P11: Phytophotodermatitis-induced bullous pemphigoid

A. Uthayakumar, M.-C. Wilmot, N. Anjum and L. Fearfield

Chelsea and Westminster Hospital, London, UK

A 68-year-old man was referred with a 6-week history of a blistering eruption on both feet, occurring within a long-standing area of vitiligo. He had applied a paste of ground figs to the patches of vitiligo on the feet and shins, and spent time barefoot outdoors on a sunny day. Within a few hours he developed erythema and pain in the patches of vitiligo on both feet, with blistering on the right forefoot. This was initially managed conservatively. After 4 weeks, he developed more blisters on the right foot extending proximally and affecting the left foot. He had a past medical history of hypertension and gastritis and took amlodipine (which was longstanding), and lansoprazole, which had been changed from omeprazole 4 weeks previously. Examination revealed healing erosions from deroofed blisters on both feet, occurring within depigmented patches of vitiligo, and two intact bullae on the right foot. A diagnostic biopsy from an intact blister showed a subepidermal blister with adjacent epidermal spongiosis, a dermal lymphohistiocytic infiltrate with eosinophilia. Direct immunofluorescence showed linear IgG and C3 along the basement membrane zone (BMZ). Indirect immunofluorescence showed anti-BMZ antibodies, which localized to the roof on salt-split-skin substrate. This led to a diagnosis of bullous pemphigoid (BP) induced by a phytophotodermatitis to fig paste. A 4-week course of topical clobetasol propionate ointment and oral doxycycline led to complete resolution. BP is a common autoimmune blistering condition characterized by autoantibodies predominantly to hemidesmosomal components of BP180 and BP230. The majority of cases are idiopathic; however, physical agents, including thermal burns, can induce BP. There is no current consensus on the pathogenic mechanism; however, one suggested mechanism is of burn-induced tissue destruction, subsequent activation of an inflammatory process and release of hemidesmosomal antigens leading to autoreactivity. Other proposed mechanisms are (i) increased vascular permeability due to local tissue damage and subsequent granulocyte activation by pre-existing low-titre autoantibodies; (ii) basement membrane modification by tissue damage and stimulation of autoantibody formation; and (iii) UV-impaired T-cell reactivity leading to autoantibody production. There are no cases of phytophotodermatitis-induced BP in the literature to date, and we propose a similar mechanism to burn-induced BP.