Francisco Colon-Fontanez, MD

Tumor necrosis factor α (TNF-α) inhibitor–induced psoriasis is a known paradoxical adverse effect of this family of medications, which includes infliximab, adalimumab, etanercept, golimumab, and certolizumab. In the pediatric population, these therapies recently gained approval for nondermatologic conditions—meaning that this phenomenon is encountered more frequently.¹ In a systematic review of TNF-α inhibitor–induced psoriasis, severe scalp involvement was associated with alopecia in 7.5% of cases.² Onset of scalp psoriasis with alopecia in patients being treated with a TNF-α inhibitor should lead to consideration of this condition.

Psoriatic alopecia is an uncommon presentation of psoriasis. Although well described, alopecia as a clinical manifestation of scalp psoriasis is not a well-known concept among clinicians and has never been widely accepted. Adding to the diagnostic challenge is that psoriatic alopecia secondary to TNF-α inhibitor–induced psoriasis rarely has been reported in adults or children.^3-5 Including our case, our review of the literature yielded 7 pediatric cases (≤18 years) of TNF-α inhibitor–induced psoriatic alopecia.^6,7 A primary literature search of PubMed articles indexed for MEDLINE was conducted using the terms psoriatic alopecia, psoriasiform alopecia, TNF-α inhibitors, infliximab, adalimumab, etanercept, golimumab, and certolizumab.

We present the case of a pediatric patient with psoriatic alopecia secondary to treatment with adalimumab for Crohn disease (CD). We also provide a review of reported cases of psoriatic alopecia induced by a TNF-α inhibitor in the literature.

Case Report

A 12-year-old girl presented to our dermatology clinic with erythematous scaly plaques on the trunk, scalp, arms, and legs of 2 months’ duration. The lesions involved approximately 15% of the body surface area. The patient’s medical history was remarkable for CD diagnosed 4 years prior to presentation of the skin lesions. She had been treated for the past 2 years with adalimumab 40 mg once every 2 weeks and azathioprine 100 mg once daily. Because her CD was poorly controlled, the dosage of adalimumab was increased to 40 mg once weekly 6 months prior to the current presentation.

Our diagnosis was TNF-α inhibitor-induced psoriasis secondary to treatment with adalimumab.

The patient was treated with mometasone lotion 0.1% for the scalp lesions and triamcinolone cream 0.1% for the body lesions. Because of the extent of the psoriasis, we recommended changing adalimumab to ustekinumab, which is approved for CD in adults but is off label in children.

At 1-month follow-up, after receiving the induction dose of ustekinumab, the patient presented with partial improvement of the skin lesions but had developed a large, alopecic, erythematous plaque with thick yellowish scales on the scalp (Figure 1). She also had a positive hair pull test. The presumptive initial diagnosis of the alopecic scalp lesion was tinea capitis, for which multiple potassium hydroxide preparations of scales were performed, all yielding negative results. In addition, histopathologic examination with hematoxylin and eosin staining was performed (Figures 2A and 2B). Sterile tissue cultures for bacteria, fungi, and acid-fast bacilli were obtained and showed no growth. Periodic acid–Schiff staining was negative for fungal structures.

A second biopsy showed a psoriasiform pattern, parakeratosis, and hypogranulosis, highly suggestive of psoriasis (Figure 2C and 2D). Based on those findings, a diagnosis of psoriatic alopecia was made. The mometasone was switched to clobetasol lotion 0.05%. The patient continued treatment with ustekinumab. At 6-month follow-up, her CD was well controlled and she showed hair regrowth in previously alopecic areas (Figure 3).

 

Comment

Psoriatic alopecia induced by a TNF-α inhibitor was first reported in 2007 in a 30-year-old woman with ankylosing spondylitis who was being treated with adalimumab.⁸ She had erythematous, scaly, alopecic plaques on the scalp and palmoplantar pustulosis. Findings on skin biopsy were compatible with psoriasis. The patient’s severe scalp psoriasis failed to respond to topical steroid treatment and adalimumab cessation. The extensive hair loss responded to cyclosporine 3 mg/kg daily.⁸

After conducting an extensive literature review, we found 26 cases of TNF-α–induced psoriatic alopecia, including the current case (Table).^6-16 The mean age at diagnosis was 27.8 years (SD, 13.6 years; range, 7–60 years). The female-to-male ratio was 3.3:1. The most common underlying condition for which TNF-α inhibitors were prescribed was CD (77% [20/26]). Psoriatic alopecia most commonly was reported secondary to treatment with infliximab (54% [14/26]), followed by adalimumab (42% [11/26]). Golimumab was the causative drug in 1 (4%) case. We did not find reports of etanercept or certolizumab having induced this manifestation. The onset of the scalp lesions occurred 2 to 46 months after starting treatment with the causative medication.

Laga et al¹⁷ reported that TNF-α inhibitor–induced psoriasis can have a variety of histopathologic findings, including typical findings of various stages of psoriasis, a lichenoid pattern mimicking remnants of lichen planus, and sterile pustular folliculitis. Our patient’s 2 scalp biopsies demonstrated results consistent with findings reported by Laga et al.¹⁷ In the first biopsy, findings were consistent with a dense neutrophilic infiltrate with negative sterile cultures and negative periodic acid–Schiff stain (sterile folliculitis), with crust and areas of parakeratosis. The second biopsy demonstrated psoriasiform hyperplasia, parakeratosis, and an absent granular layer, all typical features of psoriasis (Figure 2).

Including the current case, our review of the literature yielded 7 pediatric (ie, 0–18 years of age) cases of TNF-α inhibitor–induced psoriatic alopecia. Of the 6 previously reported pediatric cases, 5 occurred after administration of infliximab.^6,7

Similar to our case, TNF-α inhibitor–induced psoriatic alopecia was reported in a 7-year-old girl who was treated with adalimumab for juvenile idiopathic arthritis.⁶ Nine months after starting treatment, that patient presented with a tender, erythematous, eroded, and crusted alopecic plaque along with scaly plaques on the scalp. Adalimumab was discontinued, and cyclosporine and topical steroids were started. Cyclosporine was then discontinued due to partial resolution of the psoriasis; the patient was started on abatacept, with persistence of the psoriasis and alopecia. The patient was then started on oral methotrexate 12.5 mg once weekly with moderate improvement and mild to moderate exacerbations.

Tumor necrosis factor α inhibitor–induced psoriasis may occur as a result of a cytokine imbalance. A TNF-α blockade leads to upregulation of interferon α (IFN-α) and TNF-α production by plasmacytoid dendritic cells (pDCs), usually in genetically susceptible people.^6,7,9-15 The IFN-α induces maturation of myeloid dendritic cells (mDCs) responsible for increasing proinflammatory cytokines that contribute to psoriasis.¹¹ Generation of TNF-α by pDCs leads to mature or activated dendritic cells derived from pDCs through autocrine TNF-α production and paracrine IFN-α production from immature mDCs.⁹ Once pDCs mature, they are incapable of producing IFN-α; TNF-α then inhibits IFN-α production by inducing pDC maturation.¹¹ Overproduction of IFN-α during TNF-α inhibition induces expression of the chemokine receptor CXCR3 on T cells, which recruits T cells to the dermis. The T cells then produce TNF-α, causing psoriatic skin lesions.^10,11,13,14

Although TNF-α inhibitor–induced psoriatic alopecia is uncommon, the condition should be considered in female patients with underlying proinflammatory disease—CD in particular. Perman et al⁶ reported 5 cases of psoriatic alopecia in which 3 patients initially were treated with griseofulvin because of suspected tinea capitis.

Conditions with similar clinical findings should be ruled out before making a diagnosis of TNF-α inhibitor–induced psoriatic alopecia. Although clinicopathologic correlation is essential for making the diagnosis, it is possible that the histologic findings will not be specific for psoriasis.¹⁷ It is important to be aware of this condition in patients being treated with a TNF-α inhibitor as early as 2 months to 4 years or longer after starting treatment.

Previously reported cases have demonstrated various treatment options that yielded improvement or resolution of TNF-α inhibitor–induced psoriatic alopecia. These include either continuation or discontinuation of the TNF-α inhibitor combined with topical or intralesional steroids, methotrexate, or cyclosporine. Another option is to switch the TNF-α inhibitor to another biologic. Outcomes vary from patient to patient, making the physician’s clinical judgment crucial in deciding which treatment route to take. Our patient showed notable improvement when she was switched from adalimumab to ustekinumab as well as the combination of ustekinumab and clobetasol lotion 0.05%.

Conclusion

We recommend an individualized approach that provides patients with the safest and least invasive treatment option for TNF-α inhibitor–induced psoriatic alopecia. In most reported cases, the problem resolved with treatment, thereby classifying this form of alopecia as noncicatricial alopecia.

Tumor necrosis factor α (TNF-α) inhibitor–induced psoriasis is a known paradoxical adverse effect of this family of medications, which includes infliximab, adalimumab, etanercept, golimumab, and certolizumab. In the pediatric population, these therapies recently gained approval for nondermatologic conditions—meaning that this phenomenon is encountered more frequently.¹ In a systematic review of TNF-α inhibitor–induced psoriasis, severe scalp involvement was associated with alopecia in 7.5% of cases.² Onset of scalp psoriasis with alopecia in patients being treated with a TNF-α inhibitor should lead to consideration of this condition.

Psoriatic alopecia is an uncommon presentation of psoriasis. Although well described, alopecia as a clinical manifestation of scalp psoriasis is not a well-known concept among clinicians and has never been widely accepted. Adding to the diagnostic challenge is that psoriatic alopecia secondary to TNF-α inhibitor–induced psoriasis rarely has been reported in adults or children.^3-5 Including our case, our review of the literature yielded 7 pediatric cases (≤18 years) of TNF-α inhibitor–induced psoriatic alopecia.^6,7 A primary literature search of PubMed articles indexed for MEDLINE was conducted using the terms psoriatic alopecia, psoriasiform alopecia, TNF-α inhibitors, infliximab, adalimumab, etanercept, golimumab, and certolizumab.

We present the case of a pediatric patient with psoriatic alopecia secondary to treatment with adalimumab for Crohn disease (CD). We also provide a review of reported cases of psoriatic alopecia induced by a TNF-α inhibitor in the literature.

Case Report

A 12-year-old girl presented to our dermatology clinic with erythematous scaly plaques on the trunk, scalp, arms, and legs of 2 months’ duration. The lesions involved approximately 15% of the body surface area. The patient’s medical history was remarkable for CD diagnosed 4 years prior to presentation of the skin lesions. She had been treated for the past 2 years with adalimumab 40 mg once every 2 weeks and azathioprine 100 mg once daily. Because her CD was poorly controlled, the dosage of adalimumab was increased to 40 mg once weekly 6 months prior to the current presentation.

Our diagnosis was TNF-α inhibitor-induced psoriasis secondary to treatment with adalimumab.

The patient was treated with mometasone lotion 0.1% for the scalp lesions and triamcinolone cream 0.1% for the body lesions. Because of the extent of the psoriasis, we recommended changing adalimumab to ustekinumab, which is approved for CD in adults but is off label in children.

At 1-month follow-up, after receiving the induction dose of ustekinumab, the patient presented with partial improvement of the skin lesions but had developed a large, alopecic, erythematous plaque with thick yellowish scales on the scalp (Figure 1). She also had a positive hair pull test. The presumptive initial diagnosis of the alopecic scalp lesion was tinea capitis, for which multiple potassium hydroxide preparations of scales were performed, all yielding negative results. In addition, histopathologic examination with hematoxylin and eosin staining was performed (Figures 2A and 2B). Sterile tissue cultures for bacteria, fungi, and acid-fast bacilli were obtained and showed no growth. Periodic acid–Schiff staining was negative for fungal structures.

A second biopsy showed a psoriasiform pattern, parakeratosis, and hypogranulosis, highly suggestive of psoriasis (Figure 2C and 2D). Based on those findings, a diagnosis of psoriatic alopecia was made. The mometasone was switched to clobetasol lotion 0.05%. The patient continued treatment with ustekinumab. At 6-month follow-up, her CD was well controlled and she showed hair regrowth in previously alopecic areas (Figure 3).

 

Comment

Psoriatic alopecia induced by a TNF-α inhibitor was first reported in 2007 in a 30-year-old woman with ankylosing spondylitis who was being treated with adalimumab.⁸ She had erythematous, scaly, alopecic plaques on the scalp and palmoplantar pustulosis. Findings on skin biopsy were compatible with psoriasis. The patient’s severe scalp psoriasis failed to respond to topical steroid treatment and adalimumab cessation. The extensive hair loss responded to cyclosporine 3 mg/kg daily.⁸

After conducting an extensive literature review, we found 26 cases of TNF-α–induced psoriatic alopecia, including the current case (Table).^6-16 The mean age at diagnosis was 27.8 years (SD, 13.6 years; range, 7–60 years). The female-to-male ratio was 3.3:1. The most common underlying condition for which TNF-α inhibitors were prescribed was CD (77% [20/26]). Psoriatic alopecia most commonly was reported secondary to treatment with infliximab (54% [14/26]), followed by adalimumab (42% [11/26]). Golimumab was the causative drug in 1 (4%) case. We did not find reports of etanercept or certolizumab having induced this manifestation. The onset of the scalp lesions occurred 2 to 46 months after starting treatment with the causative medication.

Laga et al¹⁷ reported that TNF-α inhibitor–induced psoriasis can have a variety of histopathologic findings, including typical findings of various stages of psoriasis, a lichenoid pattern mimicking remnants of lichen planus, and sterile pustular folliculitis. Our patient’s 2 scalp biopsies demonstrated results consistent with findings reported by Laga et al.¹⁷ In the first biopsy, findings were consistent with a dense neutrophilic infiltrate with negative sterile cultures and negative periodic acid–Schiff stain (sterile folliculitis), with crust and areas of parakeratosis. The second biopsy demonstrated psoriasiform hyperplasia, parakeratosis, and an absent granular layer, all typical features of psoriasis (Figure 2).

Including the current case, our review of the literature yielded 7 pediatric (ie, 0–18 years of age) cases of TNF-α inhibitor–induced psoriatic alopecia. Of the 6 previously reported pediatric cases, 5 occurred after administration of infliximab.^6,7

Similar to our case, TNF-α inhibitor–induced psoriatic alopecia was reported in a 7-year-old girl who was treated with adalimumab for juvenile idiopathic arthritis.⁶ Nine months after starting treatment, that patient presented with a tender, erythematous, eroded, and crusted alopecic plaque along with scaly plaques on the scalp. Adalimumab was discontinued, and cyclosporine and topical steroids were started. Cyclosporine was then discontinued due to partial resolution of the psoriasis; the patient was started on abatacept, with persistence of the psoriasis and alopecia. The patient was then started on oral methotrexate 12.5 mg once weekly with moderate improvement and mild to moderate exacerbations.

Tumor necrosis factor α inhibitor–induced psoriasis may occur as a result of a cytokine imbalance. A TNF-α blockade leads to upregulation of interferon α (IFN-α) and TNF-α production by plasmacytoid dendritic cells (pDCs), usually in genetically susceptible people.^6,7,9-15 The IFN-α induces maturation of myeloid dendritic cells (mDCs) responsible for increasing proinflammatory cytokines that contribute to psoriasis.¹¹ Generation of TNF-α by pDCs leads to mature or activated dendritic cells derived from pDCs through autocrine TNF-α production and paracrine IFN-α production from immature mDCs.⁹ Once pDCs mature, they are incapable of producing IFN-α; TNF-α then inhibits IFN-α production by inducing pDC maturation.¹¹ Overproduction of IFN-α during TNF-α inhibition induces expression of the chemokine receptor CXCR3 on T cells, which recruits T cells to the dermis. The T cells then produce TNF-α, causing psoriatic skin lesions.^10,11,13,14

Although TNF-α inhibitor–induced psoriatic alopecia is uncommon, the condition should be considered in female patients with underlying proinflammatory disease—CD in particular. Perman et al⁶ reported 5 cases of psoriatic alopecia in which 3 patients initially were treated with griseofulvin because of suspected tinea capitis.

Conditions with similar clinical findings should be ruled out before making a diagnosis of TNF-α inhibitor–induced psoriatic alopecia. Although clinicopathologic correlation is essential for making the diagnosis, it is possible that the histologic findings will not be specific for psoriasis.¹⁷ It is important to be aware of this condition in patients being treated with a TNF-α inhibitor as early as 2 months to 4 years or longer after starting treatment.

Previously reported cases have demonstrated various treatment options that yielded improvement or resolution of TNF-α inhibitor–induced psoriatic alopecia. These include either continuation or discontinuation of the TNF-α inhibitor combined with topical or intralesional steroids, methotrexate, or cyclosporine. Another option is to switch the TNF-α inhibitor to another biologic. Outcomes vary from patient to patient, making the physician’s clinical judgment crucial in deciding which treatment route to take. Our patient showed notable improvement when she was switched from adalimumab to ustekinumab as well as the combination of ustekinumab and clobetasol lotion 0.05%.

Conclusion

We recommend an individualized approach that provides patients with the safest and least invasive treatment option for TNF-α inhibitor–induced psoriatic alopecia. In most reported cases, the problem resolved with treatment, thereby classifying this form of alopecia as noncicatricial alopecia.

Tumor necrosis factor α (TNF-α) inhibitor–induced psoriasis is a known paradoxical adverse effect of this family of medications, which includes infliximab, adalimumab, etanercept, golimumab, and certolizumab. In the pediatric population, these therapies recently gained approval for nondermatologic conditions—meaning that this phenomenon is encountered more frequently.¹ In a systematic review of TNF-α inhibitor–induced psoriasis, severe scalp involvement was associated with alopecia in 7.5% of cases.² Onset of scalp psoriasis with alopecia in patients being treated with a TNF-α inhibitor should lead to consideration of this condition.

Psoriatic alopecia is an uncommon presentation of psoriasis. Although well described, alopecia as a clinical manifestation of scalp psoriasis is not a well-known concept among clinicians and has never been widely accepted. Adding to the diagnostic challenge is that psoriatic alopecia secondary to TNF-α inhibitor–induced psoriasis rarely has been reported in adults or children.^3-5 Including our case, our review of the literature yielded 7 pediatric cases (≤18 years) of TNF-α inhibitor–induced psoriatic alopecia.^6,7 A primary literature search of PubMed articles indexed for MEDLINE was conducted using the terms psoriatic alopecia, psoriasiform alopecia, TNF-α inhibitors, infliximab, adalimumab, etanercept, golimumab, and certolizumab.

We present the case of a pediatric patient with psoriatic alopecia secondary to treatment with adalimumab for Crohn disease (CD). We also provide a review of reported cases of psoriatic alopecia induced by a TNF-α inhibitor in the literature.

Case Report

A 12-year-old girl presented to our dermatology clinic with erythematous scaly plaques on the trunk, scalp, arms, and legs of 2 months’ duration. The lesions involved approximately 15% of the body surface area. The patient’s medical history was remarkable for CD diagnosed 4 years prior to presentation of the skin lesions. She had been treated for the past 2 years with adalimumab 40 mg once every 2 weeks and azathioprine 100 mg once daily. Because her CD was poorly controlled, the dosage of adalimumab was increased to 40 mg once weekly 6 months prior to the current presentation.

Our diagnosis was TNF-α inhibitor-induced psoriasis secondary to treatment with adalimumab.

The patient was treated with mometasone lotion 0.1% for the scalp lesions and triamcinolone cream 0.1% for the body lesions. Because of the extent of the psoriasis, we recommended changing adalimumab to ustekinumab, which is approved for CD in adults but is off label in children.

At 1-month follow-up, after receiving the induction dose of ustekinumab, the patient presented with partial improvement of the skin lesions but had developed a large, alopecic, erythematous plaque with thick yellowish scales on the scalp (Figure 1). She also had a positive hair pull test. The presumptive initial diagnosis of the alopecic scalp lesion was tinea capitis, for which multiple potassium hydroxide preparations of scales were performed, all yielding negative results. In addition, histopathologic examination with hematoxylin and eosin staining was performed (Figures 2A and 2B). Sterile tissue cultures for bacteria, fungi, and acid-fast bacilli were obtained and showed no growth. Periodic acid–Schiff staining was negative for fungal structures.

A second biopsy showed a psoriasiform pattern, parakeratosis, and hypogranulosis, highly suggestive of psoriasis (Figure 2C and 2D). Based on those findings, a diagnosis of psoriatic alopecia was made. The mometasone was switched to clobetasol lotion 0.05%. The patient continued treatment with ustekinumab. At 6-month follow-up, her CD was well controlled and she showed hair regrowth in previously alopecic areas (Figure 3).

 

Comment

Psoriatic alopecia induced by a TNF-α inhibitor was first reported in 2007 in a 30-year-old woman with ankylosing spondylitis who was being treated with adalimumab.⁸ She had erythematous, scaly, alopecic plaques on the scalp and palmoplantar pustulosis. Findings on skin biopsy were compatible with psoriasis. The patient’s severe scalp psoriasis failed to respond to topical steroid treatment and adalimumab cessation. The extensive hair loss responded to cyclosporine 3 mg/kg daily.⁸

After conducting an extensive literature review, we found 26 cases of TNF-α–induced psoriatic alopecia, including the current case (Table).^6-16 The mean age at diagnosis was 27.8 years (SD, 13.6 years; range, 7–60 years). The female-to-male ratio was 3.3:1. The most common underlying condition for which TNF-α inhibitors were prescribed was CD (77% [20/26]). Psoriatic alopecia most commonly was reported secondary to treatment with infliximab (54% [14/26]), followed by adalimumab (42% [11/26]). Golimumab was the causative drug in 1 (4%) case. We did not find reports of etanercept or certolizumab having induced this manifestation. The onset of the scalp lesions occurred 2 to 46 months after starting treatment with the causative medication.

Laga et al¹⁷ reported that TNF-α inhibitor–induced psoriasis can have a variety of histopathologic findings, including typical findings of various stages of psoriasis, a lichenoid pattern mimicking remnants of lichen planus, and sterile pustular folliculitis. Our patient’s 2 scalp biopsies demonstrated results consistent with findings reported by Laga et al.¹⁷ In the first biopsy, findings were consistent with a dense neutrophilic infiltrate with negative sterile cultures and negative periodic acid–Schiff stain (sterile folliculitis), with crust and areas of parakeratosis. The second biopsy demonstrated psoriasiform hyperplasia, parakeratosis, and an absent granular layer, all typical features of psoriasis (Figure 2).

Including the current case, our review of the literature yielded 7 pediatric (ie, 0–18 years of age) cases of TNF-α inhibitor–induced psoriatic alopecia. Of the 6 previously reported pediatric cases, 5 occurred after administration of infliximab.^6,7

Similar to our case, TNF-α inhibitor–induced psoriatic alopecia was reported in a 7-year-old girl who was treated with adalimumab for juvenile idiopathic arthritis.⁶ Nine months after starting treatment, that patient presented with a tender, erythematous, eroded, and crusted alopecic plaque along with scaly plaques on the scalp. Adalimumab was discontinued, and cyclosporine and topical steroids were started. Cyclosporine was then discontinued due to partial resolution of the psoriasis; the patient was started on abatacept, with persistence of the psoriasis and alopecia. The patient was then started on oral methotrexate 12.5 mg once weekly with moderate improvement and mild to moderate exacerbations.

Tumor necrosis factor α inhibitor–induced psoriasis may occur as a result of a cytokine imbalance. A TNF-α blockade leads to upregulation of interferon α (IFN-α) and TNF-α production by plasmacytoid dendritic cells (pDCs), usually in genetically susceptible people.^6,7,9-15 The IFN-α induces maturation of myeloid dendritic cells (mDCs) responsible for increasing proinflammatory cytokines that contribute to psoriasis.¹¹ Generation of TNF-α by pDCs leads to mature or activated dendritic cells derived from pDCs through autocrine TNF-α production and paracrine IFN-α production from immature mDCs.⁹ Once pDCs mature, they are incapable of producing IFN-α; TNF-α then inhibits IFN-α production by inducing pDC maturation.¹¹ Overproduction of IFN-α during TNF-α inhibition induces expression of the chemokine receptor CXCR3 on T cells, which recruits T cells to the dermis. The T cells then produce TNF-α, causing psoriatic skin lesions.^10,11,13,14

Although TNF-α inhibitor–induced psoriatic alopecia is uncommon, the condition should be considered in female patients with underlying proinflammatory disease—CD in particular. Perman et al⁶ reported 5 cases of psoriatic alopecia in which 3 patients initially were treated with griseofulvin because of suspected tinea capitis.

Conditions with similar clinical findings should be ruled out before making a diagnosis of TNF-α inhibitor–induced psoriatic alopecia. Although clinicopathologic correlation is essential for making the diagnosis, it is possible that the histologic findings will not be specific for psoriasis.¹⁷ It is important to be aware of this condition in patients being treated with a TNF-α inhibitor as early as 2 months to 4 years or longer after starting treatment.

Previously reported cases have demonstrated various treatment options that yielded improvement or resolution of TNF-α inhibitor–induced psoriatic alopecia. These include either continuation or discontinuation of the TNF-α inhibitor combined with topical or intralesional steroids, methotrexate, or cyclosporine. Another option is to switch the TNF-α inhibitor to another biologic. Outcomes vary from patient to patient, making the physician’s clinical judgment crucial in deciding which treatment route to take. Our patient showed notable improvement when she was switched from adalimumab to ustekinumab as well as the combination of ustekinumab and clobetasol lotion 0.05%.

Conclusion

We recommend an individualized approach that provides patients with the safest and least invasive treatment option for TNF-α inhibitor–induced psoriatic alopecia. In most reported cases, the problem resolved with treatment, thereby classifying this form of alopecia as noncicatricial alopecia.

To the Editor:

Erosive lichen planus (LP) often is painful, debilitating, and resistant to topical therapy making it both a diagnostic and therapeutic challenge. We report the case of an elderly woman with isolated perianal erosive LP, a rare clinical manifestation. We also review cases of erosive perianal LP reported in the literature.

A 72-year-old woman was referred to our dermatology clinic for evaluation of multiple pruritic and painful perianal lesions of 1 year’s duration. The lesions had remained stable since onset, with no other reported lesions elsewhere on body, including the mucosae. Her medical history was notable for rheumatoid arthritis, osteoporosis, hypercholesterolemia, and hypertension. She was taking methotrexate, folic acid, abatacept, alendronate, atorvastatin, and lisinopril. The patient reported she had been using abatacept for 3 years and lisinopril for 2 years. Her primary care physician initially treated the lesions as hemorrhoids but referred her to a gastroenterologist when they failed to improve. Gastroenterology evaluated the patient, and a colonoscopy was performed with unremarkable results. Thus, she was referred to dermatology for further evaluation.

Physical examination revealed 2 tender, sharply defined, angulated erosions with irregular violaceous borders involving the perianal skin (Figure 1). A biopsy of one of the lesions was taken. Histopathologic examination revealed acanthosis of the epidermis with slight compact hyperkeratosis, scattered dyskeratotic keratinocytes, and a dense bandlike lymphohistiocytic infiltrate that obliterated the dermoepidermal junction (Figure 2). A diagnosis of perianal erosive LP was made. The patient was prescribed mometasone ointment 0.1% daily with notable improvement after 2 months.

Erosive LP is an extremely rare variant of LP.¹ It typically manifests as chronic painful erosions that often can progress to scarring, ulceration, and tissue destruction. Although erosive LP most commonly involves the mucosal surfaces of the genitalia and oral mucosa, it also has been reported in the palmoplantar skin, lacrimal duct, external auditory meatus, and esophagus.^2-7 However, isolated perianal involvement is extremely rare. A PubMed search of articles indexed for MEDLINE using the terms erosive or ulcerative and lichen planus and perianal revealed 10 cases of perianal erosive LP, and weak data exist regarding therapy (Table).^8-12 Of these cases, only 3 reported isolated perianal involvement.^8-10 In most reported cases, perianal involvement manifested as extremely painful and occasionally pruritic, sharply angulated erosions and ulcers arising 0.5 to 3 cm from the anus with macerated, whitish, and violaceous borders. Most of the lesions occurred unilaterally, with only 1 case of bilateral perianal involvement.¹⁰

The differential diagnosis of perianal erosions is extensive and includes cutaneous Crohn disease, extramammary Paget disease, cutaneous malignancy, herpes simplex virus, cytomegalovirus, external hemorrhoids, lichen sclerosus, Behçet disease, lichen simplex chronicus, and drug-induced lichenoid reaction, among others. It is worth emphasizing infectious processes and cutaneous malignancies in light of our patient’s immunosuppression. Perianal cytomegalovirus has been reported in the literature in association with HIV, and it is a clinically challenging diagnosis.¹³ Cutaneous malignancy associated with the use of methotrexate also was considered in the differential diagnosis for our patient, given the increased risk for nonmelanoma skin cancer with the use of immunosuppresants.¹⁴

Along with a thorough patient history and physical examination, skin biopsy and clinicopathologic correlation are key to determine the exact etiology. Histologically, LP is characterized by a lichenoid interface dermatitis with a dense bandlike lymphohistiocytic infiltrate at the dermoepidermal junction. Other distinguishing factors include irregular acanthosis, hyperkeratosis, basal cell vacuolar degeneration, and Civatte bodies. Drug-induced LP is a possibility, but it is unclear if abatacept or lisinopril may have played a role in our patient. However, absence of eosinophils and parakeratosis suggested an idiopathic rather than drug-induced etiology. In 2016, Day et al² published a clinicopathologic review of 60 cases of perianal lichenoid dermatoses in which only 17% of lesions were LP. Of note, 90% of perianal LP lesions were of the hypertrophic variant, and none were of the erosive variant, further supporting that our case represents a rare clinical manifestation of perianal LP.

Treatment of LP varies depending on the location and subtype of the lesions and is primarily aimed at improving symptoms. Topical corticosteroids are the standard treatment of LP; however, there is limited evidence regarding their efficacy for mucosal LP. Although randomized controlled trials assessing the efficacy of different interventions on oral erosive LP are available in the literature,¹⁵ there is a paucity of studies addressing this topic for genital or perianal LP. A review of the literature regarding perianal erosive LP suggests good response to high-potency topical steroids and calcineurin inhibitors with resolution of lesions within 3 to 4 weeks.^11,15-18

Erosive LP is a painful variant that can cause erosions, ulcerations, and scarring. It rarely is seen in the perianal region alone and presents a diagnostic challenge. Treatment with high-potency topical steroid therapy seems to be effective in the few cases that have been reported as well as in our case. More comprehensive data from randomized controlled trials would be needed to evaluate their efficacy compared to other therapies.

To the Editor:

Erosive lichen planus (LP) often is painful, debilitating, and resistant to topical therapy making it both a diagnostic and therapeutic challenge. We report the case of an elderly woman with isolated perianal erosive LP, a rare clinical manifestation. We also review cases of erosive perianal LP reported in the literature.

A 72-year-old woman was referred to our dermatology clinic for evaluation of multiple pruritic and painful perianal lesions of 1 year’s duration. The lesions had remained stable since onset, with no other reported lesions elsewhere on body, including the mucosae. Her medical history was notable for rheumatoid arthritis, osteoporosis, hypercholesterolemia, and hypertension. She was taking methotrexate, folic acid, abatacept, alendronate, atorvastatin, and lisinopril. The patient reported she had been using abatacept for 3 years and lisinopril for 2 years. Her primary care physician initially treated the lesions as hemorrhoids but referred her to a gastroenterologist when they failed to improve. Gastroenterology evaluated the patient, and a colonoscopy was performed with unremarkable results. Thus, she was referred to dermatology for further evaluation.

Physical examination revealed 2 tender, sharply defined, angulated erosions with irregular violaceous borders involving the perianal skin (Figure 1). A biopsy of one of the lesions was taken. Histopathologic examination revealed acanthosis of the epidermis with slight compact hyperkeratosis, scattered dyskeratotic keratinocytes, and a dense bandlike lymphohistiocytic infiltrate that obliterated the dermoepidermal junction (Figure 2). A diagnosis of perianal erosive LP was made. The patient was prescribed mometasone ointment 0.1% daily with notable improvement after 2 months.

Erosive LP is an extremely rare variant of LP.¹ It typically manifests as chronic painful erosions that often can progress to scarring, ulceration, and tissue destruction. Although erosive LP most commonly involves the mucosal surfaces of the genitalia and oral mucosa, it also has been reported in the palmoplantar skin, lacrimal duct, external auditory meatus, and esophagus.^2-7 However, isolated perianal involvement is extremely rare. A PubMed search of articles indexed for MEDLINE using the terms erosive or ulcerative and lichen planus and perianal revealed 10 cases of perianal erosive LP, and weak data exist regarding therapy (Table).^8-12 Of these cases, only 3 reported isolated perianal involvement.^8-10 In most reported cases, perianal involvement manifested as extremely painful and occasionally pruritic, sharply angulated erosions and ulcers arising 0.5 to 3 cm from the anus with macerated, whitish, and violaceous borders. Most of the lesions occurred unilaterally, with only 1 case of bilateral perianal involvement.¹⁰

The differential diagnosis of perianal erosions is extensive and includes cutaneous Crohn disease, extramammary Paget disease, cutaneous malignancy, herpes simplex virus, cytomegalovirus, external hemorrhoids, lichen sclerosus, Behçet disease, lichen simplex chronicus, and drug-induced lichenoid reaction, among others. It is worth emphasizing infectious processes and cutaneous malignancies in light of our patient’s immunosuppression. Perianal cytomegalovirus has been reported in the literature in association with HIV, and it is a clinically challenging diagnosis.¹³ Cutaneous malignancy associated with the use of methotrexate also was considered in the differential diagnosis for our patient, given the increased risk for nonmelanoma skin cancer with the use of immunosuppresants.¹⁴

Along with a thorough patient history and physical examination, skin biopsy and clinicopathologic correlation are key to determine the exact etiology. Histologically, LP is characterized by a lichenoid interface dermatitis with a dense bandlike lymphohistiocytic infiltrate at the dermoepidermal junction. Other distinguishing factors include irregular acanthosis, hyperkeratosis, basal cell vacuolar degeneration, and Civatte bodies. Drug-induced LP is a possibility, but it is unclear if abatacept or lisinopril may have played a role in our patient. However, absence of eosinophils and parakeratosis suggested an idiopathic rather than drug-induced etiology. In 2016, Day et al² published a clinicopathologic review of 60 cases of perianal lichenoid dermatoses in which only 17% of lesions were LP. Of note, 90% of perianal LP lesions were of the hypertrophic variant, and none were of the erosive variant, further supporting that our case represents a rare clinical manifestation of perianal LP.

Treatment of LP varies depending on the location and subtype of the lesions and is primarily aimed at improving symptoms. Topical corticosteroids are the standard treatment of LP; however, there is limited evidence regarding their efficacy for mucosal LP. Although randomized controlled trials assessing the efficacy of different interventions on oral erosive LP are available in the literature,¹⁵ there is a paucity of studies addressing this topic for genital or perianal LP. A review of the literature regarding perianal erosive LP suggests good response to high-potency topical steroids and calcineurin inhibitors with resolution of lesions within 3 to 4 weeks.^11,15-18

Erosive LP is a painful variant that can cause erosions, ulcerations, and scarring. It rarely is seen in the perianal region alone and presents a diagnostic challenge. Treatment with high-potency topical steroid therapy seems to be effective in the few cases that have been reported as well as in our case. More comprehensive data from randomized controlled trials would be needed to evaluate their efficacy compared to other therapies.

To the Editor:

Erosive lichen planus (LP) often is painful, debilitating, and resistant to topical therapy making it both a diagnostic and therapeutic challenge. We report the case of an elderly woman with isolated perianal erosive LP, a rare clinical manifestation. We also review cases of erosive perianal LP reported in the literature.

A 72-year-old woman was referred to our dermatology clinic for evaluation of multiple pruritic and painful perianal lesions of 1 year’s duration. The lesions had remained stable since onset, with no other reported lesions elsewhere on body, including the mucosae. Her medical history was notable for rheumatoid arthritis, osteoporosis, hypercholesterolemia, and hypertension. She was taking methotrexate, folic acid, abatacept, alendronate, atorvastatin, and lisinopril. The patient reported she had been using abatacept for 3 years and lisinopril for 2 years. Her primary care physician initially treated the lesions as hemorrhoids but referred her to a gastroenterologist when they failed to improve. Gastroenterology evaluated the patient, and a colonoscopy was performed with unremarkable results. Thus, she was referred to dermatology for further evaluation.

Physical examination revealed 2 tender, sharply defined, angulated erosions with irregular violaceous borders involving the perianal skin (Figure 1). A biopsy of one of the lesions was taken. Histopathologic examination revealed acanthosis of the epidermis with slight compact hyperkeratosis, scattered dyskeratotic keratinocytes, and a dense bandlike lymphohistiocytic infiltrate that obliterated the dermoepidermal junction (Figure 2). A diagnosis of perianal erosive LP was made. The patient was prescribed mometasone ointment 0.1% daily with notable improvement after 2 months.

Erosive LP is an extremely rare variant of LP.¹ It typically manifests as chronic painful erosions that often can progress to scarring, ulceration, and tissue destruction. Although erosive LP most commonly involves the mucosal surfaces of the genitalia and oral mucosa, it also has been reported in the palmoplantar skin, lacrimal duct, external auditory meatus, and esophagus.^2-7 However, isolated perianal involvement is extremely rare. A PubMed search of articles indexed for MEDLINE using the terms erosive or ulcerative and lichen planus and perianal revealed 10 cases of perianal erosive LP, and weak data exist regarding therapy (Table).^8-12 Of these cases, only 3 reported isolated perianal involvement.^8-10 In most reported cases, perianal involvement manifested as extremely painful and occasionally pruritic, sharply angulated erosions and ulcers arising 0.5 to 3 cm from the anus with macerated, whitish, and violaceous borders. Most of the lesions occurred unilaterally, with only 1 case of bilateral perianal involvement.¹⁰

The differential diagnosis of perianal erosions is extensive and includes cutaneous Crohn disease, extramammary Paget disease, cutaneous malignancy, herpes simplex virus, cytomegalovirus, external hemorrhoids, lichen sclerosus, Behçet disease, lichen simplex chronicus, and drug-induced lichenoid reaction, among others. It is worth emphasizing infectious processes and cutaneous malignancies in light of our patient’s immunosuppression. Perianal cytomegalovirus has been reported in the literature in association with HIV, and it is a clinically challenging diagnosis.¹³ Cutaneous malignancy associated with the use of methotrexate also was considered in the differential diagnosis for our patient, given the increased risk for nonmelanoma skin cancer with the use of immunosuppresants.¹⁴

Along with a thorough patient history and physical examination, skin biopsy and clinicopathologic correlation are key to determine the exact etiology. Histologically, LP is characterized by a lichenoid interface dermatitis with a dense bandlike lymphohistiocytic infiltrate at the dermoepidermal junction. Other distinguishing factors include irregular acanthosis, hyperkeratosis, basal cell vacuolar degeneration, and Civatte bodies. Drug-induced LP is a possibility, but it is unclear if abatacept or lisinopril may have played a role in our patient. However, absence of eosinophils and parakeratosis suggested an idiopathic rather than drug-induced etiology. In 2016, Day et al² published a clinicopathologic review of 60 cases of perianal lichenoid dermatoses in which only 17% of lesions were LP. Of note, 90% of perianal LP lesions were of the hypertrophic variant, and none were of the erosive variant, further supporting that our case represents a rare clinical manifestation of perianal LP.

Treatment of LP varies depending on the location and subtype of the lesions and is primarily aimed at improving symptoms. Topical corticosteroids are the standard treatment of LP; however, there is limited evidence regarding their efficacy for mucosal LP. Although randomized controlled trials assessing the efficacy of different interventions on oral erosive LP are available in the literature,¹⁵ there is a paucity of studies addressing this topic for genital or perianal LP. A review of the literature regarding perianal erosive LP suggests good response to high-potency topical steroids and calcineurin inhibitors with resolution of lesions within 3 to 4 weeks.^11,15-18

Erosive LP is a painful variant that can cause erosions, ulcerations, and scarring. It rarely is seen in the perianal region alone and presents a diagnostic challenge. Treatment with high-potency topical steroid therapy seems to be effective in the few cases that have been reported as well as in our case. More comprehensive data from randomized controlled trials would be needed to evaluate their efficacy compared to other therapies.