MDedge Dermatology

THE DIAGNOSIS: Trichodiscoma

Histologic evaluation revealed an unremarkable epidermal surface and a subjacent well-demarcated superficial dermal nodule showing a proliferation, sometimes fascicular, of wavy and spindled fibroblasts with some stellate forms within a variably loose fibrous stroma. Some angioplasia and vascular ectasia also were seen (Figure). A diagnosis of trichodiscoma was made based on these histologic findings.

While the patient’s personal and family history of pneumothorax originally had been attributed to other causes, the diagnosis of trichodiscoma raised suspicion for Birt-Hogg-Dubé syndrome due to the classic association of skin lesions (often trichodiscomas), renal cell carcinoma, and spontaneous pneumothorax in this condition. The patient was sent for genetic testing for the associated folliculin (FLCN) gene, which was positive and thereby confirmed the diagnosis of Birt-Hogg-Dubé syndrome. At the most recent follow-up almost 2 years after initial presentation, the lesions on the earlobe were stable. The patient has since undergone screening for abdominal and renal neoplasia with negative results, and he has had no other occurrences of pneumothorax.

Our case highlights the association between trichodiscomas and Birt-Hogg-Dubé syndrome, which necessitates screening for renal cell carcinoma, pneumothorax, and lung cysts.¹ Birt-Hogg-Dubé syndrome is an autosomal- dominant disorder of the skin and lungs that is characterized by a predisposition for renal carcinoma, pneumothorax, and colon polyps as well as cutaneous markers that include fibrofolliculomas, acrochordons, and trichodiscomas; the trichodiscomas tend to manifest as numerous smooth, flesh-colored or grayish-white papules on the face, ears, neck, and/or upper trunk.¹

Trichodiscomas are benign lesions and do not require treatment²; however, if they are cosmetically bothersome to the patient, surgical excision is an option for single lesions. For more widespread cutaneous disease, combination therapy with a CO₂ laser and erbium-doped yttrium aluminum garnet laser may be utilized.³ The differential diagnosis for trichodiscoma includes basal cell carcinoma, fibrous papule, dermal nevus, and trichofolliculoma.

Basal cell carcinoma is the most common type of skin cancer.⁴ Clinically, it typically manifests as pink or flesh-colored papules on the head or neck, often with overlying ulceration or telangiectasia. Due to its association with chronic sun exposure, the median age of diagnosis for basal cell carcinoma is 68 years. Histopathologically, basal cell carcinoma is characterized by islands or nests of atypical basaloid cells with palisading cells at the periphery.⁴ Treatment depends on the location and size of the lesion, but Mohs micrographic surgery is the most common intervention on the face and ears.⁵

In contrast, fibrous papules are benign lesions that manifest clinically as small, firm, flesh-colored papules that most commonly are found on the nose.^6,7 On dermatopathology, classic findings include fibrovascular proliferation and scattered multinucleated triangular or stellate cells in the upper dermis.⁷ Due to the benign nature of the lesion, treatment is not required⁶; however, shave excision, electrodessication, and laser therapies can be attempted if the patient chooses to pursue treatment.⁸

Dermal nevus is a type of benign acquired melanocytic nevus that manifests clinically as a light-brown to flesh-colored, dome-shaped or papillomatous papule.⁹ It typically develops in areas that are exposed to the sun, including the face.¹⁰ There also have been cases of dermal nevi on the ear.¹¹ Histopathology shows melanocytic nevus cells that have completely detached from the epidermis and are located entirely in the dermis.¹² While dermal nevi are benign and treatment is not necessary, surgical excision is an option for patients who request removal.¹³

Trichofolliculoma is a benign tumor of the adnexa that shows follicular differentiation on histopathology.¹⁴ On physical examination, it manifests as an isolated flesh-colored papule or nodule with a central pore from which tufted hairs protrude. These lesions usually appear on the face or scalp and occur more commonly in women than in men. While these may be clinically indistinguishable from trichodiscomas, the absence of protruding hair in our patient’s case makes trichofolliculoma less likely. When biopsied, histopathology classically shows a cystically dilated hair follicle with keratinous material and several mature and immature branched follicular structures. Preferred treatment for trichofolliculomas is surgical excision, and recurrence is rare.¹⁴

THE DIAGNOSIS: Trichodiscoma

Histologic evaluation revealed an unremarkable epidermal surface and a subjacent well-demarcated superficial dermal nodule showing a proliferation, sometimes fascicular, of wavy and spindled fibroblasts with some stellate forms within a variably loose fibrous stroma. Some angioplasia and vascular ectasia also were seen (Figure). A diagnosis of trichodiscoma was made based on these histologic findings.

While the patient’s personal and family history of pneumothorax originally had been attributed to other causes, the diagnosis of trichodiscoma raised suspicion for Birt-Hogg-Dubé syndrome due to the classic association of skin lesions (often trichodiscomas), renal cell carcinoma, and spontaneous pneumothorax in this condition. The patient was sent for genetic testing for the associated folliculin (FLCN) gene, which was positive and thereby confirmed the diagnosis of Birt-Hogg-Dubé syndrome. At the most recent follow-up almost 2 years after initial presentation, the lesions on the earlobe were stable. The patient has since undergone screening for abdominal and renal neoplasia with negative results, and he has had no other occurrences of pneumothorax.

Our case highlights the association between trichodiscomas and Birt-Hogg-Dubé syndrome, which necessitates screening for renal cell carcinoma, pneumothorax, and lung cysts.¹ Birt-Hogg-Dubé syndrome is an autosomal- dominant disorder of the skin and lungs that is characterized by a predisposition for renal carcinoma, pneumothorax, and colon polyps as well as cutaneous markers that include fibrofolliculomas, acrochordons, and trichodiscomas; the trichodiscomas tend to manifest as numerous smooth, flesh-colored or grayish-white papules on the face, ears, neck, and/or upper trunk.¹

Trichodiscomas are benign lesions and do not require treatment²; however, if they are cosmetically bothersome to the patient, surgical excision is an option for single lesions. For more widespread cutaneous disease, combination therapy with a CO₂ laser and erbium-doped yttrium aluminum garnet laser may be utilized.³ The differential diagnosis for trichodiscoma includes basal cell carcinoma, fibrous papule, dermal nevus, and trichofolliculoma.

Basal cell carcinoma is the most common type of skin cancer.⁴ Clinically, it typically manifests as pink or flesh-colored papules on the head or neck, often with overlying ulceration or telangiectasia. Due to its association with chronic sun exposure, the median age of diagnosis for basal cell carcinoma is 68 years. Histopathologically, basal cell carcinoma is characterized by islands or nests of atypical basaloid cells with palisading cells at the periphery.⁴ Treatment depends on the location and size of the lesion, but Mohs micrographic surgery is the most common intervention on the face and ears.⁵

In contrast, fibrous papules are benign lesions that manifest clinically as small, firm, flesh-colored papules that most commonly are found on the nose.^6,7 On dermatopathology, classic findings include fibrovascular proliferation and scattered multinucleated triangular or stellate cells in the upper dermis.⁷ Due to the benign nature of the lesion, treatment is not required⁶; however, shave excision, electrodessication, and laser therapies can be attempted if the patient chooses to pursue treatment.⁸

Dermal nevus is a type of benign acquired melanocytic nevus that manifests clinically as a light-brown to flesh-colored, dome-shaped or papillomatous papule.⁹ It typically develops in areas that are exposed to the sun, including the face.¹⁰ There also have been cases of dermal nevi on the ear.¹¹ Histopathology shows melanocytic nevus cells that have completely detached from the epidermis and are located entirely in the dermis.¹² While dermal nevi are benign and treatment is not necessary, surgical excision is an option for patients who request removal.¹³

Trichofolliculoma is a benign tumor of the adnexa that shows follicular differentiation on histopathology.¹⁴ On physical examination, it manifests as an isolated flesh-colored papule or nodule with a central pore from which tufted hairs protrude. These lesions usually appear on the face or scalp and occur more commonly in women than in men. While these may be clinically indistinguishable from trichodiscomas, the absence of protruding hair in our patient’s case makes trichofolliculoma less likely. When biopsied, histopathology classically shows a cystically dilated hair follicle with keratinous material and several mature and immature branched follicular structures. Preferred treatment for trichofolliculomas is surgical excision, and recurrence is rare.¹⁴

THE DIAGNOSIS: Trichodiscoma

Histologic evaluation revealed an unremarkable epidermal surface and a subjacent well-demarcated superficial dermal nodule showing a proliferation, sometimes fascicular, of wavy and spindled fibroblasts with some stellate forms within a variably loose fibrous stroma. Some angioplasia and vascular ectasia also were seen (Figure). A diagnosis of trichodiscoma was made based on these histologic findings.

While the patient’s personal and family history of pneumothorax originally had been attributed to other causes, the diagnosis of trichodiscoma raised suspicion for Birt-Hogg-Dubé syndrome due to the classic association of skin lesions (often trichodiscomas), renal cell carcinoma, and spontaneous pneumothorax in this condition. The patient was sent for genetic testing for the associated folliculin (FLCN) gene, which was positive and thereby confirmed the diagnosis of Birt-Hogg-Dubé syndrome. At the most recent follow-up almost 2 years after initial presentation, the lesions on the earlobe were stable. The patient has since undergone screening for abdominal and renal neoplasia with negative results, and he has had no other occurrences of pneumothorax.

Our case highlights the association between trichodiscomas and Birt-Hogg-Dubé syndrome, which necessitates screening for renal cell carcinoma, pneumothorax, and lung cysts.¹ Birt-Hogg-Dubé syndrome is an autosomal- dominant disorder of the skin and lungs that is characterized by a predisposition for renal carcinoma, pneumothorax, and colon polyps as well as cutaneous markers that include fibrofolliculomas, acrochordons, and trichodiscomas; the trichodiscomas tend to manifest as numerous smooth, flesh-colored or grayish-white papules on the face, ears, neck, and/or upper trunk.¹

Trichodiscomas are benign lesions and do not require treatment²; however, if they are cosmetically bothersome to the patient, surgical excision is an option for single lesions. For more widespread cutaneous disease, combination therapy with a CO₂ laser and erbium-doped yttrium aluminum garnet laser may be utilized.³ The differential diagnosis for trichodiscoma includes basal cell carcinoma, fibrous papule, dermal nevus, and trichofolliculoma.

Basal cell carcinoma is the most common type of skin cancer.⁴ Clinically, it typically manifests as pink or flesh-colored papules on the head or neck, often with overlying ulceration or telangiectasia. Due to its association with chronic sun exposure, the median age of diagnosis for basal cell carcinoma is 68 years. Histopathologically, basal cell carcinoma is characterized by islands or nests of atypical basaloid cells with palisading cells at the periphery.⁴ Treatment depends on the location and size of the lesion, but Mohs micrographic surgery is the most common intervention on the face and ears.⁵

In contrast, fibrous papules are benign lesions that manifest clinically as small, firm, flesh-colored papules that most commonly are found on the nose.^6,7 On dermatopathology, classic findings include fibrovascular proliferation and scattered multinucleated triangular or stellate cells in the upper dermis.⁷ Due to the benign nature of the lesion, treatment is not required⁶; however, shave excision, electrodessication, and laser therapies can be attempted if the patient chooses to pursue treatment.⁸

Dermal nevus is a type of benign acquired melanocytic nevus that manifests clinically as a light-brown to flesh-colored, dome-shaped or papillomatous papule.⁹ It typically develops in areas that are exposed to the sun, including the face.¹⁰ There also have been cases of dermal nevi on the ear.¹¹ Histopathology shows melanocytic nevus cells that have completely detached from the epidermis and are located entirely in the dermis.¹² While dermal nevi are benign and treatment is not necessary, surgical excision is an option for patients who request removal.¹³

Trichofolliculoma is a benign tumor of the adnexa that shows follicular differentiation on histopathology.¹⁴ On physical examination, it manifests as an isolated flesh-colored papule or nodule with a central pore from which tufted hairs protrude. These lesions usually appear on the face or scalp and occur more commonly in women than in men. While these may be clinically indistinguishable from trichodiscomas, the absence of protruding hair in our patient’s case makes trichofolliculoma less likely. When biopsied, histopathology classically shows a cystically dilated hair follicle with keratinous material and several mature and immature branched follicular structures. Preferred treatment for trichofolliculomas is surgical excision, and recurrence is rare.¹⁴

The advent of social media has revolutionized the way patients access and consume health information. While this increased access has its merits, it also has given rise to the proliferation of medical myths, which have considerable effects on patient-physician interactions.¹ Myths are prevalent across all fields of health care, ranging from misconceptions about disease etiology and prevention to the efficacy and safety of treatments. This influx of misinformation can derail the clinical encounter, shifting the focus from evidence-based medicine to myth-busting.² The COVID-19 pandemic exacerbated this issue, as widespread lockdowns and social distancing measures limited access to in-person medical consultations, prompting patients to increasingly turn to online sources for health information that often were unreliable, thereby bypassing professional medical advice.³ Herein, we highlight the challenges and implications of common dermatology myths and provide strategies for effectively debunking these myths to enhance patient care.

Common Dermatology Myths

In dermatology, where visible and often distressing conditions such as acne and hair loss are common, the impact of myths on patient perceptions and treatment outcomes can be particularly profound. Patients often arrive for consultations with preconceived notions that are not grounded in scientific evidence. Common dermatologic myths include eczema and the efficacy of topical corticosteroids, the causes and treatment of hair loss, and risk factors associated with skin cancer.

Eczema and Topical Corticosteroids—Topical corticosteroids for eczema are safe and effective, but nonadherence due to phobias stemming from misinformation online can impede treatment.⁴ Myths such as red skin syndrome and topical corticosteroid addiction are prevalent. Red skin syndrome refers to claims that prolonged use of topical corticosteroids causes severe redness and burning of the skin and worsening eczema symptoms upon withdrawal. Topical corticosteroid addiction suggests that patients become dependent on corticosteroids, requiring higher doses over time to maintain efficacy. These misconceptions contribute to fear and avoidance of prescribed treatments.

Eczema myths often divert focus from its true etiology as a genetic inflammatory skin disease, suggesting instead that it is caused by leaky gut or food intolerances.⁴ Risks such as skin thinning and stunted growth often are exaggerated on social media and other nonmedical platforms, though these adverse effects rarely are seen when topical corticosteroids are used appropriately under medical supervision. Misinformation often is linked to companies promoting unregulated consultations, tests, or supposedly natural treatments, including herbal remedies that may surreptitiously contain corticosteroids without clear labeling. This fosters distrust of US Food and Drug Administration– approved and dermatologist-prescribed treatments, as patients may cite concerns based on experiences with or claims about unapproved products.⁴

Sunscreen and Skin Cancer—In 2018, the American Academy of Dermatology prioritized skin cancer prevention due to suboptimal public adoption of photoprotection measures.⁵ However, the proliferation of misinformation regarding sunscreen and its potential to cause skin cancer is a more pressing issue. Myths range from claims that sunscreen is ineffective to warnings that it is dangerous, with some social media influencers even suggesting that sunscreen causes skin cancer due to toxic ingredients.⁶ Oxybenzone, typically found in chemical sunscreens, has been criticized by some advocacy groups and social media influencers as a potential hormone disruptor (ie, a chemical that could interfere with hormone production).⁷ However, no conclusive evidence has shown that oxybenzone is harmful to humans. Consumer concerns often are based on animal studies in which rats are fed oxybenzone, but mathematical modeling has indicated it would take 277 years of sunscreen use by humans to match the doses used in these studies.⁸ The false association between sunscreen use and skin cancer is based on flawed studies that found higher rates of skin cancer—including melanoma—in sunscreen users compared to those who did not use sunscreen. However, those using sunscreen also were more likely to travel to sunnier climates and engage in sunbathing, and it may have been this increased sun exposure that elevated their risk for skin cancer.⁷ It is imperative that the dermatology community counteract this type of misinformation with evidence-based advice.

Hair Loss—Some patients believe that hair loss is caused by wearing hats, frequent shampooing, or even stress in a way that oversimplifies complex physiological processes. Biotin, which commonly is added to supplements for hair, skin, and nails, has been linked to potential risks, such as interference with laboratory testing and false-positive or false-negative results in critical medical tests, which can lead to misdiagnosis or inappropriate treatment.⁹ Biotin interference can result in falsely low troponin readings, which are critical in diagnosing acute myocardial infarction. Tests for other hormones such as cortisol and parathyroid hormone also are affected, potentially impacting the evaluation and management of endocrine disorders. The US Food and Drug Administration has issued warnings for patients on this topic, emphasizing the importance of informing health care providers about any biotin supplementation prior to laboratory testing. Despite its popularity, there is no substantial scientific evidence to suggest that biotin supplementation promotes hair growth in anyone other than those with deficiency, which is quite rare.⁹

Myths and the Patient-Physician Relationship

The proliferation of medical myths and misinformation affects the dynamic between patients and dermatologists in several ways. Research across various medical fields has demonstrated that misinformation can substantially impact patient behavior and treatment adherence. Like many other specialists, dermatologists often spend considerable time during consultations with patients debunking myths and correcting misconceptions, which can detract from discussing more critical aspects of the patient’s condition and treatment plan and lead to frustration and anxiety among patients. It also can be challenging for physicians to have these conversations without alienating patients, who may distrust medical recommendations and believe that natural or alternative treatments are superior. This can lead to noncompliance with prescribed treatments, and patients may instead opt to try unproven remedies they encounter online, ultimately resulting in poorer health outcomes.

Strategies to Debunk Myths

By implementing the following strategies, dermatologists can combat the spread of myths, foster trust among patients, and promote adherence to evidence-based treatments:

• Provide educational outreach. Preemptively address myths by giving patients accurate and accessible resources. Including a dedicated section on your clinic’s website with articles, frequently asked questions, videos, and links to reputable sources can be effective. Sharing patient testimonials and before-and-after photographs to demonstrate the success of evidence-based treatments also is recommended, as real-life stories can be powerful tools in dispelling myths.
• Practice effective communication. Involve patients in the decision-making process by discussing their treatment goals, preferences, and concerns. It is important to present all options clearly, including the potential benefits and adverse effects. Discuss the expected outcomes and timelines, and be transparent about the limitations of certain treatment—honesty helps build trust and sets realistic expectations.
• Conduct structured consultations. Ensure that consultations with patients follow a structured format—history, physical examination, and discussion—to help keep the focus on evidence-based practice.
• Leverage technology. Guide patients toward reliable digital patient education tools to empower them with accurate information. Hosting live sessions on social media platforms during which patients can ask questions and receive evidence-based answers also can be beneficial.

Final Thoughts

In summary, the rise of medical myths poses a considerable challenge to dermatologic practice. By understanding the sources and impacts of these myths and employing strategies to dispel them, dermatologists can better navigate the complexities of modern patient interactions and ensure that care remains grounded in scientific evidence.

The advent of social media has revolutionized the way patients access and consume health information. While this increased access has its merits, it also has given rise to the proliferation of medical myths, which have considerable effects on patient-physician interactions.¹ Myths are prevalent across all fields of health care, ranging from misconceptions about disease etiology and prevention to the efficacy and safety of treatments. This influx of misinformation can derail the clinical encounter, shifting the focus from evidence-based medicine to myth-busting.² The COVID-19 pandemic exacerbated this issue, as widespread lockdowns and social distancing measures limited access to in-person medical consultations, prompting patients to increasingly turn to online sources for health information that often were unreliable, thereby bypassing professional medical advice.³ Herein, we highlight the challenges and implications of common dermatology myths and provide strategies for effectively debunking these myths to enhance patient care.

Common Dermatology Myths

In dermatology, where visible and often distressing conditions such as acne and hair loss are common, the impact of myths on patient perceptions and treatment outcomes can be particularly profound. Patients often arrive for consultations with preconceived notions that are not grounded in scientific evidence. Common dermatologic myths include eczema and the efficacy of topical corticosteroids, the causes and treatment of hair loss, and risk factors associated with skin cancer.

Eczema and Topical Corticosteroids—Topical corticosteroids for eczema are safe and effective, but nonadherence due to phobias stemming from misinformation online can impede treatment.⁴ Myths such as red skin syndrome and topical corticosteroid addiction are prevalent. Red skin syndrome refers to claims that prolonged use of topical corticosteroids causes severe redness and burning of the skin and worsening eczema symptoms upon withdrawal. Topical corticosteroid addiction suggests that patients become dependent on corticosteroids, requiring higher doses over time to maintain efficacy. These misconceptions contribute to fear and avoidance of prescribed treatments.

Eczema myths often divert focus from its true etiology as a genetic inflammatory skin disease, suggesting instead that it is caused by leaky gut or food intolerances.⁴ Risks such as skin thinning and stunted growth often are exaggerated on social media and other nonmedical platforms, though these adverse effects rarely are seen when topical corticosteroids are used appropriately under medical supervision. Misinformation often is linked to companies promoting unregulated consultations, tests, or supposedly natural treatments, including herbal remedies that may surreptitiously contain corticosteroids without clear labeling. This fosters distrust of US Food and Drug Administration– approved and dermatologist-prescribed treatments, as patients may cite concerns based on experiences with or claims about unapproved products.⁴

Sunscreen and Skin Cancer—In 2018, the American Academy of Dermatology prioritized skin cancer prevention due to suboptimal public adoption of photoprotection measures.⁵ However, the proliferation of misinformation regarding sunscreen and its potential to cause skin cancer is a more pressing issue. Myths range from claims that sunscreen is ineffective to warnings that it is dangerous, with some social media influencers even suggesting that sunscreen causes skin cancer due to toxic ingredients.⁶ Oxybenzone, typically found in chemical sunscreens, has been criticized by some advocacy groups and social media influencers as a potential hormone disruptor (ie, a chemical that could interfere with hormone production).⁷ However, no conclusive evidence has shown that oxybenzone is harmful to humans. Consumer concerns often are based on animal studies in which rats are fed oxybenzone, but mathematical modeling has indicated it would take 277 years of sunscreen use by humans to match the doses used in these studies.⁸ The false association between sunscreen use and skin cancer is based on flawed studies that found higher rates of skin cancer—including melanoma—in sunscreen users compared to those who did not use sunscreen. However, those using sunscreen also were more likely to travel to sunnier climates and engage in sunbathing, and it may have been this increased sun exposure that elevated their risk for skin cancer.⁷ It is imperative that the dermatology community counteract this type of misinformation with evidence-based advice.

Hair Loss—Some patients believe that hair loss is caused by wearing hats, frequent shampooing, or even stress in a way that oversimplifies complex physiological processes. Biotin, which commonly is added to supplements for hair, skin, and nails, has been linked to potential risks, such as interference with laboratory testing and false-positive or false-negative results in critical medical tests, which can lead to misdiagnosis or inappropriate treatment.⁹ Biotin interference can result in falsely low troponin readings, which are critical in diagnosing acute myocardial infarction. Tests for other hormones such as cortisol and parathyroid hormone also are affected, potentially impacting the evaluation and management of endocrine disorders. The US Food and Drug Administration has issued warnings for patients on this topic, emphasizing the importance of informing health care providers about any biotin supplementation prior to laboratory testing. Despite its popularity, there is no substantial scientific evidence to suggest that biotin supplementation promotes hair growth in anyone other than those with deficiency, which is quite rare.⁹

Myths and the Patient-Physician Relationship

The proliferation of medical myths and misinformation affects the dynamic between patients and dermatologists in several ways. Research across various medical fields has demonstrated that misinformation can substantially impact patient behavior and treatment adherence. Like many other specialists, dermatologists often spend considerable time during consultations with patients debunking myths and correcting misconceptions, which can detract from discussing more critical aspects of the patient’s condition and treatment plan and lead to frustration and anxiety among patients. It also can be challenging for physicians to have these conversations without alienating patients, who may distrust medical recommendations and believe that natural or alternative treatments are superior. This can lead to noncompliance with prescribed treatments, and patients may instead opt to try unproven remedies they encounter online, ultimately resulting in poorer health outcomes.

Strategies to Debunk Myths

By implementing the following strategies, dermatologists can combat the spread of myths, foster trust among patients, and promote adherence to evidence-based treatments:

• Provide educational outreach. Preemptively address myths by giving patients accurate and accessible resources. Including a dedicated section on your clinic’s website with articles, frequently asked questions, videos, and links to reputable sources can be effective. Sharing patient testimonials and before-and-after photographs to demonstrate the success of evidence-based treatments also is recommended, as real-life stories can be powerful tools in dispelling myths.
• Practice effective communication. Involve patients in the decision-making process by discussing their treatment goals, preferences, and concerns. It is important to present all options clearly, including the potential benefits and adverse effects. Discuss the expected outcomes and timelines, and be transparent about the limitations of certain treatment—honesty helps build trust and sets realistic expectations.
• Conduct structured consultations. Ensure that consultations with patients follow a structured format—history, physical examination, and discussion—to help keep the focus on evidence-based practice.
• Leverage technology. Guide patients toward reliable digital patient education tools to empower them with accurate information. Hosting live sessions on social media platforms during which patients can ask questions and receive evidence-based answers also can be beneficial.

Final Thoughts

In summary, the rise of medical myths poses a considerable challenge to dermatologic practice. By understanding the sources and impacts of these myths and employing strategies to dispel them, dermatologists can better navigate the complexities of modern patient interactions and ensure that care remains grounded in scientific evidence.

The advent of social media has revolutionized the way patients access and consume health information. While this increased access has its merits, it also has given rise to the proliferation of medical myths, which have considerable effects on patient-physician interactions.¹ Myths are prevalent across all fields of health care, ranging from misconceptions about disease etiology and prevention to the efficacy and safety of treatments. This influx of misinformation can derail the clinical encounter, shifting the focus from evidence-based medicine to myth-busting.² The COVID-19 pandemic exacerbated this issue, as widespread lockdowns and social distancing measures limited access to in-person medical consultations, prompting patients to increasingly turn to online sources for health information that often were unreliable, thereby bypassing professional medical advice.³ Herein, we highlight the challenges and implications of common dermatology myths and provide strategies for effectively debunking these myths to enhance patient care.

Common Dermatology Myths

In dermatology, where visible and often distressing conditions such as acne and hair loss are common, the impact of myths on patient perceptions and treatment outcomes can be particularly profound. Patients often arrive for consultations with preconceived notions that are not grounded in scientific evidence. Common dermatologic myths include eczema and the efficacy of topical corticosteroids, the causes and treatment of hair loss, and risk factors associated with skin cancer.

Eczema and Topical Corticosteroids—Topical corticosteroids for eczema are safe and effective, but nonadherence due to phobias stemming from misinformation online can impede treatment.⁴ Myths such as red skin syndrome and topical corticosteroid addiction are prevalent. Red skin syndrome refers to claims that prolonged use of topical corticosteroids causes severe redness and burning of the skin and worsening eczema symptoms upon withdrawal. Topical corticosteroid addiction suggests that patients become dependent on corticosteroids, requiring higher doses over time to maintain efficacy. These misconceptions contribute to fear and avoidance of prescribed treatments.

Eczema myths often divert focus from its true etiology as a genetic inflammatory skin disease, suggesting instead that it is caused by leaky gut or food intolerances.⁴ Risks such as skin thinning and stunted growth often are exaggerated on social media and other nonmedical platforms, though these adverse effects rarely are seen when topical corticosteroids are used appropriately under medical supervision. Misinformation often is linked to companies promoting unregulated consultations, tests, or supposedly natural treatments, including herbal remedies that may surreptitiously contain corticosteroids without clear labeling. This fosters distrust of US Food and Drug Administration– approved and dermatologist-prescribed treatments, as patients may cite concerns based on experiences with or claims about unapproved products.⁴

Sunscreen and Skin Cancer—In 2018, the American Academy of Dermatology prioritized skin cancer prevention due to suboptimal public adoption of photoprotection measures.⁵ However, the proliferation of misinformation regarding sunscreen and its potential to cause skin cancer is a more pressing issue. Myths range from claims that sunscreen is ineffective to warnings that it is dangerous, with some social media influencers even suggesting that sunscreen causes skin cancer due to toxic ingredients.⁶ Oxybenzone, typically found in chemical sunscreens, has been criticized by some advocacy groups and social media influencers as a potential hormone disruptor (ie, a chemical that could interfere with hormone production).⁷ However, no conclusive evidence has shown that oxybenzone is harmful to humans. Consumer concerns often are based on animal studies in which rats are fed oxybenzone, but mathematical modeling has indicated it would take 277 years of sunscreen use by humans to match the doses used in these studies.⁸ The false association between sunscreen use and skin cancer is based on flawed studies that found higher rates of skin cancer—including melanoma—in sunscreen users compared to those who did not use sunscreen. However, those using sunscreen also were more likely to travel to sunnier climates and engage in sunbathing, and it may have been this increased sun exposure that elevated their risk for skin cancer.⁷ It is imperative that the dermatology community counteract this type of misinformation with evidence-based advice.

Hair Loss—Some patients believe that hair loss is caused by wearing hats, frequent shampooing, or even stress in a way that oversimplifies complex physiological processes. Biotin, which commonly is added to supplements for hair, skin, and nails, has been linked to potential risks, such as interference with laboratory testing and false-positive or false-negative results in critical medical tests, which can lead to misdiagnosis or inappropriate treatment.⁹ Biotin interference can result in falsely low troponin readings, which are critical in diagnosing acute myocardial infarction. Tests for other hormones such as cortisol and parathyroid hormone also are affected, potentially impacting the evaluation and management of endocrine disorders. The US Food and Drug Administration has issued warnings for patients on this topic, emphasizing the importance of informing health care providers about any biotin supplementation prior to laboratory testing. Despite its popularity, there is no substantial scientific evidence to suggest that biotin supplementation promotes hair growth in anyone other than those with deficiency, which is quite rare.⁹

Myths and the Patient-Physician Relationship

The proliferation of medical myths and misinformation affects the dynamic between patients and dermatologists in several ways. Research across various medical fields has demonstrated that misinformation can substantially impact patient behavior and treatment adherence. Like many other specialists, dermatologists often spend considerable time during consultations with patients debunking myths and correcting misconceptions, which can detract from discussing more critical aspects of the patient’s condition and treatment plan and lead to frustration and anxiety among patients. It also can be challenging for physicians to have these conversations without alienating patients, who may distrust medical recommendations and believe that natural or alternative treatments are superior. This can lead to noncompliance with prescribed treatments, and patients may instead opt to try unproven remedies they encounter online, ultimately resulting in poorer health outcomes.

Strategies to Debunk Myths

By implementing the following strategies, dermatologists can combat the spread of myths, foster trust among patients, and promote adherence to evidence-based treatments:

• Provide educational outreach. Preemptively address myths by giving patients accurate and accessible resources. Including a dedicated section on your clinic’s website with articles, frequently asked questions, videos, and links to reputable sources can be effective. Sharing patient testimonials and before-and-after photographs to demonstrate the success of evidence-based treatments also is recommended, as real-life stories can be powerful tools in dispelling myths.
• Practice effective communication. Involve patients in the decision-making process by discussing their treatment goals, preferences, and concerns. It is important to present all options clearly, including the potential benefits and adverse effects. Discuss the expected outcomes and timelines, and be transparent about the limitations of certain treatment—honesty helps build trust and sets realistic expectations.
• Conduct structured consultations. Ensure that consultations with patients follow a structured format—history, physical examination, and discussion—to help keep the focus on evidence-based practice.
• Leverage technology. Guide patients toward reliable digital patient education tools to empower them with accurate information. Hosting live sessions on social media platforms during which patients can ask questions and receive evidence-based answers also can be beneficial.

Final Thoughts

In summary, the rise of medical myths poses a considerable challenge to dermatologic practice. By understanding the sources and impacts of these myths and employing strategies to dispel them, dermatologists can better navigate the complexities of modern patient interactions and ensure that care remains grounded in scientific evidence.

The year was 2023, and I was on my way to the American Academy of Dermatology meeting in New Orleans, Louisiana. “Geaux Tigers!” I exclaimed to a stranger as she walked by in her purple and gold shoes and scrubs. We chatted for a minute or two about Louisiana State University (LSU) football, then went our separate ways. Later that day, in the hands-on wound closures workshop, I was surprised to see my new acquaintance step up to the podium to lecture, then make rounds across the room to instruct residents. I didn’t know it at the time, but those purple and gold shoes sparked a conversation with a fellowship program director who would become one of my most valued mentors.

I didn’t set out to find a mentor that day—I simply was excited to connect with a fellow Tigers fan. But mentorship often finds us unexpectedly, and that encounter serves as a reminder that mentorship doesn’t always start in a formal setting. Sometimes it begins with a quick conversation in the right place at the right time. This story is one of many experiences that taught me valuable lessons about mentorship—its importance, how it can grow naturally, and the impact it can have.

Residency is a pivotal time in a physician’s life, filled with rapid learning, complex challenges, and new professional relationships. Amidst the long hours and heavy responsibilities, mentorship stands out as a support system for guiding residents toward professional and personal growth. Herein, I share more about my experiences with mentorship in residency, the lessons I have learned, and how they can serve as guidance for residents.

The Value of Mentorship

Mentorship in residency has been shown to have a major impact on career satisfaction, clinical confidence, and professional development.¹ A good mentor offers more than just advice—he or she can provide a model of professionalism and skills that resonates with the mentee’s own aspirations. Mentorship can help residents refine their clinical skills, navigate the complexities of patient care, engage in research, and connect with professionals in their field.²

Mentorship can be sought intentionally or arise naturally from shared interests and connections. Some residents reach out to potential mentors directly through emails, set up one-on-one meetings, or shadow them to gain firsthand experience. Others find mentorship simply by putting themselves in situations that foster these connections, such as attending conferences or lectures. Both approaches can lead to impactful relationships that shape a resident’s career and personal growth.

For residents involved in research, an effective faculty research mentor is particularly impactful. Studies show that residents who work with knowledgeable research mentors are more likely to experience success and productivity in their research efforts.³ Research mentors can provide essential guidance—from helping formulate research questions to navigating the complexities of publishing—which makes them invaluable in a resident’s academic development.

If you have interests in specific areas not heavily emphasized within your residency program (eg, transplantation dermatology, hair restoration, cutaneous lymphoma), consider checking within your broader medical community for specialists. Many dermatologists and other specialists welcome the opportunity to mentor residents who express a sincere interest in learning. By reaching out to these professionals, you not only expand your clinical knowledge but also gain access to niche areas of dermatology that can shape and refine your future practice. Often, these experiences lead to invaluable mentorships that may otherwise be unavailable within your immediate training environment.

Networking Through Professional Society Rotational and Mentorship Programs

The Women’s Dermatologic Society (https://www.womensderm.org/), the American Society for Dermatologic Surgery (https://www.asds.net/), and the American Society for Laser Medicine and Surgery (https://www.aslms.org/) all provide excellent formalized mentorship or preceptorship programs. Check their websites for application requirements and timelines. Participating in these programs is a great way to network with experts in dermatology, providing a structured way to interact with physicians who share your interests. Whether you are interested in medical dermatology, surgery, pediatrics, dermatopathology, or cosmetics, there are many mentors who greatly enjoy sharing their knowledge and experience with residents. Oftentimes, these programs include stipends to assist with costs that are awarded as accolades that can enhance your curriculum vitae. Engaging in these recognized preceptorship programs often builds lasting connections and ensures that both mentor and mentee have a vested interest in the relationship’s success.

Making Connections at Conferences and Maximizing Hands-on Learning

Professional conferences offer valuable opportunities to connect with mentors, whether you are proactively seeking mentorship or simply allowing connections to happen naturally. Conferences such as those of the American Academy of Dermatology and American Society for Dermatologic Surgery publish educational booklets and schedules online prior to the event, giving you a chance to explore both topics and speaker names ahead of time. This can be an excellent opportunity to create a day-by-day game plan, identifying sessions and lectures of interest as well as specific authors or experts you might like to meet. Planning in advance makes it easier to engage with leaders in the field, introduce yourself, and make meaningful connections.

Oftentimes, these society meetings offer hands-on courses, which are a great way to meet mentors and learn from direct instruction. Instructors for these courses often are leaders in dermatology who are passionate about teaching. With small group sizes, hands-on courses offer both technical skill-building opportunities and a chance to connect personally with instructors. Take a moment to introduce yourself and engage in a quick conversation, and if you feel it is appropriate, follow up with an email after the conference. This helps keep the connection alive beyond the event and may open doors for future mentorship opportunities.

Away Rotations

For residents looking to build specialized skills and connect with mentors outside their own program—especially those considering fellowship—away rotations can be a great tool. Though it may require using vacation time, an away rotation offers immersive learning in a particular area while providing opportunities to observe new mentors and establish relationships within a desired subspecialty or program. By simply reaching out and expressing interest, residents can connect with physicians who may become lasting mentors and advocates.

Building a Mentor-Mentee Relationship

A meaningful mentor-mentee relationship requires time, effort, and effective communication, with clear expectations around mentorship goals, time commitments, and how both parties envision the relationship evolving.⁴ Ideally, mentees should feel comfortable sharing their goals with mentors and asking for feedback. In the right context, a simple and effective practice is to send your mentor a brief update on your progress every few months. This could be a quick email sharing your latest projects, ideas, and/or achievements. By regularly checking in, you show your mentor that you are committed to growing from their guidance and respect their time.

The Lasting Impact of Mentorship

The effects of mentorship in residency extend well beyond the training years, as mentors often become lifelong guides and professional advocates for their mentees.⁵ Residency often is the last time a resident trains under the direct supervision of an attending physician, making it a unique and formative period. After graduation, many new physicians find the transition to independent practice challenging, and the “real world” can be a shock. Having a mentor during this time, or maintaining connections with mentors from residency, can be invaluable. Mentors can offer advice, act as sounding boards, and remind new graduates of the importance of being lifelong learners. These relationships help ease the transition into practice, instilling a commitment to continuous improvement and professional growth. For me, a conversation about LSU football at the AAD meeting in New Orleans exemplifies how mentorship can begin in the most unexpected ways. That casual exchange led to an away rotation, a fellowship interview, connections at national meetings, and the start of what I hope will be a lifelong friendship.

The year was 2023, and I was on my way to the American Academy of Dermatology meeting in New Orleans, Louisiana. “Geaux Tigers!” I exclaimed to a stranger as she walked by in her purple and gold shoes and scrubs. We chatted for a minute or two about Louisiana State University (LSU) football, then went our separate ways. Later that day, in the hands-on wound closures workshop, I was surprised to see my new acquaintance step up to the podium to lecture, then make rounds across the room to instruct residents. I didn’t know it at the time, but those purple and gold shoes sparked a conversation with a fellowship program director who would become one of my most valued mentors.

I didn’t set out to find a mentor that day—I simply was excited to connect with a fellow Tigers fan. But mentorship often finds us unexpectedly, and that encounter serves as a reminder that mentorship doesn’t always start in a formal setting. Sometimes it begins with a quick conversation in the right place at the right time. This story is one of many experiences that taught me valuable lessons about mentorship—its importance, how it can grow naturally, and the impact it can have.

Residency is a pivotal time in a physician’s life, filled with rapid learning, complex challenges, and new professional relationships. Amidst the long hours and heavy responsibilities, mentorship stands out as a support system for guiding residents toward professional and personal growth. Herein, I share more about my experiences with mentorship in residency, the lessons I have learned, and how they can serve as guidance for residents.

The Value of Mentorship

Mentorship in residency has been shown to have a major impact on career satisfaction, clinical confidence, and professional development.¹ A good mentor offers more than just advice—he or she can provide a model of professionalism and skills that resonates with the mentee’s own aspirations. Mentorship can help residents refine their clinical skills, navigate the complexities of patient care, engage in research, and connect with professionals in their field.²

Mentorship can be sought intentionally or arise naturally from shared interests and connections. Some residents reach out to potential mentors directly through emails, set up one-on-one meetings, or shadow them to gain firsthand experience. Others find mentorship simply by putting themselves in situations that foster these connections, such as attending conferences or lectures. Both approaches can lead to impactful relationships that shape a resident’s career and personal growth.

For residents involved in research, an effective faculty research mentor is particularly impactful. Studies show that residents who work with knowledgeable research mentors are more likely to experience success and productivity in their research efforts.³ Research mentors can provide essential guidance—from helping formulate research questions to navigating the complexities of publishing—which makes them invaluable in a resident’s academic development.

If you have interests in specific areas not heavily emphasized within your residency program (eg, transplantation dermatology, hair restoration, cutaneous lymphoma), consider checking within your broader medical community for specialists. Many dermatologists and other specialists welcome the opportunity to mentor residents who express a sincere interest in learning. By reaching out to these professionals, you not only expand your clinical knowledge but also gain access to niche areas of dermatology that can shape and refine your future practice. Often, these experiences lead to invaluable mentorships that may otherwise be unavailable within your immediate training environment.

Networking Through Professional Society Rotational and Mentorship Programs

The Women’s Dermatologic Society (https://www.womensderm.org/), the American Society for Dermatologic Surgery (https://www.asds.net/), and the American Society for Laser Medicine and Surgery (https://www.aslms.org/) all provide excellent formalized mentorship or preceptorship programs. Check their websites for application requirements and timelines. Participating in these programs is a great way to network with experts in dermatology, providing a structured way to interact with physicians who share your interests. Whether you are interested in medical dermatology, surgery, pediatrics, dermatopathology, or cosmetics, there are many mentors who greatly enjoy sharing their knowledge and experience with residents. Oftentimes, these programs include stipends to assist with costs that are awarded as accolades that can enhance your curriculum vitae. Engaging in these recognized preceptorship programs often builds lasting connections and ensures that both mentor and mentee have a vested interest in the relationship’s success.

Making Connections at Conferences and Maximizing Hands-on Learning

Professional conferences offer valuable opportunities to connect with mentors, whether you are proactively seeking mentorship or simply allowing connections to happen naturally. Conferences such as those of the American Academy of Dermatology and American Society for Dermatologic Surgery publish educational booklets and schedules online prior to the event, giving you a chance to explore both topics and speaker names ahead of time. This can be an excellent opportunity to create a day-by-day game plan, identifying sessions and lectures of interest as well as specific authors or experts you might like to meet. Planning in advance makes it easier to engage with leaders in the field, introduce yourself, and make meaningful connections.

Oftentimes, these society meetings offer hands-on courses, which are a great way to meet mentors and learn from direct instruction. Instructors for these courses often are leaders in dermatology who are passionate about teaching. With small group sizes, hands-on courses offer both technical skill-building opportunities and a chance to connect personally with instructors. Take a moment to introduce yourself and engage in a quick conversation, and if you feel it is appropriate, follow up with an email after the conference. This helps keep the connection alive beyond the event and may open doors for future mentorship opportunities.

Away Rotations

For residents looking to build specialized skills and connect with mentors outside their own program—especially those considering fellowship—away rotations can be a great tool. Though it may require using vacation time, an away rotation offers immersive learning in a particular area while providing opportunities to observe new mentors and establish relationships within a desired subspecialty or program. By simply reaching out and expressing interest, residents can connect with physicians who may become lasting mentors and advocates.

Building a Mentor-Mentee Relationship

A meaningful mentor-mentee relationship requires time, effort, and effective communication, with clear expectations around mentorship goals, time commitments, and how both parties envision the relationship evolving.⁴ Ideally, mentees should feel comfortable sharing their goals with mentors and asking for feedback. In the right context, a simple and effective practice is to send your mentor a brief update on your progress every few months. This could be a quick email sharing your latest projects, ideas, and/or achievements. By regularly checking in, you show your mentor that you are committed to growing from their guidance and respect their time.

The Lasting Impact of Mentorship

The effects of mentorship in residency extend well beyond the training years, as mentors often become lifelong guides and professional advocates for their mentees.⁵ Residency often is the last time a resident trains under the direct supervision of an attending physician, making it a unique and formative period. After graduation, many new physicians find the transition to independent practice challenging, and the “real world” can be a shock. Having a mentor during this time, or maintaining connections with mentors from residency, can be invaluable. Mentors can offer advice, act as sounding boards, and remind new graduates of the importance of being lifelong learners. These relationships help ease the transition into practice, instilling a commitment to continuous improvement and professional growth. For me, a conversation about LSU football at the AAD meeting in New Orleans exemplifies how mentorship can begin in the most unexpected ways. That casual exchange led to an away rotation, a fellowship interview, connections at national meetings, and the start of what I hope will be a lifelong friendship.

The year was 2023, and I was on my way to the American Academy of Dermatology meeting in New Orleans, Louisiana. “Geaux Tigers!” I exclaimed to a stranger as she walked by in her purple and gold shoes and scrubs. We chatted for a minute or two about Louisiana State University (LSU) football, then went our separate ways. Later that day, in the hands-on wound closures workshop, I was surprised to see my new acquaintance step up to the podium to lecture, then make rounds across the room to instruct residents. I didn’t know it at the time, but those purple and gold shoes sparked a conversation with a fellowship program director who would become one of my most valued mentors.

I didn’t set out to find a mentor that day—I simply was excited to connect with a fellow Tigers fan. But mentorship often finds us unexpectedly, and that encounter serves as a reminder that mentorship doesn’t always start in a formal setting. Sometimes it begins with a quick conversation in the right place at the right time. This story is one of many experiences that taught me valuable lessons about mentorship—its importance, how it can grow naturally, and the impact it can have.

Residency is a pivotal time in a physician’s life, filled with rapid learning, complex challenges, and new professional relationships. Amidst the long hours and heavy responsibilities, mentorship stands out as a support system for guiding residents toward professional and personal growth. Herein, I share more about my experiences with mentorship in residency, the lessons I have learned, and how they can serve as guidance for residents.

The Value of Mentorship

Mentorship in residency has been shown to have a major impact on career satisfaction, clinical confidence, and professional development.¹ A good mentor offers more than just advice—he or she can provide a model of professionalism and skills that resonates with the mentee’s own aspirations. Mentorship can help residents refine their clinical skills, navigate the complexities of patient care, engage in research, and connect with professionals in their field.²

Mentorship can be sought intentionally or arise naturally from shared interests and connections. Some residents reach out to potential mentors directly through emails, set up one-on-one meetings, or shadow them to gain firsthand experience. Others find mentorship simply by putting themselves in situations that foster these connections, such as attending conferences or lectures. Both approaches can lead to impactful relationships that shape a resident’s career and personal growth.

For residents involved in research, an effective faculty research mentor is particularly impactful. Studies show that residents who work with knowledgeable research mentors are more likely to experience success and productivity in their research efforts.³ Research mentors can provide essential guidance—from helping formulate research questions to navigating the complexities of publishing—which makes them invaluable in a resident’s academic development.

If you have interests in specific areas not heavily emphasized within your residency program (eg, transplantation dermatology, hair restoration, cutaneous lymphoma), consider checking within your broader medical community for specialists. Many dermatologists and other specialists welcome the opportunity to mentor residents who express a sincere interest in learning. By reaching out to these professionals, you not only expand your clinical knowledge but also gain access to niche areas of dermatology that can shape and refine your future practice. Often, these experiences lead to invaluable mentorships that may otherwise be unavailable within your immediate training environment.

Networking Through Professional Society Rotational and Mentorship Programs

The Women’s Dermatologic Society (https://www.womensderm.org/), the American Society for Dermatologic Surgery (https://www.asds.net/), and the American Society for Laser Medicine and Surgery (https://www.aslms.org/) all provide excellent formalized mentorship or preceptorship programs. Check their websites for application requirements and timelines. Participating in these programs is a great way to network with experts in dermatology, providing a structured way to interact with physicians who share your interests. Whether you are interested in medical dermatology, surgery, pediatrics, dermatopathology, or cosmetics, there are many mentors who greatly enjoy sharing their knowledge and experience with residents. Oftentimes, these programs include stipends to assist with costs that are awarded as accolades that can enhance your curriculum vitae. Engaging in these recognized preceptorship programs often builds lasting connections and ensures that both mentor and mentee have a vested interest in the relationship’s success.

Making Connections at Conferences and Maximizing Hands-on Learning

Professional conferences offer valuable opportunities to connect with mentors, whether you are proactively seeking mentorship or simply allowing connections to happen naturally. Conferences such as those of the American Academy of Dermatology and American Society for Dermatologic Surgery publish educational booklets and schedules online prior to the event, giving you a chance to explore both topics and speaker names ahead of time. This can be an excellent opportunity to create a day-by-day game plan, identifying sessions and lectures of interest as well as specific authors or experts you might like to meet. Planning in advance makes it easier to engage with leaders in the field, introduce yourself, and make meaningful connections.

Oftentimes, these society meetings offer hands-on courses, which are a great way to meet mentors and learn from direct instruction. Instructors for these courses often are leaders in dermatology who are passionate about teaching. With small group sizes, hands-on courses offer both technical skill-building opportunities and a chance to connect personally with instructors. Take a moment to introduce yourself and engage in a quick conversation, and if you feel it is appropriate, follow up with an email after the conference. This helps keep the connection alive beyond the event and may open doors for future mentorship opportunities.

Away Rotations

For residents looking to build specialized skills and connect with mentors outside their own program—especially those considering fellowship—away rotations can be a great tool. Though it may require using vacation time, an away rotation offers immersive learning in a particular area while providing opportunities to observe new mentors and establish relationships within a desired subspecialty or program. By simply reaching out and expressing interest, residents can connect with physicians who may become lasting mentors and advocates.

Building a Mentor-Mentee Relationship

A meaningful mentor-mentee relationship requires time, effort, and effective communication, with clear expectations around mentorship goals, time commitments, and how both parties envision the relationship evolving.⁴ Ideally, mentees should feel comfortable sharing their goals with mentors and asking for feedback. In the right context, a simple and effective practice is to send your mentor a brief update on your progress every few months. This could be a quick email sharing your latest projects, ideas, and/or achievements. By regularly checking in, you show your mentor that you are committed to growing from their guidance and respect their time.

The Lasting Impact of Mentorship

The effects of mentorship in residency extend well beyond the training years, as mentors often become lifelong guides and professional advocates for their mentees.⁵ Residency often is the last time a resident trains under the direct supervision of an attending physician, making it a unique and formative period. After graduation, many new physicians find the transition to independent practice challenging, and the “real world” can be a shock. Having a mentor during this time, or maintaining connections with mentors from residency, can be invaluable. Mentors can offer advice, act as sounding boards, and remind new graduates of the importance of being lifelong learners. These relationships help ease the transition into practice, instilling a commitment to continuous improvement and professional growth. For me, a conversation about LSU football at the AAD meeting in New Orleans exemplifies how mentorship can begin in the most unexpected ways. That casual exchange led to an away rotation, a fellowship interview, connections at national meetings, and the start of what I hope will be a lifelong friendship.

THE DIAGNOSIS: Hidradenocarcinoma

Both the original and recurrent lesions were interpreted as a chondroid syringoma, a benign adnexal tumor; however, the third biopsy of the lesion revealed a low-grade adnexal neoplasm with irregular nests of variably sized epithelial cells demonstrating mild nuclear atypia and low mitotic activity. Given the multiple recurrences, accelerated growth, and more aggressive histologic findings, the patient was referred to our clinic for surgical management.

We elected to perform modified Mohs micrographic surgery (MMS) with permanent tissue sections to enable the application of immunohistochemical stains to fully characterize the tumor. Histopathology showed a poorly circumscribed infiltrative dermal neoplasm composed of basaloid cells with a solid and cystic growth pattern in a background of hyalinized, fibrotic stroma (Figure, A and B). There were focal clear cell and squamous features as well as focal ductal differentiation (Figure, C and D). No obvious papillary structures were noted. The tumor cells were positive for D2-40, and staining for CD31 failed to reveal lymphovascular invasion. Based on the infiltrative features in conjunction with the findings from the prior biopsies, a diagnosis of hidradenocarcinoma (HAC) was made. Deep and peripheral margins were cleared after 2 stages of MMS.

Initially described in 1954, HAC is an exceedingly rare adnexal tumor of apocrine and eccrine derivation.¹ Historically, nomenclature for this entity has varied in the literature, including synonyms such as malignant nodular hidradenoma, malignant acrospiroma, solid-cystic adenocarcinoma, and malignant clear cell myoepithelioma.^2,3 Approximately 6% of all malignant eccrine tumors worldwide are HACs, which account for only 1 in 13,000 dermatopathology specimens.¹ These tumors may transform from clear cell hidradenomas (their benign counterparts) but more commonly arise de novo. Compared to benign hidradenomas, HACs are poorly circumscribed with infiltrative growth patterns on histopathology and may exhibit nuclear pleomorphism, prominent mitotic activity, necrosis, and perineural or vascular invasion.²

Clinically, HAC manifests as a 1- to 5-cm, solitary, firm, intradermal pink or violaceous nodule with possible ulceration.^2,4 The nodule often is asymptomatic but may be tender, as in our patient. There seems to be no clear anatomic site of predilection, with approximately 42% of HACs localized to the head and neck and the remainder occurring on the trunk, arms, and legs.^3,5-7 Females and males are affected equally, and lesions tend to arise in the seventh decade of life.⁷

Reports in the literature suggest that HAC is a very aggressive tumor with a generally poor prognosis.¹ Several studies have found that up to half of tumors locally recur despite aggressive surgical management, and metastasis occurs in 20% to 60% of patients.^3,8 However, a large study of US Surveillance, Epidemiology, and End Results data investigating the clinicopathologic characteristics of 289 patients with HAC revealed a more favorable prognosis.⁷ Mean overall survival and cancer-specific survival were greater than 13 years, and 10-year overall survival and cancer-specific survival rates were 60.2% and 90.5%, respectively.

Traditionally used to treat keratinocyte carcinomas, including basal cell carcinoma and squamous cell carcinoma, complete margin assessment with MMS is increasingly being utilized in the management of other cutaneous malignancies, including adnexal tumors.⁸ Due to its rarity, there remains no standard optimal treatment approach for HAC. One small retrospective study of 10 patients with HAC treated with MMS demonstrated favorable outcomes with no cases of recurrence, metastasis, or diseaserelated mortality in a mean 7-year follow-up period.⁹

Whole-body positron emission tomography/computed tomography performed in our patient approximately 1 month after MMS revealed mildly hypermetabolic left inguinal lymph nodes, which were thought to be reactive, and a question of small hypermetabolic foci in the liver. Follow-up computed tomography of the abdomen subsequently was performed and was negative for hepatic metastases. The patient will be monitored closely for local recurrence; however, the clearance of the tumor with MMS, which allowed complete margin assessment, is encouraging and supports MMS as superior to traditional surgical excision in the treatment of HAC. At his most recent examination 17 months after Mohs surgery, the patient remained tumor free.

Aggressive digital papillary adenocarcinoma (ADPA) is a rare malignant tumor originating in the sweat glands that can occur on the first toe but most commonly arises on the fingers. While both HAC and ADPA can manifest with an infiltrative growth pattern and cytologic atypia, ADPA classically reveals a well-circumscribed multinodular tumor in the dermis comprised of solid and cystic proliferation as well as papillary projections. In addition, ADPA has been described as having back-to-back glandular and ductal structures.¹⁰ Giant cell tumor of the tendon sheath is a benign fibrohistiocytic tumor that also typically manifests on the fingers but rarely can occur on the foot, including the first toe.^11,12 This tumor is more common in women and most frequently affects individuals aged 30 to 50 years.¹² Microscopically, giant cell tumor of the tendon sheath is characterized by a proliferation of osteoclastlike giant cells, epithelioid histiocytelike cells, mononuclear cells, and xanthomatous cells among collagenous bands.¹¹

Osteosarcoma is an uncommon tumor of osteoidproducing cells that usually arises in the metaphysis of long bones and manifests as a tender subcutaneous mass. It has a bimodal age distribution, peaking in adolescents and adults older than 65 years.¹³ While very rare, osteosarcoma has been reported to occur in the bones of the feet, including the phalanges.¹⁴ Given the recurrent nature of our patient’s tumor, metastasis should always be considered; however, in his case, full-body imaging was negative for additional malignancy.

THE DIAGNOSIS: Hidradenocarcinoma

Both the original and recurrent lesions were interpreted as a chondroid syringoma, a benign adnexal tumor; however, the third biopsy of the lesion revealed a low-grade adnexal neoplasm with irregular nests of variably sized epithelial cells demonstrating mild nuclear atypia and low mitotic activity. Given the multiple recurrences, accelerated growth, and more aggressive histologic findings, the patient was referred to our clinic for surgical management.

We elected to perform modified Mohs micrographic surgery (MMS) with permanent tissue sections to enable the application of immunohistochemical stains to fully characterize the tumor. Histopathology showed a poorly circumscribed infiltrative dermal neoplasm composed of basaloid cells with a solid and cystic growth pattern in a background of hyalinized, fibrotic stroma (Figure, A and B). There were focal clear cell and squamous features as well as focal ductal differentiation (Figure, C and D). No obvious papillary structures were noted. The tumor cells were positive for D2-40, and staining for CD31 failed to reveal lymphovascular invasion. Based on the infiltrative features in conjunction with the findings from the prior biopsies, a diagnosis of hidradenocarcinoma (HAC) was made. Deep and peripheral margins were cleared after 2 stages of MMS.

Initially described in 1954, HAC is an exceedingly rare adnexal tumor of apocrine and eccrine derivation.¹ Historically, nomenclature for this entity has varied in the literature, including synonyms such as malignant nodular hidradenoma, malignant acrospiroma, solid-cystic adenocarcinoma, and malignant clear cell myoepithelioma.^2,3 Approximately 6% of all malignant eccrine tumors worldwide are HACs, which account for only 1 in 13,000 dermatopathology specimens.¹ These tumors may transform from clear cell hidradenomas (their benign counterparts) but more commonly arise de novo. Compared to benign hidradenomas, HACs are poorly circumscribed with infiltrative growth patterns on histopathology and may exhibit nuclear pleomorphism, prominent mitotic activity, necrosis, and perineural or vascular invasion.²

Clinically, HAC manifests as a 1- to 5-cm, solitary, firm, intradermal pink or violaceous nodule with possible ulceration.^2,4 The nodule often is asymptomatic but may be tender, as in our patient. There seems to be no clear anatomic site of predilection, with approximately 42% of HACs localized to the head and neck and the remainder occurring on the trunk, arms, and legs.^3,5-7 Females and males are affected equally, and lesions tend to arise in the seventh decade of life.⁷

Reports in the literature suggest that HAC is a very aggressive tumor with a generally poor prognosis.¹ Several studies have found that up to half of tumors locally recur despite aggressive surgical management, and metastasis occurs in 20% to 60% of patients.^3,8 However, a large study of US Surveillance, Epidemiology, and End Results data investigating the clinicopathologic characteristics of 289 patients with HAC revealed a more favorable prognosis.⁷ Mean overall survival and cancer-specific survival were greater than 13 years, and 10-year overall survival and cancer-specific survival rates were 60.2% and 90.5%, respectively.

Traditionally used to treat keratinocyte carcinomas, including basal cell carcinoma and squamous cell carcinoma, complete margin assessment with MMS is increasingly being utilized in the management of other cutaneous malignancies, including adnexal tumors.⁸ Due to its rarity, there remains no standard optimal treatment approach for HAC. One small retrospective study of 10 patients with HAC treated with MMS demonstrated favorable outcomes with no cases of recurrence, metastasis, or diseaserelated mortality in a mean 7-year follow-up period.⁹

Whole-body positron emission tomography/computed tomography performed in our patient approximately 1 month after MMS revealed mildly hypermetabolic left inguinal lymph nodes, which were thought to be reactive, and a question of small hypermetabolic foci in the liver. Follow-up computed tomography of the abdomen subsequently was performed and was negative for hepatic metastases. The patient will be monitored closely for local recurrence; however, the clearance of the tumor with MMS, which allowed complete margin assessment, is encouraging and supports MMS as superior to traditional surgical excision in the treatment of HAC. At his most recent examination 17 months after Mohs surgery, the patient remained tumor free.

Aggressive digital papillary adenocarcinoma (ADPA) is a rare malignant tumor originating in the sweat glands that can occur on the first toe but most commonly arises on the fingers. While both HAC and ADPA can manifest with an infiltrative growth pattern and cytologic atypia, ADPA classically reveals a well-circumscribed multinodular tumor in the dermis comprised of solid and cystic proliferation as well as papillary projections. In addition, ADPA has been described as having back-to-back glandular and ductal structures.¹⁰ Giant cell tumor of the tendon sheath is a benign fibrohistiocytic tumor that also typically manifests on the fingers but rarely can occur on the foot, including the first toe.^11,12 This tumor is more common in women and most frequently affects individuals aged 30 to 50 years.¹² Microscopically, giant cell tumor of the tendon sheath is characterized by a proliferation of osteoclastlike giant cells, epithelioid histiocytelike cells, mononuclear cells, and xanthomatous cells among collagenous bands.¹¹

Osteosarcoma is an uncommon tumor of osteoidproducing cells that usually arises in the metaphysis of long bones and manifests as a tender subcutaneous mass. It has a bimodal age distribution, peaking in adolescents and adults older than 65 years.¹³ While very rare, osteosarcoma has been reported to occur in the bones of the feet, including the phalanges.¹⁴ Given the recurrent nature of our patient’s tumor, metastasis should always be considered; however, in his case, full-body imaging was negative for additional malignancy.

THE DIAGNOSIS: Hidradenocarcinoma

Both the original and recurrent lesions were interpreted as a chondroid syringoma, a benign adnexal tumor; however, the third biopsy of the lesion revealed a low-grade adnexal neoplasm with irregular nests of variably sized epithelial cells demonstrating mild nuclear atypia and low mitotic activity. Given the multiple recurrences, accelerated growth, and more aggressive histologic findings, the patient was referred to our clinic for surgical management.

We elected to perform modified Mohs micrographic surgery (MMS) with permanent tissue sections to enable the application of immunohistochemical stains to fully characterize the tumor. Histopathology showed a poorly circumscribed infiltrative dermal neoplasm composed of basaloid cells with a solid and cystic growth pattern in a background of hyalinized, fibrotic stroma (Figure, A and B). There were focal clear cell and squamous features as well as focal ductal differentiation (Figure, C and D). No obvious papillary structures were noted. The tumor cells were positive for D2-40, and staining for CD31 failed to reveal lymphovascular invasion. Based on the infiltrative features in conjunction with the findings from the prior biopsies, a diagnosis of hidradenocarcinoma (HAC) was made. Deep and peripheral margins were cleared after 2 stages of MMS.

Initially described in 1954, HAC is an exceedingly rare adnexal tumor of apocrine and eccrine derivation.¹ Historically, nomenclature for this entity has varied in the literature, including synonyms such as malignant nodular hidradenoma, malignant acrospiroma, solid-cystic adenocarcinoma, and malignant clear cell myoepithelioma.^2,3 Approximately 6% of all malignant eccrine tumors worldwide are HACs, which account for only 1 in 13,000 dermatopathology specimens.¹ These tumors may transform from clear cell hidradenomas (their benign counterparts) but more commonly arise de novo. Compared to benign hidradenomas, HACs are poorly circumscribed with infiltrative growth patterns on histopathology and may exhibit nuclear pleomorphism, prominent mitotic activity, necrosis, and perineural or vascular invasion.²

Clinically, HAC manifests as a 1- to 5-cm, solitary, firm, intradermal pink or violaceous nodule with possible ulceration.^2,4 The nodule often is asymptomatic but may be tender, as in our patient. There seems to be no clear anatomic site of predilection, with approximately 42% of HACs localized to the head and neck and the remainder occurring on the trunk, arms, and legs.^3,5-7 Females and males are affected equally, and lesions tend to arise in the seventh decade of life.⁷

Reports in the literature suggest that HAC is a very aggressive tumor with a generally poor prognosis.¹ Several studies have found that up to half of tumors locally recur despite aggressive surgical management, and metastasis occurs in 20% to 60% of patients.^3,8 However, a large study of US Surveillance, Epidemiology, and End Results data investigating the clinicopathologic characteristics of 289 patients with HAC revealed a more favorable prognosis.⁷ Mean overall survival and cancer-specific survival were greater than 13 years, and 10-year overall survival and cancer-specific survival rates were 60.2% and 90.5%, respectively.

Traditionally used to treat keratinocyte carcinomas, including basal cell carcinoma and squamous cell carcinoma, complete margin assessment with MMS is increasingly being utilized in the management of other cutaneous malignancies, including adnexal tumors.⁸ Due to its rarity, there remains no standard optimal treatment approach for HAC. One small retrospective study of 10 patients with HAC treated with MMS demonstrated favorable outcomes with no cases of recurrence, metastasis, or diseaserelated mortality in a mean 7-year follow-up period.⁹

Whole-body positron emission tomography/computed tomography performed in our patient approximately 1 month after MMS revealed mildly hypermetabolic left inguinal lymph nodes, which were thought to be reactive, and a question of small hypermetabolic foci in the liver. Follow-up computed tomography of the abdomen subsequently was performed and was negative for hepatic metastases. The patient will be monitored closely for local recurrence; however, the clearance of the tumor with MMS, which allowed complete margin assessment, is encouraging and supports MMS as superior to traditional surgical excision in the treatment of HAC. At his most recent examination 17 months after Mohs surgery, the patient remained tumor free.

Aggressive digital papillary adenocarcinoma (ADPA) is a rare malignant tumor originating in the sweat glands that can occur on the first toe but most commonly arises on the fingers. While both HAC and ADPA can manifest with an infiltrative growth pattern and cytologic atypia, ADPA classically reveals a well-circumscribed multinodular tumor in the dermis comprised of solid and cystic proliferation as well as papillary projections. In addition, ADPA has been described as having back-to-back glandular and ductal structures.¹⁰ Giant cell tumor of the tendon sheath is a benign fibrohistiocytic tumor that also typically manifests on the fingers but rarely can occur on the foot, including the first toe.^11,12 This tumor is more common in women and most frequently affects individuals aged 30 to 50 years.¹² Microscopically, giant cell tumor of the tendon sheath is characterized by a proliferation of osteoclastlike giant cells, epithelioid histiocytelike cells, mononuclear cells, and xanthomatous cells among collagenous bands.¹¹

Osteosarcoma is an uncommon tumor of osteoidproducing cells that usually arises in the metaphysis of long bones and manifests as a tender subcutaneous mass. It has a bimodal age distribution, peaking in adolescents and adults older than 65 years.¹³ While very rare, osteosarcoma has been reported to occur in the bones of the feet, including the phalanges.¹⁴ Given the recurrent nature of our patient’s tumor, metastasis should always be considered; however, in his case, full-body imaging was negative for additional malignancy.

THE DIAGNOSIS: Pemphigus Vegetans

Histopathologic examination of the biopsies from the scalp and left anterior thigh revealed suprabasal clefting with acantholytic cells extending into the follicular infundibulum with eosinophilic pustules within the epidermis. The dermis contained perivascular lymphohistiocytic and eosinophilic inflammatory infiltrates without viral cytopathic effects (Figure 1). Direct immunofluorescence revealed strong IgG and moderate IgA pericellular deposition around keratinocyte cytoplasms (Figure 2). Serologic evaluation demonstrated anti–desmoglein 3 antibodies. Based on the clinical presentation and histopathologic correlation, a diagnosis of pemphigus vegetans was made.

Pemphigus vegetans is a vesiculobullous autoimmune disease that is similar to pemphigus vulgaris but is characterized by the formation of vegetative plaques along the intertriginous areas and on the oral mucosa.¹ It is the rarest variant of all pemphigus subtypes and was first described by Neumann in 1876.² There are 2 subtypes of this variant: Hallopeau and Neumann, each with unique characteristics and physical manifestations. The Hallopeau type initially manifests with pustular lesions that rupture and evolve into erosions that commonly become infected. Gradually they merge and multiply to become more painful and vegetative.³ It has a more indolent course and typically responds well to treatment, and prolonged remission can be reached.⁴ The Neumann type is more severe and manifests with large vesiculobullous and erosive lesions that rupture and ulcerate, forming verrucous crusted vegetative plaques over the erosions.⁵ The erosions along the edge of the lesions induce new vegetation, becoming dry, hyperkeratotic, and fissured.³ The Neumann type often requires higher-dose steroids and typically is resistant to treatment.⁴ Patients can present with oral stomatitis and occasionally can develop a fissured or cerebriform appearance of the tongue, as seen in our patient (Figure 3).^1,2 Nail changes include onychorrhexis, onychomadesis, subungual pustules, and ultimately nail atrophy.⁵

Pemphigus diseases are characterized by IgG autoantibodies against desmoglein 3 and/or desmoglein 1. These are components of desmosomes that are responsible for keratinocyte adhesion, disruption of which results in the blister formation seen in pemphigus subtypes. The unique physical manifestation of pemphigus vegetans is thought to be due not only to autoantibodies against desmogleins 1 and 3 but also to autoantibodies against desmocollin 1 and 2.¹

Histopathologic examination reveals hyperkeratosis and pseudoepitheliomatous hyperplasia with acantholysis that creates a suprabasal cleft. Basal cells remain intact to the basement membrane by hemidesmosomes, resulting in a tombstone appearance. The Hallopeau type typically manifests with a large eosinophilic inflammatory response, leading to eosinophilic spongiosis and intraepidermal microabscesses. The Neumann type manifests with more of a neutrophilic and lymphocytic infiltrate, accompanied by the eosinophilic response.¹ For evaluation, obtain histopathology as well as direct immunofluorescence or enzyme-linked immunosorbent assay to look for intracellular deposition of desmoglein autoantibodies.

First-line treatment for pemphigus vulgaris and its variants is rituximab, an anti-CD20 monoclonal antibody. It has also been shown to have therapeutic benefit with combination of corticosteroids and rituximab. Corticosteroids should be given at a dose of 1 mg/kg daily for 2 to 4 weeks. Other immunosuppressive agents (steroid sparing) include azathioprine, dapsone, mycophenolate mofetil, methotrexate, cyclophosphamide, cyclosporine, and intravenous immunoglobulin. Pulse therapy with intermittent intravenous corticosteroids and immunosuppressants is another second-line therapeutic option. Topical therapeutic options include steroids, tacrolimus, and nicotinamide with oral tetracycline at onset and relapse. The goal of therapy is to maintain remission for 1 year then slowly taper treatment over another year.¹

Our patient initially was treated with prednisone, and subsequent courses of azathioprine and mycophenolate mofetil failed. He then was treated with 2 infusions of rituximab that were given 2 weeks apart. He was able to taper off the prednisone 1 month after the last infusion with complete remission of disease. He has been disease free for more than 9 months postinfusion.

Differential diagnoses for pemphigus vegetans can include bullous pemphigoid, bullous systemic lupus erythematosus, dermatitis herpetiformis, and pemphigus vulgaris. Lesion characteristics are key to differentiating pemphigus vegetans from other autoimmune blistering disorders. Bullous pemphigoid will manifest with tense blisters where pemphigus vulgaris will be flaccid; this is due to the difference in autoantibody targets between the conditions. Diagnosis depends on clinical presentation and histopathologic findings.

THE DIAGNOSIS: Pemphigus Vegetans

Histopathologic examination of the biopsies from the scalp and left anterior thigh revealed suprabasal clefting with acantholytic cells extending into the follicular infundibulum with eosinophilic pustules within the epidermis. The dermis contained perivascular lymphohistiocytic and eosinophilic inflammatory infiltrates without viral cytopathic effects (Figure 1). Direct immunofluorescence revealed strong IgG and moderate IgA pericellular deposition around keratinocyte cytoplasms (Figure 2). Serologic evaluation demonstrated anti–desmoglein 3 antibodies. Based on the clinical presentation and histopathologic correlation, a diagnosis of pemphigus vegetans was made.

Pemphigus vegetans is a vesiculobullous autoimmune disease that is similar to pemphigus vulgaris but is characterized by the formation of vegetative plaques along the intertriginous areas and on the oral mucosa.¹ It is the rarest variant of all pemphigus subtypes and was first described by Neumann in 1876.² There are 2 subtypes of this variant: Hallopeau and Neumann, each with unique characteristics and physical manifestations. The Hallopeau type initially manifests with pustular lesions that rupture and evolve into erosions that commonly become infected. Gradually they merge and multiply to become more painful and vegetative.³ It has a more indolent course and typically responds well to treatment, and prolonged remission can be reached.⁴ The Neumann type is more severe and manifests with large vesiculobullous and erosive lesions that rupture and ulcerate, forming verrucous crusted vegetative plaques over the erosions.⁵ The erosions along the edge of the lesions induce new vegetation, becoming dry, hyperkeratotic, and fissured.³ The Neumann type often requires higher-dose steroids and typically is resistant to treatment.⁴ Patients can present with oral stomatitis and occasionally can develop a fissured or cerebriform appearance of the tongue, as seen in our patient (Figure 3).^1,2 Nail changes include onychorrhexis, onychomadesis, subungual pustules, and ultimately nail atrophy.⁵

Pemphigus diseases are characterized by IgG autoantibodies against desmoglein 3 and/or desmoglein 1. These are components of desmosomes that are responsible for keratinocyte adhesion, disruption of which results in the blister formation seen in pemphigus subtypes. The unique physical manifestation of pemphigus vegetans is thought to be due not only to autoantibodies against desmogleins 1 and 3 but also to autoantibodies against desmocollin 1 and 2.¹

Histopathologic examination reveals hyperkeratosis and pseudoepitheliomatous hyperplasia with acantholysis that creates a suprabasal cleft. Basal cells remain intact to the basement membrane by hemidesmosomes, resulting in a tombstone appearance. The Hallopeau type typically manifests with a large eosinophilic inflammatory response, leading to eosinophilic spongiosis and intraepidermal microabscesses. The Neumann type manifests with more of a neutrophilic and lymphocytic infiltrate, accompanied by the eosinophilic response.¹ For evaluation, obtain histopathology as well as direct immunofluorescence or enzyme-linked immunosorbent assay to look for intracellular deposition of desmoglein autoantibodies.

First-line treatment for pemphigus vulgaris and its variants is rituximab, an anti-CD20 monoclonal antibody. It has also been shown to have therapeutic benefit with combination of corticosteroids and rituximab. Corticosteroids should be given at a dose of 1 mg/kg daily for 2 to 4 weeks. Other immunosuppressive agents (steroid sparing) include azathioprine, dapsone, mycophenolate mofetil, methotrexate, cyclophosphamide, cyclosporine, and intravenous immunoglobulin. Pulse therapy with intermittent intravenous corticosteroids and immunosuppressants is another second-line therapeutic option. Topical therapeutic options include steroids, tacrolimus, and nicotinamide with oral tetracycline at onset and relapse. The goal of therapy is to maintain remission for 1 year then slowly taper treatment over another year.¹

Our patient initially was treated with prednisone, and subsequent courses of azathioprine and mycophenolate mofetil failed. He then was treated with 2 infusions of rituximab that were given 2 weeks apart. He was able to taper off the prednisone 1 month after the last infusion with complete remission of disease. He has been disease free for more than 9 months postinfusion.

Differential diagnoses for pemphigus vegetans can include bullous pemphigoid, bullous systemic lupus erythematosus, dermatitis herpetiformis, and pemphigus vulgaris. Lesion characteristics are key to differentiating pemphigus vegetans from other autoimmune blistering disorders. Bullous pemphigoid will manifest with tense blisters where pemphigus vulgaris will be flaccid; this is due to the difference in autoantibody targets between the conditions. Diagnosis depends on clinical presentation and histopathologic findings.

THE DIAGNOSIS: Pemphigus Vegetans

Histopathologic examination of the biopsies from the scalp and left anterior thigh revealed suprabasal clefting with acantholytic cells extending into the follicular infundibulum with eosinophilic pustules within the epidermis. The dermis contained perivascular lymphohistiocytic and eosinophilic inflammatory infiltrates without viral cytopathic effects (Figure 1). Direct immunofluorescence revealed strong IgG and moderate IgA pericellular deposition around keratinocyte cytoplasms (Figure 2). Serologic evaluation demonstrated anti–desmoglein 3 antibodies. Based on the clinical presentation and histopathologic correlation, a diagnosis of pemphigus vegetans was made.

Pemphigus vegetans is a vesiculobullous autoimmune disease that is similar to pemphigus vulgaris but is characterized by the formation of vegetative plaques along the intertriginous areas and on the oral mucosa.¹ It is the rarest variant of all pemphigus subtypes and was first described by Neumann in 1876.² There are 2 subtypes of this variant: Hallopeau and Neumann, each with unique characteristics and physical manifestations. The Hallopeau type initially manifests with pustular lesions that rupture and evolve into erosions that commonly become infected. Gradually they merge and multiply to become more painful and vegetative.³ It has a more indolent course and typically responds well to treatment, and prolonged remission can be reached.⁴ The Neumann type is more severe and manifests with large vesiculobullous and erosive lesions that rupture and ulcerate, forming verrucous crusted vegetative plaques over the erosions.⁵ The erosions along the edge of the lesions induce new vegetation, becoming dry, hyperkeratotic, and fissured.³ The Neumann type often requires higher-dose steroids and typically is resistant to treatment.⁴ Patients can present with oral stomatitis and occasionally can develop a fissured or cerebriform appearance of the tongue, as seen in our patient (Figure 3).^1,2 Nail changes include onychorrhexis, onychomadesis, subungual pustules, and ultimately nail atrophy.⁵

Pemphigus diseases are characterized by IgG autoantibodies against desmoglein 3 and/or desmoglein 1. These are components of desmosomes that are responsible for keratinocyte adhesion, disruption of which results in the blister formation seen in pemphigus subtypes. The unique physical manifestation of pemphigus vegetans is thought to be due not only to autoantibodies against desmogleins 1 and 3 but also to autoantibodies against desmocollin 1 and 2.¹

Histopathologic examination reveals hyperkeratosis and pseudoepitheliomatous hyperplasia with acantholysis that creates a suprabasal cleft. Basal cells remain intact to the basement membrane by hemidesmosomes, resulting in a tombstone appearance. The Hallopeau type typically manifests with a large eosinophilic inflammatory response, leading to eosinophilic spongiosis and intraepidermal microabscesses. The Neumann type manifests with more of a neutrophilic and lymphocytic infiltrate, accompanied by the eosinophilic response.¹ For evaluation, obtain histopathology as well as direct immunofluorescence or enzyme-linked immunosorbent assay to look for intracellular deposition of desmoglein autoantibodies.

First-line treatment for pemphigus vulgaris and its variants is rituximab, an anti-CD20 monoclonal antibody. It has also been shown to have therapeutic benefit with combination of corticosteroids and rituximab. Corticosteroids should be given at a dose of 1 mg/kg daily for 2 to 4 weeks. Other immunosuppressive agents (steroid sparing) include azathioprine, dapsone, mycophenolate mofetil, methotrexate, cyclophosphamide, cyclosporine, and intravenous immunoglobulin. Pulse therapy with intermittent intravenous corticosteroids and immunosuppressants is another second-line therapeutic option. Topical therapeutic options include steroids, tacrolimus, and nicotinamide with oral tetracycline at onset and relapse. The goal of therapy is to maintain remission for 1 year then slowly taper treatment over another year.¹

Our patient initially was treated with prednisone, and subsequent courses of azathioprine and mycophenolate mofetil failed. He then was treated with 2 infusions of rituximab that were given 2 weeks apart. He was able to taper off the prednisone 1 month after the last infusion with complete remission of disease. He has been disease free for more than 9 months postinfusion.

Differential diagnoses for pemphigus vegetans can include bullous pemphigoid, bullous systemic lupus erythematosus, dermatitis herpetiformis, and pemphigus vulgaris. Lesion characteristics are key to differentiating pemphigus vegetans from other autoimmune blistering disorders. Bullous pemphigoid will manifest with tense blisters where pemphigus vulgaris will be flaccid; this is due to the difference in autoantibody targets between the conditions. Diagnosis depends on clinical presentation and histopathologic findings.

There is a direct link between psoriasis and metabolic conditions such as diabetes mellitus and obesity.¹ Exercise of varied intensity in patients with chronic inflammatory and metabolic conditions can help improve quality of life and severity of disease; however, there has not been a clear consensus on the recommended duration and types of exercise that are most advantageous.^1-5 We reviewed the literature to identify physical and mental health impacts of exercise on patients with psoriasis, and we present the recommended duration and types of exercise that are most impactful for these patients.

One indicator of the link between psoriasis and exercise is the level of peroxisome proliferator activated receptor gamma coactivator-1 α (PGC-1α) in muscle cells.² This marker reduces inflammation. When levels are low in muscle cells, an induction occurs that leads to systemic or local inflammation; however, skeletal muscle PGC-1α levels increase following exercise, indicating reduced inflammation.² The level of PGC-1α is measured through muscle biopsy and polymerase chain reaction.⁶ Another indicator of the correlation between exercise and inflammation is lipoprotein-associated phospholipase A2, which is produced by inflammatory cells and has a correlation with cardiovascular disease. Exercise reduces lipoprotein-associated phospholipase A2 levels, and a sedentary lifestyle correlates with increased levels of this marker.³ Lipoprotein-associated phospholipase A2 is measured through an enzyme-linked immunosorbent assay of the blood, with levels around 200 ng/mL considered high.⁷ Patients with psoriasis are 30% less likely to participate in physical activity compared to patients without psoriasis, which can be attributed to psychosocial impairment and other factors. Sedentary lifestyle is associated with new or worsening metabolic disease and prevalence of psoriatic lesions.¹

A metabolic equivalent task score is a classification system that measures the rate of the body’s oxygen uptake for any given activity.⁴ A score of 20.9 or more metabolic equivalent task hours of vigorous exercise per week—equal to 105 minutes of running or 180 minutes of swimming or playing tennis—is linked with a 25% to 30% risk reduction of psoriasis in women.⁴ Therefore, we recommend 30 minutes of exercise 4 to 5 times per week for women. These periods of exercise should consist mainly of activities that will not cause psoriasis flares due to excessive sweating, skin trauma, or prolonged sun exposure.⁵ Walking, yoga, and bike riding all could be good exercise options for those with psoriasis. The National Psoriasis Foundation offers guidance on physical activity in patients with psoriasis or psoriatic arthritis.⁸ Psoriasis has apparent physical and psychosocial impacts on patients that can be prevented and improved through the exercise recommendations presented in this article. Dermatologists should use these recommendations to address psoriasis in their everyday practice.

There is a direct link between psoriasis and metabolic conditions such as diabetes mellitus and obesity.¹ Exercise of varied intensity in patients with chronic inflammatory and metabolic conditions can help improve quality of life and severity of disease; however, there has not been a clear consensus on the recommended duration and types of exercise that are most advantageous.^1-5 We reviewed the literature to identify physical and mental health impacts of exercise on patients with psoriasis, and we present the recommended duration and types of exercise that are most impactful for these patients.

One indicator of the link between psoriasis and exercise is the level of peroxisome proliferator activated receptor gamma coactivator-1 α (PGC-1α) in muscle cells.² This marker reduces inflammation. When levels are low in muscle cells, an induction occurs that leads to systemic or local inflammation; however, skeletal muscle PGC-1α levels increase following exercise, indicating reduced inflammation.² The level of PGC-1α is measured through muscle biopsy and polymerase chain reaction.⁶ Another indicator of the correlation between exercise and inflammation is lipoprotein-associated phospholipase A2, which is produced by inflammatory cells and has a correlation with cardiovascular disease. Exercise reduces lipoprotein-associated phospholipase A2 levels, and a sedentary lifestyle correlates with increased levels of this marker.³ Lipoprotein-associated phospholipase A2 is measured through an enzyme-linked immunosorbent assay of the blood, with levels around 200 ng/mL considered high.⁷ Patients with psoriasis are 30% less likely to participate in physical activity compared to patients without psoriasis, which can be attributed to psychosocial impairment and other factors. Sedentary lifestyle is associated with new or worsening metabolic disease and prevalence of psoriatic lesions.¹

A metabolic equivalent task score is a classification system that measures the rate of the body’s oxygen uptake for any given activity.⁴ A score of 20.9 or more metabolic equivalent task hours of vigorous exercise per week—equal to 105 minutes of running or 180 minutes of swimming or playing tennis—is linked with a 25% to 30% risk reduction of psoriasis in women.⁴ Therefore, we recommend 30 minutes of exercise 4 to 5 times per week for women. These periods of exercise should consist mainly of activities that will not cause psoriasis flares due to excessive sweating, skin trauma, or prolonged sun exposure.⁵ Walking, yoga, and bike riding all could be good exercise options for those with psoriasis. The National Psoriasis Foundation offers guidance on physical activity in patients with psoriasis or psoriatic arthritis.⁸ Psoriasis has apparent physical and psychosocial impacts on patients that can be prevented and improved through the exercise recommendations presented in this article. Dermatologists should use these recommendations to address psoriasis in their everyday practice.

There is a direct link between psoriasis and metabolic conditions such as diabetes mellitus and obesity.¹ Exercise of varied intensity in patients with chronic inflammatory and metabolic conditions can help improve quality of life and severity of disease; however, there has not been a clear consensus on the recommended duration and types of exercise that are most advantageous.^1-5 We reviewed the literature to identify physical and mental health impacts of exercise on patients with psoriasis, and we present the recommended duration and types of exercise that are most impactful for these patients.

One indicator of the link between psoriasis and exercise is the level of peroxisome proliferator activated receptor gamma coactivator-1 α (PGC-1α) in muscle cells.² This marker reduces inflammation. When levels are low in muscle cells, an induction occurs that leads to systemic or local inflammation; however, skeletal muscle PGC-1α levels increase following exercise, indicating reduced inflammation.² The level of PGC-1α is measured through muscle biopsy and polymerase chain reaction.⁶ Another indicator of the correlation between exercise and inflammation is lipoprotein-associated phospholipase A2, which is produced by inflammatory cells and has a correlation with cardiovascular disease. Exercise reduces lipoprotein-associated phospholipase A2 levels, and a sedentary lifestyle correlates with increased levels of this marker.³ Lipoprotein-associated phospholipase A2 is measured through an enzyme-linked immunosorbent assay of the blood, with levels around 200 ng/mL considered high.⁷ Patients with psoriasis are 30% less likely to participate in physical activity compared to patients without psoriasis, which can be attributed to psychosocial impairment and other factors. Sedentary lifestyle is associated with new or worsening metabolic disease and prevalence of psoriatic lesions.¹

A metabolic equivalent task score is a classification system that measures the rate of the body’s oxygen uptake for any given activity.⁴ A score of 20.9 or more metabolic equivalent task hours of vigorous exercise per week—equal to 105 minutes of running or 180 minutes of swimming or playing tennis—is linked with a 25% to 30% risk reduction of psoriasis in women.⁴ Therefore, we recommend 30 minutes of exercise 4 to 5 times per week for women. These periods of exercise should consist mainly of activities that will not cause psoriasis flares due to excessive sweating, skin trauma, or prolonged sun exposure.⁵ Walking, yoga, and bike riding all could be good exercise options for those with psoriasis. The National Psoriasis Foundation offers guidance on physical activity in patients with psoriasis or psoriatic arthritis.⁸ Psoriasis has apparent physical and psychosocial impacts on patients that can be prevented and improved through the exercise recommendations presented in this article. Dermatologists should use these recommendations to address psoriasis in their everyday practice.

THE DIAGNOSIS: Fixed Drug Eruption

Based on the patient’s clinical presentation and history of similar eruptions, a diagnosis of levofloxacin-induced fixed drug eruption (FDE) was made. After cessation of the drug, the lesions resolved within 1 week without any residual postinflammatory hyperpigmentation.

Fixed drug eruption is an adverse cutaneous reaction characterized by the onset of a rash at a fixed location each time a specific medication is administered. Patients typically report a history of similar eruptions, often involving the upper and lower extremities, genital area, or mucous membranes. The most common causative agents vary, but retrospective analyses primarily implicate nonsteroidal anti-inflammatory drugs followed by antibiotics (eg, amoxicillin, levofloxacin, doxycycline) and antiepileptics.^1,2

While FDE can be solitary or scattered, most patients have 5 or fewer lesions, with a mean interval of 48 hours from exposure to the causative agent to onset of the rash.¹ The lesions can be differentiated by their typically solitary, well-demarcated, round or oval appearance; they also are erythematous to purple with a dusky center. The lesions may increase in size and number with each additional exposure to the offending medication.^1,3 Postinflammatory hyperpigmentation may last for weeks to months after the acute inflammatory response has resolved.

The high risk for recurrence of FDE may be explained by the presence of tissue resident memory T (TRM) cells in the affected skin that evoke a characteristic clinical manifestation upon administration of a causative agent.^2,3 Intraepidermal CD8⁺ TRM cells, which have an effectormemory phenotype, may contribute to the development of localized tissue damage; these cells demonstrate their effector function by the rapid increase in interferon gamma after challenge.² Within 24 hours of administration of the offending medication, CD8⁺ TRM cells migrate upward in the epidermis, and their activity leads to the epidermal necrosis observed with FDE. The self-limiting nature of FDE can be explained by the action of CD4+ Foxp3+ regulatory T cells that migrate similarly and induce the production of IL-10, which limits the damage inflicted by the CD8⁺ T cells.¹

Type I hypersensitivity reactions are IgE mediated; typically occur much more rapidly than FDE; and involve a raised urticarial rash, pruritus, and flushing. Urticaria is useful in identifying IgE-mediated reactions and mast cell degranulation. Previous exposure to the drug in question is required for diagnosis.⁴

Type IV delayed hypersensitivity reactions—including contact dermatitis and FDE—are mediated by T cells rather than IgE. These reactions occur at least 48 to 72 hours after drug exposure.⁴ Contact dermatitis follows exposure to an irritant but generally is limited to the site of contact and manifests with burning or stinging. Chronic contact dermatitis is characterized by erythema, scaling, and lichenification that may be associated with burning pain.

The target lesions of erythema multiforme are associated with the use of medications such as nonsteroidal anti-inflammatory drugs, antiepileptics, and antibiotics in fewer than 10% of cases. Infections are the predominant cause, with herpes simplex virus 1 being the most common etiology.⁵ Erythema multiforme lesions have 3 concentric segments: a dark red inflammatory zone surrounded by a pale ring of edema, both of which are surrounded by an erythematous halo. Lesions initially are distributed symmetrically on the extensor surfaces of the upper and lower extremities, but mucosal involvement may be present.⁵

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, involves fever and peripheral neutrophilia in addition to cutaneous erythematous eruptions and dermal neutrophilic infiltration on histopathology.⁶ Most cases are idiopathic but may occur in the setting of malignancy or drug administration. A major criterion for drug-induced Sweet syndrome is abrupt onset of painful erythematous plaques or nodules with pyrexia.⁶

THE DIAGNOSIS: Fixed Drug Eruption

Based on the patient’s clinical presentation and history of similar eruptions, a diagnosis of levofloxacin-induced fixed drug eruption (FDE) was made. After cessation of the drug, the lesions resolved within 1 week without any residual postinflammatory hyperpigmentation.

Fixed drug eruption is an adverse cutaneous reaction characterized by the onset of a rash at a fixed location each time a specific medication is administered. Patients typically report a history of similar eruptions, often involving the upper and lower extremities, genital area, or mucous membranes. The most common causative agents vary, but retrospective analyses primarily implicate nonsteroidal anti-inflammatory drugs followed by antibiotics (eg, amoxicillin, levofloxacin, doxycycline) and antiepileptics.^1,2

While FDE can be solitary or scattered, most patients have 5 or fewer lesions, with a mean interval of 48 hours from exposure to the causative agent to onset of the rash.¹ The lesions can be differentiated by their typically solitary, well-demarcated, round or oval appearance; they also are erythematous to purple with a dusky center. The lesions may increase in size and number with each additional exposure to the offending medication.^1,3 Postinflammatory hyperpigmentation may last for weeks to months after the acute inflammatory response has resolved.

The high risk for recurrence of FDE may be explained by the presence of tissue resident memory T (TRM) cells in the affected skin that evoke a characteristic clinical manifestation upon administration of a causative agent.^2,3 Intraepidermal CD8⁺ TRM cells, which have an effectormemory phenotype, may contribute to the development of localized tissue damage; these cells demonstrate their effector function by the rapid increase in interferon gamma after challenge.² Within 24 hours of administration of the offending medication, CD8⁺ TRM cells migrate upward in the epidermis, and their activity leads to the epidermal necrosis observed with FDE. The self-limiting nature of FDE can be explained by the action of CD4+ Foxp3+ regulatory T cells that migrate similarly and induce the production of IL-10, which limits the damage inflicted by the CD8⁺ T cells.¹

Type I hypersensitivity reactions are IgE mediated; typically occur much more rapidly than FDE; and involve a raised urticarial rash, pruritus, and flushing. Urticaria is useful in identifying IgE-mediated reactions and mast cell degranulation. Previous exposure to the drug in question is required for diagnosis.⁴

Type IV delayed hypersensitivity reactions—including contact dermatitis and FDE—are mediated by T cells rather than IgE. These reactions occur at least 48 to 72 hours after drug exposure.⁴ Contact dermatitis follows exposure to an irritant but generally is limited to the site of contact and manifests with burning or stinging. Chronic contact dermatitis is characterized by erythema, scaling, and lichenification that may be associated with burning pain.

The target lesions of erythema multiforme are associated with the use of medications such as nonsteroidal anti-inflammatory drugs, antiepileptics, and antibiotics in fewer than 10% of cases. Infections are the predominant cause, with herpes simplex virus 1 being the most common etiology.⁵ Erythema multiforme lesions have 3 concentric segments: a dark red inflammatory zone surrounded by a pale ring of edema, both of which are surrounded by an erythematous halo. Lesions initially are distributed symmetrically on the extensor surfaces of the upper and lower extremities, but mucosal involvement may be present.⁵

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, involves fever and peripheral neutrophilia in addition to cutaneous erythematous eruptions and dermal neutrophilic infiltration on histopathology.⁶ Most cases are idiopathic but may occur in the setting of malignancy or drug administration. A major criterion for drug-induced Sweet syndrome is abrupt onset of painful erythematous plaques or nodules with pyrexia.⁶

THE DIAGNOSIS: Fixed Drug Eruption

Based on the patient’s clinical presentation and history of similar eruptions, a diagnosis of levofloxacin-induced fixed drug eruption (FDE) was made. After cessation of the drug, the lesions resolved within 1 week without any residual postinflammatory hyperpigmentation.

Fixed drug eruption is an adverse cutaneous reaction characterized by the onset of a rash at a fixed location each time a specific medication is administered. Patients typically report a history of similar eruptions, often involving the upper and lower extremities, genital area, or mucous membranes. The most common causative agents vary, but retrospective analyses primarily implicate nonsteroidal anti-inflammatory drugs followed by antibiotics (eg, amoxicillin, levofloxacin, doxycycline) and antiepileptics.^1,2

While FDE can be solitary or scattered, most patients have 5 or fewer lesions, with a mean interval of 48 hours from exposure to the causative agent to onset of the rash.¹ The lesions can be differentiated by their typically solitary, well-demarcated, round or oval appearance; they also are erythematous to purple with a dusky center. The lesions may increase in size and number with each additional exposure to the offending medication.^1,3 Postinflammatory hyperpigmentation may last for weeks to months after the acute inflammatory response has resolved.

The high risk for recurrence of FDE may be explained by the presence of tissue resident memory T (TRM) cells in the affected skin that evoke a characteristic clinical manifestation upon administration of a causative agent.^2,3 Intraepidermal CD8⁺ TRM cells, which have an effectormemory phenotype, may contribute to the development of localized tissue damage; these cells demonstrate their effector function by the rapid increase in interferon gamma after challenge.² Within 24 hours of administration of the offending medication, CD8⁺ TRM cells migrate upward in the epidermis, and their activity leads to the epidermal necrosis observed with FDE. The self-limiting nature of FDE can be explained by the action of CD4+ Foxp3+ regulatory T cells that migrate similarly and induce the production of IL-10, which limits the damage inflicted by the CD8⁺ T cells.¹

Type I hypersensitivity reactions are IgE mediated; typically occur much more rapidly than FDE; and involve a raised urticarial rash, pruritus, and flushing. Urticaria is useful in identifying IgE-mediated reactions and mast cell degranulation. Previous exposure to the drug in question is required for diagnosis.⁴

Type IV delayed hypersensitivity reactions—including contact dermatitis and FDE—are mediated by T cells rather than IgE. These reactions occur at least 48 to 72 hours after drug exposure.⁴ Contact dermatitis follows exposure to an irritant but generally is limited to the site of contact and manifests with burning or stinging. Chronic contact dermatitis is characterized by erythema, scaling, and lichenification that may be associated with burning pain.

The target lesions of erythema multiforme are associated with the use of medications such as nonsteroidal anti-inflammatory drugs, antiepileptics, and antibiotics in fewer than 10% of cases. Infections are the predominant cause, with herpes simplex virus 1 being the most common etiology.⁵ Erythema multiforme lesions have 3 concentric segments: a dark red inflammatory zone surrounded by a pale ring of edema, both of which are surrounded by an erythematous halo. Lesions initially are distributed symmetrically on the extensor surfaces of the upper and lower extremities, but mucosal involvement may be present.⁵

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, involves fever and peripheral neutrophilia in addition to cutaneous erythematous eruptions and dermal neutrophilic infiltration on histopathology.⁶ Most cases are idiopathic but may occur in the setting of malignancy or drug administration. A major criterion for drug-induced Sweet syndrome is abrupt onset of painful erythematous plaques or nodules with pyrexia.⁶

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Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.

Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.

Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.

Androgenetic alopecia (AGA) is the most common type of hair loss after adolescence, with a high prevalence of 21.3% among males and 6.0% among females in China.¹ In men, AGA manifests as diffuse hair loss in the frontal and temporal areas of the scalp; in women, it is characterized by thinning of the hair on the top of the head with a wide part and less recession of the frontal line. Although the specific pathogenesis of AGA still is unclear, it is believed to be related mainly to genetics and androgen levels.¹ Androgenetic alopecia is not considered a life-threatening medical condition, but it can have a major impact on patients’ self-esteem and quality of life.

The prevalence of pediatric AGA has been steadily rising over the past few decades and is thought to be correlated to a hyperinsulinemic diet and elevated circulating androgens at younger ages, resulting in early onset in genetically susceptible children and adolescents.^2,3 Additionally, studies have shown that early-onset AGA is associated with metabolic syndrome,^4-6 which includes conditions such as obesity, insulin resistance, hyperglycemia, and dyslipidemia.^7,8 Furthermore, polycystic ovary syndrome (PCOS) is commonly observed in adolescent girls with early-onset AGA. The condition is associated with hormonal imbalances, particularly elevated androgens, which can contribute to the early onset of AGA. In girls, these hormonal changes may accelerate hair thinning and hair loss, making AGA a potential early indicator of underlying PCOS.^9,10

Available research on early-onset AGA in pediatric patients is limited, with most studies having a relatively small sample size and generalized findings. Data on pediatric AGA in China is scarce; therefore, the objective of this retrospective study was to analyze the clinical, laboratory, and trichoscopic features of AGA in 133 pediatric patients with AGA who visited the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University (Nanjing, China), from January 2010 to December 2023.

Methods

Study Population—Pediatric patients with early-onset AGA who were registered for outpatient consultations at the hair disease clinic of the Department of Dermatology at The First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were included. Patients aged 18 years and younger with a definitive diagnosis of AGA were selected for data collection and analysis. Any uncertain information was confirmed through telephone follow-up with patients.

Collection of Demographic Information and Laboratory Tests—Patient demographics and medical history including age, sex, age at disease onset, and duration of AGA were collected from the electronic medical record. Height and weight also were collected to calculate patients’ body mass index (BMI). Detailed laboratory test results were recorded, including assessments of sex hormone—binding globulin (SHBG), vitamin D, testosterone, and ferritin.

Analysis of Comorbidities—Due to the influence of genetic factors on body composition, there are differences in how obesity is defined across racial populations. The World Health Organization international standard defines the term overweight as a BMI greater than 25 and obese as a BMI greater than 30; however, the World Health Organization recommends a lower definition standard for these classifications in the Chinese population. China established specific BMI standards for classification of patients as overweight (24.0.27.9 kg/m²) and obese (≥28 kg/m²).¹¹ During outpatient consultations, a comprehensive medical history was obtained from each patient, including the presence of PCOS, acne, seborrheic dermatitis, hirsutism, and sleeping disorders. During routine outpatient assessments, experienced dermatologists (including W.F.) determined the presence of symptoms and confirmed the diagnosis.

Hair Loss Classification and Trichoscopy—Hair loss patterns for male patients were assessed using the basic and specific classification system, while the Ludwig scale was utilized for female patients.^12,13 Trichoscopy was utilized with high-resolution imaging systems and advanced software for image analysis, enabling precise assessment of hair in different scalp regions. Parameters such as hair density, hair diameter, percentage of terminal hairs, and percentage of vellus hair were recorded to monitor changes in hair growth for the patients.

Statistical Analysis—Categorical data were analyzed using the x² test. A P value less than .05 was considered statistically significant. All statistical analyses were conducted using SPSS software version 26 (IBM).

Results

Patient Characteristics and Hair Loss Patterns—A sample of 133 pediatric patients (60 males, 73 females) who were diagnosed with AGA at the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were selected. The mean age of the patients was 15.5 years (range, 10–18 years). The mean age was slightly lower in females compared with males (15.05 vs 16.19 years, respectively). Additionally, females showed earlier onset of the disease, with a mean age at onset of 13.41 years compared to 14.44 years in males. The time between onset of AGA symptoms and first seeking medical care ranged from 4 months to 3 years, with a mean disease duration of 1.72 years. There was no significant difference in the duration of disease between males and females (1.76 and 1.70 years, respectively). Patient characteristics by age group are summarized in eTable 1.

The pediatric patients in our study exhibited hair loss patterns similar to those typically observed in adults. Male patients typically showed diffuse thinning on the crown and varying degrees of temporal thinning, while female patients demonstrated diffuse thinning on the crown with a preserved frontal hairline; however, 5 (8.3%) male patients presented with Christmas tree– like pattern of hair loss with a preserved hairline and a thinning crown (Figures 1 and 2).

BMI and Comorbidities—Among our study sample, 27.1% (36/133) of patients were identified as overweight or obese. It came to our attention that the prevalence of patients who were overweight and obese was notably higher in patients aged older than 14 but younger than 18 years compared with those aged 14 years or younger (24.1% vs 3.0% [32/133 vs 4/133]). A more detailed analysis of patients who were overweight and obese is outlined in eTable 2.

Seborrheic dermatitis was identified as the most prevalent comorbidity associated with pediatric AGA (51.9% [69/133]), followed by acne (42.8% [57/133]), hirsutism (33.1% [44/133]), and sleep disturbances/insomnia (28.6% [38/133]). The prevalence of these comorbidities varied by age group, with a higher incidence observed among patients aged older than 14 years as compared to those aged 14 years or younger.

Family History of AGA—Our study results indicated that most (78.2% [104/133]) patients had a family history of AGA. Among males and females, 81.7% and 75.3% (49/60 and 55/73) had a positive family history, respectively. Further analysis showed that 43.3% (26/60) of males and 21.9% (16/73) of females reported AGA in their father, while 16.7% (10/60) of males and 35.6% insert (26/73) of females reported AGA in their mother. Both parents were affected in 21.7% (13/60) of male patients and 17.8% (13/73) of female patients (eTable 3).

Related Laboratory Tests of Pediatric Patients With AGA—The results of laboratory testing for vitamin D deficiency, low SHBG, high testosterone, and low ferritin levels in the study sample are outlined in eTable 4. Among the study participants, 15.9% (10/63) of females exhibited increased levels of both free and total testosterone. Low SHBG was observed in 47.1% (56/119) of patients, with a slightly higher proportion in males (48.2% [27/56] than females (46.0% [29/63]). Vitamin D deficiency was prevalent in 60.5% (72/119) of the study population, with a higher incidence rate in females (71.4%[45/63]) compared to males (48.2%[27/56]). Moreover, 21.8% (26/119) of pediatric patients had low ferritin levels, with a higher incidence rate in females (33.3%[21/63]) compared to males (8.9%[5/56]).

Female Patients With PCOS—In our study, 6 (8.2%) female patients with AGA had been diagnosed with PCOS prior to their referral to the First Affiliated Hospital of Nanjing Medical University. Information regarding their age at treatment, hair loss grade, comorbidities, and laboratory test results is provided in eTable 5.

Degree of Hair Loss at First Visit—In male pediatric patients with AGA, the majority were classified as M type according to the basic and specific classification. Specifically, the main hairloss level in males was concentrated in M1 and M2 (80.0% [48/60]), while specific type F was mainly distributed in F1 and F2 (81.7% [49/60]), and specific type V was mainly distributed in V1 and V2 (80.0% [48/60]). On the other hand, female patients were mainly (87.7% [64/73]) classified as type I or II in the Ludwig scale.

Clinical Features of Trichoscopy Examinations at First Visit—We present the trichoscopic findings of our study regarding hair characteristics, including hair density, hair diameter, terminal hair ratio, and vellus hair ratio, among male and female pediatric participants stratified into 2 age groups: 14 years or younger, and older than 14 but younger than 18 years. In males, those aged 14 years or younger had a lower average hair density than those older than 14 years but thicker hair diameter. Conversely, males aged 14 years and older were more likely to seek treatment of hair loss than those aged 14 years or younger. Among females, those older than 14 years had higher hair density, hair diameter, and terminal hair ratio than those younger than 14 years. Hair trichoscopy characteristics among pediatric patients with AGA in our study population were similar to those of adults with AGA (Figure 3).

Efficacy and Adverse Effects of Topical Minoxidil—There were 56 (42.1%) patients who had used topical minoxidil for more than 6 months: 33 (58.9%) males and 23 (41.1%) females. In terms of efficacy, 51 (91.1%) patients responded positively, demonstrating improved scalp coverage, increased hair density, or greater hair diameter. There were 2 (3.6%) cases of minor adverse reactions: 1 case of scalp itching with increased dandruff that improved with local symptomatic treatment, and 1 case of hirsutism, which improved after discontinuing the drug. Among the 28 (50.0%) pediatric patients who used topical minoxidil for more than 12 months, there were no reported adverse reactions. Overall, topical minoxidil was effective and well tolerated in pediatric patients, with mild adverse reactions.

Comment

In our study, the youngest AGA patient was 10 years old, which is slightly older than a 6-year-old patient reported in the literature.¹⁴ Females showed a higher incidence of AGA compared to males, which is consistent with some previous studies^14,15 but contradicts the findings of Gonzalez et al¹⁶ and Kim et al.¹⁷ We speculate that the differences in AGA incidence could be attributed to the diverse genetic background and racial disparities between the populations included in the study by Gonzalez et al¹⁶—primarily White patients from Europe and the United States—and our study, which included individuals from East Asia. Furthermore, variations in lifestyle and environment in Europe and the United States vs Asia (eg, dietary habits, stress, environmental pollution) may contribute to the differing sexspecific incidence rates. Additionally, our study showed that female patients tended to experience AGA at a younger age than male patients, as indicated by younger age of disease onset and at the initial visit. These findings are consistent with other studies reporting a slightly younger age of disease onset in female patients.^14,16,17 The importance lies in raising awareness among both patients and physicians about early-onset AGA, facilitating earlier detection, diagnosis, and treatment. Furthermore, our study revealed a higher prevalence of a positive family history of AGA in our study population (78.2%) compared to other studies.¹⁴ Paternal family history was more commonly observed than maternal history (81.7% and 75.3%, respectively); moreover, 19.5% of patients reported a positive family history of AGA in both parents. Therefore, it is essential to raise awareness among pediatric patients with a positive family history of AGA, as they may experience hair loss at a younger age.

Patients with AGA commonly present with concurrent skin conditions, most notably acne, seborrheic dermatitis, and hirsutism. Therefore, it is important to monitor these associated diseases and adopt appropriate treatments. Moreover, it is worth mentioning that a considerable number of pediatric patients reported experiencing sleep difficulties. It is well known that sleep disturbances can lead to hormonal abnormalities, which are also a risk factor for AGA.^18-20 Therefore, further research is needed to investigate whether treating sleep disturbances can delay onset or progression of pediatric AGA. A previous retrospective study reported a PCOS prevalence of 47.4% (9/19) in adolescent females with AGA,¹⁶ but our study observed a much lower incidence of 4.5%. This discrepancy may be due to the fact that diagnostic imaging was not required for all female patients suspected of having PCOS in our study, which may have resulted in the exclusion of some undiagnosed PCOS cases from the data analysis.

In our study, a considerable proportion of patients exhibited moderate hair loss at their first visit, and there were differences in hair density and diameter among different age groups, with female patients having finer hair than male patients. Therefore, it is necessary to raise awareness of and perform early diagnosis and treatment of AGA in pediatric patients presenting with hair loss. Upon evaluation of laboratory results, we observed a notable proportion of pediatric patients with AGA who had low levels of vitamin D, SHBG, and ferritin. Notably, female patients were more susceptible to low vitamin D levels compared with males. Screening for these indicators, particularly in female patients, could aid in the diagnosis and treatment of pediatric AGA. Surprisingly, testosterone levels did not show a significant increase in male patients with AGA. Furthermore, only a small percentage of female patients exhibited elevated testosterone levels, indicating that androgens may not play a dominant role in the pathogenesis of male pediatric AGA and that other factors and mechanisms may be involved. Although AGA has been extensively studied in adults, there is limited knowledge about its occurrence and characteristics in children and adolescents. Our study represents one of the few investigations into AGA in this population and is among the largest to explore the clinical features, laboratory testing and results, trichoscopic characteristics, and comorbidities in Chinese pediatric patients with AGA. Our findings offer valuable insights into early clinical characteristics of pediatric AGA in this specific demographic population to inform future research directions and clinical practice guidelines.

Given that we conducted a retrospective study with a relatively small sample size from a single clinic site, the generalizability of our research findings may be limited. In addition, the patients included in our study did not have frequent routine testing for metabolic and hormonal indicators to analyze further correlations between hormonal changes with severity of pediatric AGA. Future research with prospective multicenter designs and larger sample sizes are needed to increase representativeness and generalizability, and comprehensive testing is needed to validate and extend our findings. Furthermore, the psychological impact among pediatric patients with AGA warrants further investigation on early intervention to reduce psychological stress.

Besides enhancing the understanding of AGA in children and adolescents among dermatologists and pediatricians, there is a need for individualized, step-by-step, and comprehensive treatment. Initial assessment generally includes addressing hormonal disorders such as seborrheic dermatitis, folliculitis, PCOS, and acne. Some adult treatments may be effective in pediatric cases. In one study of 15 pediatric patients using minoxidil 5% daily (6 females, 4 males), 4 (66.7%) females had stable alopecia (follow-up, >6 months); 4 (44.4%) males using minoxidil 5% daily and 1 mg finasteride and 5 (55.6%) taking 1 mg of finasteride alone showed hair density gains.¹⁶ In another study,²¹ 373 adolescents with AGA (286 boys, 87 girls; age range, 10–17 years) were treated with topical minoxidil solution over an 18-month period, with 95.0% responding positively: 54.0% showed improved scalp coverage, and 41.0% experienced slower hair thinning. Topical minoxidil generally is well tolerated in pediatric patients with no significant impact on blood pressure, pulse rate, or other vital signs.²¹ The primary adverse reactions to topical minoxidil observed in clinical practice are mild scalp irritation and increased facial hair, which usually resolve upon discontinuation.²² In China, topical minoxidil (available in 2% or 5% concentrations) commonly is used in children and adolescents, with adjustments made based on treatment response and adverse effects. Despite its proven efficacy and tolerability, it is essential that adverse effects be promptly communicated to health care providers for appropriate dosage adjustments, and that concurrent conditions, such as vitamin D and iron deficiencies, be adequately managed. Encouraging patients to adhere to prescribed medications and undergo long-term follow-up typically results in favorable outcomes.

Androgenetic alopecia (AGA) is the most common type of hair loss after adolescence, with a high prevalence of 21.3% among males and 6.0% among females in China.¹ In men, AGA manifests as diffuse hair loss in the frontal and temporal areas of the scalp; in women, it is characterized by thinning of the hair on the top of the head with a wide part and less recession of the frontal line. Although the specific pathogenesis of AGA still is unclear, it is believed to be related mainly to genetics and androgen levels.¹ Androgenetic alopecia is not considered a life-threatening medical condition, but it can have a major impact on patients’ self-esteem and quality of life.

The prevalence of pediatric AGA has been steadily rising over the past few decades and is thought to be correlated to a hyperinsulinemic diet and elevated circulating androgens at younger ages, resulting in early onset in genetically susceptible children and adolescents.^2,3 Additionally, studies have shown that early-onset AGA is associated with metabolic syndrome,^4-6 which includes conditions such as obesity, insulin resistance, hyperglycemia, and dyslipidemia.^7,8 Furthermore, polycystic ovary syndrome (PCOS) is commonly observed in adolescent girls with early-onset AGA. The condition is associated with hormonal imbalances, particularly elevated androgens, which can contribute to the early onset of AGA. In girls, these hormonal changes may accelerate hair thinning and hair loss, making AGA a potential early indicator of underlying PCOS.^9,10

Available research on early-onset AGA in pediatric patients is limited, with most studies having a relatively small sample size and generalized findings. Data on pediatric AGA in China is scarce; therefore, the objective of this retrospective study was to analyze the clinical, laboratory, and trichoscopic features of AGA in 133 pediatric patients with AGA who visited the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University (Nanjing, China), from January 2010 to December 2023.

Methods

Study Population—Pediatric patients with early-onset AGA who were registered for outpatient consultations at the hair disease clinic of the Department of Dermatology at The First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were included. Patients aged 18 years and younger with a definitive diagnosis of AGA were selected for data collection and analysis. Any uncertain information was confirmed through telephone follow-up with patients.

Collection of Demographic Information and Laboratory Tests—Patient demographics and medical history including age, sex, age at disease onset, and duration of AGA were collected from the electronic medical record. Height and weight also were collected to calculate patients’ body mass index (BMI). Detailed laboratory test results were recorded, including assessments of sex hormone—binding globulin (SHBG), vitamin D, testosterone, and ferritin.

Analysis of Comorbidities—Due to the influence of genetic factors on body composition, there are differences in how obesity is defined across racial populations. The World Health Organization international standard defines the term overweight as a BMI greater than 25 and obese as a BMI greater than 30; however, the World Health Organization recommends a lower definition standard for these classifications in the Chinese population. China established specific BMI standards for classification of patients as overweight (24.0.27.9 kg/m²) and obese (≥28 kg/m²).¹¹ During outpatient consultations, a comprehensive medical history was obtained from each patient, including the presence of PCOS, acne, seborrheic dermatitis, hirsutism, and sleeping disorders. During routine outpatient assessments, experienced dermatologists (including W.F.) determined the presence of symptoms and confirmed the diagnosis.

Hair Loss Classification and Trichoscopy—Hair loss patterns for male patients were assessed using the basic and specific classification system, while the Ludwig scale was utilized for female patients.^12,13 Trichoscopy was utilized with high-resolution imaging systems and advanced software for image analysis, enabling precise assessment of hair in different scalp regions. Parameters such as hair density, hair diameter, percentage of terminal hairs, and percentage of vellus hair were recorded to monitor changes in hair growth for the patients.

Statistical Analysis—Categorical data were analyzed using the x² test. A P value less than .05 was considered statistically significant. All statistical analyses were conducted using SPSS software version 26 (IBM).

Results

Patient Characteristics and Hair Loss Patterns—A sample of 133 pediatric patients (60 males, 73 females) who were diagnosed with AGA at the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were selected. The mean age of the patients was 15.5 years (range, 10–18 years). The mean age was slightly lower in females compared with males (15.05 vs 16.19 years, respectively). Additionally, females showed earlier onset of the disease, with a mean age at onset of 13.41 years compared to 14.44 years in males. The time between onset of AGA symptoms and first seeking medical care ranged from 4 months to 3 years, with a mean disease duration of 1.72 years. There was no significant difference in the duration of disease between males and females (1.76 and 1.70 years, respectively). Patient characteristics by age group are summarized in eTable 1.

The pediatric patients in our study exhibited hair loss patterns similar to those typically observed in adults. Male patients typically showed diffuse thinning on the crown and varying degrees of temporal thinning, while female patients demonstrated diffuse thinning on the crown with a preserved frontal hairline; however, 5 (8.3%) male patients presented with Christmas tree– like pattern of hair loss with a preserved hairline and a thinning crown (Figures 1 and 2).

BMI and Comorbidities—Among our study sample, 27.1% (36/133) of patients were identified as overweight or obese. It came to our attention that the prevalence of patients who were overweight and obese was notably higher in patients aged older than 14 but younger than 18 years compared with those aged 14 years or younger (24.1% vs 3.0% [32/133 vs 4/133]). A more detailed analysis of patients who were overweight and obese is outlined in eTable 2.

Seborrheic dermatitis was identified as the most prevalent comorbidity associated with pediatric AGA (51.9% [69/133]), followed by acne (42.8% [57/133]), hirsutism (33.1% [44/133]), and sleep disturbances/insomnia (28.6% [38/133]). The prevalence of these comorbidities varied by age group, with a higher incidence observed among patients aged older than 14 years as compared to those aged 14 years or younger.

Family History of AGA—Our study results indicated that most (78.2% [104/133]) patients had a family history of AGA. Among males and females, 81.7% and 75.3% (49/60 and 55/73) had a positive family history, respectively. Further analysis showed that 43.3% (26/60) of males and 21.9% (16/73) of females reported AGA in their father, while 16.7% (10/60) of males and 35.6% insert (26/73) of females reported AGA in their mother. Both parents were affected in 21.7% (13/60) of male patients and 17.8% (13/73) of female patients (eTable 3).

Related Laboratory Tests of Pediatric Patients With AGA—The results of laboratory testing for vitamin D deficiency, low SHBG, high testosterone, and low ferritin levels in the study sample are outlined in eTable 4. Among the study participants, 15.9% (10/63) of females exhibited increased levels of both free and total testosterone. Low SHBG was observed in 47.1% (56/119) of patients, with a slightly higher proportion in males (48.2% [27/56] than females (46.0% [29/63]). Vitamin D deficiency was prevalent in 60.5% (72/119) of the study population, with a higher incidence rate in females (71.4%[45/63]) compared to males (48.2%[27/56]). Moreover, 21.8% (26/119) of pediatric patients had low ferritin levels, with a higher incidence rate in females (33.3%[21/63]) compared to males (8.9%[5/56]).

Female Patients With PCOS—In our study, 6 (8.2%) female patients with AGA had been diagnosed with PCOS prior to their referral to the First Affiliated Hospital of Nanjing Medical University. Information regarding their age at treatment, hair loss grade, comorbidities, and laboratory test results is provided in eTable 5.

Degree of Hair Loss at First Visit—In male pediatric patients with AGA, the majority were classified as M type according to the basic and specific classification. Specifically, the main hairloss level in males was concentrated in M1 and M2 (80.0% [48/60]), while specific type F was mainly distributed in F1 and F2 (81.7% [49/60]), and specific type V was mainly distributed in V1 and V2 (80.0% [48/60]). On the other hand, female patients were mainly (87.7% [64/73]) classified as type I or II in the Ludwig scale.

Clinical Features of Trichoscopy Examinations at First Visit—We present the trichoscopic findings of our study regarding hair characteristics, including hair density, hair diameter, terminal hair ratio, and vellus hair ratio, among male and female pediatric participants stratified into 2 age groups: 14 years or younger, and older than 14 but younger than 18 years. In males, those aged 14 years or younger had a lower average hair density than those older than 14 years but thicker hair diameter. Conversely, males aged 14 years and older were more likely to seek treatment of hair loss than those aged 14 years or younger. Among females, those older than 14 years had higher hair density, hair diameter, and terminal hair ratio than those younger than 14 years. Hair trichoscopy characteristics among pediatric patients with AGA in our study population were similar to those of adults with AGA (Figure 3).

Efficacy and Adverse Effects of Topical Minoxidil—There were 56 (42.1%) patients who had used topical minoxidil for more than 6 months: 33 (58.9%) males and 23 (41.1%) females. In terms of efficacy, 51 (91.1%) patients responded positively, demonstrating improved scalp coverage, increased hair density, or greater hair diameter. There were 2 (3.6%) cases of minor adverse reactions: 1 case of scalp itching with increased dandruff that improved with local symptomatic treatment, and 1 case of hirsutism, which improved after discontinuing the drug. Among the 28 (50.0%) pediatric patients who used topical minoxidil for more than 12 months, there were no reported adverse reactions. Overall, topical minoxidil was effective and well tolerated in pediatric patients, with mild adverse reactions.

Comment

In our study, the youngest AGA patient was 10 years old, which is slightly older than a 6-year-old patient reported in the literature.¹⁴ Females showed a higher incidence of AGA compared to males, which is consistent with some previous studies^14,15 but contradicts the findings of Gonzalez et al¹⁶ and Kim et al.¹⁷ We speculate that the differences in AGA incidence could be attributed to the diverse genetic background and racial disparities between the populations included in the study by Gonzalez et al¹⁶—primarily White patients from Europe and the United States—and our study, which included individuals from East Asia. Furthermore, variations in lifestyle and environment in Europe and the United States vs Asia (eg, dietary habits, stress, environmental pollution) may contribute to the differing sexspecific incidence rates. Additionally, our study showed that female patients tended to experience AGA at a younger age than male patients, as indicated by younger age of disease onset and at the initial visit. These findings are consistent with other studies reporting a slightly younger age of disease onset in female patients.^14,16,17 The importance lies in raising awareness among both patients and physicians about early-onset AGA, facilitating earlier detection, diagnosis, and treatment. Furthermore, our study revealed a higher prevalence of a positive family history of AGA in our study population (78.2%) compared to other studies.¹⁴ Paternal family history was more commonly observed than maternal history (81.7% and 75.3%, respectively); moreover, 19.5% of patients reported a positive family history of AGA in both parents. Therefore, it is essential to raise awareness among pediatric patients with a positive family history of AGA, as they may experience hair loss at a younger age.

Patients with AGA commonly present with concurrent skin conditions, most notably acne, seborrheic dermatitis, and hirsutism. Therefore, it is important to monitor these associated diseases and adopt appropriate treatments. Moreover, it is worth mentioning that a considerable number of pediatric patients reported experiencing sleep difficulties. It is well known that sleep disturbances can lead to hormonal abnormalities, which are also a risk factor for AGA.^18-20 Therefore, further research is needed to investigate whether treating sleep disturbances can delay onset or progression of pediatric AGA. A previous retrospective study reported a PCOS prevalence of 47.4% (9/19) in adolescent females with AGA,¹⁶ but our study observed a much lower incidence of 4.5%. This discrepancy may be due to the fact that diagnostic imaging was not required for all female patients suspected of having PCOS in our study, which may have resulted in the exclusion of some undiagnosed PCOS cases from the data analysis.

In our study, a considerable proportion of patients exhibited moderate hair loss at their first visit, and there were differences in hair density and diameter among different age groups, with female patients having finer hair than male patients. Therefore, it is necessary to raise awareness of and perform early diagnosis and treatment of AGA in pediatric patients presenting with hair loss. Upon evaluation of laboratory results, we observed a notable proportion of pediatric patients with AGA who had low levels of vitamin D, SHBG, and ferritin. Notably, female patients were more susceptible to low vitamin D levels compared with males. Screening for these indicators, particularly in female patients, could aid in the diagnosis and treatment of pediatric AGA. Surprisingly, testosterone levels did not show a significant increase in male patients with AGA. Furthermore, only a small percentage of female patients exhibited elevated testosterone levels, indicating that androgens may not play a dominant role in the pathogenesis of male pediatric AGA and that other factors and mechanisms may be involved. Although AGA has been extensively studied in adults, there is limited knowledge about its occurrence and characteristics in children and adolescents. Our study represents one of the few investigations into AGA in this population and is among the largest to explore the clinical features, laboratory testing and results, trichoscopic characteristics, and comorbidities in Chinese pediatric patients with AGA. Our findings offer valuable insights into early clinical characteristics of pediatric AGA in this specific demographic population to inform future research directions and clinical practice guidelines.

Given that we conducted a retrospective study with a relatively small sample size from a single clinic site, the generalizability of our research findings may be limited. In addition, the patients included in our study did not have frequent routine testing for metabolic and hormonal indicators to analyze further correlations between hormonal changes with severity of pediatric AGA. Future research with prospective multicenter designs and larger sample sizes are needed to increase representativeness and generalizability, and comprehensive testing is needed to validate and extend our findings. Furthermore, the psychological impact among pediatric patients with AGA warrants further investigation on early intervention to reduce psychological stress.

Besides enhancing the understanding of AGA in children and adolescents among dermatologists and pediatricians, there is a need for individualized, step-by-step, and comprehensive treatment. Initial assessment generally includes addressing hormonal disorders such as seborrheic dermatitis, folliculitis, PCOS, and acne. Some adult treatments may be effective in pediatric cases. In one study of 15 pediatric patients using minoxidil 5% daily (6 females, 4 males), 4 (66.7%) females had stable alopecia (follow-up, >6 months); 4 (44.4%) males using minoxidil 5% daily and 1 mg finasteride and 5 (55.6%) taking 1 mg of finasteride alone showed hair density gains.¹⁶ In another study,²¹ 373 adolescents with AGA (286 boys, 87 girls; age range, 10–17 years) were treated with topical minoxidil solution over an 18-month period, with 95.0% responding positively: 54.0% showed improved scalp coverage, and 41.0% experienced slower hair thinning. Topical minoxidil generally is well tolerated in pediatric patients with no significant impact on blood pressure, pulse rate, or other vital signs.²¹ The primary adverse reactions to topical minoxidil observed in clinical practice are mild scalp irritation and increased facial hair, which usually resolve upon discontinuation.²² In China, topical minoxidil (available in 2% or 5% concentrations) commonly is used in children and adolescents, with adjustments made based on treatment response and adverse effects. Despite its proven efficacy and tolerability, it is essential that adverse effects be promptly communicated to health care providers for appropriate dosage adjustments, and that concurrent conditions, such as vitamin D and iron deficiencies, be adequately managed. Encouraging patients to adhere to prescribed medications and undergo long-term follow-up typically results in favorable outcomes.

Androgenetic alopecia (AGA) is the most common type of hair loss after adolescence, with a high prevalence of 21.3% among males and 6.0% among females in China.¹ In men, AGA manifests as diffuse hair loss in the frontal and temporal areas of the scalp; in women, it is characterized by thinning of the hair on the top of the head with a wide part and less recession of the frontal line. Although the specific pathogenesis of AGA still is unclear, it is believed to be related mainly to genetics and androgen levels.¹ Androgenetic alopecia is not considered a life-threatening medical condition, but it can have a major impact on patients’ self-esteem and quality of life.

The prevalence of pediatric AGA has been steadily rising over the past few decades and is thought to be correlated to a hyperinsulinemic diet and elevated circulating androgens at younger ages, resulting in early onset in genetically susceptible children and adolescents.^2,3 Additionally, studies have shown that early-onset AGA is associated with metabolic syndrome,^4-6 which includes conditions such as obesity, insulin resistance, hyperglycemia, and dyslipidemia.^7,8 Furthermore, polycystic ovary syndrome (PCOS) is commonly observed in adolescent girls with early-onset AGA. The condition is associated with hormonal imbalances, particularly elevated androgens, which can contribute to the early onset of AGA. In girls, these hormonal changes may accelerate hair thinning and hair loss, making AGA a potential early indicator of underlying PCOS.^9,10

Available research on early-onset AGA in pediatric patients is limited, with most studies having a relatively small sample size and generalized findings. Data on pediatric AGA in China is scarce; therefore, the objective of this retrospective study was to analyze the clinical, laboratory, and trichoscopic features of AGA in 133 pediatric patients with AGA who visited the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University (Nanjing, China), from January 2010 to December 2023.

Methods

Study Population—Pediatric patients with early-onset AGA who were registered for outpatient consultations at the hair disease clinic of the Department of Dermatology at The First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were included. Patients aged 18 years and younger with a definitive diagnosis of AGA were selected for data collection and analysis. Any uncertain information was confirmed through telephone follow-up with patients.

Collection of Demographic Information and Laboratory Tests—Patient demographics and medical history including age, sex, age at disease onset, and duration of AGA were collected from the electronic medical record. Height and weight also were collected to calculate patients’ body mass index (BMI). Detailed laboratory test results were recorded, including assessments of sex hormone—binding globulin (SHBG), vitamin D, testosterone, and ferritin.

Analysis of Comorbidities—Due to the influence of genetic factors on body composition, there are differences in how obesity is defined across racial populations. The World Health Organization international standard defines the term overweight as a BMI greater than 25 and obese as a BMI greater than 30; however, the World Health Organization recommends a lower definition standard for these classifications in the Chinese population. China established specific BMI standards for classification of patients as overweight (24.0.27.9 kg/m²) and obese (≥28 kg/m²).¹¹ During outpatient consultations, a comprehensive medical history was obtained from each patient, including the presence of PCOS, acne, seborrheic dermatitis, hirsutism, and sleeping disorders. During routine outpatient assessments, experienced dermatologists (including W.F.) determined the presence of symptoms and confirmed the diagnosis.

Hair Loss Classification and Trichoscopy—Hair loss patterns for male patients were assessed using the basic and specific classification system, while the Ludwig scale was utilized for female patients.^12,13 Trichoscopy was utilized with high-resolution imaging systems and advanced software for image analysis, enabling precise assessment of hair in different scalp regions. Parameters such as hair density, hair diameter, percentage of terminal hairs, and percentage of vellus hair were recorded to monitor changes in hair growth for the patients.

Statistical Analysis—Categorical data were analyzed using the x² test. A P value less than .05 was considered statistically significant. All statistical analyses were conducted using SPSS software version 26 (IBM).

Results

Patient Characteristics and Hair Loss Patterns—A sample of 133 pediatric patients (60 males, 73 females) who were diagnosed with AGA at the hair disease clinic of the Department of Dermatology at the First Affiliated Hospital of Nanjing Medical University from January 2010 to December 2023 were selected. The mean age of the patients was 15.5 years (range, 10–18 years). The mean age was slightly lower in females compared with males (15.05 vs 16.19 years, respectively). Additionally, females showed earlier onset of the disease, with a mean age at onset of 13.41 years compared to 14.44 years in males. The time between onset of AGA symptoms and first seeking medical care ranged from 4 months to 3 years, with a mean disease duration of 1.72 years. There was no significant difference in the duration of disease between males and females (1.76 and 1.70 years, respectively). Patient characteristics by age group are summarized in eTable 1.

The pediatric patients in our study exhibited hair loss patterns similar to those typically observed in adults. Male patients typically showed diffuse thinning on the crown and varying degrees of temporal thinning, while female patients demonstrated diffuse thinning on the crown with a preserved frontal hairline; however, 5 (8.3%) male patients presented with Christmas tree– like pattern of hair loss with a preserved hairline and a thinning crown (Figures 1 and 2).

BMI and Comorbidities—Among our study sample, 27.1% (36/133) of patients were identified as overweight or obese. It came to our attention that the prevalence of patients who were overweight and obese was notably higher in patients aged older than 14 but younger than 18 years compared with those aged 14 years or younger (24.1% vs 3.0% [32/133 vs 4/133]). A more detailed analysis of patients who were overweight and obese is outlined in eTable 2.

Seborrheic dermatitis was identified as the most prevalent comorbidity associated with pediatric AGA (51.9% [69/133]), followed by acne (42.8% [57/133]), hirsutism (33.1% [44/133]), and sleep disturbances/insomnia (28.6% [38/133]). The prevalence of these comorbidities varied by age group, with a higher incidence observed among patients aged older than 14 years as compared to those aged 14 years or younger.

Family History of AGA—Our study results indicated that most (78.2% [104/133]) patients had a family history of AGA. Among males and females, 81.7% and 75.3% (49/60 and 55/73) had a positive family history, respectively. Further analysis showed that 43.3% (26/60) of males and 21.9% (16/73) of females reported AGA in their father, while 16.7% (10/60) of males and 35.6% insert (26/73) of females reported AGA in their mother. Both parents were affected in 21.7% (13/60) of male patients and 17.8% (13/73) of female patients (eTable 3).

Related Laboratory Tests of Pediatric Patients With AGA—The results of laboratory testing for vitamin D deficiency, low SHBG, high testosterone, and low ferritin levels in the study sample are outlined in eTable 4. Among the study participants, 15.9% (10/63) of females exhibited increased levels of both free and total testosterone. Low SHBG was observed in 47.1% (56/119) of patients, with a slightly higher proportion in males (48.2% [27/56] than females (46.0% [29/63]). Vitamin D deficiency was prevalent in 60.5% (72/119) of the study population, with a higher incidence rate in females (71.4%[45/63]) compared to males (48.2%[27/56]). Moreover, 21.8% (26/119) of pediatric patients had low ferritin levels, with a higher incidence rate in females (33.3%[21/63]) compared to males (8.9%[5/56]).

Female Patients With PCOS—In our study, 6 (8.2%) female patients with AGA had been diagnosed with PCOS prior to their referral to the First Affiliated Hospital of Nanjing Medical University. Information regarding their age at treatment, hair loss grade, comorbidities, and laboratory test results is provided in eTable 5.

Degree of Hair Loss at First Visit—In male pediatric patients with AGA, the majority were classified as M type according to the basic and specific classification. Specifically, the main hairloss level in males was concentrated in M1 and M2 (80.0% [48/60]), while specific type F was mainly distributed in F1 and F2 (81.7% [49/60]), and specific type V was mainly distributed in V1 and V2 (80.0% [48/60]). On the other hand, female patients were mainly (87.7% [64/73]) classified as type I or II in the Ludwig scale.

Clinical Features of Trichoscopy Examinations at First Visit—We present the trichoscopic findings of our study regarding hair characteristics, including hair density, hair diameter, terminal hair ratio, and vellus hair ratio, among male and female pediatric participants stratified into 2 age groups: 14 years or younger, and older than 14 but younger than 18 years. In males, those aged 14 years or younger had a lower average hair density than those older than 14 years but thicker hair diameter. Conversely, males aged 14 years and older were more likely to seek treatment of hair loss than those aged 14 years or younger. Among females, those older than 14 years had higher hair density, hair diameter, and terminal hair ratio than those younger than 14 years. Hair trichoscopy characteristics among pediatric patients with AGA in our study population were similar to those of adults with AGA (Figure 3).

Efficacy and Adverse Effects of Topical Minoxidil—There were 56 (42.1%) patients who had used topical minoxidil for more than 6 months: 33 (58.9%) males and 23 (41.1%) females. In terms of efficacy, 51 (91.1%) patients responded positively, demonstrating improved scalp coverage, increased hair density, or greater hair diameter. There were 2 (3.6%) cases of minor adverse reactions: 1 case of scalp itching with increased dandruff that improved with local symptomatic treatment, and 1 case of hirsutism, which improved after discontinuing the drug. Among the 28 (50.0%) pediatric patients who used topical minoxidil for more than 12 months, there were no reported adverse reactions. Overall, topical minoxidil was effective and well tolerated in pediatric patients, with mild adverse reactions.

Comment

In our study, the youngest AGA patient was 10 years old, which is slightly older than a 6-year-old patient reported in the literature.¹⁴ Females showed a higher incidence of AGA compared to males, which is consistent with some previous studies^14,15 but contradicts the findings of Gonzalez et al¹⁶ and Kim et al.¹⁷ We speculate that the differences in AGA incidence could be attributed to the diverse genetic background and racial disparities between the populations included in the study by Gonzalez et al¹⁶—primarily White patients from Europe and the United States—and our study, which included individuals from East Asia. Furthermore, variations in lifestyle and environment in Europe and the United States vs Asia (eg, dietary habits, stress, environmental pollution) may contribute to the differing sexspecific incidence rates. Additionally, our study showed that female patients tended to experience AGA at a younger age than male patients, as indicated by younger age of disease onset and at the initial visit. These findings are consistent with other studies reporting a slightly younger age of disease onset in female patients.^14,16,17 The importance lies in raising awareness among both patients and physicians about early-onset AGA, facilitating earlier detection, diagnosis, and treatment. Furthermore, our study revealed a higher prevalence of a positive family history of AGA in our study population (78.2%) compared to other studies.¹⁴ Paternal family history was more commonly observed than maternal history (81.7% and 75.3%, respectively); moreover, 19.5% of patients reported a positive family history of AGA in both parents. Therefore, it is essential to raise awareness among pediatric patients with a positive family history of AGA, as they may experience hair loss at a younger age.

Patients with AGA commonly present with concurrent skin conditions, most notably acne, seborrheic dermatitis, and hirsutism. Therefore, it is important to monitor these associated diseases and adopt appropriate treatments. Moreover, it is worth mentioning that a considerable number of pediatric patients reported experiencing sleep difficulties. It is well known that sleep disturbances can lead to hormonal abnormalities, which are also a risk factor for AGA.^18-20 Therefore, further research is needed to investigate whether treating sleep disturbances can delay onset or progression of pediatric AGA. A previous retrospective study reported a PCOS prevalence of 47.4% (9/19) in adolescent females with AGA,¹⁶ but our study observed a much lower incidence of 4.5%. This discrepancy may be due to the fact that diagnostic imaging was not required for all female patients suspected of having PCOS in our study, which may have resulted in the exclusion of some undiagnosed PCOS cases from the data analysis.

In our study, a considerable proportion of patients exhibited moderate hair loss at their first visit, and there were differences in hair density and diameter among different age groups, with female patients having finer hair than male patients. Therefore, it is necessary to raise awareness of and perform early diagnosis and treatment of AGA in pediatric patients presenting with hair loss. Upon evaluation of laboratory results, we observed a notable proportion of pediatric patients with AGA who had low levels of vitamin D, SHBG, and ferritin. Notably, female patients were more susceptible to low vitamin D levels compared with males. Screening for these indicators, particularly in female patients, could aid in the diagnosis and treatment of pediatric AGA. Surprisingly, testosterone levels did not show a significant increase in male patients with AGA. Furthermore, only a small percentage of female patients exhibited elevated testosterone levels, indicating that androgens may not play a dominant role in the pathogenesis of male pediatric AGA and that other factors and mechanisms may be involved. Although AGA has been extensively studied in adults, there is limited knowledge about its occurrence and characteristics in children and adolescents. Our study represents one of the few investigations into AGA in this population and is among the largest to explore the clinical features, laboratory testing and results, trichoscopic characteristics, and comorbidities in Chinese pediatric patients with AGA. Our findings offer valuable insights into early clinical characteristics of pediatric AGA in this specific demographic population to inform future research directions and clinical practice guidelines.

Given that we conducted a retrospective study with a relatively small sample size from a single clinic site, the generalizability of our research findings may be limited. In addition, the patients included in our study did not have frequent routine testing for metabolic and hormonal indicators to analyze further correlations between hormonal changes with severity of pediatric AGA. Future research with prospective multicenter designs and larger sample sizes are needed to increase representativeness and generalizability, and comprehensive testing is needed to validate and extend our findings. Furthermore, the psychological impact among pediatric patients with AGA warrants further investigation on early intervention to reduce psychological stress.

Besides enhancing the understanding of AGA in children and adolescents among dermatologists and pediatricians, there is a need for individualized, step-by-step, and comprehensive treatment. Initial assessment generally includes addressing hormonal disorders such as seborrheic dermatitis, folliculitis, PCOS, and acne. Some adult treatments may be effective in pediatric cases. In one study of 15 pediatric patients using minoxidil 5% daily (6 females, 4 males), 4 (66.7%) females had stable alopecia (follow-up, >6 months); 4 (44.4%) males using minoxidil 5% daily and 1 mg finasteride and 5 (55.6%) taking 1 mg of finasteride alone showed hair density gains.¹⁶ In another study,²¹ 373 adolescents with AGA (286 boys, 87 girls; age range, 10–17 years) were treated with topical minoxidil solution over an 18-month period, with 95.0% responding positively: 54.0% showed improved scalp coverage, and 41.0% experienced slower hair thinning. Topical minoxidil generally is well tolerated in pediatric patients with no significant impact on blood pressure, pulse rate, or other vital signs.²¹ The primary adverse reactions to topical minoxidil observed in clinical practice are mild scalp irritation and increased facial hair, which usually resolve upon discontinuation.²² In China, topical minoxidil (available in 2% or 5% concentrations) commonly is used in children and adolescents, with adjustments made based on treatment response and adverse effects. Despite its proven efficacy and tolerability, it is essential that adverse effects be promptly communicated to health care providers for appropriate dosage adjustments, and that concurrent conditions, such as vitamin D and iron deficiencies, be adequately managed. Encouraging patients to adhere to prescribed medications and undergo long-term follow-up typically results in favorable outcomes.