohort study used the COVID-19 Research Database (https://covid19researchdatabase.org/) to examine the adverse effects following the first and second doses of the mRNA vaccines in patients with and without psoriasis. The sample size for the Ad26.COV2.S vaccine was too small to analyze.

Claims were evaluated from August to October 2021 for 2 diagnoses of psoriasis prior to January 1, 2020, using the International Classification of Diseases, Tenth Revision (ICD-10) code L40.9 to increase the positive predictive value and ensure that the diagnosis preceded the COVID-19 pandemic. Patients younger than 18 years and those who did not receive 2 doses of a SARS-CoV-2 vaccine were excluded. Controls who did not have a diagnosis of psoriasis were matched for age, sex, and hypertension at a 4:1 ratio. Hypertension represented the most common comorbidity that could feasibly be controlled for in this study population. Other comorbidities recorded included obesity, type 2 diabetes mellitus, congestive heart failure, asthma, chronic obstructive pulmonary disease, chronic ischemic heart disease, rhinitis, and chronic kidney disease.

Common adverse effects as long as 30 days after vaccination were identified using ICD-10 codes. Adverse effects of interest were anaphylactic reaction, initial encounter of adverse effect of viral vaccines, fever, allergic urticaria, weakness, altered mental status, malaise, allergic reaction, chest pain, symptoms involving circulatory or respiratory systems, localized rash, axillary lymphadenopathy, infection, and myocarditis.⁵ Poisson regression was performed using Stata 17 analytical software.

We identified 4273 patients with psoriasis and 17,092 controls who received mRNA COVID-19 vaccines (Table). Adjusted odds ratios (aORs) for doses 1 and 2 were calculated for each vaccine (eTable). Adverse effects with sufficient data to generate an aOR included weakness, altered mental status, malaise, chest pain, and symptoms involving the circulatory or respiratory system. The aORs for allergic urticaria and initial encounter of adverse effect of viral vaccines were only calculated for the Moderna mRNA vaccine due to low sample size.

This study demonstrated that patients with psoriasis do not appear to have a significantly increased risk of adverse effects from mRNA SARS-CoV-2 vaccines. Although the ORs in this study were not significant, most recorded adverse effects demonstrated an aOR less than 1, suggesting that there might be a lower risk of certain adverse effects in psoriasis patients. This could be explained by the immunomodulatory effects of certain systemic psoriasis treatments that might influence the adverse effect presentation.

The study is limited by the lack of treatment data, small sample size, and the fact that it did not assess flares or worsening of psoriasis with the vaccines. Underreporting of adverse effects by patients and underdiagnosis of adverse effects secondary to SARS-CoV-2 vaccines due to its novel nature, incompletely understood consequences, and limited ICD-10 codes associated with adverse effects all contributed to the small sample size.

Our findings suggest that the risk for immediate adverse effects from the mRNA SARS-CoV-2 vaccines is not increased among psoriasis patients. However, the impact of immunomodulatory agents on vaccine efficacy and expected adverse effects should be investigated. As more individuals receive the COVID-19 vaccine, the adverse effect profile in patients with psoriasis is an important area of investigation.

Consultations and referrals are an important component of many dermatology practices. There are several families of consultation codes that can be utilized based on the setting and format of the patient encounter. In this article, I describe appropriate use of 3 families of consultation codes and recent updates in these areas.

Consultation Definitions

For all of these code sets, the same definition of consultationapplies—namely that the encounter is provided at the request of another physician, other qualified health care professional, or other appropriate source (eg, nonclinical social worker, educator, lawyer, insurance company) for a specific condition or problem. Importantly, a consultation initiated by a patient or family, or both, and not requested by one of the professionals listed above is not reported using a consultation code.¹

The consultant’s opinion and any services that were ordered or performed also must be communicated to the requesting provider. The type of communication required varies based on the consultation code set in question.

Outpatient Consultation Codes

Outpatient consultation CPT (Current Procedural Terminology) codes (99241-99245) are a family of codes that can be utilized for evaluation of a new patient or an existing patient with a new problem in the outpatient setting. These codes are not reimbursed by the Centers for Medicare & Medicaid Services, but some private payers do recognize and reimburse for them.²

The consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹ Modifier -32 should not be used for a second request by a patient or a patient’s family.¹

This family of codes has been revised in tandem with other evaluation and management (E/M) code sets; changes went into effect January 1, 2023. These updates are part of the ongoing effort to update code wording and structures to reflect guiding principles of the American Medical Association when redesigning E/M codes. These principles include decreasing administrative burden and the need for audits, decreasing unnecessary documentation that is not needed for patient care, and ensuring that payment for E/M is resource based.³ Updated code language and payment structure is found in Table 1.^1,2 The main updates to these codes include:

• Code 99241 was deleted. This was in line with removal of 99201 from the outpatient E/M family set.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 99417 can be utilized.

Inpatient Consultation Codes

Similar to the outpatient consultation codes, the inpatient consultation codes also have been revised as part of E/M updates; revisions went into effect January 1, 2023. Also, as with the outpatient consultation codes, the consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹

When inpatient consultations are performed, 2 code families generally are utilized. For initial consultation, initial inpatient consultation codes (99251-99255) are used; for any follow-up encounters performed while the patient is an inpatient, subsequent inpatient consultation codes (99231-99233) are used. The subsequent code family is the same that is utilized for all subsequent care within the inpatient or observation care setting, regardless of how the care was initiated.¹

“Initial service” is when the patient has not received any professional services from either the physician or other qualified health care professional or from another physician or other qualified health care professional ofthe exact same specialty and subspecialty who belongs to the same group practice during the inpatient, observation, or nursing facility admission and stay. “Subsequent service” is when the patient has received professional service(s) from either the physician or other qualified health care professional or from another physician or other qualified health care professional.¹ Updated code language and payment structure is found in Table 2.^1,2 Major changes include:

• Code 99251 was deleted. This is in line with deletion of a new low-level patient encounter in the outpatient E/M family set and consultation code family set, as noted above.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 993X0 can be utilized.

Interprofessional Consultation Codes

An additional code family that can be utilized for consultations is the interprofessional consultation codes. These codes can be utilized when assisting in the diagnosis or management, or both, of a patient without face-to-face contact. These codes are listed in Table 3.^2,4 For all of these codes, the consultation is performed by telephone, internet or electronic health record, or a combination of these means. The consultation can be for a new problem or a worsening existing problem. The patient can be a new or established patient to the consultant. Documentation should be performed in the patient’s medical record, including the reason for the request.

To bill for interprofessional consultation, the consultant should not have seen the patient in a face-to-face encounter within the prior 14 days or see them in the following 14 days. The codes should not be reported more than once in a 7-day period or more than once in a 14-day period in the case of code 99452.⁴ For codes 99446 to 99449, more than 50% of the time spent by the consulting physician must be devoted to verbal or internet discussion, or both, with the referring physician. For code 99451, service time is based on total review and interprofessional communication time.⁴ The correct code is chosen based on the following parameters:

• 99446-99449: Describes interprofessional consultation services, which include both a written and a verbal report to the patient’s treating or requesting physician or qualified health care professional. These codes can be utilized by a consulting physician. The correct code is chosen based on time spent by the consulting physician.

• 99451: Describes an interprofessional consultation service, which includes a written report to the patient’s treating or requesting physician or qualified health care professional. This code can be utilized by a consulting physician once 5 minutes of consultative discussion and review has been performed.

• 99452: Describes an interprofessional consultation service provided by the requesting physician. This code can be utilized when a requesting physician spends 16 to 30 minutes in medical consultative discussion and review.

Final Thoughts

Consultation codes can be an important part of a dermatologist’s practice. Differences exist between consultation code sets based on the encounter setting and whether the encounter was performed with or without face-to-face contact. In addition, updates to the E/M inpatient and outpatient consultation codes went into effect January 1, 2023. It is important to understand those changes to correctly bill for these encounters.

Consultations and referrals are an important component of many dermatology practices. There are several families of consultation codes that can be utilized based on the setting and format of the patient encounter. In this article, I describe appropriate use of 3 families of consultation codes and recent updates in these areas.

Consultation Definitions

For all of these code sets, the same definition of consultationapplies—namely that the encounter is provided at the request of another physician, other qualified health care professional, or other appropriate source (eg, nonclinical social worker, educator, lawyer, insurance company) for a specific condition or problem. Importantly, a consultation initiated by a patient or family, or both, and not requested by one of the professionals listed above is not reported using a consultation code.¹

The consultant’s opinion and any services that were ordered or performed also must be communicated to the requesting provider. The type of communication required varies based on the consultation code set in question.

Outpatient Consultation Codes

Outpatient consultation CPT (Current Procedural Terminology) codes (99241-99245) are a family of codes that can be utilized for evaluation of a new patient or an existing patient with a new problem in the outpatient setting. These codes are not reimbursed by the Centers for Medicare & Medicaid Services, but some private payers do recognize and reimburse for them.²

The consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹ Modifier -32 should not be used for a second request by a patient or a patient’s family.¹

This family of codes has been revised in tandem with other evaluation and management (E/M) code sets; changes went into effect January 1, 2023. These updates are part of the ongoing effort to update code wording and structures to reflect guiding principles of the American Medical Association when redesigning E/M codes. These principles include decreasing administrative burden and the need for audits, decreasing unnecessary documentation that is not needed for patient care, and ensuring that payment for E/M is resource based.³ Updated code language and payment structure is found in Table 1.^1,2 The main updates to these codes include:

• Code 99241 was deleted. This was in line with removal of 99201 from the outpatient E/M family set.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 99417 can be utilized.

Inpatient Consultation Codes

Similar to the outpatient consultation codes, the inpatient consultation codes also have been revised as part of E/M updates; revisions went into effect January 1, 2023. Also, as with the outpatient consultation codes, the consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹

When inpatient consultations are performed, 2 code families generally are utilized. For initial consultation, initial inpatient consultation codes (99251-99255) are used; for any follow-up encounters performed while the patient is an inpatient, subsequent inpatient consultation codes (99231-99233) are used. The subsequent code family is the same that is utilized for all subsequent care within the inpatient or observation care setting, regardless of how the care was initiated.¹

“Initial service” is when the patient has not received any professional services from either the physician or other qualified health care professional or from another physician or other qualified health care professional ofthe exact same specialty and subspecialty who belongs to the same group practice during the inpatient, observation, or nursing facility admission and stay. “Subsequent service” is when the patient has received professional service(s) from either the physician or other qualified health care professional or from another physician or other qualified health care professional.¹ Updated code language and payment structure is found in Table 2.^1,2 Major changes include:

• Code 99251 was deleted. This is in line with deletion of a new low-level patient encounter in the outpatient E/M family set and consultation code family set, as noted above.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 993X0 can be utilized.

Interprofessional Consultation Codes

An additional code family that can be utilized for consultations is the interprofessional consultation codes. These codes can be utilized when assisting in the diagnosis or management, or both, of a patient without face-to-face contact. These codes are listed in Table 3.^2,4 For all of these codes, the consultation is performed by telephone, internet or electronic health record, or a combination of these means. The consultation can be for a new problem or a worsening existing problem. The patient can be a new or established patient to the consultant. Documentation should be performed in the patient’s medical record, including the reason for the request.

To bill for interprofessional consultation, the consultant should not have seen the patient in a face-to-face encounter within the prior 14 days or see them in the following 14 days. The codes should not be reported more than once in a 7-day period or more than once in a 14-day period in the case of code 99452.⁴ For codes 99446 to 99449, more than 50% of the time spent by the consulting physician must be devoted to verbal or internet discussion, or both, with the referring physician. For code 99451, service time is based on total review and interprofessional communication time.⁴ The correct code is chosen based on the following parameters:

• 99446-99449: Describes interprofessional consultation services, which include both a written and a verbal report to the patient’s treating or requesting physician or qualified health care professional. These codes can be utilized by a consulting physician. The correct code is chosen based on time spent by the consulting physician.

• 99451: Describes an interprofessional consultation service, which includes a written report to the patient’s treating or requesting physician or qualified health care professional. This code can be utilized by a consulting physician once 5 minutes of consultative discussion and review has been performed.

• 99452: Describes an interprofessional consultation service provided by the requesting physician. This code can be utilized when a requesting physician spends 16 to 30 minutes in medical consultative discussion and review.

Final Thoughts

Consultation codes can be an important part of a dermatologist’s practice. Differences exist between consultation code sets based on the encounter setting and whether the encounter was performed with or without face-to-face contact. In addition, updates to the E/M inpatient and outpatient consultation codes went into effect January 1, 2023. It is important to understand those changes to correctly bill for these encounters.

Consultations and referrals are an important component of many dermatology practices. There are several families of consultation codes that can be utilized based on the setting and format of the patient encounter. In this article, I describe appropriate use of 3 families of consultation codes and recent updates in these areas.

Consultation Definitions

For all of these code sets, the same definition of consultationapplies—namely that the encounter is provided at the request of another physician, other qualified health care professional, or other appropriate source (eg, nonclinical social worker, educator, lawyer, insurance company) for a specific condition or problem. Importantly, a consultation initiated by a patient or family, or both, and not requested by one of the professionals listed above is not reported using a consultation code.¹

The consultant’s opinion and any services that were ordered or performed also must be communicated to the requesting provider. The type of communication required varies based on the consultation code set in question.

Outpatient Consultation Codes

Outpatient consultation CPT (Current Procedural Terminology) codes (99241-99245) are a family of codes that can be utilized for evaluation of a new patient or an existing patient with a new problem in the outpatient setting. These codes are not reimbursed by the Centers for Medicare & Medicaid Services, but some private payers do recognize and reimburse for them.²

The consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹ Modifier -32 should not be used for a second request by a patient or a patient’s family.¹

This family of codes has been revised in tandem with other evaluation and management (E/M) code sets; changes went into effect January 1, 2023. These updates are part of the ongoing effort to update code wording and structures to reflect guiding principles of the American Medical Association when redesigning E/M codes. These principles include decreasing administrative burden and the need for audits, decreasing unnecessary documentation that is not needed for patient care, and ensuring that payment for E/M is resource based.³ Updated code language and payment structure is found in Table 1.^1,2 The main updates to these codes include:

• Code 99241 was deleted. This was in line with removal of 99201 from the outpatient E/M family set.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 99417 can be utilized.

Inpatient Consultation Codes

Similar to the outpatient consultation codes, the inpatient consultation codes also have been revised as part of E/M updates; revisions went into effect January 1, 2023. Also, as with the outpatient consultation codes, the consultant’s opinion and any services that were ordered or performed must be communicated by written report to the requesting physician, other qualified health care professional, or other appropriate source. If a consultation is mandated (eg, by a third-party payer), then modifier -32 also should be reported.¹

When inpatient consultations are performed, 2 code families generally are utilized. For initial consultation, initial inpatient consultation codes (99251-99255) are used; for any follow-up encounters performed while the patient is an inpatient, subsequent inpatient consultation codes (99231-99233) are used. The subsequent code family is the same that is utilized for all subsequent care within the inpatient or observation care setting, regardless of how the care was initiated.¹

“Initial service” is when the patient has not received any professional services from either the physician or other qualified health care professional or from another physician or other qualified health care professional ofthe exact same specialty and subspecialty who belongs to the same group practice during the inpatient, observation, or nursing facility admission and stay. “Subsequent service” is when the patient has received professional service(s) from either the physician or other qualified health care professional or from another physician or other qualified health care professional.¹ Updated code language and payment structure is found in Table 2.^1,2 Major changes include:

• Code 99251 was deleted. This is in line with deletion of a new low-level patient encounter in the outpatient E/M family set and consultation code family set, as noted above.

• Level of service is now based solely on either time on the date of encounter or medical decision-making.

• Definitions regarding medical decision-making are in line with those utilized for outpatient E/M codes.

• If coding by time and the maximum amount of time has been exceeded by 15 or more minutes, prolonged services code 993X0 can be utilized.

Interprofessional Consultation Codes

An additional code family that can be utilized for consultations is the interprofessional consultation codes. These codes can be utilized when assisting in the diagnosis or management, or both, of a patient without face-to-face contact. These codes are listed in Table 3.^2,4 For all of these codes, the consultation is performed by telephone, internet or electronic health record, or a combination of these means. The consultation can be for a new problem or a worsening existing problem. The patient can be a new or established patient to the consultant. Documentation should be performed in the patient’s medical record, including the reason for the request.

To bill for interprofessional consultation, the consultant should not have seen the patient in a face-to-face encounter within the prior 14 days or see them in the following 14 days. The codes should not be reported more than once in a 7-day period or more than once in a 14-day period in the case of code 99452.⁴ For codes 99446 to 99449, more than 50% of the time spent by the consulting physician must be devoted to verbal or internet discussion, or both, with the referring physician. For code 99451, service time is based on total review and interprofessional communication time.⁴ The correct code is chosen based on the following parameters:

• 99446-99449: Describes interprofessional consultation services, which include both a written and a verbal report to the patient’s treating or requesting physician or qualified health care professional. These codes can be utilized by a consulting physician. The correct code is chosen based on time spent by the consulting physician.

• 99451: Describes an interprofessional consultation service, which includes a written report to the patient’s treating or requesting physician or qualified health care professional. This code can be utilized by a consulting physician once 5 minutes of consultative discussion and review has been performed.

• 99452: Describes an interprofessional consultation service provided by the requesting physician. This code can be utilized when a requesting physician spends 16 to 30 minutes in medical consultative discussion and review.

Final Thoughts

Consultation codes can be an important part of a dermatologist’s practice. Differences exist between consultation code sets based on the encounter setting and whether the encounter was performed with or without face-to-face contact. In addition, updates to the E/M inpatient and outpatient consultation codes went into effect January 1, 2023. It is important to understand those changes to correctly bill for these encounters.

New treatments for psoriasis constitute an embarrassment of riches compared to any other area of dermatology. Despite the many advances over the last 25 years, additional topical and systemic treatments have recently become available. Gosh, it’s great!

In May 2022, once-daily tapinarof cream 1% was approved for the topical treatment of plaque psoriasis in adults.¹ Tapinarof was identified as a metabolite made by bacteria symbiotic to a nematode, allowing the nematode to infect insects.² Tapinarof’s anti-inflammatory effect extends to mammals. The drug works by activating the aryl hydrocarbon receptor, downregulating proinflammatory cytokines such as IL-17, and normalizing the expression of skin barrier proteins such as filaggrin.² In two 12-week, phase 3, randomized trials with 510 and 515 patients, respectively, 35% to 40% of tapinarof-treated psoriasis patients were clear or almost clear compared with only 6% of patients in the placebo group. The drug appears safe; common adverse events (AEs) included folliculitis, nasopharyngitis, contact dermatitis, headache, upper respiratory tract infection, and pruritus.³

A second new topical treatment for plaque psoriasis was approved in July 2022—once-daily roflumilast 0.3% cream—for patients 12 years and older.⁴ Similar to apremilast, roflumilast is a phosphodiesterase 4 inhibitor that blocks the degradation of cAMP and reduces the downstream production of inflammatory molecules implicated in psoriasis.⁵ In two 8-week, phase 3 clinical trials (ClinicalTrials.gov Identifiers NCT04211363 and NCT04211389)(N=881), approximately 40% of roflumilast-treated patients were clear or almost clear vs approximately 6% in the placebo group. Topical roflumilast was well-tolerated; the most common AEs included diarrhea, headache, insomnia, nausea, application-site pain, upper respiratory tract infection, and urinary tract infection.⁶

We have so many patients—and many more people with psoriasis who are not yet patients—with limited psoriasis who would be amenable to topical treatment but who are not responding to current treatments. There is considerable enthusiasm for the new topicals, but it is still questionable how much they will help our patients. The main reason the current topicals fail is poor adherence to the treatment. If we give these new treatments to patients who used existing topicals and failed, thereby inadvertently selecting patients with poor adherence to topicals, it will be surprising if the new treatments live up to expectations. Perhaps tapinarof and roflumilast will revolutionize the management of localized psoriasis; perhaps their impact will be similar to topical crisaborole— exciting in trials and less practical in real life. It may be that apremilast, which is now approved for psoriasis of any severity, will make a bigger difference for patients who can access it for limited psoriasis.

Deucravacitinib is a once-daily oral selective tyrosine kinase 2 inhibitor that blocks IL-23 and type I interferon signaling. It was approved for adults with moderate to severe plaque psoriasis in September 2021.⁷ We know patients want oral treatment; they ask for apremilast even though injections may be much more potent. In a 16-week, phase 3 clinical trial comparing daily deucravacitinib (n=332), apremilast (n=168), and placebo (n=166), rates of clear or almost clear were approximately 55% in the deucravacitinib group, 32% in the apremilast group, and 7% with placebo. The most common AEs included nasopharyngitis, upper respiratory tract infection, headache, diarrhea, and nausea.⁸ Although deucravacitinib is much more effective than apremilast, deucravacitinib will require monitoring and may have some risk for viral reactivation of herpes simplex and zoster (and hopefully not much else). Whether physicians view it as a replacement for apremilast, which requires no laboratory monitoring, remains to be seen.

Bimekizumab, a humanized monoclonal IgG1 antibody expected to receive US Food and Drug Administration approval in the coming months, inhibits both IL-17A and IL-17F and may become our most effective treatment of psoriasis. Although we are probably not hungering for a more effective psoriasis treatment (given our current embarrassment of riches), bimekizumab’s remarkably high efficacy for psoriatic arthritis may be a quantum leap forward, especially if no new safety signals are identified; bimekizumab treatment is associated with a higher risk of oral candidiasis than other currently available IL-17 antagonists.⁹ Biosimilars may reduce the cost of psoriasis management to the health system, but it seems unlikely that biosimilars will allow us to help patients who we cannot already help with the existing extensive psoriasis treatment armamentarium.

New treatments for psoriasis constitute an embarrassment of riches compared to any other area of dermatology. Despite the many advances over the last 25 years, additional topical and systemic treatments have recently become available. Gosh, it’s great!

In May 2022, once-daily tapinarof cream 1% was approved for the topical treatment of plaque psoriasis in adults.¹ Tapinarof was identified as a metabolite made by bacteria symbiotic to a nematode, allowing the nematode to infect insects.² Tapinarof’s anti-inflammatory effect extends to mammals. The drug works by activating the aryl hydrocarbon receptor, downregulating proinflammatory cytokines such as IL-17, and normalizing the expression of skin barrier proteins such as filaggrin.² In two 12-week, phase 3, randomized trials with 510 and 515 patients, respectively, 35% to 40% of tapinarof-treated psoriasis patients were clear or almost clear compared with only 6% of patients in the placebo group. The drug appears safe; common adverse events (AEs) included folliculitis, nasopharyngitis, contact dermatitis, headache, upper respiratory tract infection, and pruritus.³

A second new topical treatment for plaque psoriasis was approved in July 2022—once-daily roflumilast 0.3% cream—for patients 12 years and older.⁴ Similar to apremilast, roflumilast is a phosphodiesterase 4 inhibitor that blocks the degradation of cAMP and reduces the downstream production of inflammatory molecules implicated in psoriasis.⁵ In two 8-week, phase 3 clinical trials (ClinicalTrials.gov Identifiers NCT04211363 and NCT04211389)(N=881), approximately 40% of roflumilast-treated patients were clear or almost clear vs approximately 6% in the placebo group. Topical roflumilast was well-tolerated; the most common AEs included diarrhea, headache, insomnia, nausea, application-site pain, upper respiratory tract infection, and urinary tract infection.⁶

We have so many patients—and many more people with psoriasis who are not yet patients—with limited psoriasis who would be amenable to topical treatment but who are not responding to current treatments. There is considerable enthusiasm for the new topicals, but it is still questionable how much they will help our patients. The main reason the current topicals fail is poor adherence to the treatment. If we give these new treatments to patients who used existing topicals and failed, thereby inadvertently selecting patients with poor adherence to topicals, it will be surprising if the new treatments live up to expectations. Perhaps tapinarof and roflumilast will revolutionize the management of localized psoriasis; perhaps their impact will be similar to topical crisaborole— exciting in trials and less practical in real life. It may be that apremilast, which is now approved for psoriasis of any severity, will make a bigger difference for patients who can access it for limited psoriasis.

Deucravacitinib is a once-daily oral selective tyrosine kinase 2 inhibitor that blocks IL-23 and type I interferon signaling. It was approved for adults with moderate to severe plaque psoriasis in September 2021.⁷ We know patients want oral treatment; they ask for apremilast even though injections may be much more potent. In a 16-week, phase 3 clinical trial comparing daily deucravacitinib (n=332), apremilast (n=168), and placebo (n=166), rates of clear or almost clear were approximately 55% in the deucravacitinib group, 32% in the apremilast group, and 7% with placebo. The most common AEs included nasopharyngitis, upper respiratory tract infection, headache, diarrhea, and nausea.⁸ Although deucravacitinib is much more effective than apremilast, deucravacitinib will require monitoring and may have some risk for viral reactivation of herpes simplex and zoster (and hopefully not much else). Whether physicians view it as a replacement for apremilast, which requires no laboratory monitoring, remains to be seen.

Bimekizumab, a humanized monoclonal IgG1 antibody expected to receive US Food and Drug Administration approval in the coming months, inhibits both IL-17A and IL-17F and may become our most effective treatment of psoriasis. Although we are probably not hungering for a more effective psoriasis treatment (given our current embarrassment of riches), bimekizumab’s remarkably high efficacy for psoriatic arthritis may be a quantum leap forward, especially if no new safety signals are identified; bimekizumab treatment is associated with a higher risk of oral candidiasis than other currently available IL-17 antagonists.⁹ Biosimilars may reduce the cost of psoriasis management to the health system, but it seems unlikely that biosimilars will allow us to help patients who we cannot already help with the existing extensive psoriasis treatment armamentarium.

New treatments for psoriasis constitute an embarrassment of riches compared to any other area of dermatology. Despite the many advances over the last 25 years, additional topical and systemic treatments have recently become available. Gosh, it’s great!

In May 2022, once-daily tapinarof cream 1% was approved for the topical treatment of plaque psoriasis in adults.¹ Tapinarof was identified as a metabolite made by bacteria symbiotic to a nematode, allowing the nematode to infect insects.² Tapinarof’s anti-inflammatory effect extends to mammals. The drug works by activating the aryl hydrocarbon receptor, downregulating proinflammatory cytokines such as IL-17, and normalizing the expression of skin barrier proteins such as filaggrin.² In two 12-week, phase 3, randomized trials with 510 and 515 patients, respectively, 35% to 40% of tapinarof-treated psoriasis patients were clear or almost clear compared with only 6% of patients in the placebo group. The drug appears safe; common adverse events (AEs) included folliculitis, nasopharyngitis, contact dermatitis, headache, upper respiratory tract infection, and pruritus.³

A second new topical treatment for plaque psoriasis was approved in July 2022—once-daily roflumilast 0.3% cream—for patients 12 years and older.⁴ Similar to apremilast, roflumilast is a phosphodiesterase 4 inhibitor that blocks the degradation of cAMP and reduces the downstream production of inflammatory molecules implicated in psoriasis.⁵ In two 8-week, phase 3 clinical trials (ClinicalTrials.gov Identifiers NCT04211363 and NCT04211389)(N=881), approximately 40% of roflumilast-treated patients were clear or almost clear vs approximately 6% in the placebo group. Topical roflumilast was well-tolerated; the most common AEs included diarrhea, headache, insomnia, nausea, application-site pain, upper respiratory tract infection, and urinary tract infection.⁶

We have so many patients—and many more people with psoriasis who are not yet patients—with limited psoriasis who would be amenable to topical treatment but who are not responding to current treatments. There is considerable enthusiasm for the new topicals, but it is still questionable how much they will help our patients. The main reason the current topicals fail is poor adherence to the treatment. If we give these new treatments to patients who used existing topicals and failed, thereby inadvertently selecting patients with poor adherence to topicals, it will be surprising if the new treatments live up to expectations. Perhaps tapinarof and roflumilast will revolutionize the management of localized psoriasis; perhaps their impact will be similar to topical crisaborole— exciting in trials and less practical in real life. It may be that apremilast, which is now approved for psoriasis of any severity, will make a bigger difference for patients who can access it for limited psoriasis.

Deucravacitinib is a once-daily oral selective tyrosine kinase 2 inhibitor that blocks IL-23 and type I interferon signaling. It was approved for adults with moderate to severe plaque psoriasis in September 2021.⁷ We know patients want oral treatment; they ask for apremilast even though injections may be much more potent. In a 16-week, phase 3 clinical trial comparing daily deucravacitinib (n=332), apremilast (n=168), and placebo (n=166), rates of clear or almost clear were approximately 55% in the deucravacitinib group, 32% in the apremilast group, and 7% with placebo. The most common AEs included nasopharyngitis, upper respiratory tract infection, headache, diarrhea, and nausea.⁸ Although deucravacitinib is much more effective than apremilast, deucravacitinib will require monitoring and may have some risk for viral reactivation of herpes simplex and zoster (and hopefully not much else). Whether physicians view it as a replacement for apremilast, which requires no laboratory monitoring, remains to be seen.

Bimekizumab, a humanized monoclonal IgG1 antibody expected to receive US Food and Drug Administration approval in the coming months, inhibits both IL-17A and IL-17F and may become our most effective treatment of psoriasis. Although we are probably not hungering for a more effective psoriasis treatment (given our current embarrassment of riches), bimekizumab’s remarkably high efficacy for psoriatic arthritis may be a quantum leap forward, especially if no new safety signals are identified; bimekizumab treatment is associated with a higher risk of oral candidiasis than other currently available IL-17 antagonists.⁹ Biosimilars may reduce the cost of psoriasis management to the health system, but it seems unlikely that biosimilars will allow us to help patients who we cannot already help with the existing extensive psoriasis treatment armamentarium.