Cutis

THE DIAGNOSIS: Granuloma Faciale

Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.¹ Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.¹ Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.²

Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.^1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.¹ Oral dapsone is given at a dose of 50 mg to 150 mg once daily.¹ Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.¹

The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.⁴ Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.⁵ The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.⁶ Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.⁷

THE DIAGNOSIS: Granuloma Faciale

Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.¹ Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.¹ Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.²

Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.^1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.¹ Oral dapsone is given at a dose of 50 mg to 150 mg once daily.¹ Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.¹

The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.⁴ Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.⁵ The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.⁶ Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.⁷

THE DIAGNOSIS: Granuloma Faciale

Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.¹ Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.¹ Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.²

Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.^1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.¹ Oral dapsone is given at a dose of 50 mg to 150 mg once daily.¹ Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.¹

The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.⁴ Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.⁵ The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.⁶ Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.⁷

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

To the Editor:

Psoriasis is a chronic systemic inflammatory disease that affects 1% to 3% of the global population.^1,2 Due to dysregulation of the immune system, patients with HIV who have concurrent moderate to severe psoriasis present a clinical therapeutic challenge for dermatologists. Recent guidelines from the American Academy of Dermatology recommended avoiding certain systemic treatments (eg, methotrexate, cyclosporine) in patients who are HIV positive due to their immunosuppressive effects, as well as cautious use of certain biologics in populations with HIV.³ Traditional therapies for managing psoriasis in patients with HIV have included topical agents, antiretroviral therapy (ART), phototherapy, and acitretin; however, phototherapy can be logistically cumbersome for patients, and in the setting of ART, acitretin has the potential to exacerbate hypertriglyceridemia as well as other undesirable adverse effects.³

Apremilast is a phosphodiesterase 4 inhibitor that has emerged as a promising alternative in patients with HIV who require treatment for psoriasis. It has demonstrated clinical efficacy in psoriasis and has minimal immunosuppressive risk.⁴ Despite its potential in this population, reports of apremilast used in patients who are HIV positive are rare, and these patients often are excluded from larges studies. In this study, we reviewed the literature to evaluate outcomes and adverse events in patients with HIV who underwent psoriasis treatment with apremilast.

A search of PubMed articles indexed for MEDLINE from the inception of the database through January 2023 was conducted using the terms psoriasis, human immunodeficiency virus, acquired immunodeficiency syndrome, therapy, apremilast, and adverse events. The inclusion criteria were articles that reported patients with HIV and psoriasis undergoing treatment with apremilast with subsequent follow-up to delineate potential outcomes and adverse effects. Non–English language articles were excluded.

Our search of the literature yielded 7 patients with HIV and psoriasis who were treated with apremilast (eTable).^5-11 All of the patients were male and ranged in age from 31 to 55 years, and all had pretreatment CD4 cell counts greater than 450 cells/mm³. All but 1 patient were confirmed to have undergone ART prior to treatment with apremilast, and all were treated using the traditional apremilast titration from 10 mg to 30 mg orally twice daily.

The mean pretreatment Psoriasis Area and Severity Index (PASI) score in the patients we evaluated was 12.2, with an average reduction in PASI score of 9.3. This equated to achievement of PASI 75 or greater (ie, representing at least a 75% improvement in psoriasis) in 4 (57.1%) patients, with clinical improvement confirmed in all 7 patients (100.0%)(eTable). The average follow-up time was 9.7 months (range, 6 weeks to 24 months). Only 1 (14.3%) patient experienced any adverse effects, which included self-resolving diarrhea and respiratory infections (nonopportunistic) over a follow-up period of 2 years.⁶ Of note, gastrointestinal upset is common with apremilast and usually improves over time.¹²

Apremilast represents a safe and effective alternative systemic therapy for patients with HIV and psoriasis.⁴ As a phosphodiesterase 4 inhibitor, apremilast leads to increased levels of cyclic adenosine monophosphate, which restores an equilibrium between proinflammatory (eg, tumor necrosis factors, interferons, IL-2, IL-6, IL-12, IL-23) and anti-inflammatory (eg, IL-10) cytokines.¹³ Unlike most biologics that target and inhibit a specific proinflammatory cytokine, apremilast’s homeostatic mechanism may explain its minimal immunosuppressive adverse effects.

In the majority of patients we evaluated, initiation of apremilast led to documented clinical improvement. It is worth noting that some patients presented with a relevant medical history and/or comorbidities such as hepatitis and metabolic conditions (eg, obesity, type 2 diabetes mellitus, hypertriglyceridemia). Despite these comorbidities, initiation of apremilast therapy in these patients led to clinical improvement of psoriasis overall. Notable cases from our study included a 41-year-old man with concurrent hepatitis B and psoriatic arthritis who achieved PASI 90 after 24 weeks of apremilast therapy⁸; a 46-year-old man with concurrent hepatitis C who went from 8% to 1.5% body surface area affected after 5 months of treatment with apremilast⁵; and a 54-year-old man with concurrent obesity, type 2 diabetes mellitus, and hypertriglyceridemia who went from a PASI score of 10.2 to 4.1 after 3 months of apremilast treatment and maintained a PASI score of 2.7 at 2 years’ follow up (eTable).⁶

Limitations of this study included the small sample size and homogeneous demographic consisting only of adult males, which restrict the external validity of the findings. Despite limitations, apremilast was utilized effectively for patients with both psoriasis and psoriatic arthritis. The observed effectiveness of apremilast in multiple forms of psoriasis provides valuable insights into the drug’s versatility in this patient population.

The use of apremilast for treatment of psoriasis in patients with HIV represents an important therapeutic development. Its effectiveness in reducing psoriasis symptoms in these immunocompromised patients makes it a viable alternative to traditional systemic therapies that might be contraindicated in this population. While larger studies would be ideal, the exclusion of patients with HIV from clinical trials presents an obstacle and therefore makes case series and reviews helpful for clinicians in bridging the gap with respect to treatment options for these patients. Apremilast may be a safe and effective medication for patients with HIV and psoriasis who require systemic therapy to treat their skin disease.

To the Editor:

Psoriasis is a chronic systemic inflammatory disease that affects 1% to 3% of the global population.^1,2 Due to dysregulation of the immune system, patients with HIV who have concurrent moderate to severe psoriasis present a clinical therapeutic challenge for dermatologists. Recent guidelines from the American Academy of Dermatology recommended avoiding certain systemic treatments (eg, methotrexate, cyclosporine) in patients who are HIV positive due to their immunosuppressive effects, as well as cautious use of certain biologics in populations with HIV.³ Traditional therapies for managing psoriasis in patients with HIV have included topical agents, antiretroviral therapy (ART), phototherapy, and acitretin; however, phototherapy can be logistically cumbersome for patients, and in the setting of ART, acitretin has the potential to exacerbate hypertriglyceridemia as well as other undesirable adverse effects.³

Apremilast is a phosphodiesterase 4 inhibitor that has emerged as a promising alternative in patients with HIV who require treatment for psoriasis. It has demonstrated clinical efficacy in psoriasis and has minimal immunosuppressive risk.⁴ Despite its potential in this population, reports of apremilast used in patients who are HIV positive are rare, and these patients often are excluded from larges studies. In this study, we reviewed the literature to evaluate outcomes and adverse events in patients with HIV who underwent psoriasis treatment with apremilast.

A search of PubMed articles indexed for MEDLINE from the inception of the database through January 2023 was conducted using the terms psoriasis, human immunodeficiency virus, acquired immunodeficiency syndrome, therapy, apremilast, and adverse events. The inclusion criteria were articles that reported patients with HIV and psoriasis undergoing treatment with apremilast with subsequent follow-up to delineate potential outcomes and adverse effects. Non–English language articles were excluded.

Our search of the literature yielded 7 patients with HIV and psoriasis who were treated with apremilast (eTable).^5-11 All of the patients were male and ranged in age from 31 to 55 years, and all had pretreatment CD4 cell counts greater than 450 cells/mm³. All but 1 patient were confirmed to have undergone ART prior to treatment with apremilast, and all were treated using the traditional apremilast titration from 10 mg to 30 mg orally twice daily.

The mean pretreatment Psoriasis Area and Severity Index (PASI) score in the patients we evaluated was 12.2, with an average reduction in PASI score of 9.3. This equated to achievement of PASI 75 or greater (ie, representing at least a 75% improvement in psoriasis) in 4 (57.1%) patients, with clinical improvement confirmed in all 7 patients (100.0%)(eTable). The average follow-up time was 9.7 months (range, 6 weeks to 24 months). Only 1 (14.3%) patient experienced any adverse effects, which included self-resolving diarrhea and respiratory infections (nonopportunistic) over a follow-up period of 2 years.⁶ Of note, gastrointestinal upset is common with apremilast and usually improves over time.¹²

Apremilast represents a safe and effective alternative systemic therapy for patients with HIV and psoriasis.⁴ As a phosphodiesterase 4 inhibitor, apremilast leads to increased levels of cyclic adenosine monophosphate, which restores an equilibrium between proinflammatory (eg, tumor necrosis factors, interferons, IL-2, IL-6, IL-12, IL-23) and anti-inflammatory (eg, IL-10) cytokines.¹³ Unlike most biologics that target and inhibit a specific proinflammatory cytokine, apremilast’s homeostatic mechanism may explain its minimal immunosuppressive adverse effects.

In the majority of patients we evaluated, initiation of apremilast led to documented clinical improvement. It is worth noting that some patients presented with a relevant medical history and/or comorbidities such as hepatitis and metabolic conditions (eg, obesity, type 2 diabetes mellitus, hypertriglyceridemia). Despite these comorbidities, initiation of apremilast therapy in these patients led to clinical improvement of psoriasis overall. Notable cases from our study included a 41-year-old man with concurrent hepatitis B and psoriatic arthritis who achieved PASI 90 after 24 weeks of apremilast therapy⁸; a 46-year-old man with concurrent hepatitis C who went from 8% to 1.5% body surface area affected after 5 months of treatment with apremilast⁵; and a 54-year-old man with concurrent obesity, type 2 diabetes mellitus, and hypertriglyceridemia who went from a PASI score of 10.2 to 4.1 after 3 months of apremilast treatment and maintained a PASI score of 2.7 at 2 years’ follow up (eTable).⁶

Limitations of this study included the small sample size and homogeneous demographic consisting only of adult males, which restrict the external validity of the findings. Despite limitations, apremilast was utilized effectively for patients with both psoriasis and psoriatic arthritis. The observed effectiveness of apremilast in multiple forms of psoriasis provides valuable insights into the drug’s versatility in this patient population.

The use of apremilast for treatment of psoriasis in patients with HIV represents an important therapeutic development. Its effectiveness in reducing psoriasis symptoms in these immunocompromised patients makes it a viable alternative to traditional systemic therapies that might be contraindicated in this population. While larger studies would be ideal, the exclusion of patients with HIV from clinical trials presents an obstacle and therefore makes case series and reviews helpful for clinicians in bridging the gap with respect to treatment options for these patients. Apremilast may be a safe and effective medication for patients with HIV and psoriasis who require systemic therapy to treat their skin disease.

To the Editor:

Psoriasis is a chronic systemic inflammatory disease that affects 1% to 3% of the global population.^1,2 Due to dysregulation of the immune system, patients with HIV who have concurrent moderate to severe psoriasis present a clinical therapeutic challenge for dermatologists. Recent guidelines from the American Academy of Dermatology recommended avoiding certain systemic treatments (eg, methotrexate, cyclosporine) in patients who are HIV positive due to their immunosuppressive effects, as well as cautious use of certain biologics in populations with HIV.³ Traditional therapies for managing psoriasis in patients with HIV have included topical agents, antiretroviral therapy (ART), phototherapy, and acitretin; however, phototherapy can be logistically cumbersome for patients, and in the setting of ART, acitretin has the potential to exacerbate hypertriglyceridemia as well as other undesirable adverse effects.³

Apremilast is a phosphodiesterase 4 inhibitor that has emerged as a promising alternative in patients with HIV who require treatment for psoriasis. It has demonstrated clinical efficacy in psoriasis and has minimal immunosuppressive risk.⁴ Despite its potential in this population, reports of apremilast used in patients who are HIV positive are rare, and these patients often are excluded from larges studies. In this study, we reviewed the literature to evaluate outcomes and adverse events in patients with HIV who underwent psoriasis treatment with apremilast.

A search of PubMed articles indexed for MEDLINE from the inception of the database through January 2023 was conducted using the terms psoriasis, human immunodeficiency virus, acquired immunodeficiency syndrome, therapy, apremilast, and adverse events. The inclusion criteria were articles that reported patients with HIV and psoriasis undergoing treatment with apremilast with subsequent follow-up to delineate potential outcomes and adverse effects. Non–English language articles were excluded.

Our search of the literature yielded 7 patients with HIV and psoriasis who were treated with apremilast (eTable).^5-11 All of the patients were male and ranged in age from 31 to 55 years, and all had pretreatment CD4 cell counts greater than 450 cells/mm³. All but 1 patient were confirmed to have undergone ART prior to treatment with apremilast, and all were treated using the traditional apremilast titration from 10 mg to 30 mg orally twice daily.

The mean pretreatment Psoriasis Area and Severity Index (PASI) score in the patients we evaluated was 12.2, with an average reduction in PASI score of 9.3. This equated to achievement of PASI 75 or greater (ie, representing at least a 75% improvement in psoriasis) in 4 (57.1%) patients, with clinical improvement confirmed in all 7 patients (100.0%)(eTable). The average follow-up time was 9.7 months (range, 6 weeks to 24 months). Only 1 (14.3%) patient experienced any adverse effects, which included self-resolving diarrhea and respiratory infections (nonopportunistic) over a follow-up period of 2 years.⁶ Of note, gastrointestinal upset is common with apremilast and usually improves over time.¹²

Apremilast represents a safe and effective alternative systemic therapy for patients with HIV and psoriasis.⁴ As a phosphodiesterase 4 inhibitor, apremilast leads to increased levels of cyclic adenosine monophosphate, which restores an equilibrium between proinflammatory (eg, tumor necrosis factors, interferons, IL-2, IL-6, IL-12, IL-23) and anti-inflammatory (eg, IL-10) cytokines.¹³ Unlike most biologics that target and inhibit a specific proinflammatory cytokine, apremilast’s homeostatic mechanism may explain its minimal immunosuppressive adverse effects.

In the majority of patients we evaluated, initiation of apremilast led to documented clinical improvement. It is worth noting that some patients presented with a relevant medical history and/or comorbidities such as hepatitis and metabolic conditions (eg, obesity, type 2 diabetes mellitus, hypertriglyceridemia). Despite these comorbidities, initiation of apremilast therapy in these patients led to clinical improvement of psoriasis overall. Notable cases from our study included a 41-year-old man with concurrent hepatitis B and psoriatic arthritis who achieved PASI 90 after 24 weeks of apremilast therapy⁸; a 46-year-old man with concurrent hepatitis C who went from 8% to 1.5% body surface area affected after 5 months of treatment with apremilast⁵; and a 54-year-old man with concurrent obesity, type 2 diabetes mellitus, and hypertriglyceridemia who went from a PASI score of 10.2 to 4.1 after 3 months of apremilast treatment and maintained a PASI score of 2.7 at 2 years’ follow up (eTable).⁶

Limitations of this study included the small sample size and homogeneous demographic consisting only of adult males, which restrict the external validity of the findings. Despite limitations, apremilast was utilized effectively for patients with both psoriasis and psoriatic arthritis. The observed effectiveness of apremilast in multiple forms of psoriasis provides valuable insights into the drug’s versatility in this patient population.

The use of apremilast for treatment of psoriasis in patients with HIV represents an important therapeutic development. Its effectiveness in reducing psoriasis symptoms in these immunocompromised patients makes it a viable alternative to traditional systemic therapies that might be contraindicated in this population. While larger studies would be ideal, the exclusion of patients with HIV from clinical trials presents an obstacle and therefore makes case series and reviews helpful for clinicians in bridging the gap with respect to treatment options for these patients. Apremilast may be a safe and effective medication for patients with HIV and psoriasis who require systemic therapy to treat their skin disease.

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Health care costs continue to increase in 2025 while physician reimbursement continues to decrease. Of the $4.5 trillion spent on health care in 2022, only 20% was spent on physician and clinical services.¹ Since 2001, practice expense has risen 47%, while the Consumer Price Index has risen 73%; adjusted for inflation, physician reimbursement has declined 30% since 2001.²

The formula for Medicare payments for physician services, calculated by multiplying the conversion factor (CF) by the relative value unit (RVU), was developed by the Centers for Medicare & Medicaid Services (CMS) in 1992. The combination of the physician’s work, the practice’s expense, and the cost of professional liability insurance make up RVUs, which are aligned by geographic index adjustments.³ The 2024 CF was $32.75, compared to $32.00 in 1992. The proposed 2025 CF is $32.35, which is a 10% decrease since 2019 and a 2.8% decrease relative to the 2024 Medicare Physician Fee Schedule (MPFS). The 2.8% cut is due to expiration of the 2.93% temporary payment increase for services provided by the Consolidated Appropriations Act 2024 and the supplemental relief provided from March 9, 2024, to December 31, 2024.⁴ If the CF had increased with inflation, it would have been $71.15 in 2024.⁴

Declining reimbursement rates for physician services undermine the ability of physician practices to keep their doors open in the face of increased operating costs. Faced with the widening gap between what Medicare pays for physician services and the cost of delivering value-based, quality care, physicians are urging Congress to pass a reform package to permanently strengthen Medicare.

Herein, an overview of key coding updates and changes, telehealth flexibilities, and a new dermatologyfocused Merit-based Incentive Payment System (MIPS) Value Pathways is provided.

Update on the Medicare Economic Index Postponement

Developed in 1975, the Medicare Economic Index (MEI) is a measure of practice cost inflation. It is a yearly calculation that estimates the annual changes in physicians’ operating costs to determine appropriate Medicare physician payment updates.⁵ The MEI is composed of physician practice costs (eg, staff salaries, office space, malpractice insurance) and physician compensation (direct earnings by the physician). Both are used to calculate adjustments to Medicare physician payments to account for inflationary increases in health care costs. The MEI for 2025 is projected to increase by 3.5%, while physician payment continues to dwindle.⁵ This disparity between rising costs and declining physician payments will impact patient access to medical care. Physicians may choose to stop accepting Medicare and other health insurance, face the possibility of closing or selling their practices, or even decide to leave the profession.

The CMS has continued to delay implementation of the 2017 MEI cost weights (which currently are based on 2006 data⁵) for RVUs in the MPFS rate setting for 2025 pending completion of the American Medical Association (AMA) Physician Practice Information Survey.⁶ The AMA contracted with an independent research company to conduct the survey, which will be used to update the MEI. Survey data will be shared with the CMS in early 2025.⁶

Future of Telehealth is Uncertain

On January 1, 2025, many telehealth flexibilities were set to expire; however, Congress passed an extension of the current telehealth policy flexibilities that have been in place since the COVID-19 pandemic through March 31, 2025.⁷ The CMS recognizes concerns about maintaining access to Medicare telehealth services once the statutory flexibilities expire; however, it maintains that it has limited statutory authority to extend these Medicare telehealth flexibilities.⁸ There will be originating site requirements and geographic location restrictions. Clinicians working in a federally qualified health center or a rural health clinic would not be affected.⁸

The CMS rejected adoption of 16 of 17 new Current Procedural Terminology (CPT) codes (98000–98016) for telemedicine evaluation and management (E/M) services, rendering them nonreimbursable.⁸ Physicians should continue to use the standard E/M codes 99202 through 99215 for telehealth visits. The CMS only approved code 99016, which will replace Healthcare Common Procedure Coding System code G2012, for brief virtual check-in encounters. The CMS specified that CPT codes 99441 through 99443, which describe telephone E/M services, have been removed and are no longer valid for billing. Asynchronous communication (eg, store-and-forward technology via an electronic health record portal) will continue to be reported using the online digital E/M service codes 99421, 99422, and 99423.⁸

Practitioners can use their enrolled practice location instead of their home address when providing telehealth services from home.⁸ Teaching physicians will continue to be allowed to have a virtual presence for purposes of billing for services involving residents in all teaching settings, but only when the service is furnished remotely (ie, the patient, resident, and teaching physician all are in separate locations). The use of real-time audio and video technology for direct supervision has been extended through December 31, 2025, allowing practitioners to be immediately available virtually. The CMS also plans to permanently allow virtual supervision for lower-risk services that typically do not require the billing practitioner’s physical presence or extensive direction (eg, diagnostic tests, behavioral health, dermatology, therapy).⁸

It is essential to verify the reimbursement policies and billing guidelines of individual payers, as some may adopt policies that differ from the AMA and CMS guidelines.

When to Use Modifiers -59 and -76

Modifiers -59 and -76 are used when billing for multiple procedures on the same day and can be confused. These modifiers help clarify situations in which procedures might appear redundant or improperly coded, reducing the risk for claim denials and ensuring compliance with coding guidelines. Use modifier -59 when a procedure or service is distinct or separate from other services performed on the same day (eg, cryosurgery of 4 actinic keratoses and a tangential biopsy of a nevus). Use modifier -76 when a physician performs the exact same procedure multiple times on the same patient on the same day (eg, removing 2 nevi on the face with the same excision code or performing multiple biopsies on different areas on the skin).⁹

What Are the Medical Team Conference CPT Codes?

Dermatologists frequently manage complex medical and surgical cases and actively participate in tumor boards and multidisciplinary teams conferences. It is essential to be familiar with the relevant CPT codes that can be used in these scenarios: CPT code 99366 can be used when the medical team conference occurs face-to-face with the patient present, and CPT code 99367 can be used for a medical team conference with an interdisciplinary group of health care professionals from different specialties, each of whom provides direct care to the patient.¹⁰ For CPT code 99367, the patient and/or family are not present during the meeting, which lasts a minimum of 30 minutes or more and requires participation by a physician. Current Procedural Terminology code 99368 can be used for participation in the medical team conference by a nonphysician qualified health care professional. The reporting participants need to document their participation in the medical team conference as well as their contributed information that explains the case and subsequent treatment recommendations.¹⁰

No more than 1 individual from the same specialty may report CPT codes 99366 through 99368 at the same encounter.¹⁰ Codes 99366 through 99368 should not be reported when participation in the medical team conference is part of a facility or contractually provided by the facility such as group therapy.¹⁰ The medical team conference starts at the beginning of the review of an individual patient and ends at the conclusion of the review for coding purposes. Time related to record-keeping or report generation does not need to be reported. The reporting participant needs to be present for the entire conference. The time reported is not limited to the time that the participant is communicating with other team members or the patient and/or their family/ caregiver(s). Time reported for medical team conferences may not be used in the determination for other services, such as care plan oversight (99374-99380), prolonged services (99358, 99359), psychotherapy, or any E/M service. When the patient is present for any part of the duration of the team conference, nonphysician qualified health care professionals (eg, speech-language pathologists, physical therapists, occupational therapists, social workers, dietitians) report the medical team conference face-to-face with code 99366.¹⁰

Update on Excimer Laser CPT Codes

The CMS rejected values recommended for CPT codes (96920-96922) by the Relative Value Scale Update Committee, proposing lower work RVUs of 0.83, 0.90, and 1.15, respectively (Table).^2,11 The CPT panel did not recognize the strength of the literature supporting the expanded use of the codes for conditions other than psoriasis. Report the use of excimer laser for treatment of vitiligo, atopic dermatitis, and alopecia areata using CPT code 96999 (unlisted special dermatological service or procedure).¹¹

Update on the New G2211 Code

Healthcare Common Procedure Coding System code G2211 is an add-on complexity code that can be reported with all outpatient E/M visits to better account for additional resources associated with primary care or similarly ongoing medical care related to a patient’s single serious condition or complex condition.¹² It can be billed if the physician is serving as the continuing focal point for all the patient's health care service needs, acting as the central point of contact for the patient’s ongoing medical care, and managing all aspects of their health needs over time. It is not restricted based on specialty, but it is determined based on the nature of the physician-patient relationship.¹²

Code G2211 should not be used for the following scenarios: (1) care provided by a clinician with a discrete, routine, or time-limited relationship with the patient, such as a routine skin examination or an acute allergic contact dermatitis; (2) conditions in which comorbidities are not present or addressed; (3) when the billing clinician has not assumed responsibility for ongoing medical care with consistency and continuity over time; and (4) visits billed with modifier -25.¹² In the 2025 MPFS, the CMS is proposing to allow payment of G2211 when the code is reported by the same practitioner on the same day as an annual wellness visit, vaccine administration, or any Medicare Part B preventive service furnished in the office or outpatient setting (ie, creating a limited exception to the prohibition of using this code with modifier -25).²

Documentation in the medical record must support reporting code G2211 and indicate a medically reasonable and necessary reason for the additional RVUs (0.33 and additional payment of $16.05).¹²

Underutilization of Z Codes for Social Determinants of Health

Barriers to documentation of social determinants of health (SDOH)–related International Classification of Diseases, Tenth Revision, Z codes (Z55-Z66)(eTable 1), include lack of clarity on who can document patients’ social needs, lack of systems and processes for documenting and coding SDOH, unfamiliarity with these Z codes, and a low prioritization of collecting these data.¹³ Documentation of a SDOH-related Z code relevant to a patient encounter is considered moderate risk and can have a major impact on a patient’s overall health, unmet social needs, and outcomes.¹³ If the other 2 medical decision-making elements (ie, number and complexity of problems addressed along with amount and/or complexity of data to be reviewed and analyzed) for the E/M visit also are moderate, then the encounter can be coded as level 4.¹³

New Codes for Alopecia and Acne Surgery

New International Classification of Diseases, Tenth Revision, Clinical Modification, codes for alopecia have been developed through collaboration of the American Academy of Dermatology Association and the Scarring Alopecia Foundation (eTable 2). Cutaneous extraction—previously coded as acne surgery (CPT code 10040)—will now be listed in the 2026 CPT coding manual as “extraction” (eg, marsupialization, opening of multiple milia, acne comedones, cysts, pustules).¹⁴

Quality Payment Program Update

The MIPS performance threshold will remain at 75 for the 2025 performance period, impacting the 2027 payment year.¹⁵ The MIPS Value Pathways will be available but optional in 2025, and the CMS plans to fully replace MIPS by 2029. The goal for the MVPs is to reduce the administrative burden of MIPS for physicians and their staff while simplifying reporting; however, there are several concerns. The MIPS Value Pathways build on the MIPS’s flawed processes; compare the cost for one condition to the quality of another; continue to be burdensome to physicians; have not demonstrated improved patient care; are a broad, one-size-fits-all model that could lead to inequity based on practice mix; and are not clinically relevant to physicians and patients.¹⁵

Beginning in 2025, dermatologists also will have access to a new high-priority quality measure—Melanoma: Tracking and Evaluation of Recurrence—and the Melanoma: Continuity of Care–Recall System measure (MIPS measure 137) will be removed starting in 2025.¹⁵

What Can Dermatologists Do?

With the fifth consecutive year of payment cuts, the cumulative reduction to physician payments has reached an untenable level, and physicians cannot continue to absorb the reductions, which impact access and ability to provide patient care. Members of the American Academy of Dermatology Association must urge members of Congress to stop the cuts and find a permanent solution to fix Medicare physician payment by asking their representatives to cosponsor the following bills in the US House of Representatives and Senate¹⁶:

• HR 10073—The Medicare Patient Access and Practice Stabilization Act of 2024 would stop the 2.8% cut to the 2025 MPFS and provide a positive inflationary adjustment for physician practices equal to 50% of the 2025 MEI, which comes down to an increase of approximately 1.8%.¹⁷
• HR 2424—The Strengthening Medicare for Patients and Providers Act would provide an annual inflation update equal to the MEI for Medicare physician payments.¹⁸
• HR 6371—The Provider Reimbursement Stability Act would revise budget neutrality policies that contribute to eroding Medicare physician reimbursement.¹⁹
• S 4935—The Physician Fee Stabilization Act would increase the budget neutrality trigger from $20 million to $53 million.²⁰

Advocacy is critically important: be engaged and get involved in grassroots efforts to protect access to health care, as these cuts do nothing to curb health care costs.

Final Thoughts

Congress has failed to address declining Medicare reimbursement rates, allowing cuts that jeopardize patient access to care as physicians close or sell their practices. It is important for dermatologists to attend the American Medical Association’s National Advocacy Conference in February 2025, which will feature an event on fixing Medicare. Dermatologists also can join prominent House members in urging Congress to reverse Medicare cuts and reform the physician payment system as well as write to their representatives and share how these cuts impact their practices and patients.

Health care costs continue to increase in 2025 while physician reimbursement continues to decrease. Of the $4.5 trillion spent on health care in 2022, only 20% was spent on physician and clinical services.¹ Since 2001, practice expense has risen 47%, while the Consumer Price Index has risen 73%; adjusted for inflation, physician reimbursement has declined 30% since 2001.²

The formula for Medicare payments for physician services, calculated by multiplying the conversion factor (CF) by the relative value unit (RVU), was developed by the Centers for Medicare & Medicaid Services (CMS) in 1992. The combination of the physician’s work, the practice’s expense, and the cost of professional liability insurance make up RVUs, which are aligned by geographic index adjustments.³ The 2024 CF was $32.75, compared to $32.00 in 1992. The proposed 2025 CF is $32.35, which is a 10% decrease since 2019 and a 2.8% decrease relative to the 2024 Medicare Physician Fee Schedule (MPFS). The 2.8% cut is due to expiration of the 2.93% temporary payment increase for services provided by the Consolidated Appropriations Act 2024 and the supplemental relief provided from March 9, 2024, to December 31, 2024.⁴ If the CF had increased with inflation, it would have been $71.15 in 2024.⁴

Declining reimbursement rates for physician services undermine the ability of physician practices to keep their doors open in the face of increased operating costs. Faced with the widening gap between what Medicare pays for physician services and the cost of delivering value-based, quality care, physicians are urging Congress to pass a reform package to permanently strengthen Medicare.

Herein, an overview of key coding updates and changes, telehealth flexibilities, and a new dermatologyfocused Merit-based Incentive Payment System (MIPS) Value Pathways is provided.

Update on the Medicare Economic Index Postponement

Developed in 1975, the Medicare Economic Index (MEI) is a measure of practice cost inflation. It is a yearly calculation that estimates the annual changes in physicians’ operating costs to determine appropriate Medicare physician payment updates.⁵ The MEI is composed of physician practice costs (eg, staff salaries, office space, malpractice insurance) and physician compensation (direct earnings by the physician). Both are used to calculate adjustments to Medicare physician payments to account for inflationary increases in health care costs. The MEI for 2025 is projected to increase by 3.5%, while physician payment continues to dwindle.⁵ This disparity between rising costs and declining physician payments will impact patient access to medical care. Physicians may choose to stop accepting Medicare and other health insurance, face the possibility of closing or selling their practices, or even decide to leave the profession.

The CMS has continued to delay implementation of the 2017 MEI cost weights (which currently are based on 2006 data⁵) for RVUs in the MPFS rate setting for 2025 pending completion of the American Medical Association (AMA) Physician Practice Information Survey.⁶ The AMA contracted with an independent research company to conduct the survey, which will be used to update the MEI. Survey data will be shared with the CMS in early 2025.⁶

Future of Telehealth is Uncertain

On January 1, 2025, many telehealth flexibilities were set to expire; however, Congress passed an extension of the current telehealth policy flexibilities that have been in place since the COVID-19 pandemic through March 31, 2025.⁷ The CMS recognizes concerns about maintaining access to Medicare telehealth services once the statutory flexibilities expire; however, it maintains that it has limited statutory authority to extend these Medicare telehealth flexibilities.⁸ There will be originating site requirements and geographic location restrictions. Clinicians working in a federally qualified health center or a rural health clinic would not be affected.⁸

The CMS rejected adoption of 16 of 17 new Current Procedural Terminology (CPT) codes (98000–98016) for telemedicine evaluation and management (E/M) services, rendering them nonreimbursable.⁸ Physicians should continue to use the standard E/M codes 99202 through 99215 for telehealth visits. The CMS only approved code 99016, which will replace Healthcare Common Procedure Coding System code G2012, for brief virtual check-in encounters. The CMS specified that CPT codes 99441 through 99443, which describe telephone E/M services, have been removed and are no longer valid for billing. Asynchronous communication (eg, store-and-forward technology via an electronic health record portal) will continue to be reported using the online digital E/M service codes 99421, 99422, and 99423.⁸

Practitioners can use their enrolled practice location instead of their home address when providing telehealth services from home.⁸ Teaching physicians will continue to be allowed to have a virtual presence for purposes of billing for services involving residents in all teaching settings, but only when the service is furnished remotely (ie, the patient, resident, and teaching physician all are in separate locations). The use of real-time audio and video technology for direct supervision has been extended through December 31, 2025, allowing practitioners to be immediately available virtually. The CMS also plans to permanently allow virtual supervision for lower-risk services that typically do not require the billing practitioner’s physical presence or extensive direction (eg, diagnostic tests, behavioral health, dermatology, therapy).⁸

It is essential to verify the reimbursement policies and billing guidelines of individual payers, as some may adopt policies that differ from the AMA and CMS guidelines.

When to Use Modifiers -59 and -76

Modifiers -59 and -76 are used when billing for multiple procedures on the same day and can be confused. These modifiers help clarify situations in which procedures might appear redundant or improperly coded, reducing the risk for claim denials and ensuring compliance with coding guidelines. Use modifier -59 when a procedure or service is distinct or separate from other services performed on the same day (eg, cryosurgery of 4 actinic keratoses and a tangential biopsy of a nevus). Use modifier -76 when a physician performs the exact same procedure multiple times on the same patient on the same day (eg, removing 2 nevi on the face with the same excision code or performing multiple biopsies on different areas on the skin).⁹

What Are the Medical Team Conference CPT Codes?

Dermatologists frequently manage complex medical and surgical cases and actively participate in tumor boards and multidisciplinary teams conferences. It is essential to be familiar with the relevant CPT codes that can be used in these scenarios: CPT code 99366 can be used when the medical team conference occurs face-to-face with the patient present, and CPT code 99367 can be used for a medical team conference with an interdisciplinary group of health care professionals from different specialties, each of whom provides direct care to the patient.¹⁰ For CPT code 99367, the patient and/or family are not present during the meeting, which lasts a minimum of 30 minutes or more and requires participation by a physician. Current Procedural Terminology code 99368 can be used for participation in the medical team conference by a nonphysician qualified health care professional. The reporting participants need to document their participation in the medical team conference as well as their contributed information that explains the case and subsequent treatment recommendations.¹⁰

No more than 1 individual from the same specialty may report CPT codes 99366 through 99368 at the same encounter.¹⁰ Codes 99366 through 99368 should not be reported when participation in the medical team conference is part of a facility or contractually provided by the facility such as group therapy.¹⁰ The medical team conference starts at the beginning of the review of an individual patient and ends at the conclusion of the review for coding purposes. Time related to record-keeping or report generation does not need to be reported. The reporting participant needs to be present for the entire conference. The time reported is not limited to the time that the participant is communicating with other team members or the patient and/or their family/ caregiver(s). Time reported for medical team conferences may not be used in the determination for other services, such as care plan oversight (99374-99380), prolonged services (99358, 99359), psychotherapy, or any E/M service. When the patient is present for any part of the duration of the team conference, nonphysician qualified health care professionals (eg, speech-language pathologists, physical therapists, occupational therapists, social workers, dietitians) report the medical team conference face-to-face with code 99366.¹⁰

Update on Excimer Laser CPT Codes

The CMS rejected values recommended for CPT codes (96920-96922) by the Relative Value Scale Update Committee, proposing lower work RVUs of 0.83, 0.90, and 1.15, respectively (Table).^2,11 The CPT panel did not recognize the strength of the literature supporting the expanded use of the codes for conditions other than psoriasis. Report the use of excimer laser for treatment of vitiligo, atopic dermatitis, and alopecia areata using CPT code 96999 (unlisted special dermatological service or procedure).¹¹

Update on the New G2211 Code

Healthcare Common Procedure Coding System code G2211 is an add-on complexity code that can be reported with all outpatient E/M visits to better account for additional resources associated with primary care or similarly ongoing medical care related to a patient’s single serious condition or complex condition.¹² It can be billed if the physician is serving as the continuing focal point for all the patient's health care service needs, acting as the central point of contact for the patient’s ongoing medical care, and managing all aspects of their health needs over time. It is not restricted based on specialty, but it is determined based on the nature of the physician-patient relationship.¹²

Code G2211 should not be used for the following scenarios: (1) care provided by a clinician with a discrete, routine, or time-limited relationship with the patient, such as a routine skin examination or an acute allergic contact dermatitis; (2) conditions in which comorbidities are not present or addressed; (3) when the billing clinician has not assumed responsibility for ongoing medical care with consistency and continuity over time; and (4) visits billed with modifier -25.¹² In the 2025 MPFS, the CMS is proposing to allow payment of G2211 when the code is reported by the same practitioner on the same day as an annual wellness visit, vaccine administration, or any Medicare Part B preventive service furnished in the office or outpatient setting (ie, creating a limited exception to the prohibition of using this code with modifier -25).²

Documentation in the medical record must support reporting code G2211 and indicate a medically reasonable and necessary reason for the additional RVUs (0.33 and additional payment of $16.05).¹²

Underutilization of Z Codes for Social Determinants of Health

Barriers to documentation of social determinants of health (SDOH)–related International Classification of Diseases, Tenth Revision, Z codes (Z55-Z66)(eTable 1), include lack of clarity on who can document patients’ social needs, lack of systems and processes for documenting and coding SDOH, unfamiliarity with these Z codes, and a low prioritization of collecting these data.¹³ Documentation of a SDOH-related Z code relevant to a patient encounter is considered moderate risk and can have a major impact on a patient’s overall health, unmet social needs, and outcomes.¹³ If the other 2 medical decision-making elements (ie, number and complexity of problems addressed along with amount and/or complexity of data to be reviewed and analyzed) for the E/M visit also are moderate, then the encounter can be coded as level 4.¹³

New Codes for Alopecia and Acne Surgery

New International Classification of Diseases, Tenth Revision, Clinical Modification, codes for alopecia have been developed through collaboration of the American Academy of Dermatology Association and the Scarring Alopecia Foundation (eTable 2). Cutaneous extraction—previously coded as acne surgery (CPT code 10040)—will now be listed in the 2026 CPT coding manual as “extraction” (eg, marsupialization, opening of multiple milia, acne comedones, cysts, pustules).¹⁴

Quality Payment Program Update

The MIPS performance threshold will remain at 75 for the 2025 performance period, impacting the 2027 payment year.¹⁵ The MIPS Value Pathways will be available but optional in 2025, and the CMS plans to fully replace MIPS by 2029. The goal for the MVPs is to reduce the administrative burden of MIPS for physicians and their staff while simplifying reporting; however, there are several concerns. The MIPS Value Pathways build on the MIPS’s flawed processes; compare the cost for one condition to the quality of another; continue to be burdensome to physicians; have not demonstrated improved patient care; are a broad, one-size-fits-all model that could lead to inequity based on practice mix; and are not clinically relevant to physicians and patients.¹⁵

Beginning in 2025, dermatologists also will have access to a new high-priority quality measure—Melanoma: Tracking and Evaluation of Recurrence—and the Melanoma: Continuity of Care–Recall System measure (MIPS measure 137) will be removed starting in 2025.¹⁵

What Can Dermatologists Do?

With the fifth consecutive year of payment cuts, the cumulative reduction to physician payments has reached an untenable level, and physicians cannot continue to absorb the reductions, which impact access and ability to provide patient care. Members of the American Academy of Dermatology Association must urge members of Congress to stop the cuts and find a permanent solution to fix Medicare physician payment by asking their representatives to cosponsor the following bills in the US House of Representatives and Senate¹⁶:

• HR 10073—The Medicare Patient Access and Practice Stabilization Act of 2024 would stop the 2.8% cut to the 2025 MPFS and provide a positive inflationary adjustment for physician practices equal to 50% of the 2025 MEI, which comes down to an increase of approximately 1.8%.¹⁷
• HR 2424—The Strengthening Medicare for Patients and Providers Act would provide an annual inflation update equal to the MEI for Medicare physician payments.¹⁸
• HR 6371—The Provider Reimbursement Stability Act would revise budget neutrality policies that contribute to eroding Medicare physician reimbursement.¹⁹
• S 4935—The Physician Fee Stabilization Act would increase the budget neutrality trigger from $20 million to $53 million.²⁰

Advocacy is critically important: be engaged and get involved in grassroots efforts to protect access to health care, as these cuts do nothing to curb health care costs.

Final Thoughts

Congress has failed to address declining Medicare reimbursement rates, allowing cuts that jeopardize patient access to care as physicians close or sell their practices. It is important for dermatologists to attend the American Medical Association’s National Advocacy Conference in February 2025, which will feature an event on fixing Medicare. Dermatologists also can join prominent House members in urging Congress to reverse Medicare cuts and reform the physician payment system as well as write to their representatives and share how these cuts impact their practices and patients.

Health care costs continue to increase in 2025 while physician reimbursement continues to decrease. Of the $4.5 trillion spent on health care in 2022, only 20% was spent on physician and clinical services.¹ Since 2001, practice expense has risen 47%, while the Consumer Price Index has risen 73%; adjusted for inflation, physician reimbursement has declined 30% since 2001.²

The formula for Medicare payments for physician services, calculated by multiplying the conversion factor (CF) by the relative value unit (RVU), was developed by the Centers for Medicare & Medicaid Services (CMS) in 1992. The combination of the physician’s work, the practice’s expense, and the cost of professional liability insurance make up RVUs, which are aligned by geographic index adjustments.³ The 2024 CF was $32.75, compared to $32.00 in 1992. The proposed 2025 CF is $32.35, which is a 10% decrease since 2019 and a 2.8% decrease relative to the 2024 Medicare Physician Fee Schedule (MPFS). The 2.8% cut is due to expiration of the 2.93% temporary payment increase for services provided by the Consolidated Appropriations Act 2024 and the supplemental relief provided from March 9, 2024, to December 31, 2024.⁴ If the CF had increased with inflation, it would have been $71.15 in 2024.⁴

Declining reimbursement rates for physician services undermine the ability of physician practices to keep their doors open in the face of increased operating costs. Faced with the widening gap between what Medicare pays for physician services and the cost of delivering value-based, quality care, physicians are urging Congress to pass a reform package to permanently strengthen Medicare.

Herein, an overview of key coding updates and changes, telehealth flexibilities, and a new dermatologyfocused Merit-based Incentive Payment System (MIPS) Value Pathways is provided.

Update on the Medicare Economic Index Postponement

Developed in 1975, the Medicare Economic Index (MEI) is a measure of practice cost inflation. It is a yearly calculation that estimates the annual changes in physicians’ operating costs to determine appropriate Medicare physician payment updates.⁵ The MEI is composed of physician practice costs (eg, staff salaries, office space, malpractice insurance) and physician compensation (direct earnings by the physician). Both are used to calculate adjustments to Medicare physician payments to account for inflationary increases in health care costs. The MEI for 2025 is projected to increase by 3.5%, while physician payment continues to dwindle.⁵ This disparity between rising costs and declining physician payments will impact patient access to medical care. Physicians may choose to stop accepting Medicare and other health insurance, face the possibility of closing or selling their practices, or even decide to leave the profession.

The CMS has continued to delay implementation of the 2017 MEI cost weights (which currently are based on 2006 data⁵) for RVUs in the MPFS rate setting for 2025 pending completion of the American Medical Association (AMA) Physician Practice Information Survey.⁶ The AMA contracted with an independent research company to conduct the survey, which will be used to update the MEI. Survey data will be shared with the CMS in early 2025.⁶

Future of Telehealth is Uncertain

On January 1, 2025, many telehealth flexibilities were set to expire; however, Congress passed an extension of the current telehealth policy flexibilities that have been in place since the COVID-19 pandemic through March 31, 2025.⁷ The CMS recognizes concerns about maintaining access to Medicare telehealth services once the statutory flexibilities expire; however, it maintains that it has limited statutory authority to extend these Medicare telehealth flexibilities.⁸ There will be originating site requirements and geographic location restrictions. Clinicians working in a federally qualified health center or a rural health clinic would not be affected.⁸

The CMS rejected adoption of 16 of 17 new Current Procedural Terminology (CPT) codes (98000–98016) for telemedicine evaluation and management (E/M) services, rendering them nonreimbursable.⁸ Physicians should continue to use the standard E/M codes 99202 through 99215 for telehealth visits. The CMS only approved code 99016, which will replace Healthcare Common Procedure Coding System code G2012, for brief virtual check-in encounters. The CMS specified that CPT codes 99441 through 99443, which describe telephone E/M services, have been removed and are no longer valid for billing. Asynchronous communication (eg, store-and-forward technology via an electronic health record portal) will continue to be reported using the online digital E/M service codes 99421, 99422, and 99423.⁸

Practitioners can use their enrolled practice location instead of their home address when providing telehealth services from home.⁸ Teaching physicians will continue to be allowed to have a virtual presence for purposes of billing for services involving residents in all teaching settings, but only when the service is furnished remotely (ie, the patient, resident, and teaching physician all are in separate locations). The use of real-time audio and video technology for direct supervision has been extended through December 31, 2025, allowing practitioners to be immediately available virtually. The CMS also plans to permanently allow virtual supervision for lower-risk services that typically do not require the billing practitioner’s physical presence or extensive direction (eg, diagnostic tests, behavioral health, dermatology, therapy).⁸

It is essential to verify the reimbursement policies and billing guidelines of individual payers, as some may adopt policies that differ from the AMA and CMS guidelines.

When to Use Modifiers -59 and -76

Modifiers -59 and -76 are used when billing for multiple procedures on the same day and can be confused. These modifiers help clarify situations in which procedures might appear redundant or improperly coded, reducing the risk for claim denials and ensuring compliance with coding guidelines. Use modifier -59 when a procedure or service is distinct or separate from other services performed on the same day (eg, cryosurgery of 4 actinic keratoses and a tangential biopsy of a nevus). Use modifier -76 when a physician performs the exact same procedure multiple times on the same patient on the same day (eg, removing 2 nevi on the face with the same excision code or performing multiple biopsies on different areas on the skin).⁹

What Are the Medical Team Conference CPT Codes?

Dermatologists frequently manage complex medical and surgical cases and actively participate in tumor boards and multidisciplinary teams conferences. It is essential to be familiar with the relevant CPT codes that can be used in these scenarios: CPT code 99366 can be used when the medical team conference occurs face-to-face with the patient present, and CPT code 99367 can be used for a medical team conference with an interdisciplinary group of health care professionals from different specialties, each of whom provides direct care to the patient.¹⁰ For CPT code 99367, the patient and/or family are not present during the meeting, which lasts a minimum of 30 minutes or more and requires participation by a physician. Current Procedural Terminology code 99368 can be used for participation in the medical team conference by a nonphysician qualified health care professional. The reporting participants need to document their participation in the medical team conference as well as their contributed information that explains the case and subsequent treatment recommendations.¹⁰

No more than 1 individual from the same specialty may report CPT codes 99366 through 99368 at the same encounter.¹⁰ Codes 99366 through 99368 should not be reported when participation in the medical team conference is part of a facility or contractually provided by the facility such as group therapy.¹⁰ The medical team conference starts at the beginning of the review of an individual patient and ends at the conclusion of the review for coding purposes. Time related to record-keeping or report generation does not need to be reported. The reporting participant needs to be present for the entire conference. The time reported is not limited to the time that the participant is communicating with other team members or the patient and/or their family/ caregiver(s). Time reported for medical team conferences may not be used in the determination for other services, such as care plan oversight (99374-99380), prolonged services (99358, 99359), psychotherapy, or any E/M service. When the patient is present for any part of the duration of the team conference, nonphysician qualified health care professionals (eg, speech-language pathologists, physical therapists, occupational therapists, social workers, dietitians) report the medical team conference face-to-face with code 99366.¹⁰

Update on Excimer Laser CPT Codes

The CMS rejected values recommended for CPT codes (96920-96922) by the Relative Value Scale Update Committee, proposing lower work RVUs of 0.83, 0.90, and 1.15, respectively (Table).^2,11 The CPT panel did not recognize the strength of the literature supporting the expanded use of the codes for conditions other than psoriasis. Report the use of excimer laser for treatment of vitiligo, atopic dermatitis, and alopecia areata using CPT code 96999 (unlisted special dermatological service or procedure).¹¹

Update on the New G2211 Code

Healthcare Common Procedure Coding System code G2211 is an add-on complexity code that can be reported with all outpatient E/M visits to better account for additional resources associated with primary care or similarly ongoing medical care related to a patient’s single serious condition or complex condition.¹² It can be billed if the physician is serving as the continuing focal point for all the patient's health care service needs, acting as the central point of contact for the patient’s ongoing medical care, and managing all aspects of their health needs over time. It is not restricted based on specialty, but it is determined based on the nature of the physician-patient relationship.¹²

Code G2211 should not be used for the following scenarios: (1) care provided by a clinician with a discrete, routine, or time-limited relationship with the patient, such as a routine skin examination or an acute allergic contact dermatitis; (2) conditions in which comorbidities are not present or addressed; (3) when the billing clinician has not assumed responsibility for ongoing medical care with consistency and continuity over time; and (4) visits billed with modifier -25.¹² In the 2025 MPFS, the CMS is proposing to allow payment of G2211 when the code is reported by the same practitioner on the same day as an annual wellness visit, vaccine administration, or any Medicare Part B preventive service furnished in the office or outpatient setting (ie, creating a limited exception to the prohibition of using this code with modifier -25).²

Documentation in the medical record must support reporting code G2211 and indicate a medically reasonable and necessary reason for the additional RVUs (0.33 and additional payment of $16.05).¹²

Underutilization of Z Codes for Social Determinants of Health

Barriers to documentation of social determinants of health (SDOH)–related International Classification of Diseases, Tenth Revision, Z codes (Z55-Z66)(eTable 1), include lack of clarity on who can document patients’ social needs, lack of systems and processes for documenting and coding SDOH, unfamiliarity with these Z codes, and a low prioritization of collecting these data.¹³ Documentation of a SDOH-related Z code relevant to a patient encounter is considered moderate risk and can have a major impact on a patient’s overall health, unmet social needs, and outcomes.¹³ If the other 2 medical decision-making elements (ie, number and complexity of problems addressed along with amount and/or complexity of data to be reviewed and analyzed) for the E/M visit also are moderate, then the encounter can be coded as level 4.¹³

New Codes for Alopecia and Acne Surgery

New International Classification of Diseases, Tenth Revision, Clinical Modification, codes for alopecia have been developed through collaboration of the American Academy of Dermatology Association and the Scarring Alopecia Foundation (eTable 2). Cutaneous extraction—previously coded as acne surgery (CPT code 10040)—will now be listed in the 2026 CPT coding manual as “extraction” (eg, marsupialization, opening of multiple milia, acne comedones, cysts, pustules).¹⁴

Quality Payment Program Update

The MIPS performance threshold will remain at 75 for the 2025 performance period, impacting the 2027 payment year.¹⁵ The MIPS Value Pathways will be available but optional in 2025, and the CMS plans to fully replace MIPS by 2029. The goal for the MVPs is to reduce the administrative burden of MIPS for physicians and their staff while simplifying reporting; however, there are several concerns. The MIPS Value Pathways build on the MIPS’s flawed processes; compare the cost for one condition to the quality of another; continue to be burdensome to physicians; have not demonstrated improved patient care; are a broad, one-size-fits-all model that could lead to inequity based on practice mix; and are not clinically relevant to physicians and patients.¹⁵

Beginning in 2025, dermatologists also will have access to a new high-priority quality measure—Melanoma: Tracking and Evaluation of Recurrence—and the Melanoma: Continuity of Care–Recall System measure (MIPS measure 137) will be removed starting in 2025.¹⁵

What Can Dermatologists Do?

With the fifth consecutive year of payment cuts, the cumulative reduction to physician payments has reached an untenable level, and physicians cannot continue to absorb the reductions, which impact access and ability to provide patient care. Members of the American Academy of Dermatology Association must urge members of Congress to stop the cuts and find a permanent solution to fix Medicare physician payment by asking their representatives to cosponsor the following bills in the US House of Representatives and Senate¹⁶:

• HR 10073—The Medicare Patient Access and Practice Stabilization Act of 2024 would stop the 2.8% cut to the 2025 MPFS and provide a positive inflationary adjustment for physician practices equal to 50% of the 2025 MEI, which comes down to an increase of approximately 1.8%.¹⁷
• HR 2424—The Strengthening Medicare for Patients and Providers Act would provide an annual inflation update equal to the MEI for Medicare physician payments.¹⁸
• HR 6371—The Provider Reimbursement Stability Act would revise budget neutrality policies that contribute to eroding Medicare physician reimbursement.¹⁹
• S 4935—The Physician Fee Stabilization Act would increase the budget neutrality trigger from $20 million to $53 million.²⁰

Advocacy is critically important: be engaged and get involved in grassroots efforts to protect access to health care, as these cuts do nothing to curb health care costs.

Final Thoughts

Congress has failed to address declining Medicare reimbursement rates, allowing cuts that jeopardize patient access to care as physicians close or sell their practices. It is important for dermatologists to attend the American Medical Association’s National Advocacy Conference in February 2025, which will feature an event on fixing Medicare. Dermatologists also can join prominent House members in urging Congress to reverse Medicare cuts and reform the physician payment system as well as write to their representatives and share how these cuts impact their practices and patients.

THE DIAGNOSIS: Diffuse Dermal Angiomatosis

Diffuse dermal angiomatosis (DDA) is a rare benign condition that manifests as tender, indurated, erythematous or violaceous plaques that can develop ulceration and necrosis. It typically occurs in areas susceptible to chronic hypoxia, such as the arms and legs, as was seen in our patient, as well as on large pendulous breasts in females. This condition is a distinct variant of reactive angioendotheliomatosis associated with smoking, trauma, underlying vaso-occlusion, and hypercoagulability.^1,2 Risk factors include a history of smoking as well as conditions associated with chronic hypoxia, such as severe peripheral vascular disease, subclavian artery stenosis, hypercoagulable states, monoclonal gammopathy, steal syndrome from an arteriovenous fistula, end-stage renal failure, calciphylaxis, and obesity.¹

Histopathology of DDA reveals a diffuse dermal proliferation of capillaries due to upregulation of vascular endothelial growth factor secondary to chronic ischemia and hypoxia.^1,2 Small, well-formed capillaries surrounded by pericytes dissect through dermal collagen into the subcutis (eFigure 1). Spindle-shaped cells with vacuolated cytoplasm and scattered extravasated erythrocytes with hemosiderin may be observed.² Cellular atypia generally is not seen.^2,3 Diffuse dermal angiomatosis is characterized by positive CD31, CD34, and ERG immunostaining1 and HHV-8 and D2-40 negativity.² In our patient, the areas suggestive of connective tissue calciumlike depositions were concerning for dystrophic calcification related to end-stage renal disease. Although Von Kossa staining failed to highlight vascular calcifications, early calciphylaxis from end-stage renal disease could not be excluded.

The main goal of DDA treatment is to target tissue hypoxia, and primary preventive measures aim to reduce risk factors associated with atherosclerosis.¹ Treatment options for DDA include revascularization, reduction mammoplasty, excision, isotretinoin, oral corticosteroids, smoking cessation, pentoxifylline plus aspirin, and management of underlying calciphylaxis.^1,2 Spontaneous resolution of DDA rarely has been reported.¹

Acroangiodermatitis, also known as pseudo–Kaposi sarcoma (KS), is a rare angioproliferative disorder that often is associated with vascular anomalies.^4,5 It is divided into 2 main variants: Mali type, which is associated with chronic venous insufficiency, and Stewart-Bluefarb type, associated with arteriovenous malformations.⁴ This condition is characterized by red to violaceous macules, papules, or plaques that may become ulcerated or coalesce to form larger confluent patches, typically arising on the lower extremities.^4,6,7 Histopathology of acroangiodermatitis reveals circumscribed lobular proliferation of thick-walled dermal vessels (eFigure 2), in contrast to the diffuse dermal proliferation of endothelial cells between collagen bundles seen in DDA.^2,3,6

Angiosarcoma is a rare, highly aggressive vascular tumor that originates from vascular or lymphatic endothelial cells. It typically manifests with raised, bruiselike, erythematous to violaceous papules or plaques.^8,9 Histopathologically, the hallmark feature of angiosarcoma is abnormal, pleomorphic, malignant endothelial cells with pale, light, eosinophilic cytoplasm and hyperchromatic nuclei (eFigure 3).^2,9 In poorly differentiated cases, malignant endothelial cells may exhibit an epithelioid morphology with areas of hemorrhage and necrosis.⁹ Immunohistochemistry is positive for ERG, CD34, CD31, vascular endothelial growth factor, and D2-40.^2,9

Kaposi sarcoma is a soft tissue malignancy known to occur in immunosuppressed patients such as individuals with AIDS or those undergoing immunosuppressive therapy for organ transplantation.¹⁰ There are 4 major forms of KS: classic (appearing on the lower extremities in elderly men of Mediterranean and Eastern European descent), endemic (occurring in children specifically in Africa with generalized lymph node involvement), HIV/ AIDS–related (occurring in patients not taking highly active antiretroviral therapy with diffuse involvement of the skin and internal organs), and iatrogenic (occurring in immunosuppressed patients with diffuse involvement of the skin and internal organs).^10,11 Kaposi sarcoma presents as multiple reddish brown, raised or flat, painless, nonblanching mucocutaneous lesions that occasionally can ulcerate and bleed.¹¹ Histopathologic features of KS include vascular proliferation in the dermis with diffuse slitlike lumen formation with the promontory sign, hyaline globules, hemosiderin accumulation, and an inflammatory component that often contains plasma cells (eFigure 4).^2,11 Kaposi sarcoma is characterized by positive staining for CD31, CD34, D2-40, and HHV-8; the last 2 are an important distinction from DDA.²

Targetoid hemosiderotic hemangioma, also known as hobnail hemangioma, is a benign vascular lesion that typically manifests as a solitary, brown to violaceous papule or plaque on the trunk or extremities.¹² It is sometimes surrounded by a pale area and a peripheral ecchymotic ring, giving the lesion a targetoid appearance.^12,13 Histopathologic features include dilated, thin-walled vessels with prominent endothelial hobnailing in the papillary dermis, slit-shaped vascular channels between collagen bundles in the deeper dermis, and an interstitial lymphocytic infiltrate with extravasated erythrocytes and hemosiderin deposits (eFigure 5).^12,14 The etiology of targetoid hemosiderotic hemangioma remains unclear. Chronic inflammation, trauma, exposure to ionizing radiation, and vascular obstruction have been suggested as inciting factors, though many cases have been reported without a history of cutaneous injury.^12,13 Studies suggest a lymphatic origin instead of its original classification as a hemangioma.^13,15 The endothelial cells stain positive with CD31 and may stain with D2-40 and CD34.^13,15

THE DIAGNOSIS: Diffuse Dermal Angiomatosis

Diffuse dermal angiomatosis (DDA) is a rare benign condition that manifests as tender, indurated, erythematous or violaceous plaques that can develop ulceration and necrosis. It typically occurs in areas susceptible to chronic hypoxia, such as the arms and legs, as was seen in our patient, as well as on large pendulous breasts in females. This condition is a distinct variant of reactive angioendotheliomatosis associated with smoking, trauma, underlying vaso-occlusion, and hypercoagulability.^1,2 Risk factors include a history of smoking as well as conditions associated with chronic hypoxia, such as severe peripheral vascular disease, subclavian artery stenosis, hypercoagulable states, monoclonal gammopathy, steal syndrome from an arteriovenous fistula, end-stage renal failure, calciphylaxis, and obesity.¹

Histopathology of DDA reveals a diffuse dermal proliferation of capillaries due to upregulation of vascular endothelial growth factor secondary to chronic ischemia and hypoxia.^1,2 Small, well-formed capillaries surrounded by pericytes dissect through dermal collagen into the subcutis (eFigure 1). Spindle-shaped cells with vacuolated cytoplasm and scattered extravasated erythrocytes with hemosiderin may be observed.² Cellular atypia generally is not seen.^2,3 Diffuse dermal angiomatosis is characterized by positive CD31, CD34, and ERG immunostaining1 and HHV-8 and D2-40 negativity.² In our patient, the areas suggestive of connective tissue calciumlike depositions were concerning for dystrophic calcification related to end-stage renal disease. Although Von Kossa staining failed to highlight vascular calcifications, early calciphylaxis from end-stage renal disease could not be excluded.

The main goal of DDA treatment is to target tissue hypoxia, and primary preventive measures aim to reduce risk factors associated with atherosclerosis.¹ Treatment options for DDA include revascularization, reduction mammoplasty, excision, isotretinoin, oral corticosteroids, smoking cessation, pentoxifylline plus aspirin, and management of underlying calciphylaxis.^1,2 Spontaneous resolution of DDA rarely has been reported.¹

Acroangiodermatitis, also known as pseudo–Kaposi sarcoma (KS), is a rare angioproliferative disorder that often is associated with vascular anomalies.^4,5 It is divided into 2 main variants: Mali type, which is associated with chronic venous insufficiency, and Stewart-Bluefarb type, associated with arteriovenous malformations.⁴ This condition is characterized by red to violaceous macules, papules, or plaques that may become ulcerated or coalesce to form larger confluent patches, typically arising on the lower extremities.^4,6,7 Histopathology of acroangiodermatitis reveals circumscribed lobular proliferation of thick-walled dermal vessels (eFigure 2), in contrast to the diffuse dermal proliferation of endothelial cells between collagen bundles seen in DDA.^2,3,6

Angiosarcoma is a rare, highly aggressive vascular tumor that originates from vascular or lymphatic endothelial cells. It typically manifests with raised, bruiselike, erythematous to violaceous papules or plaques.^8,9 Histopathologically, the hallmark feature of angiosarcoma is abnormal, pleomorphic, malignant endothelial cells with pale, light, eosinophilic cytoplasm and hyperchromatic nuclei (eFigure 3).^2,9 In poorly differentiated cases, malignant endothelial cells may exhibit an epithelioid morphology with areas of hemorrhage and necrosis.⁹ Immunohistochemistry is positive for ERG, CD34, CD31, vascular endothelial growth factor, and D2-40.^2,9

Kaposi sarcoma is a soft tissue malignancy known to occur in immunosuppressed patients such as individuals with AIDS or those undergoing immunosuppressive therapy for organ transplantation.¹⁰ There are 4 major forms of KS: classic (appearing on the lower extremities in elderly men of Mediterranean and Eastern European descent), endemic (occurring in children specifically in Africa with generalized lymph node involvement), HIV/ AIDS–related (occurring in patients not taking highly active antiretroviral therapy with diffuse involvement of the skin and internal organs), and iatrogenic (occurring in immunosuppressed patients with diffuse involvement of the skin and internal organs).^10,11 Kaposi sarcoma presents as multiple reddish brown, raised or flat, painless, nonblanching mucocutaneous lesions that occasionally can ulcerate and bleed.¹¹ Histopathologic features of KS include vascular proliferation in the dermis with diffuse slitlike lumen formation with the promontory sign, hyaline globules, hemosiderin accumulation, and an inflammatory component that often contains plasma cells (eFigure 4).^2,11 Kaposi sarcoma is characterized by positive staining for CD31, CD34, D2-40, and HHV-8; the last 2 are an important distinction from DDA.²

Targetoid hemosiderotic hemangioma, also known as hobnail hemangioma, is a benign vascular lesion that typically manifests as a solitary, brown to violaceous papule or plaque on the trunk or extremities.¹² It is sometimes surrounded by a pale area and a peripheral ecchymotic ring, giving the lesion a targetoid appearance.^12,13 Histopathologic features include dilated, thin-walled vessels with prominent endothelial hobnailing in the papillary dermis, slit-shaped vascular channels between collagen bundles in the deeper dermis, and an interstitial lymphocytic infiltrate with extravasated erythrocytes and hemosiderin deposits (eFigure 5).^12,14 The etiology of targetoid hemosiderotic hemangioma remains unclear. Chronic inflammation, trauma, exposure to ionizing radiation, and vascular obstruction have been suggested as inciting factors, though many cases have been reported without a history of cutaneous injury.^12,13 Studies suggest a lymphatic origin instead of its original classification as a hemangioma.^13,15 The endothelial cells stain positive with CD31 and may stain with D2-40 and CD34.^13,15

THE DIAGNOSIS: Diffuse Dermal Angiomatosis

Diffuse dermal angiomatosis (DDA) is a rare benign condition that manifests as tender, indurated, erythematous or violaceous plaques that can develop ulceration and necrosis. It typically occurs in areas susceptible to chronic hypoxia, such as the arms and legs, as was seen in our patient, as well as on large pendulous breasts in females. This condition is a distinct variant of reactive angioendotheliomatosis associated with smoking, trauma, underlying vaso-occlusion, and hypercoagulability.^1,2 Risk factors include a history of smoking as well as conditions associated with chronic hypoxia, such as severe peripheral vascular disease, subclavian artery stenosis, hypercoagulable states, monoclonal gammopathy, steal syndrome from an arteriovenous fistula, end-stage renal failure, calciphylaxis, and obesity.¹

Histopathology of DDA reveals a diffuse dermal proliferation of capillaries due to upregulation of vascular endothelial growth factor secondary to chronic ischemia and hypoxia.^1,2 Small, well-formed capillaries surrounded by pericytes dissect through dermal collagen into the subcutis (eFigure 1). Spindle-shaped cells with vacuolated cytoplasm and scattered extravasated erythrocytes with hemosiderin may be observed.² Cellular atypia generally is not seen.^2,3 Diffuse dermal angiomatosis is characterized by positive CD31, CD34, and ERG immunostaining1 and HHV-8 and D2-40 negativity.² In our patient, the areas suggestive of connective tissue calciumlike depositions were concerning for dystrophic calcification related to end-stage renal disease. Although Von Kossa staining failed to highlight vascular calcifications, early calciphylaxis from end-stage renal disease could not be excluded.

The main goal of DDA treatment is to target tissue hypoxia, and primary preventive measures aim to reduce risk factors associated with atherosclerosis.¹ Treatment options for DDA include revascularization, reduction mammoplasty, excision, isotretinoin, oral corticosteroids, smoking cessation, pentoxifylline plus aspirin, and management of underlying calciphylaxis.^1,2 Spontaneous resolution of DDA rarely has been reported.¹

Acroangiodermatitis, also known as pseudo–Kaposi sarcoma (KS), is a rare angioproliferative disorder that often is associated with vascular anomalies.^4,5 It is divided into 2 main variants: Mali type, which is associated with chronic venous insufficiency, and Stewart-Bluefarb type, associated with arteriovenous malformations.⁴ This condition is characterized by red to violaceous macules, papules, or plaques that may become ulcerated or coalesce to form larger confluent patches, typically arising on the lower extremities.^4,6,7 Histopathology of acroangiodermatitis reveals circumscribed lobular proliferation of thick-walled dermal vessels (eFigure 2), in contrast to the diffuse dermal proliferation of endothelial cells between collagen bundles seen in DDA.^2,3,6

Angiosarcoma is a rare, highly aggressive vascular tumor that originates from vascular or lymphatic endothelial cells. It typically manifests with raised, bruiselike, erythematous to violaceous papules or plaques.^8,9 Histopathologically, the hallmark feature of angiosarcoma is abnormal, pleomorphic, malignant endothelial cells with pale, light, eosinophilic cytoplasm and hyperchromatic nuclei (eFigure 3).^2,9 In poorly differentiated cases, malignant endothelial cells may exhibit an epithelioid morphology with areas of hemorrhage and necrosis.⁹ Immunohistochemistry is positive for ERG, CD34, CD31, vascular endothelial growth factor, and D2-40.^2,9

Kaposi sarcoma is a soft tissue malignancy known to occur in immunosuppressed patients such as individuals with AIDS or those undergoing immunosuppressive therapy for organ transplantation.¹⁰ There are 4 major forms of KS: classic (appearing on the lower extremities in elderly men of Mediterranean and Eastern European descent), endemic (occurring in children specifically in Africa with generalized lymph node involvement), HIV/ AIDS–related (occurring in patients not taking highly active antiretroviral therapy with diffuse involvement of the skin and internal organs), and iatrogenic (occurring in immunosuppressed patients with diffuse involvement of the skin and internal organs).^10,11 Kaposi sarcoma presents as multiple reddish brown, raised or flat, painless, nonblanching mucocutaneous lesions that occasionally can ulcerate and bleed.¹¹ Histopathologic features of KS include vascular proliferation in the dermis with diffuse slitlike lumen formation with the promontory sign, hyaline globules, hemosiderin accumulation, and an inflammatory component that often contains plasma cells (eFigure 4).^2,11 Kaposi sarcoma is characterized by positive staining for CD31, CD34, D2-40, and HHV-8; the last 2 are an important distinction from DDA.²

Targetoid hemosiderotic hemangioma, also known as hobnail hemangioma, is a benign vascular lesion that typically manifests as a solitary, brown to violaceous papule or plaque on the trunk or extremities.¹² It is sometimes surrounded by a pale area and a peripheral ecchymotic ring, giving the lesion a targetoid appearance.^12,13 Histopathologic features include dilated, thin-walled vessels with prominent endothelial hobnailing in the papillary dermis, slit-shaped vascular channels between collagen bundles in the deeper dermis, and an interstitial lymphocytic infiltrate with extravasated erythrocytes and hemosiderin deposits (eFigure 5).^12,14 The etiology of targetoid hemosiderotic hemangioma remains unclear. Chronic inflammation, trauma, exposure to ionizing radiation, and vascular obstruction have been suggested as inciting factors, though many cases have been reported without a history of cutaneous injury.^12,13 Studies suggest a lymphatic origin instead of its original classification as a hemangioma.^13,15 The endothelial cells stain positive with CD31 and may stain with D2-40 and CD34.^13,15

Dermatopathology education, which comprises approximately 30% of the dermatology residency curriculum, is crucial for the holistic training of dermatology residents to diagnose and manage a range of dermatologic conditions.¹ Additionally, dermatopathology is the topic of one of the 4 American Board of Dermatology CORE Exam modules, further highlighting the need for comprehensive education in this area. A variety of resources including virtual dermatopathology and conventional microscopy training currently are used in residency programs for dermatopathology education.^2,3 Although used less frequently, social media platforms such as Instagram also are used to aid in dermatopathology education for a wider audience.⁴ Other online resources, including the American Society of Dermatopathology website (www.asdp.org) and DermpathAtlas.com, are excellent tools for medical students, residents, and fellows to develop their knowledge.⁵ While these resources are accessible, they must be directly sought out by the student and utilized on their own time. Additionally, if medical students do not have a strong understanding of the basics of dermatopathology, they may not have the foundation required to benefit from these resources.

Dermatopathology education is critical for the overall practice of dermatology, yet most dermatology residency programs may not be incorporating dermatopathology education early enough in training. One study evaluating the timing and length of dermatopathology education during residency reported that fewer than 40% (20/51) of dermatology residency programs allocate 3 or more weeks to dermatopathology education during the second postgraduate year.¹ Despite Ackerman6 advocating for early dermatopathology exposure to best prepare medical students to recognize and manage certain dermatologic conditions, the majority of exposure still seems to occur during postgraduate year 4.¹ Furthermore, current primary care residents feel that their medical school training did not sufficiently prepare them to diagnose and manage dermatologic conditions, with only 37% (93/252) reporting feeling adequately prepared.^7,8 Medical students also reported a lack of confidence in overall dermatology knowledge, with 89% (72/81) reporting they felt neutral, slightly confident, or not at all confident when asked to diagnose skin lesions.⁹ In the same study, the average score was 46.6% (7/15 questions answered correctly) when 74 participants were assessed via a multiple choice quiz on dermatologic diagnosis and treatment, further demonstrating the lack of general dermatology comfort among medical students.⁹ This likely stems from limited dermatology curriculum in medical schools, demonstrating the need for further dermatology education as a whole in medical school.¹⁰

Ensuring robust dermatopathology education in medical school and the first year of dermatology residency has the potential to better prepare medical students for the transition into dermatology residency and clinical practice. We created an introductory dermatopathology lecture and presented it to medical students and first year dermatology residents to improve dermatopathology knowledge and confidence in learners early in their dermatology training.

Structure of the Lecture

Participants included first-year dermatology residents and fourth-year medical students rotating with the Wayne State University Department of Dermatology (Detroit, Michigan). The same facilitator (H.O.) taught each of the lectures, and all lectures were conducted via Zoom at the beginning of the month from May 2024 through November 2024. A total of 7 lectures were given. The lecture was formatted so that a histologic image was shown, then learners expressed their thoughts about what the image was showing before the answer was given. This format allowed participants to view the images on their own device screen and allowed the facilitator to annotate the images. The lecture was divided into 3 sections: (1) cell types and basic structures, (2) anatomic slides, and (3) common diagnoses. Each session lasted approximately 45 minutes.

Section 1: Cell Types and Basic Structures—The first section covered the fundamental cell types (neutrophils, lymphocytes, plasma cells, melanocytes, and eosinophils) along with glandular structures (apocrine, eccrine, and sebaceous). The session was designed to follow a retention and allow learners to think through each slide. First, participants were shown histologic images of each cell type and were asked to identify what type of cell was being shown. On the following slide, key features of each cell type were highlighted. Next, participants similarly were shown images of the glandular structures followed by key features of each. The section concluded with a review of the layers of the skin (stratum corneum, stratum granulosum, stratum lucidum, stratum spinosum, and stratum basale). A histologic image was shown, and the facilitator discussed how to distinguish the layers.

Section 2: Anatomic Sites—This section focused on key pathologic features for differentiating body surfaces, including the scalp, face, eyelids, ears, areolae, palms and soles, and mucosae. Participants initially were shown an image of a hematoxylin and eosin–stained slide from a specific body surface and then were asked to identify structures that may serve as a clue to the anatomic location. If the participants were not sure, they were given hints; for example, when participants were shown an image of the ear and were unsure of the location, the facilitator circled cartilage and asked them to identify the structure. In most cases, once participants named this structure, they were able to recognize that the location was the ear.

Section 3: Common Diagnoses—This section addressed frequently encountered diagnoses in dermatopathology, including basal cell carcinoma, squamous cell carcinoma, squamous cell carcinoma in situ, epidermoid cyst, pilar cyst, seborrheic keratosis, solar lentigo, melanocytic nevus, melanoma, verruca vulgaris, spongiotic dermatitis, psoriasis, and lichen planus. It followed the same format of the first section: participants were shown an hemotoxyllin and eosin–stained image and then were asked to discuss what the diagnosis could be and why. Hints were given if participants struggled to come up with the correct diagnosis. A few slides also were dedicated to distinguishing benign nevi, dysplastic nevi, and melanoma.

Pretest and Posttest Results

Residents participated in the lecture as part of their first-year orientation, and medical students participated during their dermatology rotation. All participants were invited to complete a pretest and a posttest before and after the lecture, respectively. Both assessments were optional and anonymous. The pretest was completed electronically and consisted of 10 knowledge-based, multiple-choice questions that included a histopathologic image and asked, “What is the most likely diagnosis?,” “What is the predominant cell type?,” and “Where was this specimen taken from?” In addition to the knowledge-based questions, participants also were asked to rate their confidence in dermatopathology on a 5-point Likert scale ranging from 1 (not confident at all) to 5 (extremely confident). Participants completed the entire pretest before any information on the topic was provided. After the lecture, participants were asked to complete a posttest identical to the pretest and to rate their confidence in dermatopathology again on the same scale. The posttest included an additional question asking participants to rate the helpfulness of the lecture on a Likert scale ranging from 1 (not helpful at all) to 5 (extremely helpful). Participants completed the posttest within 48 hours of the lecture.

Overall, 15 learners participated in the pretest and 12 in the posttest. Of the 15 pretest participants, 3 were first-year residents and 12 were medical students. Similarly, in the posttest, 2 respondents were first-year residents and 10 were medical students. All responses contained complete pretests and posttests. The mean score on the pretest was 62%, whereas the mean score on the posttest was 75%. A paired t test indicated a statistically significant improvement (P=.017). In addition, the mean rating for confidence in dermatopathology knowledge before the lecture was 1.5 prior to the lecture and 2.6 after the lecture. A paired t test demonstrated statistical significance (P=.010). The mean rating of the helpfulness of the lecture was 4.67. The majority (91.7% [11/12]) of the participants gave a rating of 4 or 5.

Impact of the Lecture on Dermatopathology Knowledge

There is a gap in dermatopathology education early in medical training. Our introductory lecture led to higher post test scores and increased confidence in dermatopathology among medical students and dermatology residents, demonstrating the effectiveness of this kind of program in bridging this education gap. The majority of participants in our lecture said they found the session helpful. A previously published article called for early implementation of dermatology education as a whole in the medical curriculum due to lack of knowledge and confidence, and our introductory lecture may help to bridge this gap.⁸ Increasing dermatopathology content for medical students and first-year dermatology residents can expand knowledge, as shown by the increased scores on the posttest, and better supports learners transitioning to dermatology residency, where dermatopathology constitutes a large part of the overall curriculum.² More comprehensive knowledge of dermatopathology early in dermatology training also may help to better prepare residents to accurately diagnose and manage dermatologic conditions.

Pretest scores showed that the average confidence rating in dermatopathology among participants in our lecture was 1.5, which is rather low. This is consistent with prior studies that have found that residents feel that medical school inadequately prepared them for dermatology residency.^7,8 More than 87% (71/81) of medical students surveyed felt they received inadequate general dermatology training in medical school.⁹ This supports the proposed educational gap that is impacting confidence in overall dermatology knowledge, which includes dermatopathology. In our study, the average confidence rating increased by 1.1 points after the lecture, which was statistically significant (P=.010) and demonstrates that an introductory lecture serves as a feasible intervention to improve confidence in this area.

The feedback we received from participants in our lecture shows the benefits of an introductory interactive lecture with virtual dermatopathology images. Ngo et al2 highlighted how residents perceive virtual images to be superior to conventional microscopy for dermatopathology, which we utilized in our lecture. This method is not only cost effective but also provides a simple way for learners and facilitators to point out key findings on histopathology slides.²

Final Thoughts

Overall, implementing dermatopathology education early in training has a measurable impact on dermatopathology knowledge and confidence among medical students and first-year dermatology residents. An interactive lecture with virtual images similar to the one we describe here may better prepare learners for the transition to dermatology residency by addressing the educational gap in dermatopathology early in training.

Dermatopathology education, which comprises approximately 30% of the dermatology residency curriculum, is crucial for the holistic training of dermatology residents to diagnose and manage a range of dermatologic conditions.¹ Additionally, dermatopathology is the topic of one of the 4 American Board of Dermatology CORE Exam modules, further highlighting the need for comprehensive education in this area. A variety of resources including virtual dermatopathology and conventional microscopy training currently are used in residency programs for dermatopathology education.^2,3 Although used less frequently, social media platforms such as Instagram also are used to aid in dermatopathology education for a wider audience.⁴ Other online resources, including the American Society of Dermatopathology website (www.asdp.org) and DermpathAtlas.com, are excellent tools for medical students, residents, and fellows to develop their knowledge.⁵ While these resources are accessible, they must be directly sought out by the student and utilized on their own time. Additionally, if medical students do not have a strong understanding of the basics of dermatopathology, they may not have the foundation required to benefit from these resources.

Dermatopathology education is critical for the overall practice of dermatology, yet most dermatology residency programs may not be incorporating dermatopathology education early enough in training. One study evaluating the timing and length of dermatopathology education during residency reported that fewer than 40% (20/51) of dermatology residency programs allocate 3 or more weeks to dermatopathology education during the second postgraduate year.¹ Despite Ackerman6 advocating for early dermatopathology exposure to best prepare medical students to recognize and manage certain dermatologic conditions, the majority of exposure still seems to occur during postgraduate year 4.¹ Furthermore, current primary care residents feel that their medical school training did not sufficiently prepare them to diagnose and manage dermatologic conditions, with only 37% (93/252) reporting feeling adequately prepared.^7,8 Medical students also reported a lack of confidence in overall dermatology knowledge, with 89% (72/81) reporting they felt neutral, slightly confident, or not at all confident when asked to diagnose skin lesions.⁹ In the same study, the average score was 46.6% (7/15 questions answered correctly) when 74 participants were assessed via a multiple choice quiz on dermatologic diagnosis and treatment, further demonstrating the lack of general dermatology comfort among medical students.⁹ This likely stems from limited dermatology curriculum in medical schools, demonstrating the need for further dermatology education as a whole in medical school.¹⁰

Ensuring robust dermatopathology education in medical school and the first year of dermatology residency has the potential to better prepare medical students for the transition into dermatology residency and clinical practice. We created an introductory dermatopathology lecture and presented it to medical students and first year dermatology residents to improve dermatopathology knowledge and confidence in learners early in their dermatology training.

Structure of the Lecture

Participants included first-year dermatology residents and fourth-year medical students rotating with the Wayne State University Department of Dermatology (Detroit, Michigan). The same facilitator (H.O.) taught each of the lectures, and all lectures were conducted via Zoom at the beginning of the month from May 2024 through November 2024. A total of 7 lectures were given. The lecture was formatted so that a histologic image was shown, then learners expressed their thoughts about what the image was showing before the answer was given. This format allowed participants to view the images on their own device screen and allowed the facilitator to annotate the images. The lecture was divided into 3 sections: (1) cell types and basic structures, (2) anatomic slides, and (3) common diagnoses. Each session lasted approximately 45 minutes.

Section 1: Cell Types and Basic Structures—The first section covered the fundamental cell types (neutrophils, lymphocytes, plasma cells, melanocytes, and eosinophils) along with glandular structures (apocrine, eccrine, and sebaceous). The session was designed to follow a retention and allow learners to think through each slide. First, participants were shown histologic images of each cell type and were asked to identify what type of cell was being shown. On the following slide, key features of each cell type were highlighted. Next, participants similarly were shown images of the glandular structures followed by key features of each. The section concluded with a review of the layers of the skin (stratum corneum, stratum granulosum, stratum lucidum, stratum spinosum, and stratum basale). A histologic image was shown, and the facilitator discussed how to distinguish the layers.

Section 2: Anatomic Sites—This section focused on key pathologic features for differentiating body surfaces, including the scalp, face, eyelids, ears, areolae, palms and soles, and mucosae. Participants initially were shown an image of a hematoxylin and eosin–stained slide from a specific body surface and then were asked to identify structures that may serve as a clue to the anatomic location. If the participants were not sure, they were given hints; for example, when participants were shown an image of the ear and were unsure of the location, the facilitator circled cartilage and asked them to identify the structure. In most cases, once participants named this structure, they were able to recognize that the location was the ear.

Section 3: Common Diagnoses—This section addressed frequently encountered diagnoses in dermatopathology, including basal cell carcinoma, squamous cell carcinoma, squamous cell carcinoma in situ, epidermoid cyst, pilar cyst, seborrheic keratosis, solar lentigo, melanocytic nevus, melanoma, verruca vulgaris, spongiotic dermatitis, psoriasis, and lichen planus. It followed the same format of the first section: participants were shown an hemotoxyllin and eosin–stained image and then were asked to discuss what the diagnosis could be and why. Hints were given if participants struggled to come up with the correct diagnosis. A few slides also were dedicated to distinguishing benign nevi, dysplastic nevi, and melanoma.

Pretest and Posttest Results

Residents participated in the lecture as part of their first-year orientation, and medical students participated during their dermatology rotation. All participants were invited to complete a pretest and a posttest before and after the lecture, respectively. Both assessments were optional and anonymous. The pretest was completed electronically and consisted of 10 knowledge-based, multiple-choice questions that included a histopathologic image and asked, “What is the most likely diagnosis?,” “What is the predominant cell type?,” and “Where was this specimen taken from?” In addition to the knowledge-based questions, participants also were asked to rate their confidence in dermatopathology on a 5-point Likert scale ranging from 1 (not confident at all) to 5 (extremely confident). Participants completed the entire pretest before any information on the topic was provided. After the lecture, participants were asked to complete a posttest identical to the pretest and to rate their confidence in dermatopathology again on the same scale. The posttest included an additional question asking participants to rate the helpfulness of the lecture on a Likert scale ranging from 1 (not helpful at all) to 5 (extremely helpful). Participants completed the posttest within 48 hours of the lecture.

Overall, 15 learners participated in the pretest and 12 in the posttest. Of the 15 pretest participants, 3 were first-year residents and 12 were medical students. Similarly, in the posttest, 2 respondents were first-year residents and 10 were medical students. All responses contained complete pretests and posttests. The mean score on the pretest was 62%, whereas the mean score on the posttest was 75%. A paired t test indicated a statistically significant improvement (P=.017). In addition, the mean rating for confidence in dermatopathology knowledge before the lecture was 1.5 prior to the lecture and 2.6 after the lecture. A paired t test demonstrated statistical significance (P=.010). The mean rating of the helpfulness of the lecture was 4.67. The majority (91.7% [11/12]) of the participants gave a rating of 4 or 5.

Impact of the Lecture on Dermatopathology Knowledge

There is a gap in dermatopathology education early in medical training. Our introductory lecture led to higher post test scores and increased confidence in dermatopathology among medical students and dermatology residents, demonstrating the effectiveness of this kind of program in bridging this education gap. The majority of participants in our lecture said they found the session helpful. A previously published article called for early implementation of dermatology education as a whole in the medical curriculum due to lack of knowledge and confidence, and our introductory lecture may help to bridge this gap.⁸ Increasing dermatopathology content for medical students and first-year dermatology residents can expand knowledge, as shown by the increased scores on the posttest, and better supports learners transitioning to dermatology residency, where dermatopathology constitutes a large part of the overall curriculum.² More comprehensive knowledge of dermatopathology early in dermatology training also may help to better prepare residents to accurately diagnose and manage dermatologic conditions.

Pretest scores showed that the average confidence rating in dermatopathology among participants in our lecture was 1.5, which is rather low. This is consistent with prior studies that have found that residents feel that medical school inadequately prepared them for dermatology residency.^7,8 More than 87% (71/81) of medical students surveyed felt they received inadequate general dermatology training in medical school.⁹ This supports the proposed educational gap that is impacting confidence in overall dermatology knowledge, which includes dermatopathology. In our study, the average confidence rating increased by 1.1 points after the lecture, which was statistically significant (P=.010) and demonstrates that an introductory lecture serves as a feasible intervention to improve confidence in this area.

The feedback we received from participants in our lecture shows the benefits of an introductory interactive lecture with virtual dermatopathology images. Ngo et al2 highlighted how residents perceive virtual images to be superior to conventional microscopy for dermatopathology, which we utilized in our lecture. This method is not only cost effective but also provides a simple way for learners and facilitators to point out key findings on histopathology slides.²

Final Thoughts

Overall, implementing dermatopathology education early in training has a measurable impact on dermatopathology knowledge and confidence among medical students and first-year dermatology residents. An interactive lecture with virtual images similar to the one we describe here may better prepare learners for the transition to dermatology residency by addressing the educational gap in dermatopathology early in training.

Dermatopathology education, which comprises approximately 30% of the dermatology residency curriculum, is crucial for the holistic training of dermatology residents to diagnose and manage a range of dermatologic conditions.¹ Additionally, dermatopathology is the topic of one of the 4 American Board of Dermatology CORE Exam modules, further highlighting the need for comprehensive education in this area. A variety of resources including virtual dermatopathology and conventional microscopy training currently are used in residency programs for dermatopathology education.^2,3 Although used less frequently, social media platforms such as Instagram also are used to aid in dermatopathology education for a wider audience.⁴ Other online resources, including the American Society of Dermatopathology website (www.asdp.org) and DermpathAtlas.com, are excellent tools for medical students, residents, and fellows to develop their knowledge.⁵ While these resources are accessible, they must be directly sought out by the student and utilized on their own time. Additionally, if medical students do not have a strong understanding of the basics of dermatopathology, they may not have the foundation required to benefit from these resources.

Dermatopathology education is critical for the overall practice of dermatology, yet most dermatology residency programs may not be incorporating dermatopathology education early enough in training. One study evaluating the timing and length of dermatopathology education during residency reported that fewer than 40% (20/51) of dermatology residency programs allocate 3 or more weeks to dermatopathology education during the second postgraduate year.¹ Despite Ackerman6 advocating for early dermatopathology exposure to best prepare medical students to recognize and manage certain dermatologic conditions, the majority of exposure still seems to occur during postgraduate year 4.¹ Furthermore, current primary care residents feel that their medical school training did not sufficiently prepare them to diagnose and manage dermatologic conditions, with only 37% (93/252) reporting feeling adequately prepared.^7,8 Medical students also reported a lack of confidence in overall dermatology knowledge, with 89% (72/81) reporting they felt neutral, slightly confident, or not at all confident when asked to diagnose skin lesions.⁹ In the same study, the average score was 46.6% (7/15 questions answered correctly) when 74 participants were assessed via a multiple choice quiz on dermatologic diagnosis and treatment, further demonstrating the lack of general dermatology comfort among medical students.⁹ This likely stems from limited dermatology curriculum in medical schools, demonstrating the need for further dermatology education as a whole in medical school.¹⁰

Ensuring robust dermatopathology education in medical school and the first year of dermatology residency has the potential to better prepare medical students for the transition into dermatology residency and clinical practice. We created an introductory dermatopathology lecture and presented it to medical students and first year dermatology residents to improve dermatopathology knowledge and confidence in learners early in their dermatology training.

Structure of the Lecture

Participants included first-year dermatology residents and fourth-year medical students rotating with the Wayne State University Department of Dermatology (Detroit, Michigan). The same facilitator (H.O.) taught each of the lectures, and all lectures were conducted via Zoom at the beginning of the month from May 2024 through November 2024. A total of 7 lectures were given. The lecture was formatted so that a histologic image was shown, then learners expressed their thoughts about what the image was showing before the answer was given. This format allowed participants to view the images on their own device screen and allowed the facilitator to annotate the images. The lecture was divided into 3 sections: (1) cell types and basic structures, (2) anatomic slides, and (3) common diagnoses. Each session lasted approximately 45 minutes.

Section 1: Cell Types and Basic Structures—The first section covered the fundamental cell types (neutrophils, lymphocytes, plasma cells, melanocytes, and eosinophils) along with glandular structures (apocrine, eccrine, and sebaceous). The session was designed to follow a retention and allow learners to think through each slide. First, participants were shown histologic images of each cell type and were asked to identify what type of cell was being shown. On the following slide, key features of each cell type were highlighted. Next, participants similarly were shown images of the glandular structures followed by key features of each. The section concluded with a review of the layers of the skin (stratum corneum, stratum granulosum, stratum lucidum, stratum spinosum, and stratum basale). A histologic image was shown, and the facilitator discussed how to distinguish the layers.

Section 2: Anatomic Sites—This section focused on key pathologic features for differentiating body surfaces, including the scalp, face, eyelids, ears, areolae, palms and soles, and mucosae. Participants initially were shown an image of a hematoxylin and eosin–stained slide from a specific body surface and then were asked to identify structures that may serve as a clue to the anatomic location. If the participants were not sure, they were given hints; for example, when participants were shown an image of the ear and were unsure of the location, the facilitator circled cartilage and asked them to identify the structure. In most cases, once participants named this structure, they were able to recognize that the location was the ear.

Section 3: Common Diagnoses—This section addressed frequently encountered diagnoses in dermatopathology, including basal cell carcinoma, squamous cell carcinoma, squamous cell carcinoma in situ, epidermoid cyst, pilar cyst, seborrheic keratosis, solar lentigo, melanocytic nevus, melanoma, verruca vulgaris, spongiotic dermatitis, psoriasis, and lichen planus. It followed the same format of the first section: participants were shown an hemotoxyllin and eosin–stained image and then were asked to discuss what the diagnosis could be and why. Hints were given if participants struggled to come up with the correct diagnosis. A few slides also were dedicated to distinguishing benign nevi, dysplastic nevi, and melanoma.

Pretest and Posttest Results

Residents participated in the lecture as part of their first-year orientation, and medical students participated during their dermatology rotation. All participants were invited to complete a pretest and a posttest before and after the lecture, respectively. Both assessments were optional and anonymous. The pretest was completed electronically and consisted of 10 knowledge-based, multiple-choice questions that included a histopathologic image and asked, “What is the most likely diagnosis?,” “What is the predominant cell type?,” and “Where was this specimen taken from?” In addition to the knowledge-based questions, participants also were asked to rate their confidence in dermatopathology on a 5-point Likert scale ranging from 1 (not confident at all) to 5 (extremely confident). Participants completed the entire pretest before any information on the topic was provided. After the lecture, participants were asked to complete a posttest identical to the pretest and to rate their confidence in dermatopathology again on the same scale. The posttest included an additional question asking participants to rate the helpfulness of the lecture on a Likert scale ranging from 1 (not helpful at all) to 5 (extremely helpful). Participants completed the posttest within 48 hours of the lecture.

Overall, 15 learners participated in the pretest and 12 in the posttest. Of the 15 pretest participants, 3 were first-year residents and 12 were medical students. Similarly, in the posttest, 2 respondents were first-year residents and 10 were medical students. All responses contained complete pretests and posttests. The mean score on the pretest was 62%, whereas the mean score on the posttest was 75%. A paired t test indicated a statistically significant improvement (P=.017). In addition, the mean rating for confidence in dermatopathology knowledge before the lecture was 1.5 prior to the lecture and 2.6 after the lecture. A paired t test demonstrated statistical significance (P=.010). The mean rating of the helpfulness of the lecture was 4.67. The majority (91.7% [11/12]) of the participants gave a rating of 4 or 5.

Impact of the Lecture on Dermatopathology Knowledge

There is a gap in dermatopathology education early in medical training. Our introductory lecture led to higher post test scores and increased confidence in dermatopathology among medical students and dermatology residents, demonstrating the effectiveness of this kind of program in bridging this education gap. The majority of participants in our lecture said they found the session helpful. A previously published article called for early implementation of dermatology education as a whole in the medical curriculum due to lack of knowledge and confidence, and our introductory lecture may help to bridge this gap.⁸ Increasing dermatopathology content for medical students and first-year dermatology residents can expand knowledge, as shown by the increased scores on the posttest, and better supports learners transitioning to dermatology residency, where dermatopathology constitutes a large part of the overall curriculum.² More comprehensive knowledge of dermatopathology early in dermatology training also may help to better prepare residents to accurately diagnose and manage dermatologic conditions.

Pretest scores showed that the average confidence rating in dermatopathology among participants in our lecture was 1.5, which is rather low. This is consistent with prior studies that have found that residents feel that medical school inadequately prepared them for dermatology residency.^7,8 More than 87% (71/81) of medical students surveyed felt they received inadequate general dermatology training in medical school.⁹ This supports the proposed educational gap that is impacting confidence in overall dermatology knowledge, which includes dermatopathology. In our study, the average confidence rating increased by 1.1 points after the lecture, which was statistically significant (P=.010) and demonstrates that an introductory lecture serves as a feasible intervention to improve confidence in this area.

The feedback we received from participants in our lecture shows the benefits of an introductory interactive lecture with virtual dermatopathology images. Ngo et al2 highlighted how residents perceive virtual images to be superior to conventional microscopy for dermatopathology, which we utilized in our lecture. This method is not only cost effective but also provides a simple way for learners and facilitators to point out key findings on histopathology slides.²

Final Thoughts

Overall, implementing dermatopathology education early in training has a measurable impact on dermatopathology knowledge and confidence among medical students and first-year dermatology residents. An interactive lecture with virtual images similar to the one we describe here may better prepare learners for the transition to dermatology residency by addressing the educational gap in dermatopathology early in training.

Practice Gap

Dermatology encompasses a wide range of procedures performed in both clinical and surgical settings. One comprehensive review of ergonomics in dermatologic surgery found a high prevalence of musculoskeletal injuries (MSIs).¹ A survey conducted in 2010 revealed that 90% of dermatologic surgeons experienced MSIs, which commonly resulted in neck, shoulder, and/or back pain.²

Prolonged abnormal static postures and repetitive motions, which are common in dermatologic practice, can lead to muscle imbalances and focal muscular ischemia, increasing physicians’ susceptibility to MSIs. When muscle fibers experience enough repeated focal ischemia, they may enter a constant state of contraction leading to myofascial pain syndrome (MPS); these painful areas are known as trigger points and often are refractory to traditional stretching.³

Musculoskeletal injuries can potentially impact dermatologists’ career longevity and satisfaction. To date, the literature on techniques and exercises that may prevent or alleviate MSIs is limited.^1,4 We collaborated with a colleague in physical therapy (R.P.) to present stretching, mobility, and strengthening techniques and exercises dermatologists can perform both in and outside the procedure room to potentially reduce pain and prevent future MSIs.

The Techniques

Stretching and Mobility Exercises—When dermatologists adopt abnormal static postures, they are at risk for muscular imbalances caused by repetitive flexion and/or rotation in one direction. Over time, these repetitive movements can result in loss of flexibility in the direction opposite to that in which they are consistently positioned.³ Regular stretching offers physiologic benefits such as maintaining joint range of motion, increasing blood flow to muscles, and increasing synovial fluid production—all of which contribute to reduced risk for MSIs.³ Multiple studies and a systematic review have found that regular stretching throughout the day serves as an effective method for preventing and mitigating MSI pain in health care providers.^1,3-5

Considering the directional manner of MSIs induced by prolonged static positions, the most benefit will be derived from stretches or extension in the opposite direction of that in which the practitioner usually works. For most dermatologic surgeons, stretches should target the trapezius muscles, shoulders, and cervical musculature. Techniques such as the neck and shoulder combination stretch, the upper trapezius stretch, and the downward shoulder blade squeeze stretch can be performed regularly throughout the day.^3,4 To perform the neck and shoulder combination stretch, place the arm in flexion to shoulder height and bend the elbow at a 90° angle. Gently pull the arm across the front of the body, point the head gazing in the direction of the shoulder being stretched, and hold for 10 to 20 seconds. Repeat with the other side (eFigure 1).

Some surgeons may experience pain that is refractory to stretching, potentially indicating the presence of MPS.³ Managing MPS via stretching alone may be a challenge. Physical therapists utilize various techniques to manually massage the tissue, but self-myofascial release—which involves the use of a tool such as a dense foam roller or massage ball, both of which can easily be purchased—may be convenient and effective for busy providers. To perform this technique, the operator lies with their back on a dense foam roller positioned perpendicular to the body and uses their legs to undulate or roll back and forth in a smooth motion (Figure 1). This may help to alleviate myofascial pain in the spinal intrinsic muscles, which often are prone to injury due to posture; it also warms the fascia and breaks up adhesions. Self-myofascial release may have similar acute analgesic effects to classic stretching while also helping to alleviate MPS.

Strengthening Exercises—Musculoskeletal injuries often begin with fatigue in postural stabilizing muscles of the trunk and shoulders, leading the dermatologist to assume a slouched posture. Dermatologists should perform strengthening exercises targeting the trunk and shoulder girdle, which help to promote good working posture while optimizing the function of the arms and hands. Ideally, dermatologists should incorporate strengthening exercises 3 to 4 times per week in combination with daily stretching.

The 4-point kneeling alternate arm and leg extensions technique targets many muscle groups that commonly are affected in dermatologists and dermatologic surgeons. While on all fours, the operator positions the hands under the shoulders and the knees under the hips. The neck remains in line with the back with the eyes facing the floor. The abdominal muscles are then pulled up and in while simultaneously extending the left arm and right leg until both are parallel to the floor. This position should be held for 5 seconds and then repeated with the opposite contralateral extremities (Figure 2). Exercises specific to each muscle group also can be performed, such as planks to enhance truncal stability or scapular wall clocks to strengthen the shoulder girdle (eFigure 2). To perform scapular wall clocks, wrap a single resistance band around both wrists. Next, press the hands and elbows gently into a wall pointing superiorly and imagine there is a clock on the wall with 12 o’clock at the top and 6 o’clock at the bottom. Press the wrists outward on the band, keep the elbows straight, and reach out with the right hand while keeping the left hand stable. Move the right hand to the 1-, 3-, and 5-o’clock positions. Repeat with the left hand while holding the right hand stable. Move the left hand to the 11-, 9-, 7-, and 6-o’clock positions. Repeat these steps for 3 to 5 sets.

It is important to note that a decreased flow of oxygen and nutrients to muscles contributes to MSIs. Aerobic exercises increase blood flow and improve the ability of the muscles to utilize oxygen. Engaging in an enjoyable aerobic activity (eg, walking, running, swimming, cycling) 3 to 4 times per week can help prevent MSIs; however, as with any new exercise regimen (including the strengthening techniques described here), it is important to consult your primary care physician before getting started.

Practice Implications

As dermatologists progress in their careers, implementation of these techniques can mitigate MSIs and their sequelae. The long-term benefits of stretching, mobility, and strengthening exercises are dependent on having ergonomically suitable environmental factors. In addition to their own mechanics and posture, dermatologists must consider all elements that may affect the ergonomics of their daily practice, including operating room layout, instrumentation and workflow, and patient positioning. Through a consistent approach to prevention using the techniques described here, dermatologists can minimize the risk for MSIs and foster sustainability in their careers.

Practice Gap

Dermatology encompasses a wide range of procedures performed in both clinical and surgical settings. One comprehensive review of ergonomics in dermatologic surgery found a high prevalence of musculoskeletal injuries (MSIs).¹ A survey conducted in 2010 revealed that 90% of dermatologic surgeons experienced MSIs, which commonly resulted in neck, shoulder, and/or back pain.²

Prolonged abnormal static postures and repetitive motions, which are common in dermatologic practice, can lead to muscle imbalances and focal muscular ischemia, increasing physicians’ susceptibility to MSIs. When muscle fibers experience enough repeated focal ischemia, they may enter a constant state of contraction leading to myofascial pain syndrome (MPS); these painful areas are known as trigger points and often are refractory to traditional stretching.³

Musculoskeletal injuries can potentially impact dermatologists’ career longevity and satisfaction. To date, the literature on techniques and exercises that may prevent or alleviate MSIs is limited.^1,4 We collaborated with a colleague in physical therapy (R.P.) to present stretching, mobility, and strengthening techniques and exercises dermatologists can perform both in and outside the procedure room to potentially reduce pain and prevent future MSIs.

The Techniques

Stretching and Mobility Exercises—When dermatologists adopt abnormal static postures, they are at risk for muscular imbalances caused by repetitive flexion and/or rotation in one direction. Over time, these repetitive movements can result in loss of flexibility in the direction opposite to that in which they are consistently positioned.³ Regular stretching offers physiologic benefits such as maintaining joint range of motion, increasing blood flow to muscles, and increasing synovial fluid production—all of which contribute to reduced risk for MSIs.³ Multiple studies and a systematic review have found that regular stretching throughout the day serves as an effective method for preventing and mitigating MSI pain in health care providers.^1,3-5

Considering the directional manner of MSIs induced by prolonged static positions, the most benefit will be derived from stretches or extension in the opposite direction of that in which the practitioner usually works. For most dermatologic surgeons, stretches should target the trapezius muscles, shoulders, and cervical musculature. Techniques such as the neck and shoulder combination stretch, the upper trapezius stretch, and the downward shoulder blade squeeze stretch can be performed regularly throughout the day.^3,4 To perform the neck and shoulder combination stretch, place the arm in flexion to shoulder height and bend the elbow at a 90° angle. Gently pull the arm across the front of the body, point the head gazing in the direction of the shoulder being stretched, and hold for 10 to 20 seconds. Repeat with the other side (eFigure 1).

Some surgeons may experience pain that is refractory to stretching, potentially indicating the presence of MPS.³ Managing MPS via stretching alone may be a challenge. Physical therapists utilize various techniques to manually massage the tissue, but self-myofascial release—which involves the use of a tool such as a dense foam roller or massage ball, both of which can easily be purchased—may be convenient and effective for busy providers. To perform this technique, the operator lies with their back on a dense foam roller positioned perpendicular to the body and uses their legs to undulate or roll back and forth in a smooth motion (Figure 1). This may help to alleviate myofascial pain in the spinal intrinsic muscles, which often are prone to injury due to posture; it also warms the fascia and breaks up adhesions. Self-myofascial release may have similar acute analgesic effects to classic stretching while also helping to alleviate MPS.

Strengthening Exercises—Musculoskeletal injuries often begin with fatigue in postural stabilizing muscles of the trunk and shoulders, leading the dermatologist to assume a slouched posture. Dermatologists should perform strengthening exercises targeting the trunk and shoulder girdle, which help to promote good working posture while optimizing the function of the arms and hands. Ideally, dermatologists should incorporate strengthening exercises 3 to 4 times per week in combination with daily stretching.

The 4-point kneeling alternate arm and leg extensions technique targets many muscle groups that commonly are affected in dermatologists and dermatologic surgeons. While on all fours, the operator positions the hands under the shoulders and the knees under the hips. The neck remains in line with the back with the eyes facing the floor. The abdominal muscles are then pulled up and in while simultaneously extending the left arm and right leg until both are parallel to the floor. This position should be held for 5 seconds and then repeated with the opposite contralateral extremities (Figure 2). Exercises specific to each muscle group also can be performed, such as planks to enhance truncal stability or scapular wall clocks to strengthen the shoulder girdle (eFigure 2). To perform scapular wall clocks, wrap a single resistance band around both wrists. Next, press the hands and elbows gently into a wall pointing superiorly and imagine there is a clock on the wall with 12 o’clock at the top and 6 o’clock at the bottom. Press the wrists outward on the band, keep the elbows straight, and reach out with the right hand while keeping the left hand stable. Move the right hand to the 1-, 3-, and 5-o’clock positions. Repeat with the left hand while holding the right hand stable. Move the left hand to the 11-, 9-, 7-, and 6-o’clock positions. Repeat these steps for 3 to 5 sets.

It is important to note that a decreased flow of oxygen and nutrients to muscles contributes to MSIs. Aerobic exercises increase blood flow and improve the ability of the muscles to utilize oxygen. Engaging in an enjoyable aerobic activity (eg, walking, running, swimming, cycling) 3 to 4 times per week can help prevent MSIs; however, as with any new exercise regimen (including the strengthening techniques described here), it is important to consult your primary care physician before getting started.

Practice Implications

As dermatologists progress in their careers, implementation of these techniques can mitigate MSIs and their sequelae. The long-term benefits of stretching, mobility, and strengthening exercises are dependent on having ergonomically suitable environmental factors. In addition to their own mechanics and posture, dermatologists must consider all elements that may affect the ergonomics of their daily practice, including operating room layout, instrumentation and workflow, and patient positioning. Through a consistent approach to prevention using the techniques described here, dermatologists can minimize the risk for MSIs and foster sustainability in their careers.

Practice Gap

Dermatology encompasses a wide range of procedures performed in both clinical and surgical settings. One comprehensive review of ergonomics in dermatologic surgery found a high prevalence of musculoskeletal injuries (MSIs).¹ A survey conducted in 2010 revealed that 90% of dermatologic surgeons experienced MSIs, which commonly resulted in neck, shoulder, and/or back pain.²

Prolonged abnormal static postures and repetitive motions, which are common in dermatologic practice, can lead to muscle imbalances and focal muscular ischemia, increasing physicians’ susceptibility to MSIs. When muscle fibers experience enough repeated focal ischemia, they may enter a constant state of contraction leading to myofascial pain syndrome (MPS); these painful areas are known as trigger points and often are refractory to traditional stretching.³

Musculoskeletal injuries can potentially impact dermatologists’ career longevity and satisfaction. To date, the literature on techniques and exercises that may prevent or alleviate MSIs is limited.^1,4 We collaborated with a colleague in physical therapy (R.P.) to present stretching, mobility, and strengthening techniques and exercises dermatologists can perform both in and outside the procedure room to potentially reduce pain and prevent future MSIs.

The Techniques

Stretching and Mobility Exercises—When dermatologists adopt abnormal static postures, they are at risk for muscular imbalances caused by repetitive flexion and/or rotation in one direction. Over time, these repetitive movements can result in loss of flexibility in the direction opposite to that in which they are consistently positioned.³ Regular stretching offers physiologic benefits such as maintaining joint range of motion, increasing blood flow to muscles, and increasing synovial fluid production—all of which contribute to reduced risk for MSIs.³ Multiple studies and a systematic review have found that regular stretching throughout the day serves as an effective method for preventing and mitigating MSI pain in health care providers.^1,3-5

Considering the directional manner of MSIs induced by prolonged static positions, the most benefit will be derived from stretches or extension in the opposite direction of that in which the practitioner usually works. For most dermatologic surgeons, stretches should target the trapezius muscles, shoulders, and cervical musculature. Techniques such as the neck and shoulder combination stretch, the upper trapezius stretch, and the downward shoulder blade squeeze stretch can be performed regularly throughout the day.^3,4 To perform the neck and shoulder combination stretch, place the arm in flexion to shoulder height and bend the elbow at a 90° angle. Gently pull the arm across the front of the body, point the head gazing in the direction of the shoulder being stretched, and hold for 10 to 20 seconds. Repeat with the other side (eFigure 1).

Some surgeons may experience pain that is refractory to stretching, potentially indicating the presence of MPS.³ Managing MPS via stretching alone may be a challenge. Physical therapists utilize various techniques to manually massage the tissue, but self-myofascial release—which involves the use of a tool such as a dense foam roller or massage ball, both of which can easily be purchased—may be convenient and effective for busy providers. To perform this technique, the operator lies with their back on a dense foam roller positioned perpendicular to the body and uses their legs to undulate or roll back and forth in a smooth motion (Figure 1). This may help to alleviate myofascial pain in the spinal intrinsic muscles, which often are prone to injury due to posture; it also warms the fascia and breaks up adhesions. Self-myofascial release may have similar acute analgesic effects to classic stretching while also helping to alleviate MPS.

Strengthening Exercises—Musculoskeletal injuries often begin with fatigue in postural stabilizing muscles of the trunk and shoulders, leading the dermatologist to assume a slouched posture. Dermatologists should perform strengthening exercises targeting the trunk and shoulder girdle, which help to promote good working posture while optimizing the function of the arms and hands. Ideally, dermatologists should incorporate strengthening exercises 3 to 4 times per week in combination with daily stretching.

The 4-point kneeling alternate arm and leg extensions technique targets many muscle groups that commonly are affected in dermatologists and dermatologic surgeons. While on all fours, the operator positions the hands under the shoulders and the knees under the hips. The neck remains in line with the back with the eyes facing the floor. The abdominal muscles are then pulled up and in while simultaneously extending the left arm and right leg until both are parallel to the floor. This position should be held for 5 seconds and then repeated with the opposite contralateral extremities (Figure 2). Exercises specific to each muscle group also can be performed, such as planks to enhance truncal stability or scapular wall clocks to strengthen the shoulder girdle (eFigure 2). To perform scapular wall clocks, wrap a single resistance band around both wrists. Next, press the hands and elbows gently into a wall pointing superiorly and imagine there is a clock on the wall with 12 o’clock at the top and 6 o’clock at the bottom. Press the wrists outward on the band, keep the elbows straight, and reach out with the right hand while keeping the left hand stable. Move the right hand to the 1-, 3-, and 5-o’clock positions. Repeat with the left hand while holding the right hand stable. Move the left hand to the 11-, 9-, 7-, and 6-o’clock positions. Repeat these steps for 3 to 5 sets.

It is important to note that a decreased flow of oxygen and nutrients to muscles contributes to MSIs. Aerobic exercises increase blood flow and improve the ability of the muscles to utilize oxygen. Engaging in an enjoyable aerobic activity (eg, walking, running, swimming, cycling) 3 to 4 times per week can help prevent MSIs; however, as with any new exercise regimen (including the strengthening techniques described here), it is important to consult your primary care physician before getting started.

Practice Implications

As dermatologists progress in their careers, implementation of these techniques can mitigate MSIs and their sequelae. The long-term benefits of stretching, mobility, and strengthening exercises are dependent on having ergonomically suitable environmental factors. In addition to their own mechanics and posture, dermatologists must consider all elements that may affect the ergonomics of their daily practice, including operating room layout, instrumentation and workflow, and patient positioning. Through a consistent approach to prevention using the techniques described here, dermatologists can minimize the risk for MSIs and foster sustainability in their careers.

THE COMPARISON

• A A Black woman with dermatosis papulosa nigra manifesting as a cluster of light brown flat seborrheic keratoses that covered the cheeks and lateral face and extended to the neck.
• B A Black man with dermatosis papulosa nigra manifesting as small black papules on the cheeks and eyelids involving the central face.

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones.^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided.

Epidemiology

The incidence of SKs increases with age.^3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹

Key Clinical Features

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules.² Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters.^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4

Worth Noting

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.⁴ The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions.^4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigator-blinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P=.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful.

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹²

Health Disparity Highlight

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address—and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden.

THE COMPARISON

• A A Black woman with dermatosis papulosa nigra manifesting as a cluster of light brown flat seborrheic keratoses that covered the cheeks and lateral face and extended to the neck.
• B A Black man with dermatosis papulosa nigra manifesting as small black papules on the cheeks and eyelids involving the central face.

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones.^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided.

Epidemiology

The incidence of SKs increases with age.^3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹

Key Clinical Features

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules.² Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters.^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4

Worth Noting

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.⁴ The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions.^4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigator-blinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P=.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful.

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹²

Health Disparity Highlight

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address—and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden.

THE COMPARISON

• A A Black woman with dermatosis papulosa nigra manifesting as a cluster of light brown flat seborrheic keratoses that covered the cheeks and lateral face and extended to the neck.
• B A Black man with dermatosis papulosa nigra manifesting as small black papules on the cheeks and eyelids involving the central face.

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones.^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided.

Epidemiology

The incidence of SKs increases with age.^3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹

Key Clinical Features

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules.² Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters.^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4

Worth Noting

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.⁴ The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions.^4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigator-blinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P=.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful.

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹²

Health Disparity Highlight

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address—and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden.