DP03: Alopecia areata-like histopathology in lupus: follicular and stromal clues to diagnosis

Nikolina Lalagianni,¹ David A. Fenton,¹ Anoud Zidan^1,2 and Catherine M. Stefanato^1,2

¹St John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust, London, UK; and ²Department of Dermatopathology, St John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust, London, UK

Alopecia in systemic lupus erythematosus (SLE) may present with the chronic discoid scarring variant or the nonscarring pattern of diffuse telogen effluvium. A third patchy nonscarring pattern may occur, with clinical and histopathological features mimicking those of alopecia areata (AA). A peribulbar lymphoid cell infiltrate with a shift out of anagen similar to AA was observed in all cases; however, abundant deposition of acid mucopolysaccharide (mucin) in the deep dermis, a finding not seen in AA but characteristic of lupus, was present. A 43-year-old woman with type VI skin presented with a 1 year history of a solitary, coin-shaped asymptomatic patch of hair loss affecting the vertex of her scalp. Clinical examination revealed a discrete, round patch of hair loss with broken black hair in the centre. A subtle central atrophy and hyperpigmentation were noticeable, as was mild peripheral erythema. Histopathology showed increased numbers of telogen hair follicles, hair follicle miniaturization, peribulbar lymphoid cell infiltrate and pigment casts. Colloidal iron stain showed increases of mucin in the deep dermis and subcutis. The histological features were consistent with AA, but the presence of mucin raised a suspicion of SLE. This was clinically unsuspected. Blood tests subsequently revealed high titres of antinuclear antibodies. A 30-year-old systemically well man presented with asymptomatic patchy hair loss. The clinical suspicion was to rule out lupus. Horizontal sections of a 4-mm punch biopsy from the left posterior scalp showed nonscarring alopecia with active peribulbar lymphoid cell infiltrate, consistent with AA. However, colloidal iron stain revealed abundant deep dermal interstitial mucin, confirming the clinical suspicion of lupus. A 38-year-old woman with a history of systemic symptoms, lymphadenopathy and Raynaud phenomenon had a scalp biopsy with horizontal sections showing nonscarring alopecia with a ‘shift out of anagen’ with increased telogen hair follicles, peribulbar lymphoid cell infiltrate with nuclear dust, plasma cells and pigment casts. Abundant deep dermal mucin was confirmed by colloidal iron, consistent with the clinical impression of SLE. Assessment of interstitial dermal mucin in the setting of AA-like histopathology should be an integral part of histological examination, as it may unmask the diagnosis of lupus. Autoimmune screening is advisable in such cases as part of laboratory investigations.