Co‐localization of alopecia areata and lichen planopilaris in a patient receiving immunosuppressants: A rare case

Background AA is an acquired dermatosis distributed universally, with multifactorial etiology. It affects the hair follicle with or without nail involvement, resulting in an acute nonscarring alopecia with a relapsing course.1 Being a relatively common skin disease, LPP (lichen planopilaris) is initiated by a chronic lymphocytic inflammation that selectively destructs the hair follicles and eventually leads to scarring alopecia. Also, even though there is enough literature available for the co‐existence of AA and LPP with each other and their association with other autoimmune conditions, there are only very few reports on the anatomical concomitance of both disorders.3 Aims Although the incidence of not only one but two autoimmune diseases in an immunosuppressed individual is very unusual, we hereby report a case of co‐localization of AA and LPP in a patient receiving immunosuppression due to a previous history of SLE (Systemic lupus erythematosus). Patients A 37‐year‐old woman, housewife, presented to our office with general alopecia on the scalp since about two years ago (Figure 1), particularly on the vertex which was accompanied by mild itching and trichodynia. She had a history of hypothyroidism and lupus erythematosus arthritis. She had been receiving long‐term treatment with prednisolone, hydroxychloroquine, azathioprine, and levothyroxine but had not been treated for hair loss. Despite being on all of the above‐mentioned immunosuppressants, the patient developed AA and LPP which are both immune‐mediated diseases. Results In addition to continuing her oral immunosuppressants, the patient was treated with Minoxidil 5% and Clobetasol solution as well as a higher dose of Azathioprine than she was receiving beforehand. Approximately, 3 months into the treatment, the follicular hyperkeratosis and scalp erythema resolved. Also, hair growth could be seen on AA spots. Conclusion Our case report is indicating the possibly mutual immunopathogenesis of these two T cell–mediated disorders. Furthermore, we want to bring attention to the probability of new autoimmune diseases occurring even during treatment with immunosuppressive medications.