BH12 Granulomatous alopecia areata

Abstract

A 46-year-old woman with Fitzpatrick skin type V presented with sudden-onset accelerated diffuse hair loss. Her other relevant medical history included Graves disease. Trichoscopy showed black dots, broken hairs with exclamation mark-like hairs and yellow dots. She was provisionally diagnosed with diffuse alopecia areata (AA). Laboratory work-up, including complete blood count, liver/renal parameters, antinuclear antibody and complement screen did not reveal any abnormality. Thyroid function and adjusted calcium level were all within the normal range. She had slight iron, folate and vitamin D deficiencies, which were treated with the appropriate supplements. A biopsy was taken from the scalp, and histological examination showed a nonscarring process with miniaturization, significant telogen shift and peribulbar granulomatous inflammation. Subsequent syphilis serology was negative, and serum angiotensin-converting enzyme was within normal limits. No clinical features of sarcoidosis or syphilis were observed. After careful clinicopathological correlation, she was diagnosed with granulomatous AA. We planned to treat her with diphencyprone; however, her hair grew back spontaneously after 2 months. AA is a nonscarring hair loss that can commonly affect the scalp and beard, as well as any hair-bearing surface on the body. It is a T-cell-mediated disease with characteristic histological features, including peribulbar lymphocytic inflammation with or without eosinophils, follicular miniaturization and an increase in catagen/telogen hairs. Peribulbar granulomatous inflammation is a rare histopathological finding in AA. In the context of alopecia, other conditions associated with histopathological granulomatous findings include sarcoidosis, syphilis and various forms of inflammatory and cicatrizing alopecia. To our knowledge, only five other cases of granulomatous AA have been reported. Notably, we describe the first case from the UK and only the second case internationally to show spontaneous resolution, suggesting that the prognosis of granulomatous AA is not dissimilar to histologically typical AA. To summarize, we have described a clinically typical AA with atypical histopathological findings. Granulomatous inflammation should not preclude a diagnosis of AA. This demonstrates the importance of clinicopathological correlation as the histopathology of alopecia could potentially be misleading.