Cutis

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁷

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁷

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁷

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.

THE DIAGNOSIS: Pseudopsoriatic Nails With Pterygium Inversum Unguis

Based on the clinical findings and the patient’s history of gel manicures, a diagnosis of pseudopsoriatic nails with pterygium inversum unguis (PIU) was made. The patient was advised to avoid gel manicures and any other chemical or mechanical trauma to the nails. No other treatment was administered. Improvements including healthy nail growth and disappearing color and structure changes within the nail plates were noted at 2 months’ follow-up.

The durability and availability of gel manicures has been increasingly popular due to their ideal cosmetic results. A gel manicure involves applying a gel nail polish (GNP) containing acrylate or methacrylate monomers that harden after exposure to UV light through a photopolymerization reaction. Acrylate polymers including ethylene glycol dimethacrylate, 2-hydroxyethyl acrylate, 2-hydroxyethyl methacrylate, 2-hydroxypropyl methacrylate, methyl methacrylate, and tetrahydrofurfuryl methacrylate are known to cause allergic contact dermatitis in patients who wear acrylate-based GNP.¹Hydroxyethyl methacrylate is the most common sensitizer among these acrylates. Fingertip dry dermatitis, fissured painful pulpitis of the fingers, and periungual erythema are the most common manifestations of methacrylate allergy; however, there also are reports of onycholysis and onychodystrophy in patients with severe allergic contact dermatitis caused by acrylates.^2,3

In contrast to common public misconception that GNP may strengthen the nails, scientific evidence has shown otherwise. Besides allergic contact dermatitis, mechanical damage and UV-induced skin manifestations have been reported in association with GNP.^1,3,4 Pseudopsoriatic nails are characterized by onycholysis accompanied by subungual hyperkeratosis, closely resembling the nail findings seen in psoriasis. This condition may occur due to mechanical damage and acrylate sensitization.^2,4 Pterygium inversum unguis, also known as ventral pterygium, occurs as a result of hyponychium trauma due to either application or removal processes of GNP and/ or exposure to chemical ingredients and is one of the most striking clinical manifestations of GNP use.⁵ In our patient, all fingernails were affected by PIU.

Patients presenting with pseudopsoriatic nail changes and/or PIU should be questioned about potential exposure to GNP and/or sculpted nails, also known as custom artificial nails or nail prostheses. Diagnosis primarily is made clinically, but microbial cultures or skin biopsy may be required to exclude psoriasis and fungal infections in some patients. Patch testing with acrylate series in particular also is necessary in patients presenting with hand dermatitis. As it is the most common contact sensitizer in the acrylic material of the GNPs, screening for 2-hydroxyethyl methacrylate allergy is recommended in these patients.¹ Almost all adverse effects related to use of GNP may be reversible upon discontinuation of exposure.

THE DIAGNOSIS: Pseudopsoriatic Nails With Pterygium Inversum Unguis

Based on the clinical findings and the patient’s history of gel manicures, a diagnosis of pseudopsoriatic nails with pterygium inversum unguis (PIU) was made. The patient was advised to avoid gel manicures and any other chemical or mechanical trauma to the nails. No other treatment was administered. Improvements including healthy nail growth and disappearing color and structure changes within the nail plates were noted at 2 months’ follow-up.

The durability and availability of gel manicures has been increasingly popular due to their ideal cosmetic results. A gel manicure involves applying a gel nail polish (GNP) containing acrylate or methacrylate monomers that harden after exposure to UV light through a photopolymerization reaction. Acrylate polymers including ethylene glycol dimethacrylate, 2-hydroxyethyl acrylate, 2-hydroxyethyl methacrylate, 2-hydroxypropyl methacrylate, methyl methacrylate, and tetrahydrofurfuryl methacrylate are known to cause allergic contact dermatitis in patients who wear acrylate-based GNP.¹Hydroxyethyl methacrylate is the most common sensitizer among these acrylates. Fingertip dry dermatitis, fissured painful pulpitis of the fingers, and periungual erythema are the most common manifestations of methacrylate allergy; however, there also are reports of onycholysis and onychodystrophy in patients with severe allergic contact dermatitis caused by acrylates.^2,3

In contrast to common public misconception that GNP may strengthen the nails, scientific evidence has shown otherwise. Besides allergic contact dermatitis, mechanical damage and UV-induced skin manifestations have been reported in association with GNP.^1,3,4 Pseudopsoriatic nails are characterized by onycholysis accompanied by subungual hyperkeratosis, closely resembling the nail findings seen in psoriasis. This condition may occur due to mechanical damage and acrylate sensitization.^2,4 Pterygium inversum unguis, also known as ventral pterygium, occurs as a result of hyponychium trauma due to either application or removal processes of GNP and/ or exposure to chemical ingredients and is one of the most striking clinical manifestations of GNP use.⁵ In our patient, all fingernails were affected by PIU.

Patients presenting with pseudopsoriatic nail changes and/or PIU should be questioned about potential exposure to GNP and/or sculpted nails, also known as custom artificial nails or nail prostheses. Diagnosis primarily is made clinically, but microbial cultures or skin biopsy may be required to exclude psoriasis and fungal infections in some patients. Patch testing with acrylate series in particular also is necessary in patients presenting with hand dermatitis. As it is the most common contact sensitizer in the acrylic material of the GNPs, screening for 2-hydroxyethyl methacrylate allergy is recommended in these patients.¹ Almost all adverse effects related to use of GNP may be reversible upon discontinuation of exposure.

THE DIAGNOSIS: Pseudopsoriatic Nails With Pterygium Inversum Unguis

Based on the clinical findings and the patient’s history of gel manicures, a diagnosis of pseudopsoriatic nails with pterygium inversum unguis (PIU) was made. The patient was advised to avoid gel manicures and any other chemical or mechanical trauma to the nails. No other treatment was administered. Improvements including healthy nail growth and disappearing color and structure changes within the nail plates were noted at 2 months’ follow-up.

The durability and availability of gel manicures has been increasingly popular due to their ideal cosmetic results. A gel manicure involves applying a gel nail polish (GNP) containing acrylate or methacrylate monomers that harden after exposure to UV light through a photopolymerization reaction. Acrylate polymers including ethylene glycol dimethacrylate, 2-hydroxyethyl acrylate, 2-hydroxyethyl methacrylate, 2-hydroxypropyl methacrylate, methyl methacrylate, and tetrahydrofurfuryl methacrylate are known to cause allergic contact dermatitis in patients who wear acrylate-based GNP.¹Hydroxyethyl methacrylate is the most common sensitizer among these acrylates. Fingertip dry dermatitis, fissured painful pulpitis of the fingers, and periungual erythema are the most common manifestations of methacrylate allergy; however, there also are reports of onycholysis and onychodystrophy in patients with severe allergic contact dermatitis caused by acrylates.^2,3

In contrast to common public misconception that GNP may strengthen the nails, scientific evidence has shown otherwise. Besides allergic contact dermatitis, mechanical damage and UV-induced skin manifestations have been reported in association with GNP.^1,3,4 Pseudopsoriatic nails are characterized by onycholysis accompanied by subungual hyperkeratosis, closely resembling the nail findings seen in psoriasis. This condition may occur due to mechanical damage and acrylate sensitization.^2,4 Pterygium inversum unguis, also known as ventral pterygium, occurs as a result of hyponychium trauma due to either application or removal processes of GNP and/ or exposure to chemical ingredients and is one of the most striking clinical manifestations of GNP use.⁵ In our patient, all fingernails were affected by PIU.

Patients presenting with pseudopsoriatic nail changes and/or PIU should be questioned about potential exposure to GNP and/or sculpted nails, also known as custom artificial nails or nail prostheses. Diagnosis primarily is made clinically, but microbial cultures or skin biopsy may be required to exclude psoriasis and fungal infections in some patients. Patch testing with acrylate series in particular also is necessary in patients presenting with hand dermatitis. As it is the most common contact sensitizer in the acrylic material of the GNPs, screening for 2-hydroxyethyl methacrylate allergy is recommended in these patients.¹ Almost all adverse effects related to use of GNP may be reversible upon discontinuation of exposure.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

To the Editor:

Segmental vitiligo (SV) accounts for a minority of vitiligo cases and most frequently occurs in children.¹ It characteristically manifests unilaterally and affects a single body area with a sharp midline demarcation. In contrast to nonsegmental vitiligo (NSV), SV typically stabilizes early in the disease progression.¹ The pathophysiology of this vitiligo subtype is not well established, but possible autoinflammatory mechanisms associated with somatic mosaicism, neuronal mechanisms, and/or microvascular skin-homing have been proposed.² We present the case of a pediatric patient with segmental vitiligo of the right hemiface treated with a combination of a topical calcineurin inhibitor and narrow-band UVB (NB-UVB) phototherapy.

An otherwise healthy 7-year-old boy presented to the dermatology department for evaluation of depigmented macules and patches affecting the right hemiface (temporal, periorbital, malar, perioral, preauricular, and mandibular regions) and neck associated with homolateral leukotrichia of the scalp and facial hair as well as the eyelashes of 5 years’ duration. The findings were consistent with SV (Figure 1). The patient previously had been diagnosed based on the clinical findings and treated with continuous application of topical calcineurin inhibitors plus oral cyclosporine (3 mg/kg/d) for 1 year, but the response was poor. The condition had a severe impact on the patient’s quality of life and social relationships. Therapeutic options were discussed with the patient’s caregivers, and ultimately NB-UVB phototherapy was started twice weekly with 10% increases in the dose at each treatment. Topical tacrolimus ointment (1 mg/g) also was started, and the cyclosporine was stopped. Evaluation of treatment progress occurred every 3 months, with progressive repigmentation of the patches following a perifollicular pattern. After 6 months of phototherapy, there was notable repigmentation of the affected areas, particularly in the malar, perioral, and perinasal regions (Figure 2) and the therapeutic response improved after 1 year of treatment (Figure 3). No adverse events were noted during the treatment period.

Segmental vitiligo lacks consistently effective treatment options. This subtype of vitiligo is classically resistant to conventional therapeutic options. Surgery may be a more effective and long-lasting treatment option but is not suitable for every patient.^1,3 Janus kinase (JAK) inhibitors are the newest treatment options being explored for topical and systemic treatment of vitiligo, with promising results in active and stable NSV lesions^4,5; however, SV rarely is represented in case reports and clinical trials. The topical JAK inhibitor ruxolitinib has been approved for use in NSV,⁵ and a phase 2 trial with oral ritlecitinib only included patients with NSV.⁴ Furthermore, JAK inhibitors have been studied and approved for children aged 12 years or older as well as for adults,^4,5 but younger age groups (4-10 years)—in whom SV most frequently manifests, as in our patient—have been excluded from these studies.¹ We present a novel case of SV of the right hemiface in a child that was successfully treated with NB-UVB phototherapy in association with topical calcineurin inhibitors.

The role of phototherapy for the treatment of vitiligo has been well documented, and it frequently is combined with other therapeutic modalities, such as topical anti-inflammatory drugs or, most recently, laser and micrografting techniques.^6,7 The most frequently used modality is NB-UVB. In the active phase, it performs an immunomodulatory role, while in the stable phase, it stimulates migration and activity of perilesional and hair follicle melanocytes.⁸ Initiating therapy early is advisable, particularly during the first 6 months of progression, as there is a higher probability of response^1,3,8; nevertheless, a good response was achieved despite the 5-year evolution of vitiligo in our patient. This is a safe option for a skin condition that may begin early in life and require long-term treatment.⁸ A main concern would be an increased risk for skin cancer associated with repeated NB-UVB exposure, which has not been verified in a recent analysis.⁹

Segmental vitiligo can considerably impact the patient’s quality of life, affecting social interactions and self-perception, particularly in younger patients with facial involvement; thus, effective and safe therapeutic strategies adapted to the individual and their vitiligo lesions should be discussed. Classical treatment options remain valid and provide good results for some patients; therefore, they should not be disregarded even with the rise of innovative therapies.

To the Editor:

Segmental vitiligo (SV) accounts for a minority of vitiligo cases and most frequently occurs in children.¹ It characteristically manifests unilaterally and affects a single body area with a sharp midline demarcation. In contrast to nonsegmental vitiligo (NSV), SV typically stabilizes early in the disease progression.¹ The pathophysiology of this vitiligo subtype is not well established, but possible autoinflammatory mechanisms associated with somatic mosaicism, neuronal mechanisms, and/or microvascular skin-homing have been proposed.² We present the case of a pediatric patient with segmental vitiligo of the right hemiface treated with a combination of a topical calcineurin inhibitor and narrow-band UVB (NB-UVB) phototherapy.

An otherwise healthy 7-year-old boy presented to the dermatology department for evaluation of depigmented macules and patches affecting the right hemiface (temporal, periorbital, malar, perioral, preauricular, and mandibular regions) and neck associated with homolateral leukotrichia of the scalp and facial hair as well as the eyelashes of 5 years’ duration. The findings were consistent with SV (Figure 1). The patient previously had been diagnosed based on the clinical findings and treated with continuous application of topical calcineurin inhibitors plus oral cyclosporine (3 mg/kg/d) for 1 year, but the response was poor. The condition had a severe impact on the patient’s quality of life and social relationships. Therapeutic options were discussed with the patient’s caregivers, and ultimately NB-UVB phototherapy was started twice weekly with 10% increases in the dose at each treatment. Topical tacrolimus ointment (1 mg/g) also was started, and the cyclosporine was stopped. Evaluation of treatment progress occurred every 3 months, with progressive repigmentation of the patches following a perifollicular pattern. After 6 months of phototherapy, there was notable repigmentation of the affected areas, particularly in the malar, perioral, and perinasal regions (Figure 2) and the therapeutic response improved after 1 year of treatment (Figure 3). No adverse events were noted during the treatment period.

Segmental vitiligo lacks consistently effective treatment options. This subtype of vitiligo is classically resistant to conventional therapeutic options. Surgery may be a more effective and long-lasting treatment option but is not suitable for every patient.^1,3 Janus kinase (JAK) inhibitors are the newest treatment options being explored for topical and systemic treatment of vitiligo, with promising results in active and stable NSV lesions^4,5; however, SV rarely is represented in case reports and clinical trials. The topical JAK inhibitor ruxolitinib has been approved for use in NSV,⁵ and a phase 2 trial with oral ritlecitinib only included patients with NSV.⁴ Furthermore, JAK inhibitors have been studied and approved for children aged 12 years or older as well as for adults,^4,5 but younger age groups (4-10 years)—in whom SV most frequently manifests, as in our patient—have been excluded from these studies.¹ We present a novel case of SV of the right hemiface in a child that was successfully treated with NB-UVB phototherapy in association with topical calcineurin inhibitors.

The role of phototherapy for the treatment of vitiligo has been well documented, and it frequently is combined with other therapeutic modalities, such as topical anti-inflammatory drugs or, most recently, laser and micrografting techniques.^6,7 The most frequently used modality is NB-UVB. In the active phase, it performs an immunomodulatory role, while in the stable phase, it stimulates migration and activity of perilesional and hair follicle melanocytes.⁸ Initiating therapy early is advisable, particularly during the first 6 months of progression, as there is a higher probability of response^1,3,8; nevertheless, a good response was achieved despite the 5-year evolution of vitiligo in our patient. This is a safe option for a skin condition that may begin early in life and require long-term treatment.⁸ A main concern would be an increased risk for skin cancer associated with repeated NB-UVB exposure, which has not been verified in a recent analysis.⁹

Segmental vitiligo can considerably impact the patient’s quality of life, affecting social interactions and self-perception, particularly in younger patients with facial involvement; thus, effective and safe therapeutic strategies adapted to the individual and their vitiligo lesions should be discussed. Classical treatment options remain valid and provide good results for some patients; therefore, they should not be disregarded even with the rise of innovative therapies.

To the Editor:

Segmental vitiligo (SV) accounts for a minority of vitiligo cases and most frequently occurs in children.¹ It characteristically manifests unilaterally and affects a single body area with a sharp midline demarcation. In contrast to nonsegmental vitiligo (NSV), SV typically stabilizes early in the disease progression.¹ The pathophysiology of this vitiligo subtype is not well established, but possible autoinflammatory mechanisms associated with somatic mosaicism, neuronal mechanisms, and/or microvascular skin-homing have been proposed.² We present the case of a pediatric patient with segmental vitiligo of the right hemiface treated with a combination of a topical calcineurin inhibitor and narrow-band UVB (NB-UVB) phototherapy.

An otherwise healthy 7-year-old boy presented to the dermatology department for evaluation of depigmented macules and patches affecting the right hemiface (temporal, periorbital, malar, perioral, preauricular, and mandibular regions) and neck associated with homolateral leukotrichia of the scalp and facial hair as well as the eyelashes of 5 years’ duration. The findings were consistent with SV (Figure 1). The patient previously had been diagnosed based on the clinical findings and treated with continuous application of topical calcineurin inhibitors plus oral cyclosporine (3 mg/kg/d) for 1 year, but the response was poor. The condition had a severe impact on the patient’s quality of life and social relationships. Therapeutic options were discussed with the patient’s caregivers, and ultimately NB-UVB phototherapy was started twice weekly with 10% increases in the dose at each treatment. Topical tacrolimus ointment (1 mg/g) also was started, and the cyclosporine was stopped. Evaluation of treatment progress occurred every 3 months, with progressive repigmentation of the patches following a perifollicular pattern. After 6 months of phototherapy, there was notable repigmentation of the affected areas, particularly in the malar, perioral, and perinasal regions (Figure 2) and the therapeutic response improved after 1 year of treatment (Figure 3). No adverse events were noted during the treatment period.

Segmental vitiligo lacks consistently effective treatment options. This subtype of vitiligo is classically resistant to conventional therapeutic options. Surgery may be a more effective and long-lasting treatment option but is not suitable for every patient.^1,3 Janus kinase (JAK) inhibitors are the newest treatment options being explored for topical and systemic treatment of vitiligo, with promising results in active and stable NSV lesions^4,5; however, SV rarely is represented in case reports and clinical trials. The topical JAK inhibitor ruxolitinib has been approved for use in NSV,⁵ and a phase 2 trial with oral ritlecitinib only included patients with NSV.⁴ Furthermore, JAK inhibitors have been studied and approved for children aged 12 years or older as well as for adults,^4,5 but younger age groups (4-10 years)—in whom SV most frequently manifests, as in our patient—have been excluded from these studies.¹ We present a novel case of SV of the right hemiface in a child that was successfully treated with NB-UVB phototherapy in association with topical calcineurin inhibitors.

The role of phototherapy for the treatment of vitiligo has been well documented, and it frequently is combined with other therapeutic modalities, such as topical anti-inflammatory drugs or, most recently, laser and micrografting techniques.^6,7 The most frequently used modality is NB-UVB. In the active phase, it performs an immunomodulatory role, while in the stable phase, it stimulates migration and activity of perilesional and hair follicle melanocytes.⁸ Initiating therapy early is advisable, particularly during the first 6 months of progression, as there is a higher probability of response^1,3,8; nevertheless, a good response was achieved despite the 5-year evolution of vitiligo in our patient. This is a safe option for a skin condition that may begin early in life and require long-term treatment.⁸ A main concern would be an increased risk for skin cancer associated with repeated NB-UVB exposure, which has not been verified in a recent analysis.⁹

Segmental vitiligo can considerably impact the patient’s quality of life, affecting social interactions and self-perception, particularly in younger patients with facial involvement; thus, effective and safe therapeutic strategies adapted to the individual and their vitiligo lesions should be discussed. Classical treatment options remain valid and provide good results for some patients; therefore, they should not be disregarded even with the rise of innovative therapies.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

Accurate procedural coding is essential to appropriate reimbursement and regulatory compliance in dermatology. This article reviews commonly misunderstood areas of procedural coding, including new biopsy codes; coding for shave removals, destruction, excision and repair, and adjacent tissue transfer (flap closure); the National Correct Coding Initiative; Medicare payment edits; Mohs micrographic surgery (MMS) codes; and correct use of key modifiers. Practical guidance is provided to help avoid frequent errors.

NEW BIOPSY CODES

The most common questions about procedural coding relate to the new Current Procedural Terminology (CPT) biopsy codes, which are reported based on method of removal. Primary codes include the following:

• 11102: tangential biopsy of skin (eg, shave, scoop, saucerize, curette) for a single lesion
• 11104: punch biopsy of skin, including simple closure, when performed, for a single lesion
• 11106: incisional biopsy of skin (eg, wedge), including simple closure, when performed, for a single lesion

Add-on codes are used for each separate or additional lesion:

• 11103: tangential biopsy
• 11105: punch biopsy
• 11107: incisional biopsy

When multiple biopsy types are performed on the same date of service, only one primary code is reported along with add-on codes for any additional biopsies. The primary code reported should have the highest relative value unit (generally incisional > punch > tangential) plus the add-on codes for additional biopsies performed. Sampling of the stratum corneum only (eg, skin scraping or tape stripping) does not constitute a skin biopsy and is not reportable as a procedure.

SHAVE REMOVAL CODES

Shave removal codes are appropriate when the intent is removal of the entire lesion and there is only dermis remaining at the base of the wound. Tangential biopsy codes are appropriate when the intent is to sample a portion of a lesion for diagnosis. If saucerization of a lesion is appropriate and only fat remains at the base of the wound, the procedure is correctly coded as an excision. If any dermis remains at the base of the wound, the procedure is properly coded as shave removal. Shave codes do not distinguish between benign and malignant lesions and do not include the margin of normal skin, only the diameter of the lesion itself.

DESTRUCTION CODES

Destruction codes include both premalignant and benign lesions and may be reported as add-on codes or standalone codes, depending on lesion type and number. The 17000 series is used for destruction of premalignant lesions such as actinic keratosis, large cell acanthoma, actinic cheilitis, and porokeratosis:

• 17000: destruction of the first premalignant lesion
• 17003: destruction of each additional premalignant lesion (up to 13 lesions); reported in addition to 17000
• 17004: destruction of 15 or more premalignant lesions; reported as a standalone code (not in addition to 17000)

The following codes are used for destruction of benign lesions:

• 17110: destruction of benign lesions (up to 14 lesions)
• 17111: destruction of 15 or more benign lesions; reported as a standalone code (not in addition to 17110)

EXCISION AND REPAIR CODES

Individual excisions are reported separately, while repairs are reported as the sum of the lengths within grouped anatomic zones. The groupings differ for intermediate and complex closures, so be sure to refer to your coding manual. Intermediate or complex closures should be reported separately for skin excisions, whereas simple closures are already included in the excision code and are not reported separately. Excision diameter includes the margins necessary to ensure complete removal of the tumor for both benign and malignant tumors. For neoplasms of uncertain behavior, defer billing until pathology results are available to ensure accurate reporting as either a benign or malignant tumor excision. Lesion size is measured prior to excision and includes the lesion plus the narrowest intended clinical margin; this measurement reflects the width of the excised specimen rather than the length of the repair.

Malignant tumor excisions continue to be worth more because of the greater risk and preservice and postservice work involved. Only about 50% of payment relates to the procedure itself; the other 50% relates to risk and preoperative and postoperative counseling as well as bundled follow-up visits in the global period. That accounts for the difference in compensation for benign vs malignant tumors as well as the 50% multiple surgical reduction for multiple lesions, as the equipment and cognitive portion bundled into the procedure are not separate for each procedure.

Historically, Medicare has bundled complex closures with benign excisions under 0.5 cm. Medicare also applies medically unlikely edits that may limit payment when more than 5 excisions, closures, or destruction procedures (excluding add-on codes) are reported on the same date of service. Medicare may pay for the additional procedures if a copy of the record and a letter of medical necessity are included.

CODING FOR ADJACENT TISSUE TRANSFER (FLAP CLOSURE)

When reporting adjacent tissue transfers, the total size of the defect includes primary and secondary defects when calculating the area of the flap. The areas of the primary and secondary defects are added together when the flap represents a single repair. The sums are reported separately if they are distinct repairs. Adjacent tissue transfer already includes payment for the excision of malignant or benign lesions. Do not code separately for the excision.

CORRECT CODING INITIATIVE

On January 1, 1996, the Medicare program implemented the National Correct Coding Initiative (https://www.cms.gov/national-correct-coding-initiative-ncci), employing nearly 83,000 code edits, in an attempt to eliminate unbundling or other inappropriate reporting of CPT codes. When procedures are performed on separate and distinct lesions, a modifier is required to bypass the edit that would otherwise deny payment for the second procedure. Medicare publishes lists of paired codes (column 1 paired with column 2). The code in column 2 is the one that requires modifier 59 or 79.

MEDICARE PAYMENT EDITS

Mutually Exclusive Edits

Mutually exclusive edits seek to identify services that cannot reasonably be performed in the same session. The “comprehensive” code will be paid and the “component” code disallowed.

Medically Unlikely Edits

The Centers for Medicare & Medicaid Services stop paying when multiples of a procedure exceed the medically unlikely edits, but payment may be made if accompanied by a copy of the medical record and letter of medical necessity. A common example would be a transplant recipient requiring destruction of many malignant lesions in a single session, exceeding the medically unlikely edits for the procedure.

MOHS MICROGRAPHIC SURGERY CODES

Mohs micrographic surgery codes require that a single physician act as both surgeon and pathologist. Do not report 88305 separately, as the pathology interpretation is already included in the MMS reimbursement. Repairs, grafts, and adjacent tissue transfer are separately reportable with the CPT codes for MMS.

The CPT codes for MMS include skin biopsy and excision services (11102-11107, 11600-11646, and 17260-17286); however, if a suspected skin cancer is biopsied for pathologic diagnosis prior to MMS, the biopsy (11102-11107) and frozen section pathology (88331) may be reported separately utilizing modifier 59 or 58 to distinguish the diagnostic biopsy from the definitive MMS. The biopsy should not duplicate a prior biopsy unless that biopsy result cannot be located; it must be performed before MMS and must determine the subsequent procedure. Although CPT indicates that modifier 59 should be used, it also is acceptable to utilize modifier 58 to indicate that the diagnostic skin biopsy and MMS were staged or planned procedures. This may be appropriate in the following scenarios:

• The lesion for which MMS is planned has not been biopsied within the previous 60 days,
• The surgeon cannot obtain a pathology report, with reasonable effort, from the referring physician, or
• The biopsy is performed on a lesion that is not associated with the MMS.

KEY MODIFIERS AND HOW THEY ARE USED

Modifiers are essential tools in dermatology coding that are used to indicate when procedures or evaluation and management (E/M) services are distinct, staged, bilateral, or related to specific global periods. Correct application ensures accurate reimbursement, prevents claim denials, and reflects the true work performed. The following list summarizes commonly used modifiers and guidance for their proper use.

Modifier 59: Distinct Procedural Service

Modifier 59 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

When code 17000 is paired with the new biopsy codes, modifier 59 is paired with code 17000.

Modifier 79: Distinct Procedural Service During a Postoperative Period

Modifier 79 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

Modifier 58: Staged or Planned Procedure

Modifier 58 is most commonly used when a staged excision is planned in advance or when a positive tumor margin requires further excision during a global period.

Modifier 25: Significant, Separately Identifiable E/M Service

Modifier 25 is defined as a significant and separately identifiable E/M service performed by the same physician on the same day as a procedure or other service. It is used to describe a separate, distinctly identifiable E/M service rendered during the same visit as another procedure. The modifier must be appended to the E/M code. The decision to perform a 0- or 10-day global procedure on the same date of service is already bundled into the payment for the procedure and does not qualify as a separate billable service.

Modifier 24: Unrelated E/M Service During a Postoperative Period

Modifier 24 is defined as an unrelated E/M service performed by the same physician during a postoperative period. It is used when a separate, unrelated E/M service is provided during the global period of a surgical procedure.

Modifiers 24 and 25: Documentation and Distinction

The CPT definition of modifier 25 states that an E/M service may be prompted by the system or condition for which a separate procedure or service is needed. Neither modifier requires a separate diagnosis; however, both require clearly distinguishable cognitive services beyond those typically associated with the procedure itself. This includes evaluation beyond the examination of the lesion, discussion of risks, benefits, and alternatives, and the decision to perform a 0- or 10-day global procedure.

Modifier 50: Bilateral Procedure

Modifier 50 is defined as a bilateral procedure and is used when the same procedure is performed on both sides of the body, such as application of Unna boots. When reporting this modifier, specify the quantity applied. Because Unna boots may be required on the arms as well as the legs, the billing system cannot determine how many were applied unless the quantity is clearly indicated.

Modifier 57: Decision for Surgery

Modifier 57 is reported when an E/M service involves the decision to perform a 90-day global procedure on the same date of service. For 10-day global procedures, the decision to perform surgery on the same day does not justify a separate E/M service. The global period timing begins at midnight, with the 10-day global starting on the day of the procedure and the 90-day global starting the day before the procedure; for example, if an excision is performed today and an adjacent tissue transfer is performed tomorrow, the excision is considered within the global period.

FINAL THOUGHTS

Physicians remain responsible for accurately selecting diagnosis and procedure codes that reflect medically necessary services, and CPT codes continue to define the procedures that are reported. The Relative Value Scale Update Committee determines the value of each procedure based on physician survey data, including time and follow-up visit utilization, as well as practice expense, which represents a substantial portion of each code’s value. Our specialty relies on dedicated volunteers who devote significant time and effort to ensuring accurate representation of the work we perform for our patients. When the opportunity arises, please thank them for their service.

Accurate procedural coding is essential to appropriate reimbursement and regulatory compliance in dermatology. This article reviews commonly misunderstood areas of procedural coding, including new biopsy codes; coding for shave removals, destruction, excision and repair, and adjacent tissue transfer (flap closure); the National Correct Coding Initiative; Medicare payment edits; Mohs micrographic surgery (MMS) codes; and correct use of key modifiers. Practical guidance is provided to help avoid frequent errors.

NEW BIOPSY CODES

The most common questions about procedural coding relate to the new Current Procedural Terminology (CPT) biopsy codes, which are reported based on method of removal. Primary codes include the following:

• 11102: tangential biopsy of skin (eg, shave, scoop, saucerize, curette) for a single lesion
• 11104: punch biopsy of skin, including simple closure, when performed, for a single lesion
• 11106: incisional biopsy of skin (eg, wedge), including simple closure, when performed, for a single lesion

Add-on codes are used for each separate or additional lesion:

• 11103: tangential biopsy
• 11105: punch biopsy
• 11107: incisional biopsy

When multiple biopsy types are performed on the same date of service, only one primary code is reported along with add-on codes for any additional biopsies. The primary code reported should have the highest relative value unit (generally incisional > punch > tangential) plus the add-on codes for additional biopsies performed. Sampling of the stratum corneum only (eg, skin scraping or tape stripping) does not constitute a skin biopsy and is not reportable as a procedure.

SHAVE REMOVAL CODES

Shave removal codes are appropriate when the intent is removal of the entire lesion and there is only dermis remaining at the base of the wound. Tangential biopsy codes are appropriate when the intent is to sample a portion of a lesion for diagnosis. If saucerization of a lesion is appropriate and only fat remains at the base of the wound, the procedure is correctly coded as an excision. If any dermis remains at the base of the wound, the procedure is properly coded as shave removal. Shave codes do not distinguish between benign and malignant lesions and do not include the margin of normal skin, only the diameter of the lesion itself.

DESTRUCTION CODES

Destruction codes include both premalignant and benign lesions and may be reported as add-on codes or standalone codes, depending on lesion type and number. The 17000 series is used for destruction of premalignant lesions such as actinic keratosis, large cell acanthoma, actinic cheilitis, and porokeratosis:

• 17000: destruction of the first premalignant lesion
• 17003: destruction of each additional premalignant lesion (up to 13 lesions); reported in addition to 17000
• 17004: destruction of 15 or more premalignant lesions; reported as a standalone code (not in addition to 17000)

The following codes are used for destruction of benign lesions:

• 17110: destruction of benign lesions (up to 14 lesions)
• 17111: destruction of 15 or more benign lesions; reported as a standalone code (not in addition to 17110)

EXCISION AND REPAIR CODES

Individual excisions are reported separately, while repairs are reported as the sum of the lengths within grouped anatomic zones. The groupings differ for intermediate and complex closures, so be sure to refer to your coding manual. Intermediate or complex closures should be reported separately for skin excisions, whereas simple closures are already included in the excision code and are not reported separately. Excision diameter includes the margins necessary to ensure complete removal of the tumor for both benign and malignant tumors. For neoplasms of uncertain behavior, defer billing until pathology results are available to ensure accurate reporting as either a benign or malignant tumor excision. Lesion size is measured prior to excision and includes the lesion plus the narrowest intended clinical margin; this measurement reflects the width of the excised specimen rather than the length of the repair.

Malignant tumor excisions continue to be worth more because of the greater risk and preservice and postservice work involved. Only about 50% of payment relates to the procedure itself; the other 50% relates to risk and preoperative and postoperative counseling as well as bundled follow-up visits in the global period. That accounts for the difference in compensation for benign vs malignant tumors as well as the 50% multiple surgical reduction for multiple lesions, as the equipment and cognitive portion bundled into the procedure are not separate for each procedure.

Historically, Medicare has bundled complex closures with benign excisions under 0.5 cm. Medicare also applies medically unlikely edits that may limit payment when more than 5 excisions, closures, or destruction procedures (excluding add-on codes) are reported on the same date of service. Medicare may pay for the additional procedures if a copy of the record and a letter of medical necessity are included.

CODING FOR ADJACENT TISSUE TRANSFER (FLAP CLOSURE)

When reporting adjacent tissue transfers, the total size of the defect includes primary and secondary defects when calculating the area of the flap. The areas of the primary and secondary defects are added together when the flap represents a single repair. The sums are reported separately if they are distinct repairs. Adjacent tissue transfer already includes payment for the excision of malignant or benign lesions. Do not code separately for the excision.

CORRECT CODING INITIATIVE

On January 1, 1996, the Medicare program implemented the National Correct Coding Initiative (https://www.cms.gov/national-correct-coding-initiative-ncci), employing nearly 83,000 code edits, in an attempt to eliminate unbundling or other inappropriate reporting of CPT codes. When procedures are performed on separate and distinct lesions, a modifier is required to bypass the edit that would otherwise deny payment for the second procedure. Medicare publishes lists of paired codes (column 1 paired with column 2). The code in column 2 is the one that requires modifier 59 or 79.

MEDICARE PAYMENT EDITS

Mutually Exclusive Edits

Mutually exclusive edits seek to identify services that cannot reasonably be performed in the same session. The “comprehensive” code will be paid and the “component” code disallowed.

Medically Unlikely Edits

The Centers for Medicare & Medicaid Services stop paying when multiples of a procedure exceed the medically unlikely edits, but payment may be made if accompanied by a copy of the medical record and letter of medical necessity. A common example would be a transplant recipient requiring destruction of many malignant lesions in a single session, exceeding the medically unlikely edits for the procedure.

MOHS MICROGRAPHIC SURGERY CODES

Mohs micrographic surgery codes require that a single physician act as both surgeon and pathologist. Do not report 88305 separately, as the pathology interpretation is already included in the MMS reimbursement. Repairs, grafts, and adjacent tissue transfer are separately reportable with the CPT codes for MMS.

The CPT codes for MMS include skin biopsy and excision services (11102-11107, 11600-11646, and 17260-17286); however, if a suspected skin cancer is biopsied for pathologic diagnosis prior to MMS, the biopsy (11102-11107) and frozen section pathology (88331) may be reported separately utilizing modifier 59 or 58 to distinguish the diagnostic biopsy from the definitive MMS. The biopsy should not duplicate a prior biopsy unless that biopsy result cannot be located; it must be performed before MMS and must determine the subsequent procedure. Although CPT indicates that modifier 59 should be used, it also is acceptable to utilize modifier 58 to indicate that the diagnostic skin biopsy and MMS were staged or planned procedures. This may be appropriate in the following scenarios:

• The lesion for which MMS is planned has not been biopsied within the previous 60 days,
• The surgeon cannot obtain a pathology report, with reasonable effort, from the referring physician, or
• The biopsy is performed on a lesion that is not associated with the MMS.

KEY MODIFIERS AND HOW THEY ARE USED

Modifiers are essential tools in dermatology coding that are used to indicate when procedures or evaluation and management (E/M) services are distinct, staged, bilateral, or related to specific global periods. Correct application ensures accurate reimbursement, prevents claim denials, and reflects the true work performed. The following list summarizes commonly used modifiers and guidance for their proper use.

Modifier 59: Distinct Procedural Service

Modifier 59 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

When code 17000 is paired with the new biopsy codes, modifier 59 is paired with code 17000.

Modifier 79: Distinct Procedural Service During a Postoperative Period

Modifier 79 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

Modifier 58: Staged or Planned Procedure

Modifier 58 is most commonly used when a staged excision is planned in advance or when a positive tumor margin requires further excision during a global period.

Modifier 25: Significant, Separately Identifiable E/M Service

Modifier 25 is defined as a significant and separately identifiable E/M service performed by the same physician on the same day as a procedure or other service. It is used to describe a separate, distinctly identifiable E/M service rendered during the same visit as another procedure. The modifier must be appended to the E/M code. The decision to perform a 0- or 10-day global procedure on the same date of service is already bundled into the payment for the procedure and does not qualify as a separate billable service.

Modifier 24: Unrelated E/M Service During a Postoperative Period

Modifier 24 is defined as an unrelated E/M service performed by the same physician during a postoperative period. It is used when a separate, unrelated E/M service is provided during the global period of a surgical procedure.

Modifiers 24 and 25: Documentation and Distinction

The CPT definition of modifier 25 states that an E/M service may be prompted by the system or condition for which a separate procedure or service is needed. Neither modifier requires a separate diagnosis; however, both require clearly distinguishable cognitive services beyond those typically associated with the procedure itself. This includes evaluation beyond the examination of the lesion, discussion of risks, benefits, and alternatives, and the decision to perform a 0- or 10-day global procedure.

Modifier 50: Bilateral Procedure

Modifier 50 is defined as a bilateral procedure and is used when the same procedure is performed on both sides of the body, such as application of Unna boots. When reporting this modifier, specify the quantity applied. Because Unna boots may be required on the arms as well as the legs, the billing system cannot determine how many were applied unless the quantity is clearly indicated.

Modifier 57: Decision for Surgery

Modifier 57 is reported when an E/M service involves the decision to perform a 90-day global procedure on the same date of service. For 10-day global procedures, the decision to perform surgery on the same day does not justify a separate E/M service. The global period timing begins at midnight, with the 10-day global starting on the day of the procedure and the 90-day global starting the day before the procedure; for example, if an excision is performed today and an adjacent tissue transfer is performed tomorrow, the excision is considered within the global period.

FINAL THOUGHTS

Physicians remain responsible for accurately selecting diagnosis and procedure codes that reflect medically necessary services, and CPT codes continue to define the procedures that are reported. The Relative Value Scale Update Committee determines the value of each procedure based on physician survey data, including time and follow-up visit utilization, as well as practice expense, which represents a substantial portion of each code’s value. Our specialty relies on dedicated volunteers who devote significant time and effort to ensuring accurate representation of the work we perform for our patients. When the opportunity arises, please thank them for their service.

Accurate procedural coding is essential to appropriate reimbursement and regulatory compliance in dermatology. This article reviews commonly misunderstood areas of procedural coding, including new biopsy codes; coding for shave removals, destruction, excision and repair, and adjacent tissue transfer (flap closure); the National Correct Coding Initiative; Medicare payment edits; Mohs micrographic surgery (MMS) codes; and correct use of key modifiers. Practical guidance is provided to help avoid frequent errors.

NEW BIOPSY CODES

The most common questions about procedural coding relate to the new Current Procedural Terminology (CPT) biopsy codes, which are reported based on method of removal. Primary codes include the following:

• 11102: tangential biopsy of skin (eg, shave, scoop, saucerize, curette) for a single lesion
• 11104: punch biopsy of skin, including simple closure, when performed, for a single lesion
• 11106: incisional biopsy of skin (eg, wedge), including simple closure, when performed, for a single lesion

Add-on codes are used for each separate or additional lesion:

• 11103: tangential biopsy
• 11105: punch biopsy
• 11107: incisional biopsy

When multiple biopsy types are performed on the same date of service, only one primary code is reported along with add-on codes for any additional biopsies. The primary code reported should have the highest relative value unit (generally incisional > punch > tangential) plus the add-on codes for additional biopsies performed. Sampling of the stratum corneum only (eg, skin scraping or tape stripping) does not constitute a skin biopsy and is not reportable as a procedure.

SHAVE REMOVAL CODES

Shave removal codes are appropriate when the intent is removal of the entire lesion and there is only dermis remaining at the base of the wound. Tangential biopsy codes are appropriate when the intent is to sample a portion of a lesion for diagnosis. If saucerization of a lesion is appropriate and only fat remains at the base of the wound, the procedure is correctly coded as an excision. If any dermis remains at the base of the wound, the procedure is properly coded as shave removal. Shave codes do not distinguish between benign and malignant lesions and do not include the margin of normal skin, only the diameter of the lesion itself.

DESTRUCTION CODES

Destruction codes include both premalignant and benign lesions and may be reported as add-on codes or standalone codes, depending on lesion type and number. The 17000 series is used for destruction of premalignant lesions such as actinic keratosis, large cell acanthoma, actinic cheilitis, and porokeratosis:

• 17000: destruction of the first premalignant lesion
• 17003: destruction of each additional premalignant lesion (up to 13 lesions); reported in addition to 17000
• 17004: destruction of 15 or more premalignant lesions; reported as a standalone code (not in addition to 17000)

The following codes are used for destruction of benign lesions:

• 17110: destruction of benign lesions (up to 14 lesions)
• 17111: destruction of 15 or more benign lesions; reported as a standalone code (not in addition to 17110)

EXCISION AND REPAIR CODES

Individual excisions are reported separately, while repairs are reported as the sum of the lengths within grouped anatomic zones. The groupings differ for intermediate and complex closures, so be sure to refer to your coding manual. Intermediate or complex closures should be reported separately for skin excisions, whereas simple closures are already included in the excision code and are not reported separately. Excision diameter includes the margins necessary to ensure complete removal of the tumor for both benign and malignant tumors. For neoplasms of uncertain behavior, defer billing until pathology results are available to ensure accurate reporting as either a benign or malignant tumor excision. Lesion size is measured prior to excision and includes the lesion plus the narrowest intended clinical margin; this measurement reflects the width of the excised specimen rather than the length of the repair.

Malignant tumor excisions continue to be worth more because of the greater risk and preservice and postservice work involved. Only about 50% of payment relates to the procedure itself; the other 50% relates to risk and preoperative and postoperative counseling as well as bundled follow-up visits in the global period. That accounts for the difference in compensation for benign vs malignant tumors as well as the 50% multiple surgical reduction for multiple lesions, as the equipment and cognitive portion bundled into the procedure are not separate for each procedure.

Historically, Medicare has bundled complex closures with benign excisions under 0.5 cm. Medicare also applies medically unlikely edits that may limit payment when more than 5 excisions, closures, or destruction procedures (excluding add-on codes) are reported on the same date of service. Medicare may pay for the additional procedures if a copy of the record and a letter of medical necessity are included.

CODING FOR ADJACENT TISSUE TRANSFER (FLAP CLOSURE)

When reporting adjacent tissue transfers, the total size of the defect includes primary and secondary defects when calculating the area of the flap. The areas of the primary and secondary defects are added together when the flap represents a single repair. The sums are reported separately if they are distinct repairs. Adjacent tissue transfer already includes payment for the excision of malignant or benign lesions. Do not code separately for the excision.

CORRECT CODING INITIATIVE

On January 1, 1996, the Medicare program implemented the National Correct Coding Initiative (https://www.cms.gov/national-correct-coding-initiative-ncci), employing nearly 83,000 code edits, in an attempt to eliminate unbundling or other inappropriate reporting of CPT codes. When procedures are performed on separate and distinct lesions, a modifier is required to bypass the edit that would otherwise deny payment for the second procedure. Medicare publishes lists of paired codes (column 1 paired with column 2). The code in column 2 is the one that requires modifier 59 or 79.

MEDICARE PAYMENT EDITS

Mutually Exclusive Edits

Mutually exclusive edits seek to identify services that cannot reasonably be performed in the same session. The “comprehensive” code will be paid and the “component” code disallowed.

Medically Unlikely Edits

The Centers for Medicare & Medicaid Services stop paying when multiples of a procedure exceed the medically unlikely edits, but payment may be made if accompanied by a copy of the medical record and letter of medical necessity. A common example would be a transplant recipient requiring destruction of many malignant lesions in a single session, exceeding the medically unlikely edits for the procedure.

MOHS MICROGRAPHIC SURGERY CODES

Mohs micrographic surgery codes require that a single physician act as both surgeon and pathologist. Do not report 88305 separately, as the pathology interpretation is already included in the MMS reimbursement. Repairs, grafts, and adjacent tissue transfer are separately reportable with the CPT codes for MMS.

The CPT codes for MMS include skin biopsy and excision services (11102-11107, 11600-11646, and 17260-17286); however, if a suspected skin cancer is biopsied for pathologic diagnosis prior to MMS, the biopsy (11102-11107) and frozen section pathology (88331) may be reported separately utilizing modifier 59 or 58 to distinguish the diagnostic biopsy from the definitive MMS. The biopsy should not duplicate a prior biopsy unless that biopsy result cannot be located; it must be performed before MMS and must determine the subsequent procedure. Although CPT indicates that modifier 59 should be used, it also is acceptable to utilize modifier 58 to indicate that the diagnostic skin biopsy and MMS were staged or planned procedures. This may be appropriate in the following scenarios:

• The lesion for which MMS is planned has not been biopsied within the previous 60 days,
• The surgeon cannot obtain a pathology report, with reasonable effort, from the referring physician, or
• The biopsy is performed on a lesion that is not associated with the MMS.

KEY MODIFIERS AND HOW THEY ARE USED

Modifiers are essential tools in dermatology coding that are used to indicate when procedures or evaluation and management (E/M) services are distinct, staged, bilateral, or related to specific global periods. Correct application ensures accurate reimbursement, prevents claim denials, and reflects the true work performed. The following list summarizes commonly used modifiers and guidance for their proper use.

Modifier 59: Distinct Procedural Service

Modifier 59 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

When code 17000 is paired with the new biopsy codes, modifier 59 is paired with code 17000.

Modifier 79: Distinct Procedural Service During a Postoperative Period

Modifier 79 is used to clearly designate when distinct, independent, and separate multiple procedures are provided. The procedure must not be a component of another procedure. Examples include:

• Different procedures or surgeries
• Surgery on different sites or organ systems
• Separate incision/excision
• Separate lesions

Modifier 58: Staged or Planned Procedure

Modifier 58 is most commonly used when a staged excision is planned in advance or when a positive tumor margin requires further excision during a global period.

Modifier 25: Significant, Separately Identifiable E/M Service

Modifier 25 is defined as a significant and separately identifiable E/M service performed by the same physician on the same day as a procedure or other service. It is used to describe a separate, distinctly identifiable E/M service rendered during the same visit as another procedure. The modifier must be appended to the E/M code. The decision to perform a 0- or 10-day global procedure on the same date of service is already bundled into the payment for the procedure and does not qualify as a separate billable service.

Modifier 24: Unrelated E/M Service During a Postoperative Period

Modifier 24 is defined as an unrelated E/M service performed by the same physician during a postoperative period. It is used when a separate, unrelated E/M service is provided during the global period of a surgical procedure.

Modifiers 24 and 25: Documentation and Distinction

The CPT definition of modifier 25 states that an E/M service may be prompted by the system or condition for which a separate procedure or service is needed. Neither modifier requires a separate diagnosis; however, both require clearly distinguishable cognitive services beyond those typically associated with the procedure itself. This includes evaluation beyond the examination of the lesion, discussion of risks, benefits, and alternatives, and the decision to perform a 0- or 10-day global procedure.

Modifier 50: Bilateral Procedure

Modifier 50 is defined as a bilateral procedure and is used when the same procedure is performed on both sides of the body, such as application of Unna boots. When reporting this modifier, specify the quantity applied. Because Unna boots may be required on the arms as well as the legs, the billing system cannot determine how many were applied unless the quantity is clearly indicated.

Modifier 57: Decision for Surgery

Modifier 57 is reported when an E/M service involves the decision to perform a 90-day global procedure on the same date of service. For 10-day global procedures, the decision to perform surgery on the same day does not justify a separate E/M service. The global period timing begins at midnight, with the 10-day global starting on the day of the procedure and the 90-day global starting the day before the procedure; for example, if an excision is performed today and an adjacent tissue transfer is performed tomorrow, the excision is considered within the global period.

FINAL THOUGHTS

Physicians remain responsible for accurately selecting diagnosis and procedure codes that reflect medically necessary services, and CPT codes continue to define the procedures that are reported. The Relative Value Scale Update Committee determines the value of each procedure based on physician survey data, including time and follow-up visit utilization, as well as practice expense, which represents a substantial portion of each code’s value. Our specialty relies on dedicated volunteers who devote significant time and effort to ensuring accurate representation of the work we perform for our patients. When the opportunity arises, please thank them for their service.