Cutis

THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.¹ Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.^2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).¹

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.^1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.⁴ Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,⁵ as well as to the lungs.⁶ Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.⁴

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.⁷ Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.⁸ Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.^7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.⁹ While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).¹ Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).^10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.¹ Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.¹² Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.¹³ Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.¹⁴ The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.¹⁵

THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.¹ Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.^2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).¹

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.^1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.⁴ Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,⁵ as well as to the lungs.⁶ Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.⁴

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.⁷ Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.⁸ Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.^7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.⁹ While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).¹ Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).^10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.¹ Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.¹² Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.¹³ Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.¹⁴ The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.¹⁵

THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.¹ Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.^2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).¹

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.^1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.⁴ Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,⁵ as well as to the lungs.⁶ Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.⁴

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.⁷ Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.⁸ Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.^7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.⁹ While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).¹ Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).^10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.¹ Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.¹² Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.¹³ Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.¹⁴ The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.¹⁵

Dermatologists have long relied on oral antibiotics to manage moderate to severe acne^1-4; however, it is critical to reassess how these medications are used in clinical practice as concerns about antibiotic resistance grow.⁵ The question is not whether antibiotics are effective for acne treatment—we know they are—but how to optimize their use to balance clinical benefit with responsible prescribing. Resistance in Cutibacterium acnes has been well documented in laboratory settings, but clinical treatment failure due to resistance remains rare and difficult to quantify.^6,7 Still, minimizing unnecessary exposure is good clinical practice. Whether antibiotic resistance ultimately proves to drive clinical failure or remains largely theoretical, stewardship safeguards future treatment options.

In this article, we present a practical, expert-based framework aligned with American Academy of Dermatology (AAD) guidelines to support responsible antibiotic use in acne management. Seven prescribing principles are outlined to help clinicians maintain efficacy while minimizing resistance risk. Mechanisms of resistance in C acnes and broader microbiome impacts also are discussed.

MECHANISMS OF RESISTANCE IN ACNE THERAPY

Antibiotic resistance in acne primarily involves C acnes and arises through selective pressure from prolonged or subtherapeutic antibiotic exposure. Resistance mechanisms include point mutations in ribosomal binding sites, leading to decreased binding affinity for tetracyclines and macrolides as well as efflux pump activation and biofilm formation.^8,9 Over time, resistant strains may proliferate and outcompete susceptible populations, potentially contributing to reduced clinical efficacy. Importantly, the use of broad-spectrum antibiotics may disrupt the skin and gut microbiota, promoting resistance among nontarget organisms.⁵ These concerns underscore the importance of limiting antibiotic use to appropriate indications, combining antibiotics with adjunctive nonantibiotic therapies, and avoiding monotherapy.

PRESCRIBING PRINCIPLES FOR RESPONSIBLE ORAL ANTIBIOTIC USE IN ACNE

The following principles are derived from our clinical experience and are aligned with AAD guidelines on acne treatment.¹⁰ This practical framework supports safe, effective, and streamlined prescribing.

Reserve Oral Antibiotics for Appropriate Cases

Oral antibiotics should be considered for patients with moderate to severe inflammatory acne when rapid anti-inflammatory control is needed. They are not indicated for comedonal or mild papulopustular acne. Before initiating treatment, clinicians should weigh the potential benefits against the risks associated with antibiotic exposure, including resistance and microbiome disruption.

Combine Oral Antibiotics With Topical Retinoids

Oral antibiotics should not be used as monotherapy. Topical retinoids should be initiated concurrently with oral antibiotics to maximize anti-inflammatory benefit, support transition to maintenance therapy, and reduce risk for resistance.

Consider Adding an Adjunctive Topical Antimicrobial Agent

Adjunctive topical antimicrobials can help reduce bacterial load. Benzoyl peroxide remains a first-line option due to its bactericidal activity and lack of resistance induction; however, recent product recalls involving benzene contamination may have raised safety concerns among some clinicians and patients.^11,12 While no definitive harm has been established, alternative topical agents approved by the US Food and Drug Administration (eg, azelaic acid) may be used based on shared decision-making, tolerability, cost, access, and patient preference. Use of topical antibiotics (eg, clindamycin, erythromycin) as monotherapy is discouraged due to their higher resistance potential, which is consistent with AAD guidance.

Limit Treatment Duration to 12 Weeks or Less

Antibiotic use should be time limited, with discontinuation ideally within 8 to 12 weeks as clinical improvement is demonstrated. Repeated or prolonged courses should be avoided to minimize risk for resistance.

Simplify Treatment Regimens to Enhance Adherence

Regimen simplicity improves adherence, especially in adolescents. A two-agent regimen of an oral antibiotic and a topical retinoid typically is sufficient during the induction phase.^13,14

Select Narrower-Spectrum Antibiotics When Feasible

Using a narrower-spectrum antibiotic may help minimize disruption to nontarget microbiota.^15,16 Sarecycline has shown narrower in vitro activity within the tetracycline class,^17,18 though clinical decisions should be informed by access, availability, and cost. Regardless of the agent used (eg, doxycycline, minocycline, or sarecycline), all antibiotics should be used judiciously and for the shortest effective duration.

Use Systemic Nonantibiotic Therapies When Appropriate

If there is inadequate response to oral antibiotic therapy, consider switching to systemic nonantibiotic options. Hormonal therapy may be appropriate for select female patients. Oral isotretinoin should be considered for patients with severe, recalcitrant, or scarring acne. Cycling between antibiotic classes without clear benefit is discouraged.

FINAL THOUGHTS

Oral antibiotics remain a foundational component in the management of moderate to severe acne; however, their use must be intentional, time limited, and guided by best practices to minimize the emergence of antimicrobial resistance. By adhering to the prescribing principles we have outlined here, which are rooted in clinical expertise and consistent with AAD guidelines, dermatologists can preserve antibiotic efficacy, optimize patient outcomes, and reduce long-term microbiologic risks. Stewardship is not about withholding treatment; it is about optimizing care today to protect treatment options for tomorrow.

Dermatologists have long relied on oral antibiotics to manage moderate to severe acne^1-4; however, it is critical to reassess how these medications are used in clinical practice as concerns about antibiotic resistance grow.⁵ The question is not whether antibiotics are effective for acne treatment—we know they are—but how to optimize their use to balance clinical benefit with responsible prescribing. Resistance in Cutibacterium acnes has been well documented in laboratory settings, but clinical treatment failure due to resistance remains rare and difficult to quantify.^6,7 Still, minimizing unnecessary exposure is good clinical practice. Whether antibiotic resistance ultimately proves to drive clinical failure or remains largely theoretical, stewardship safeguards future treatment options.

In this article, we present a practical, expert-based framework aligned with American Academy of Dermatology (AAD) guidelines to support responsible antibiotic use in acne management. Seven prescribing principles are outlined to help clinicians maintain efficacy while minimizing resistance risk. Mechanisms of resistance in C acnes and broader microbiome impacts also are discussed.

MECHANISMS OF RESISTANCE IN ACNE THERAPY

Antibiotic resistance in acne primarily involves C acnes and arises through selective pressure from prolonged or subtherapeutic antibiotic exposure. Resistance mechanisms include point mutations in ribosomal binding sites, leading to decreased binding affinity for tetracyclines and macrolides as well as efflux pump activation and biofilm formation.^8,9 Over time, resistant strains may proliferate and outcompete susceptible populations, potentially contributing to reduced clinical efficacy. Importantly, the use of broad-spectrum antibiotics may disrupt the skin and gut microbiota, promoting resistance among nontarget organisms.⁵ These concerns underscore the importance of limiting antibiotic use to appropriate indications, combining antibiotics with adjunctive nonantibiotic therapies, and avoiding monotherapy.

PRESCRIBING PRINCIPLES FOR RESPONSIBLE ORAL ANTIBIOTIC USE IN ACNE

The following principles are derived from our clinical experience and are aligned with AAD guidelines on acne treatment.¹⁰ This practical framework supports safe, effective, and streamlined prescribing.

Reserve Oral Antibiotics for Appropriate Cases

Oral antibiotics should be considered for patients with moderate to severe inflammatory acne when rapid anti-inflammatory control is needed. They are not indicated for comedonal or mild papulopustular acne. Before initiating treatment, clinicians should weigh the potential benefits against the risks associated with antibiotic exposure, including resistance and microbiome disruption.

Combine Oral Antibiotics With Topical Retinoids

Oral antibiotics should not be used as monotherapy. Topical retinoids should be initiated concurrently with oral antibiotics to maximize anti-inflammatory benefit, support transition to maintenance therapy, and reduce risk for resistance.

Consider Adding an Adjunctive Topical Antimicrobial Agent

Adjunctive topical antimicrobials can help reduce bacterial load. Benzoyl peroxide remains a first-line option due to its bactericidal activity and lack of resistance induction; however, recent product recalls involving benzene contamination may have raised safety concerns among some clinicians and patients.^11,12 While no definitive harm has been established, alternative topical agents approved by the US Food and Drug Administration (eg, azelaic acid) may be used based on shared decision-making, tolerability, cost, access, and patient preference. Use of topical antibiotics (eg, clindamycin, erythromycin) as monotherapy is discouraged due to their higher resistance potential, which is consistent with AAD guidance.

Limit Treatment Duration to 12 Weeks or Less

Antibiotic use should be time limited, with discontinuation ideally within 8 to 12 weeks as clinical improvement is demonstrated. Repeated or prolonged courses should be avoided to minimize risk for resistance.

Simplify Treatment Regimens to Enhance Adherence

Regimen simplicity improves adherence, especially in adolescents. A two-agent regimen of an oral antibiotic and a topical retinoid typically is sufficient during the induction phase.^13,14

Select Narrower-Spectrum Antibiotics When Feasible

Using a narrower-spectrum antibiotic may help minimize disruption to nontarget microbiota.^15,16 Sarecycline has shown narrower in vitro activity within the tetracycline class,^17,18 though clinical decisions should be informed by access, availability, and cost. Regardless of the agent used (eg, doxycycline, minocycline, or sarecycline), all antibiotics should be used judiciously and for the shortest effective duration.

Use Systemic Nonantibiotic Therapies When Appropriate

If there is inadequate response to oral antibiotic therapy, consider switching to systemic nonantibiotic options. Hormonal therapy may be appropriate for select female patients. Oral isotretinoin should be considered for patients with severe, recalcitrant, or scarring acne. Cycling between antibiotic classes without clear benefit is discouraged.

FINAL THOUGHTS

Oral antibiotics remain a foundational component in the management of moderate to severe acne; however, their use must be intentional, time limited, and guided by best practices to minimize the emergence of antimicrobial resistance. By adhering to the prescribing principles we have outlined here, which are rooted in clinical expertise and consistent with AAD guidelines, dermatologists can preserve antibiotic efficacy, optimize patient outcomes, and reduce long-term microbiologic risks. Stewardship is not about withholding treatment; it is about optimizing care today to protect treatment options for tomorrow.

Dermatologists have long relied on oral antibiotics to manage moderate to severe acne^1-4; however, it is critical to reassess how these medications are used in clinical practice as concerns about antibiotic resistance grow.⁵ The question is not whether antibiotics are effective for acne treatment—we know they are—but how to optimize their use to balance clinical benefit with responsible prescribing. Resistance in Cutibacterium acnes has been well documented in laboratory settings, but clinical treatment failure due to resistance remains rare and difficult to quantify.^6,7 Still, minimizing unnecessary exposure is good clinical practice. Whether antibiotic resistance ultimately proves to drive clinical failure or remains largely theoretical, stewardship safeguards future treatment options.

In this article, we present a practical, expert-based framework aligned with American Academy of Dermatology (AAD) guidelines to support responsible antibiotic use in acne management. Seven prescribing principles are outlined to help clinicians maintain efficacy while minimizing resistance risk. Mechanisms of resistance in C acnes and broader microbiome impacts also are discussed.

MECHANISMS OF RESISTANCE IN ACNE THERAPY

Antibiotic resistance in acne primarily involves C acnes and arises through selective pressure from prolonged or subtherapeutic antibiotic exposure. Resistance mechanisms include point mutations in ribosomal binding sites, leading to decreased binding affinity for tetracyclines and macrolides as well as efflux pump activation and biofilm formation.^8,9 Over time, resistant strains may proliferate and outcompete susceptible populations, potentially contributing to reduced clinical efficacy. Importantly, the use of broad-spectrum antibiotics may disrupt the skin and gut microbiota, promoting resistance among nontarget organisms.⁵ These concerns underscore the importance of limiting antibiotic use to appropriate indications, combining antibiotics with adjunctive nonantibiotic therapies, and avoiding monotherapy.

PRESCRIBING PRINCIPLES FOR RESPONSIBLE ORAL ANTIBIOTIC USE IN ACNE

The following principles are derived from our clinical experience and are aligned with AAD guidelines on acne treatment.¹⁰ This practical framework supports safe, effective, and streamlined prescribing.

Reserve Oral Antibiotics for Appropriate Cases

Oral antibiotics should be considered for patients with moderate to severe inflammatory acne when rapid anti-inflammatory control is needed. They are not indicated for comedonal or mild papulopustular acne. Before initiating treatment, clinicians should weigh the potential benefits against the risks associated with antibiotic exposure, including resistance and microbiome disruption.

Combine Oral Antibiotics With Topical Retinoids

Oral antibiotics should not be used as monotherapy. Topical retinoids should be initiated concurrently with oral antibiotics to maximize anti-inflammatory benefit, support transition to maintenance therapy, and reduce risk for resistance.

Consider Adding an Adjunctive Topical Antimicrobial Agent

Adjunctive topical antimicrobials can help reduce bacterial load. Benzoyl peroxide remains a first-line option due to its bactericidal activity and lack of resistance induction; however, recent product recalls involving benzene contamination may have raised safety concerns among some clinicians and patients.^11,12 While no definitive harm has been established, alternative topical agents approved by the US Food and Drug Administration (eg, azelaic acid) may be used based on shared decision-making, tolerability, cost, access, and patient preference. Use of topical antibiotics (eg, clindamycin, erythromycin) as monotherapy is discouraged due to their higher resistance potential, which is consistent with AAD guidance.

Limit Treatment Duration to 12 Weeks or Less

Antibiotic use should be time limited, with discontinuation ideally within 8 to 12 weeks as clinical improvement is demonstrated. Repeated or prolonged courses should be avoided to minimize risk for resistance.

Simplify Treatment Regimens to Enhance Adherence

Regimen simplicity improves adherence, especially in adolescents. A two-agent regimen of an oral antibiotic and a topical retinoid typically is sufficient during the induction phase.^13,14

Select Narrower-Spectrum Antibiotics When Feasible

Using a narrower-spectrum antibiotic may help minimize disruption to nontarget microbiota.^15,16 Sarecycline has shown narrower in vitro activity within the tetracycline class,^17,18 though clinical decisions should be informed by access, availability, and cost. Regardless of the agent used (eg, doxycycline, minocycline, or sarecycline), all antibiotics should be used judiciously and for the shortest effective duration.

Use Systemic Nonantibiotic Therapies When Appropriate

If there is inadequate response to oral antibiotic therapy, consider switching to systemic nonantibiotic options. Hormonal therapy may be appropriate for select female patients. Oral isotretinoin should be considered for patients with severe, recalcitrant, or scarring acne. Cycling between antibiotic classes without clear benefit is discouraged.

FINAL THOUGHTS

Oral antibiotics remain a foundational component in the management of moderate to severe acne; however, their use must be intentional, time limited, and guided by best practices to minimize the emergence of antimicrobial resistance. By adhering to the prescribing principles we have outlined here, which are rooted in clinical expertise and consistent with AAD guidelines, dermatologists can preserve antibiotic efficacy, optimize patient outcomes, and reduce long-term microbiologic risks. Stewardship is not about withholding treatment; it is about optimizing care today to protect treatment options for tomorrow.

Practice Gap

Lipoatrophy associated with HIV is characterized by loss of adipose tissue in distinctive anatomic areas, most prominently in the nasolabial folds, temples, and medial cheeks.¹ This adverse effect further stigmatizes patients with HIV, and its association with highly active antiretroviral therapy (HAART)—specifically protease inhibitors—may contribute to suboptimal adherence to treatment.^1,2 Moreover, this finding is not uncommon: The prevalence of facial lipoatrophy after receiving HAART can range from 28% in patients treated for less than 5 years to 54% in those treated for a median of 10 years.² The associated stigma, notable decrease in quality of life, and known affiliation as an adverse effect of HAART make correction of facial lipoatrophy in patients with HIV an important management option.

Poly-L-lactic acid is approved by the US Food and Drug Administration for addressing fat loss due to HAART in patients with HIV.^2,3 When used as a dermal filler for correction of facial lipoatrophy, PLLA is well tolerated and has been shown to improve quality of life.^2,3 Poly-L-lactic acid is available for clinical use as microparticles of lyophilized alpha hydroxy acid polymers. Once injected (after the carrier substance is absorbed), PLLA induces an inflammatory response that ultimately leads to the production of new collagen.³ Unfortunately, PLLA microparticles often obstruct needles and make the product difficult to use, potentially hindering effective injection; thus, it is in the best interest of the patient to mitigate needle obstruction during this procedure. In this article, we describe a simple and effective way to mitigate this problem by utilizing a water bath to warm the filler prior to injection.

Technique

The required supplies include a thermostatic water bath, reconstituted PLLA, a syringe, and a 26-gauge injection needle. Because laboratory-grade heated water baths typically cost between $300 and $3000,⁴ we recommend using a more affordable, commercially available thermostatic water bath (eg, baby bottle warmer)(Figure 1) to warm the filler prior to injection, as the optimal temperature for this technique can still be achieved while remaining cost effective. Vials of PLLA reconstituted with 7 mL of sterile water and 2 mL lidocaine hydrochloride 1% should be labeled with the date of reconstitution and manually agitated for 30 seconds. The reconstituted product should be stored for 24 hours to ensure even suspension and powder saturation.⁵ On the day of the procedure, the vial should be placed into the water bath (heated to 100 °C) for 10 minutes prior to injection (Figure 2) and agitated again immediately before withdrawal into the syringe. The clinician then should sterilize the rubber top and draw the product from the warmed vial using the same size needle that will be used for injection. Although a larger gauge needle may make drawing up the product easier in typical practice, drawing and injecting with the same gauge needle helps prevent larger particles from clogging a smaller injection needle. Using a 26-gauge injection needle for withdrawal further reduces clogging by serving as a filter to prevent larger product particles from entering the injection syringe. The vials of PLLA can be kept in the water bath throughout the procedure between uses to keep the filler at a consistent temperature.

Practice Implications

Although many clinicians reduce needle obstructions by warming PLLA before injection, a published protocol currently is not available. One consideration when utilizing this technique is the limited data on the clinical stability and efficacy of PLLA at varying temperatures. Two studies recommend bringing the reconstituted vial to room temperature prior to injection, while others have documented an endothermic melting point in the range of 120 °C to 180 °C for PLLA, which lies well above the physiologic temperature readily achievable by baby bottle warmers.^6,7 Easily accessible bottle warmers can maintain the suspension at approximately 100 °C, keeping it in its crystalline polymer form and preventing melting. With this technique, the authors observed an improvement in efficacy due to fewer clogged needles, resulting in the delivery of more filler to the patient. In addition to comparable clinical results to not warming the product, our experience has shown that warming the PLLA prior to injection is not associated with increased patient discomfort and is well tolerated. Furthermore, patients experience less bruising and bleeding, as fewer needle sticks are necessary. This combination of a consistently heated filler with the added benefit of needle filtration yields dramatically fewer needle obstructions, fewer needle sticks, and increased patient satisfaction, improving the experience of patients with HIV-associated lipoatrophy seeking correction.

Practice Gap

Lipoatrophy associated with HIV is characterized by loss of adipose tissue in distinctive anatomic areas, most prominently in the nasolabial folds, temples, and medial cheeks.¹ This adverse effect further stigmatizes patients with HIV, and its association with highly active antiretroviral therapy (HAART)—specifically protease inhibitors—may contribute to suboptimal adherence to treatment.^1,2 Moreover, this finding is not uncommon: The prevalence of facial lipoatrophy after receiving HAART can range from 28% in patients treated for less than 5 years to 54% in those treated for a median of 10 years.² The associated stigma, notable decrease in quality of life, and known affiliation as an adverse effect of HAART make correction of facial lipoatrophy in patients with HIV an important management option.

Poly-L-lactic acid is approved by the US Food and Drug Administration for addressing fat loss due to HAART in patients with HIV.^2,3 When used as a dermal filler for correction of facial lipoatrophy, PLLA is well tolerated and has been shown to improve quality of life.^2,3 Poly-L-lactic acid is available for clinical use as microparticles of lyophilized alpha hydroxy acid polymers. Once injected (after the carrier substance is absorbed), PLLA induces an inflammatory response that ultimately leads to the production of new collagen.³ Unfortunately, PLLA microparticles often obstruct needles and make the product difficult to use, potentially hindering effective injection; thus, it is in the best interest of the patient to mitigate needle obstruction during this procedure. In this article, we describe a simple and effective way to mitigate this problem by utilizing a water bath to warm the filler prior to injection.

Technique

The required supplies include a thermostatic water bath, reconstituted PLLA, a syringe, and a 26-gauge injection needle. Because laboratory-grade heated water baths typically cost between $300 and $3000,⁴ we recommend using a more affordable, commercially available thermostatic water bath (eg, baby bottle warmer)(Figure 1) to warm the filler prior to injection, as the optimal temperature for this technique can still be achieved while remaining cost effective. Vials of PLLA reconstituted with 7 mL of sterile water and 2 mL lidocaine hydrochloride 1% should be labeled with the date of reconstitution and manually agitated for 30 seconds. The reconstituted product should be stored for 24 hours to ensure even suspension and powder saturation.⁵ On the day of the procedure, the vial should be placed into the water bath (heated to 100 °C) for 10 minutes prior to injection (Figure 2) and agitated again immediately before withdrawal into the syringe. The clinician then should sterilize the rubber top and draw the product from the warmed vial using the same size needle that will be used for injection. Although a larger gauge needle may make drawing up the product easier in typical practice, drawing and injecting with the same gauge needle helps prevent larger particles from clogging a smaller injection needle. Using a 26-gauge injection needle for withdrawal further reduces clogging by serving as a filter to prevent larger product particles from entering the injection syringe. The vials of PLLA can be kept in the water bath throughout the procedure between uses to keep the filler at a consistent temperature.

Practice Implications

Although many clinicians reduce needle obstructions by warming PLLA before injection, a published protocol currently is not available. One consideration when utilizing this technique is the limited data on the clinical stability and efficacy of PLLA at varying temperatures. Two studies recommend bringing the reconstituted vial to room temperature prior to injection, while others have documented an endothermic melting point in the range of 120 °C to 180 °C for PLLA, which lies well above the physiologic temperature readily achievable by baby bottle warmers.^6,7 Easily accessible bottle warmers can maintain the suspension at approximately 100 °C, keeping it in its crystalline polymer form and preventing melting. With this technique, the authors observed an improvement in efficacy due to fewer clogged needles, resulting in the delivery of more filler to the patient. In addition to comparable clinical results to not warming the product, our experience has shown that warming the PLLA prior to injection is not associated with increased patient discomfort and is well tolerated. Furthermore, patients experience less bruising and bleeding, as fewer needle sticks are necessary. This combination of a consistently heated filler with the added benefit of needle filtration yields dramatically fewer needle obstructions, fewer needle sticks, and increased patient satisfaction, improving the experience of patients with HIV-associated lipoatrophy seeking correction.

Practice Gap

Lipoatrophy associated with HIV is characterized by loss of adipose tissue in distinctive anatomic areas, most prominently in the nasolabial folds, temples, and medial cheeks.¹ This adverse effect further stigmatizes patients with HIV, and its association with highly active antiretroviral therapy (HAART)—specifically protease inhibitors—may contribute to suboptimal adherence to treatment.^1,2 Moreover, this finding is not uncommon: The prevalence of facial lipoatrophy after receiving HAART can range from 28% in patients treated for less than 5 years to 54% in those treated for a median of 10 years.² The associated stigma, notable decrease in quality of life, and known affiliation as an adverse effect of HAART make correction of facial lipoatrophy in patients with HIV an important management option.

Poly-L-lactic acid is approved by the US Food and Drug Administration for addressing fat loss due to HAART in patients with HIV.^2,3 When used as a dermal filler for correction of facial lipoatrophy, PLLA is well tolerated and has been shown to improve quality of life.^2,3 Poly-L-lactic acid is available for clinical use as microparticles of lyophilized alpha hydroxy acid polymers. Once injected (after the carrier substance is absorbed), PLLA induces an inflammatory response that ultimately leads to the production of new collagen.³ Unfortunately, PLLA microparticles often obstruct needles and make the product difficult to use, potentially hindering effective injection; thus, it is in the best interest of the patient to mitigate needle obstruction during this procedure. In this article, we describe a simple and effective way to mitigate this problem by utilizing a water bath to warm the filler prior to injection.

Technique

The required supplies include a thermostatic water bath, reconstituted PLLA, a syringe, and a 26-gauge injection needle. Because laboratory-grade heated water baths typically cost between $300 and $3000,⁴ we recommend using a more affordable, commercially available thermostatic water bath (eg, baby bottle warmer)(Figure 1) to warm the filler prior to injection, as the optimal temperature for this technique can still be achieved while remaining cost effective. Vials of PLLA reconstituted with 7 mL of sterile water and 2 mL lidocaine hydrochloride 1% should be labeled with the date of reconstitution and manually agitated for 30 seconds. The reconstituted product should be stored for 24 hours to ensure even suspension and powder saturation.⁵ On the day of the procedure, the vial should be placed into the water bath (heated to 100 °C) for 10 minutes prior to injection (Figure 2) and agitated again immediately before withdrawal into the syringe. The clinician then should sterilize the rubber top and draw the product from the warmed vial using the same size needle that will be used for injection. Although a larger gauge needle may make drawing up the product easier in typical practice, drawing and injecting with the same gauge needle helps prevent larger particles from clogging a smaller injection needle. Using a 26-gauge injection needle for withdrawal further reduces clogging by serving as a filter to prevent larger product particles from entering the injection syringe. The vials of PLLA can be kept in the water bath throughout the procedure between uses to keep the filler at a consistent temperature.

Practice Implications

Although many clinicians reduce needle obstructions by warming PLLA before injection, a published protocol currently is not available. One consideration when utilizing this technique is the limited data on the clinical stability and efficacy of PLLA at varying temperatures. Two studies recommend bringing the reconstituted vial to room temperature prior to injection, while others have documented an endothermic melting point in the range of 120 °C to 180 °C for PLLA, which lies well above the physiologic temperature readily achievable by baby bottle warmers.^6,7 Easily accessible bottle warmers can maintain the suspension at approximately 100 °C, keeping it in its crystalline polymer form and preventing melting. With this technique, the authors observed an improvement in efficacy due to fewer clogged needles, resulting in the delivery of more filler to the patient. In addition to comparable clinical results to not warming the product, our experience has shown that warming the PLLA prior to injection is not associated with increased patient discomfort and is well tolerated. Furthermore, patients experience less bruising and bleeding, as fewer needle sticks are necessary. This combination of a consistently heated filler with the added benefit of needle filtration yields dramatically fewer needle obstructions, fewer needle sticks, and increased patient satisfaction, improving the experience of patients with HIV-associated lipoatrophy seeking correction.

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (<1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, >35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (>5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (<1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, >35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (>5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (<1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, >35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (>5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

To the Editor:

Residency applicants, especially in competitive specialties such as dermatology, face major financial barriers due to the high costs of applications, interviews, and away rotations.¹ While several studies have examined application costs of other specialties, few have analyzed expenses associated with dermatology applications.^1,2 There are no data examining costs following the start of the COVID-19 pandemic in 2020; thus, our study evaluated dermatology application cost trends from 2021 to 2024 and compared them to other specialties to identify strategies to reduce the financial burden on applicants.

Self-reported total application costs, application fees, interview expenses, and away rotation costs from 2021 to 2024 were collected from the Texas Seeking Transparency in Application to Residency (STAR) database powered by the UT Southwestern Medical Center (Dallas, Texas).³ The mean total application expenses per year were compared among specialties, and an analysis of variance was used to determine if the differences were statistically significant.

The number of applicants who recorded information in the Texas STAR database was 110 in 2021, 163 in 2022, 136 in 2023, and 129 in 2024.³ The total dermatology application expenses increased from $2805 in 2021 to $6231 in 2024; interview costs increased from $404 in 2021 to $911 in 2024; and away rotation costs increased from $850 in 2021 to $3812 in 2024 (all P<.05)(Table). There was no significant change in application fees during the study period ($2176 in 2021 to $2125 in 2024 [P=.58]). Dermatology had the fourth highest average total cost over the study period compared to all other specialties, increasing from $2250 in 2021 to $5250 in 2024, following orthopedic surgery ($2250 in 2021 to $6750 in 2024), plastic surgery ($2250 in 2021 to $9750 in 2024), and neurosurgery ($1750 in 2021 to $11,250 in 2024).

Our study found that dermatology residency application costs have increased significantly from 2021 to 2024, primarily driven by rising interview and away rotation expenses (both P<.05). This trend places dermatology among the most expensive fields to apply to for residency. A cross-sectional survey of dermatology residency program directors identified away rotations as one of the top 5 selection criteria, underscoring their importance in the matching process.⁴ In addition, a cross-sectional analysis of 345 dermatology residents found that 26.2% matched at institutions where they had mentors, including those they connected with through away rotations.^5,6 Overall, the high cost of away rotations partially may reflect the competitive nature of the specialty, as building connections at programs may enhance the chances of matching. These costs also can vary based on geography, as rotating in high-cost urban centers can be more expensive than in rural areas; however, rural rotations may be less common due to limited program availability and applicant preferences. For example, nearly 50% of 2024 Electronic Residency Application Service applicants indicated a preference for urban settings, while fewer than 5% selected rural settings.⁷ Additionally, the high costs associated with applying to residency programs and completing away rotations can disproportionately impact students from rural backgrounds and underrepresented minorities, who may have fewer financial resources.

In our study, the lower application-related expenses in 2021 (during the pandemic) compared to those of 2024 (postpandemic) likely stem from the Association of American Medical Colleges’ recommendation to conduct virtual interviews during the pandemic.⁸ In 2024, some dermatology programs returned to in-person interviews, with some applicants consequently incurring higher costs related to travel, lodging, and other associated expenses.⁸ A cost-analysis study of 4153 dermatology applicants from 2016 to 2021 found that the average application costs were $1759 per applicant during the pandemic, when virtual interviews replaced in-person ones, whereas costs were $8476 per applicant during periods with in-person interviews and no COVID-19 restrictions.² However, we did not observe a significant change in application fees over our study period, likely because the pandemic did not affect application numbers. A cross-sectional analysis of dermatology applicants during the pandemic similarly reported reductions in application-related expenses during the period when interviews were conducted virtually,⁹ supporting the trend observed in our study. Overall, our findings taken together with other studies highlight the pandemic’s role in reducing expenses and underscore the potential for exploring additional cost-saving measures.

Implementing strategies to reduce these financial burdens—including virtual interviews, increasing student funding for away rotations, and limiting the number of applications individual students can submit—could help alleviate socioeconomic disparities. The new signaling system for residency programs aims to reduce the number of applications submitted, as applicants typically receive interviews only from the limited number of programs they signal, reducing overall application costs. However, our data from the Texas STAR database suggest that application numbers remained relatively stable from 2021 to 2024, indicating that, despite signaling, many applicants still may apply broadly in hopes of improving their chances in an increasingly competitive field. Although a definitive solution to reducing the financial burden on dermatology applicants remains elusive, these strategies can raise awareness and encourage important dialogues.

Limitations of our study include the voluntary nature of the Texas STAR survey, leading to potential voluntary response bias, as well as the small sample size. Students who choose to submit cost data may differ systematically from those who do not; for example, students who match may be more likely to report their outcomes, while those who do not match may be less likely to participate, potentially introducing selection bias. In addition, general awareness of the Texas STAR survey may vary across institutions and among students, further limiting the number of students who participate. Additionally, 2021 was the only presignaling year included, making it difficult to assess longer-term trends. Despite these limitations, the Texas STAR database remains a valuable resource for analyzing general residency application expenses and trends, as it offers comprehensive data from more than 100 medical schools and includes many variables.³

In conclusion, our study found that total dermatology residency application costs have increased significantly from 2021 to 2024 (all P<.05), making dermatology among the most expensive specialties for applying. This study sets the foundation for future survey-based research for applicants and program directors on strategies to alleviate financial burdens.

To the Editor:

Residency applicants, especially in competitive specialties such as dermatology, face major financial barriers due to the high costs of applications, interviews, and away rotations.¹ While several studies have examined application costs of other specialties, few have analyzed expenses associated with dermatology applications.^1,2 There are no data examining costs following the start of the COVID-19 pandemic in 2020; thus, our study evaluated dermatology application cost trends from 2021 to 2024 and compared them to other specialties to identify strategies to reduce the financial burden on applicants.

Self-reported total application costs, application fees, interview expenses, and away rotation costs from 2021 to 2024 were collected from the Texas Seeking Transparency in Application to Residency (STAR) database powered by the UT Southwestern Medical Center (Dallas, Texas).³ The mean total application expenses per year were compared among specialties, and an analysis of variance was used to determine if the differences were statistically significant.

The number of applicants who recorded information in the Texas STAR database was 110 in 2021, 163 in 2022, 136 in 2023, and 129 in 2024.³ The total dermatology application expenses increased from $2805 in 2021 to $6231 in 2024; interview costs increased from $404 in 2021 to $911 in 2024; and away rotation costs increased from $850 in 2021 to $3812 in 2024 (all P<.05)(Table). There was no significant change in application fees during the study period ($2176 in 2021 to $2125 in 2024 [P=.58]). Dermatology had the fourth highest average total cost over the study period compared to all other specialties, increasing from $2250 in 2021 to $5250 in 2024, following orthopedic surgery ($2250 in 2021 to $6750 in 2024), plastic surgery ($2250 in 2021 to $9750 in 2024), and neurosurgery ($1750 in 2021 to $11,250 in 2024).

Our study found that dermatology residency application costs have increased significantly from 2021 to 2024, primarily driven by rising interview and away rotation expenses (both P<.05). This trend places dermatology among the most expensive fields to apply to for residency. A cross-sectional survey of dermatology residency program directors identified away rotations as one of the top 5 selection criteria, underscoring their importance in the matching process.⁴ In addition, a cross-sectional analysis of 345 dermatology residents found that 26.2% matched at institutions where they had mentors, including those they connected with through away rotations.^5,6 Overall, the high cost of away rotations partially may reflect the competitive nature of the specialty, as building connections at programs may enhance the chances of matching. These costs also can vary based on geography, as rotating in high-cost urban centers can be more expensive than in rural areas; however, rural rotations may be less common due to limited program availability and applicant preferences. For example, nearly 50% of 2024 Electronic Residency Application Service applicants indicated a preference for urban settings, while fewer than 5% selected rural settings.⁷ Additionally, the high costs associated with applying to residency programs and completing away rotations can disproportionately impact students from rural backgrounds and underrepresented minorities, who may have fewer financial resources.

In our study, the lower application-related expenses in 2021 (during the pandemic) compared to those of 2024 (postpandemic) likely stem from the Association of American Medical Colleges’ recommendation to conduct virtual interviews during the pandemic.⁸ In 2024, some dermatology programs returned to in-person interviews, with some applicants consequently incurring higher costs related to travel, lodging, and other associated expenses.⁸ A cost-analysis study of 4153 dermatology applicants from 2016 to 2021 found that the average application costs were $1759 per applicant during the pandemic, when virtual interviews replaced in-person ones, whereas costs were $8476 per applicant during periods with in-person interviews and no COVID-19 restrictions.² However, we did not observe a significant change in application fees over our study period, likely because the pandemic did not affect application numbers. A cross-sectional analysis of dermatology applicants during the pandemic similarly reported reductions in application-related expenses during the period when interviews were conducted virtually,⁹ supporting the trend observed in our study. Overall, our findings taken together with other studies highlight the pandemic’s role in reducing expenses and underscore the potential for exploring additional cost-saving measures.

Implementing strategies to reduce these financial burdens—including virtual interviews, increasing student funding for away rotations, and limiting the number of applications individual students can submit—could help alleviate socioeconomic disparities. The new signaling system for residency programs aims to reduce the number of applications submitted, as applicants typically receive interviews only from the limited number of programs they signal, reducing overall application costs. However, our data from the Texas STAR database suggest that application numbers remained relatively stable from 2021 to 2024, indicating that, despite signaling, many applicants still may apply broadly in hopes of improving their chances in an increasingly competitive field. Although a definitive solution to reducing the financial burden on dermatology applicants remains elusive, these strategies can raise awareness and encourage important dialogues.

Limitations of our study include the voluntary nature of the Texas STAR survey, leading to potential voluntary response bias, as well as the small sample size. Students who choose to submit cost data may differ systematically from those who do not; for example, students who match may be more likely to report their outcomes, while those who do not match may be less likely to participate, potentially introducing selection bias. In addition, general awareness of the Texas STAR survey may vary across institutions and among students, further limiting the number of students who participate. Additionally, 2021 was the only presignaling year included, making it difficult to assess longer-term trends. Despite these limitations, the Texas STAR database remains a valuable resource for analyzing general residency application expenses and trends, as it offers comprehensive data from more than 100 medical schools and includes many variables.³

In conclusion, our study found that total dermatology residency application costs have increased significantly from 2021 to 2024 (all P<.05), making dermatology among the most expensive specialties for applying. This study sets the foundation for future survey-based research for applicants and program directors on strategies to alleviate financial burdens.

To the Editor:

Residency applicants, especially in competitive specialties such as dermatology, face major financial barriers due to the high costs of applications, interviews, and away rotations.¹ While several studies have examined application costs of other specialties, few have analyzed expenses associated with dermatology applications.^1,2 There are no data examining costs following the start of the COVID-19 pandemic in 2020; thus, our study evaluated dermatology application cost trends from 2021 to 2024 and compared them to other specialties to identify strategies to reduce the financial burden on applicants.

Self-reported total application costs, application fees, interview expenses, and away rotation costs from 2021 to 2024 were collected from the Texas Seeking Transparency in Application to Residency (STAR) database powered by the UT Southwestern Medical Center (Dallas, Texas).³ The mean total application expenses per year were compared among specialties, and an analysis of variance was used to determine if the differences were statistically significant.

The number of applicants who recorded information in the Texas STAR database was 110 in 2021, 163 in 2022, 136 in 2023, and 129 in 2024.³ The total dermatology application expenses increased from $2805 in 2021 to $6231 in 2024; interview costs increased from $404 in 2021 to $911 in 2024; and away rotation costs increased from $850 in 2021 to $3812 in 2024 (all P<.05)(Table). There was no significant change in application fees during the study period ($2176 in 2021 to $2125 in 2024 [P=.58]). Dermatology had the fourth highest average total cost over the study period compared to all other specialties, increasing from $2250 in 2021 to $5250 in 2024, following orthopedic surgery ($2250 in 2021 to $6750 in 2024), plastic surgery ($2250 in 2021 to $9750 in 2024), and neurosurgery ($1750 in 2021 to $11,250 in 2024).

Our study found that dermatology residency application costs have increased significantly from 2021 to 2024, primarily driven by rising interview and away rotation expenses (both P<.05). This trend places dermatology among the most expensive fields to apply to for residency. A cross-sectional survey of dermatology residency program directors identified away rotations as one of the top 5 selection criteria, underscoring their importance in the matching process.⁴ In addition, a cross-sectional analysis of 345 dermatology residents found that 26.2% matched at institutions where they had mentors, including those they connected with through away rotations.^5,6 Overall, the high cost of away rotations partially may reflect the competitive nature of the specialty, as building connections at programs may enhance the chances of matching. These costs also can vary based on geography, as rotating in high-cost urban centers can be more expensive than in rural areas; however, rural rotations may be less common due to limited program availability and applicant preferences. For example, nearly 50% of 2024 Electronic Residency Application Service applicants indicated a preference for urban settings, while fewer than 5% selected rural settings.⁷ Additionally, the high costs associated with applying to residency programs and completing away rotations can disproportionately impact students from rural backgrounds and underrepresented minorities, who may have fewer financial resources.

In our study, the lower application-related expenses in 2021 (during the pandemic) compared to those of 2024 (postpandemic) likely stem from the Association of American Medical Colleges’ recommendation to conduct virtual interviews during the pandemic.⁸ In 2024, some dermatology programs returned to in-person interviews, with some applicants consequently incurring higher costs related to travel, lodging, and other associated expenses.⁸ A cost-analysis study of 4153 dermatology applicants from 2016 to 2021 found that the average application costs were $1759 per applicant during the pandemic, when virtual interviews replaced in-person ones, whereas costs were $8476 per applicant during periods with in-person interviews and no COVID-19 restrictions.² However, we did not observe a significant change in application fees over our study period, likely because the pandemic did not affect application numbers. A cross-sectional analysis of dermatology applicants during the pandemic similarly reported reductions in application-related expenses during the period when interviews were conducted virtually,⁹ supporting the trend observed in our study. Overall, our findings taken together with other studies highlight the pandemic’s role in reducing expenses and underscore the potential for exploring additional cost-saving measures.

Implementing strategies to reduce these financial burdens—including virtual interviews, increasing student funding for away rotations, and limiting the number of applications individual students can submit—could help alleviate socioeconomic disparities. The new signaling system for residency programs aims to reduce the number of applications submitted, as applicants typically receive interviews only from the limited number of programs they signal, reducing overall application costs. However, our data from the Texas STAR database suggest that application numbers remained relatively stable from 2021 to 2024, indicating that, despite signaling, many applicants still may apply broadly in hopes of improving their chances in an increasingly competitive field. Although a definitive solution to reducing the financial burden on dermatology applicants remains elusive, these strategies can raise awareness and encourage important dialogues.

Limitations of our study include the voluntary nature of the Texas STAR survey, leading to potential voluntary response bias, as well as the small sample size. Students who choose to submit cost data may differ systematically from those who do not; for example, students who match may be more likely to report their outcomes, while those who do not match may be less likely to participate, potentially introducing selection bias. In addition, general awareness of the Texas STAR survey may vary across institutions and among students, further limiting the number of students who participate. Additionally, 2021 was the only presignaling year included, making it difficult to assess longer-term trends. Despite these limitations, the Texas STAR database remains a valuable resource for analyzing general residency application expenses and trends, as it offers comprehensive data from more than 100 medical schools and includes many variables.³

In conclusion, our study found that total dermatology residency application costs have increased significantly from 2021 to 2024 (all P<.05), making dermatology among the most expensive specialties for applying. This study sets the foundation for future survey-based research for applicants and program directors on strategies to alleviate financial burdens.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

The Diagnosis: Juvenile Xanthogranuloma

Given the patient’s age, clinical features of the lesion, and characteristic setting-sun pattern on dermoscopy, a diagnosis of juvenile xanthogranuloma (JXG) was made. The patient showed no other signs of neurofibromatosis type 1 (NF1) or systemic disease and was managed conservatively with observation and routine follow-up. Minimal growth of the lesion was noted at 1-year follow-up, and he was meeting all age-appropriate developmental milestones and showed no other symptoms consistent with NF1. 

Juvenile xanthogranuloma is the most common childhood non–Langerhans cell histiocytosis. While it typically manifests as an isolated condition, JXG also can be associated with NF1 as well as juvenile myelomonocytic leukemia.^1-3 Neurofibromatosis type 1 is a multisystem disorder with variable clinical manifestations that commonly is associated with skin findings such as café au lait macules, intertriginous freckling, and neurofibromas, in addition to JXG.^2,3 Diagnosis of JXG should prompt noninvasive evaluation for further signs and symptoms of NF1, including thorough patient and family history and physical examination to identify other characteristic cutaneous findings, and can include consideration of slit lamp eye examination and radiography for identification of osseous findings. 

The pathogenesis of JXG is not fully known, though there is evidence that it may be associated with a mutation in the mitogen-activated protein kinase pathway.¹ The majority of cases appear in the first year of life.⁴ Clinically, JXG can manifest with extracutaneous lesions, including on the eyes and lungs.^5-7 Juvenile xanthogranuloma can be noninvasively diagnosed with dermoscopy. As seen in our patient, dermoscopic findings include a red-yellow or yellow-orange background with an erythematous border, typically described as a setting-sun pattern.^4,8 Biopsy can confirm the diagnosis; however, given the usually benign course, this often is unnecessary. Most pediatric patients with cutaneous manifestations have a self-limited course with regression over several months to years. Generally, no treatment is required for cutaneous manifestations alone; however, lesions can be removed for aesthetic concerns. For those with systemic involvement, a range of other treatments have been used, including chemotherapy, radiotherapy, systemic corticosteroids, and cyclosporine.^6,7 

The differential diagnosis for JXG includes Brooke-Spiegler syndrome, Fabry disease, solitary cutaneous mastocytoma, and tuberous sclerosis complex. Brooke-Spiegler syndrome is an autosomal-dominant condition characterized by the growth of adnexal neoplasms, including trichoepitheliomas, cylindromas, and spiradenomas. These lesions usually manifest on the face but can include other areas such as the trunk.⁹ Fabry disease is an X-linked recessive lysosomal storage disorder with cutaneous manifestations such as angiokeratoma corporis diffusum and hypohidrosis. Patients also may present with systemic symptoms including hypertension and renal and cardiovascular disease.¹⁰ Mastocytosis encompasses several clinical disorders defined by mast cell hyperplasia and accumulation in various organ systems, and solitary cutaneous mastocytoma is the most common manifestation in children.^11,12 Cutaneous mastocytoma can manifest as a single red-brown or yellow papule, usually located on the arms or legs.¹³ Solitary cutaneous mastocytomas in pediatric patients typically are diagnosed based on clinical appearance and the formation of a wheal upon firm palpation (Darier sign).^11-13 Our patient did not demonstrate the Darier sign, and the lesion was asymptomatic. Tuberous sclerosis complex is an autosomal-dominant neurocutaneous disorder with neurologic and skin findings that occur early in the disease course and include facial angiofibromas, hypomelanotic macules, shagreen patches, and café-au-lait macules.¹⁴

The Diagnosis: Juvenile Xanthogranuloma

Given the patient’s age, clinical features of the lesion, and characteristic setting-sun pattern on dermoscopy, a diagnosis of juvenile xanthogranuloma (JXG) was made. The patient showed no other signs of neurofibromatosis type 1 (NF1) or systemic disease and was managed conservatively with observation and routine follow-up. Minimal growth of the lesion was noted at 1-year follow-up, and he was meeting all age-appropriate developmental milestones and showed no other symptoms consistent with NF1. 

Juvenile xanthogranuloma is the most common childhood non–Langerhans cell histiocytosis. While it typically manifests as an isolated condition, JXG also can be associated with NF1 as well as juvenile myelomonocytic leukemia.^1-3 Neurofibromatosis type 1 is a multisystem disorder with variable clinical manifestations that commonly is associated with skin findings such as café au lait macules, intertriginous freckling, and neurofibromas, in addition to JXG.^2,3 Diagnosis of JXG should prompt noninvasive evaluation for further signs and symptoms of NF1, including thorough patient and family history and physical examination to identify other characteristic cutaneous findings, and can include consideration of slit lamp eye examination and radiography for identification of osseous findings. 

The pathogenesis of JXG is not fully known, though there is evidence that it may be associated with a mutation in the mitogen-activated protein kinase pathway.¹ The majority of cases appear in the first year of life.⁴ Clinically, JXG can manifest with extracutaneous lesions, including on the eyes and lungs.^5-7 Juvenile xanthogranuloma can be noninvasively diagnosed with dermoscopy. As seen in our patient, dermoscopic findings include a red-yellow or yellow-orange background with an erythematous border, typically described as a setting-sun pattern.^4,8 Biopsy can confirm the diagnosis; however, given the usually benign course, this often is unnecessary. Most pediatric patients with cutaneous manifestations have a self-limited course with regression over several months to years. Generally, no treatment is required for cutaneous manifestations alone; however, lesions can be removed for aesthetic concerns. For those with systemic involvement, a range of other treatments have been used, including chemotherapy, radiotherapy, systemic corticosteroids, and cyclosporine.^6,7 

The differential diagnosis for JXG includes Brooke-Spiegler syndrome, Fabry disease, solitary cutaneous mastocytoma, and tuberous sclerosis complex. Brooke-Spiegler syndrome is an autosomal-dominant condition characterized by the growth of adnexal neoplasms, including trichoepitheliomas, cylindromas, and spiradenomas. These lesions usually manifest on the face but can include other areas such as the trunk.⁹ Fabry disease is an X-linked recessive lysosomal storage disorder with cutaneous manifestations such as angiokeratoma corporis diffusum and hypohidrosis. Patients also may present with systemic symptoms including hypertension and renal and cardiovascular disease.¹⁰ Mastocytosis encompasses several clinical disorders defined by mast cell hyperplasia and accumulation in various organ systems, and solitary cutaneous mastocytoma is the most common manifestation in children.^11,12 Cutaneous mastocytoma can manifest as a single red-brown or yellow papule, usually located on the arms or legs.¹³ Solitary cutaneous mastocytomas in pediatric patients typically are diagnosed based on clinical appearance and the formation of a wheal upon firm palpation (Darier sign).^11-13 Our patient did not demonstrate the Darier sign, and the lesion was asymptomatic. Tuberous sclerosis complex is an autosomal-dominant neurocutaneous disorder with neurologic and skin findings that occur early in the disease course and include facial angiofibromas, hypomelanotic macules, shagreen patches, and café-au-lait macules.¹⁴

The Diagnosis: Juvenile Xanthogranuloma

Given the patient’s age, clinical features of the lesion, and characteristic setting-sun pattern on dermoscopy, a diagnosis of juvenile xanthogranuloma (JXG) was made. The patient showed no other signs of neurofibromatosis type 1 (NF1) or systemic disease and was managed conservatively with observation and routine follow-up. Minimal growth of the lesion was noted at 1-year follow-up, and he was meeting all age-appropriate developmental milestones and showed no other symptoms consistent with NF1. 

Juvenile xanthogranuloma is the most common childhood non–Langerhans cell histiocytosis. While it typically manifests as an isolated condition, JXG also can be associated with NF1 as well as juvenile myelomonocytic leukemia.^1-3 Neurofibromatosis type 1 is a multisystem disorder with variable clinical manifestations that commonly is associated with skin findings such as café au lait macules, intertriginous freckling, and neurofibromas, in addition to JXG.^2,3 Diagnosis of JXG should prompt noninvasive evaluation for further signs and symptoms of NF1, including thorough patient and family history and physical examination to identify other characteristic cutaneous findings, and can include consideration of slit lamp eye examination and radiography for identification of osseous findings. 

The pathogenesis of JXG is not fully known, though there is evidence that it may be associated with a mutation in the mitogen-activated protein kinase pathway.¹ The majority of cases appear in the first year of life.⁴ Clinically, JXG can manifest with extracutaneous lesions, including on the eyes and lungs.^5-7 Juvenile xanthogranuloma can be noninvasively diagnosed with dermoscopy. As seen in our patient, dermoscopic findings include a red-yellow or yellow-orange background with an erythematous border, typically described as a setting-sun pattern.^4,8 Biopsy can confirm the diagnosis; however, given the usually benign course, this often is unnecessary. Most pediatric patients with cutaneous manifestations have a self-limited course with regression over several months to years. Generally, no treatment is required for cutaneous manifestations alone; however, lesions can be removed for aesthetic concerns. For those with systemic involvement, a range of other treatments have been used, including chemotherapy, radiotherapy, systemic corticosteroids, and cyclosporine.^6,7 

The differential diagnosis for JXG includes Brooke-Spiegler syndrome, Fabry disease, solitary cutaneous mastocytoma, and tuberous sclerosis complex. Brooke-Spiegler syndrome is an autosomal-dominant condition characterized by the growth of adnexal neoplasms, including trichoepitheliomas, cylindromas, and spiradenomas. These lesions usually manifest on the face but can include other areas such as the trunk.⁹ Fabry disease is an X-linked recessive lysosomal storage disorder with cutaneous manifestations such as angiokeratoma corporis diffusum and hypohidrosis. Patients also may present with systemic symptoms including hypertension and renal and cardiovascular disease.¹⁰ Mastocytosis encompasses several clinical disorders defined by mast cell hyperplasia and accumulation in various organ systems, and solitary cutaneous mastocytoma is the most common manifestation in children.^11,12 Cutaneous mastocytoma can manifest as a single red-brown or yellow papule, usually located on the arms or legs.¹³ Solitary cutaneous mastocytomas in pediatric patients typically are diagnosed based on clinical appearance and the formation of a wheal upon firm palpation (Darier sign).^11-13 Our patient did not demonstrate the Darier sign, and the lesion was asymptomatic. Tuberous sclerosis complex is an autosomal-dominant neurocutaneous disorder with neurologic and skin findings that occur early in the disease course and include facial angiofibromas, hypomelanotic macules, shagreen patches, and café-au-lait macules.¹⁴

The patient was diagnosed with erythema ab igne based on characteristic skin findings on physical examination along with a convincing history of chronic localized heat exposure. Erythema ab igne manifests as a persistent reticulated, erythematous, or hyperpigmented rash at sites of chronic heat exposure.¹ Commonplace items that emit heat such as electric heaters, car heaters, heating pads, hot water bottles, and, in our case, laptops also emit infrared radiation, which can lead to changes in the skin with long-term exposure.² Because exposure to these sources often is limited to one area of the body, erythema ab igne usually manifests locally, as exemplified in this case. Chronic heat exposure and infrared radiation from these sources are thought to induce hyperthermia below the threshold for a thermal burn, and the cutaneous findings correspond with the dermal venous plexus.³

Diagnosis of erythema ab igne primarily is made clinically based on characteristic skin findings and exposure history. Relevant history may include occupations with prolonged heat exposure, such as baking, silversmithing, or foundry work. Heat exposure also may result from cultural practices such as cupping with moxibustion.⁴ Additionally, repeated use of heating pads or hot water bottles for pain relief by patients diagnosed with chronic pain or an underlying illness may contribute to development of erythema ab igne.^1,4

Biopsy was not needed for diagnosis of this patient, but if the presentation is equivocal and history of potential exposures is unclear, a biopsy may be taken. A hematoxylin and eosin stain would reveal dilation of small vascular channels in the superficial dermis, contributing to the classic reticulated appearance. Biopsy findings also would reveal either an interface dermatitis or pigment incontinence containing melanin-laden macrophages correlating to either the erythema or hyperpigmentation, respectively.⁴

The prognosis for erythema ab igne is excellent, especially if diagnosed early. Treatment involves removal of the inciting heat source.¹ The discoloration may resolve within a few months to years or may persist. If the hyperpigmentation is persistent, patients may consider laser treatments or lightening agents such as topical hydroquinone or topical tretinoin.⁴ However, if undiagnosed, patients may be at risk for development of a cutaneous malignancy, such as squamous cell carcinoma, Merkel cell carcinoma, poorly differentiated carcinoma, or cutaneous marginal zone lymphoma.^2,4 Malignant transformation has been reported to occur decades after the initial skin eruption, although the risk is rare⁵; however, due to this risk, patients with erythema ab igne should be followed regularly and screened for new lesions in the affected areas.

The patient was diagnosed with erythema ab igne based on characteristic skin findings on physical examination along with a convincing history of chronic localized heat exposure. Erythema ab igne manifests as a persistent reticulated, erythematous, or hyperpigmented rash at sites of chronic heat exposure.¹ Commonplace items that emit heat such as electric heaters, car heaters, heating pads, hot water bottles, and, in our case, laptops also emit infrared radiation, which can lead to changes in the skin with long-term exposure.² Because exposure to these sources often is limited to one area of the body, erythema ab igne usually manifests locally, as exemplified in this case. Chronic heat exposure and infrared radiation from these sources are thought to induce hyperthermia below the threshold for a thermal burn, and the cutaneous findings correspond with the dermal venous plexus.³

Diagnosis of erythema ab igne primarily is made clinically based on characteristic skin findings and exposure history. Relevant history may include occupations with prolonged heat exposure, such as baking, silversmithing, or foundry work. Heat exposure also may result from cultural practices such as cupping with moxibustion.⁴ Additionally, repeated use of heating pads or hot water bottles for pain relief by patients diagnosed with chronic pain or an underlying illness may contribute to development of erythema ab igne.^1,4

Biopsy was not needed for diagnosis of this patient, but if the presentation is equivocal and history of potential exposures is unclear, a biopsy may be taken. A hematoxylin and eosin stain would reveal dilation of small vascular channels in the superficial dermis, contributing to the classic reticulated appearance. Biopsy findings also would reveal either an interface dermatitis or pigment incontinence containing melanin-laden macrophages correlating to either the erythema or hyperpigmentation, respectively.⁴

The prognosis for erythema ab igne is excellent, especially if diagnosed early. Treatment involves removal of the inciting heat source.¹ The discoloration may resolve within a few months to years or may persist. If the hyperpigmentation is persistent, patients may consider laser treatments or lightening agents such as topical hydroquinone or topical tretinoin.⁴ However, if undiagnosed, patients may be at risk for development of a cutaneous malignancy, such as squamous cell carcinoma, Merkel cell carcinoma, poorly differentiated carcinoma, or cutaneous marginal zone lymphoma.^2,4 Malignant transformation has been reported to occur decades after the initial skin eruption, although the risk is rare⁵; however, due to this risk, patients with erythema ab igne should be followed regularly and screened for new lesions in the affected areas.

The patient was diagnosed with erythema ab igne based on characteristic skin findings on physical examination along with a convincing history of chronic localized heat exposure. Erythema ab igne manifests as a persistent reticulated, erythematous, or hyperpigmented rash at sites of chronic heat exposure.¹ Commonplace items that emit heat such as electric heaters, car heaters, heating pads, hot water bottles, and, in our case, laptops also emit infrared radiation, which can lead to changes in the skin with long-term exposure.² Because exposure to these sources often is limited to one area of the body, erythema ab igne usually manifests locally, as exemplified in this case. Chronic heat exposure and infrared radiation from these sources are thought to induce hyperthermia below the threshold for a thermal burn, and the cutaneous findings correspond with the dermal venous plexus.³

Diagnosis of erythema ab igne primarily is made clinically based on characteristic skin findings and exposure history. Relevant history may include occupations with prolonged heat exposure, such as baking, silversmithing, or foundry work. Heat exposure also may result from cultural practices such as cupping with moxibustion.⁴ Additionally, repeated use of heating pads or hot water bottles for pain relief by patients diagnosed with chronic pain or an underlying illness may contribute to development of erythema ab igne.^1,4

Biopsy was not needed for diagnosis of this patient, but if the presentation is equivocal and history of potential exposures is unclear, a biopsy may be taken. A hematoxylin and eosin stain would reveal dilation of small vascular channels in the superficial dermis, contributing to the classic reticulated appearance. Biopsy findings also would reveal either an interface dermatitis or pigment incontinence containing melanin-laden macrophages correlating to either the erythema or hyperpigmentation, respectively.⁴

The prognosis for erythema ab igne is excellent, especially if diagnosed early. Treatment involves removal of the inciting heat source.¹ The discoloration may resolve within a few months to years or may persist. If the hyperpigmentation is persistent, patients may consider laser treatments or lightening agents such as topical hydroquinone or topical tretinoin.⁴ However, if undiagnosed, patients may be at risk for development of a cutaneous malignancy, such as squamous cell carcinoma, Merkel cell carcinoma, poorly differentiated carcinoma, or cutaneous marginal zone lymphoma.^2,4 Malignant transformation has been reported to occur decades after the initial skin eruption, although the risk is rare⁵; however, due to this risk, patients with erythema ab igne should be followed regularly and screened for new lesions in the affected areas.

Are you seeing any increase or trends in cutaneous adverse effects related to the use of GLP-1 agonists in your practice?

DR. SHIELDS: The use of GLP-1 agonists is increasing substantially across numerous populations. Patients are using these medications not only for weight management and diabetes control but also for blood pressure modulation and cardiovascular risk reduction. The market size is expected to grow at a rate of about 6% until 2027. While severe cutaneous adverse effects still are considered relatively rare with GLP-1 agonist use, mild adverse effects are quite common. Dermatologists should be familiar with these effects and how to manage them. Rare but serious cutaneous reactions include morbilliform drug eruptions, dermal hypersensitivity reactions, panniculitis, and bullous pemphigoid. It is thought that some GLP-1 agonists may cause more skin reactions than others; for example, exenatide extended-release has been associated with cutaneous adverse events more frequently than other GLP-1 agonists in a recent comprehensive literature review.

Do you see a role for dermatologists in monitoring or managing the downstream dermatologic effects of GLP-1 agonists over the next few years?

DR. SHIELDS: Absolutely. When patients develop a drug eruption, bullous pemphigoid, or eosinophilic panniculitis, dermatologists are going to be the ones to diagnose and manage therapy. Awareness of these adverse effects is crucial to timely and thoughtful discussions surrounding medication discontinuation vs a “treat through” approach.

Do you recommend coordinating with endocrinologists or obesity medicine specialists when managing shared patients on GLP-1s (particularly if skin concerns arise)?

DR. SHIELDS: Yes. This is crucial to patient success. Co-management can provide clarity around the indication for therapy and allow for a thoughtful risk-benefit discussion with the patient, primary care physician, endocrinologist, cardiologist, etc. In my practice, I have found that many patients do not want to stop therapy even when they develop cutaneous adverse effects. There are options to transition therapy or treat through in some cases, but having a comprehensive monitoring and therapy plan is critical.

Have you encountered cases in which rapid weight loss from GLP-1s worsened conditions such as loose skin, cellulite, or facial lipoatrophy, leading to new aesthetic concerns? How would you recommend counseling and/or treating affected patients?

DR. SHIELDS: Accelerated facial aging is a noticeable adverse effect in patients who undergo treatment with GLP-1 agonists, especially when used off-label for weight loss. Localized loss of facial fat can result in altered facial proportions and excess skin. There are multiple additional mechanisms that may underlie accelerated facial aging in patients on GLP-1s, and really we are just beginning to scratch the surface of why and how this happens. Understanding these mechanisms will open the door to downstream preventive and therapeutic options. If patients experience new aesthetic concerns, I currently work with them to adjust their medication to slow weight loss, recommend improved nutrition and hydration, encourage exercise and weight training to maintain muscle mass, and engage my cosmetic dermatology colleagues to discuss procedures such as dermal fillers.

All patients starting GLP-1 agonists should be thoroughly counseled on risks and adverse effects of their medication. These are well reported and should be considered carefully. Starting with lower medication dosing in conjunction with slow escalation and careful monitoring can be helpful in combatting these adverse effects.

Are you seeing any increase or trends in cutaneous adverse effects related to the use of GLP-1 agonists in your practice?

DR. SHIELDS: The use of GLP-1 agonists is increasing substantially across numerous populations. Patients are using these medications not only for weight management and diabetes control but also for blood pressure modulation and cardiovascular risk reduction. The market size is expected to grow at a rate of about 6% until 2027. While severe cutaneous adverse effects still are considered relatively rare with GLP-1 agonist use, mild adverse effects are quite common. Dermatologists should be familiar with these effects and how to manage them. Rare but serious cutaneous reactions include morbilliform drug eruptions, dermal hypersensitivity reactions, panniculitis, and bullous pemphigoid. It is thought that some GLP-1 agonists may cause more skin reactions than others; for example, exenatide extended-release has been associated with cutaneous adverse events more frequently than other GLP-1 agonists in a recent comprehensive literature review.

Do you see a role for dermatologists in monitoring or managing the downstream dermatologic effects of GLP-1 agonists over the next few years?

DR. SHIELDS: Absolutely. When patients develop a drug eruption, bullous pemphigoid, or eosinophilic panniculitis, dermatologists are going to be the ones to diagnose and manage therapy. Awareness of these adverse effects is crucial to timely and thoughtful discussions surrounding medication discontinuation vs a “treat through” approach.

Do you recommend coordinating with endocrinologists or obesity medicine specialists when managing shared patients on GLP-1s (particularly if skin concerns arise)?

DR. SHIELDS: Yes. This is crucial to patient success. Co-management can provide clarity around the indication for therapy and allow for a thoughtful risk-benefit discussion with the patient, primary care physician, endocrinologist, cardiologist, etc. In my practice, I have found that many patients do not want to stop therapy even when they develop cutaneous adverse effects. There are options to transition therapy or treat through in some cases, but having a comprehensive monitoring and therapy plan is critical.

Have you encountered cases in which rapid weight loss from GLP-1s worsened conditions such as loose skin, cellulite, or facial lipoatrophy, leading to new aesthetic concerns? How would you recommend counseling and/or treating affected patients?

DR. SHIELDS: Accelerated facial aging is a noticeable adverse effect in patients who undergo treatment with GLP-1 agonists, especially when used off-label for weight loss. Localized loss of facial fat can result in altered facial proportions and excess skin. There are multiple additional mechanisms that may underlie accelerated facial aging in patients on GLP-1s, and really we are just beginning to scratch the surface of why and how this happens. Understanding these mechanisms will open the door to downstream preventive and therapeutic options. If patients experience new aesthetic concerns, I currently work with them to adjust their medication to slow weight loss, recommend improved nutrition and hydration, encourage exercise and weight training to maintain muscle mass, and engage my cosmetic dermatology colleagues to discuss procedures such as dermal fillers.

All patients starting GLP-1 agonists should be thoroughly counseled on risks and adverse effects of their medication. These are well reported and should be considered carefully. Starting with lower medication dosing in conjunction with slow escalation and careful monitoring can be helpful in combatting these adverse effects.

Are you seeing any increase or trends in cutaneous adverse effects related to the use of GLP-1 agonists in your practice?

DR. SHIELDS: The use of GLP-1 agonists is increasing substantially across numerous populations. Patients are using these medications not only for weight management and diabetes control but also for blood pressure modulation and cardiovascular risk reduction. The market size is expected to grow at a rate of about 6% until 2027. While severe cutaneous adverse effects still are considered relatively rare with GLP-1 agonist use, mild adverse effects are quite common. Dermatologists should be familiar with these effects and how to manage them. Rare but serious cutaneous reactions include morbilliform drug eruptions, dermal hypersensitivity reactions, panniculitis, and bullous pemphigoid. It is thought that some GLP-1 agonists may cause more skin reactions than others; for example, exenatide extended-release has been associated with cutaneous adverse events more frequently than other GLP-1 agonists in a recent comprehensive literature review.

Do you see a role for dermatologists in monitoring or managing the downstream dermatologic effects of GLP-1 agonists over the next few years?

DR. SHIELDS: Absolutely. When patients develop a drug eruption, bullous pemphigoid, or eosinophilic panniculitis, dermatologists are going to be the ones to diagnose and manage therapy. Awareness of these adverse effects is crucial to timely and thoughtful discussions surrounding medication discontinuation vs a “treat through” approach.

Do you recommend coordinating with endocrinologists or obesity medicine specialists when managing shared patients on GLP-1s (particularly if skin concerns arise)?

DR. SHIELDS: Yes. This is crucial to patient success. Co-management can provide clarity around the indication for therapy and allow for a thoughtful risk-benefit discussion with the patient, primary care physician, endocrinologist, cardiologist, etc. In my practice, I have found that many patients do not want to stop therapy even when they develop cutaneous adverse effects. There are options to transition therapy or treat through in some cases, but having a comprehensive monitoring and therapy plan is critical.

Have you encountered cases in which rapid weight loss from GLP-1s worsened conditions such as loose skin, cellulite, or facial lipoatrophy, leading to new aesthetic concerns? How would you recommend counseling and/or treating affected patients?

DR. SHIELDS: Accelerated facial aging is a noticeable adverse effect in patients who undergo treatment with GLP-1 agonists, especially when used off-label for weight loss. Localized loss of facial fat can result in altered facial proportions and excess skin. There are multiple additional mechanisms that may underlie accelerated facial aging in patients on GLP-1s, and really we are just beginning to scratch the surface of why and how this happens. Understanding these mechanisms will open the door to downstream preventive and therapeutic options. If patients experience new aesthetic concerns, I currently work with them to adjust their medication to slow weight loss, recommend improved nutrition and hydration, encourage exercise and weight training to maintain muscle mass, and engage my cosmetic dermatology colleagues to discuss procedures such as dermal fillers.

All patients starting GLP-1 agonists should be thoroughly counseled on risks and adverse effects of their medication. These are well reported and should be considered carefully. Starting with lower medication dosing in conjunction with slow escalation and careful monitoring can be helpful in combatting these adverse effects.