CD21: Probable ‘baboon syndrome’ triggered by hormone replacement therapy

Abstract

CD21 Probable ‘baboon syndrome’ triggered by hormone replacement therapy M. Stanciu, A. Hollywood, O. McFeely, L. Paul and M. O’Connell University Hospital Waterford, Waterford, Ireland A 50-year-old postmenopausal female was referred to dermatology from general surgeon colleagues with a 3-year history of atypical recurrent buttock cellulitis. The patient presented with severe, well-demarcated erythema of the buttocks, natal cleft and lower back. There was associated pruritis and severe pain, resulting in difficulty sitting upright. A mildly elevated white cell count (11 9 10 cells L) and neutrophil count (8 81 9 10 cells L), and high C-reactive protein (105 7 mg L) were observed on her initial medical admission. Blood cultures and wound swabs were negative. No pyrexia was identified. She was treated with intravenous or oral antibiotics every 2 months, over the course of the 3 years, requiring four hospital admissions and multiple general practitioner visits. Investigations prior to her referral to dermatology included magnetic resonance imaging of the pelvis, ultrasound of buttocks, colonoscopy with terminal ileum biopsy and random colonic biopsy, and the resection of two benign perianal polyps. No underlying cause was identified. On presentation to dermatology, clinical history and clinical photographs were suggestive of a symmetrical drug-related intertriginous and flexural exanthema (SDRIFE). A thorough drug history revealed that hormone replacement therapy (HRT) had been started in the month prior to the onset of the rash. The patient was trialled off HRT, with no recurrence of the rash over 4 months. She was then rechallenged with HRT and the rash recurred after 3 weeks. She is now 8 months postcessation of HRT and is in complete remission. SDRIFE represents an erythematous flexural reaction to systemic drugs. Over 50 causative medications are known, but antibiotics are the most common trigger. Latency is usually hours to days and it can occur regardless of prior exposure to the drug. It typically presents as pruritic, erythematous papules, which coalesce to produce a symmetrical, well-demarcated erythema on the buttocks. It can also present as a V-shaped erythema of the lower abdomen, groins and thighs. The gold standard for diagnosing SDRIFE is through withdrawal of the suspected drug followed by a rechallenge, which was demonstrated in our case. To our knowledge, this is the first case reported in the literature of SDRIFE caused by HRT. CD22 A perplexing recurrent exfoliative eruption in a child E. Rudd, E. Williamson and A. Tewari King’s College Hospital NHS Foundation Trust, London, UK A 6-year-old boy with a past medical history of atopic dermatitis presented 6 months ago with fever and a flexural exanthem that started around the neck and extended to affect the armpits and groin. It progressed to a superficial widespread skin peeling and he was treated for a presumed diagnosis of staphylococcal-scalded skin syndrome with oral flucloxacillin, topical emollients and Dermol 500 to wash with. The rash resolved within 2 weeks. He was asked to continue with the Dermol 500 and emollients. However, 4 weeks later he returned with flexural erythema and then exfoliation affecting the whole body, leaving normal skin. This resulted in significant psychological distress and, after a further 6 weeks, the same episode reoccurred. Presumed infective in origin, with likely superficial acantholysis causing the clinical presentation, his antiseptic wash was switched to Hibiscrub (4% chlorhexidine). Skin biopsy revealed a spongiotic dermatitis. Swabs, blood profile, cultures and echocardiogram were normal. He re-presented to dermatology with anterior neck erythema and early signs of skin desquamation around the armpits. He was discussed at a regional dermatology meeting and a diagnosis of chlorhexidine-induced dermatitis was raised. The patient’s mother was advised to stop Hibiscrub and switch to Hydromol ointment to wash and moisturize with. Three months later the patient has not re-presented to our clinic and on direct questioning has not had a further eruption. Chlorhexidine cleaves bacterial cell walls, resulting in rapid bacterial cell death (https://www.chlorhexidinefacts.com/mechanism-of-ac tion.html). We suspect that in our patient’s case it was probably causing cleavage of the stratum corneum, resulting in a widespread exfoliative dermatitis. This has been a diagnosis of exclusion; no infective source for the skin presentation was identified. In addition, cessation of use resulted in rapid and complete improvement. Cutaneous contact allergy to chlorhexidine is well described in the literature (Magdaleno-Tapial J, Mart ınez-Dom enech A, Valenzuela-O~ nate C et al. Allergic contact dermatitis to chlorhexidine in pediatric patients. Pediatr Dermatol 2019; 36: 540–1) but rarely reported in children (Toholka R, Nixon R. Allergic contact dermatitis to chlorhexidine. Australas J Dermatol 2013; 54: 303–6) and typically presents with an urticaria, a cellulitis-like eruption or eczema. We report a case of a paediatric patient presenting with an exfoliative dermatitis secondary to chlorhexidine use (Dermol 500 and Hibiscrub), with no further skin breakouts once the agent was stopped.