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Aggravated crusted scabies: case report A 26-year-old woman experienced an aggravation of crusted scabies (CS) during treatment with risankizumab, betamethasone and clobetasol [duration of treatments to reaction onset not stated]. The woman with Down’s syndrome presented to the Emergency Department (ED) with a severe inflammatory and ichthyosiform dermatosis, which was affecting her face and extremities. She was under consultation with dermatologist for 2 years for psoriasislike lesions. Initially her hands developed various degrees of hyperkeratosis as well as pachyonychia on the nails. Afterwards, progressively hyperkeratotic ichthyosis-like lesions developed on the fingers and the limbs. The lesions were non-pruritic and there was no identifiable scratch lesions. She had never presented with any dermatological problems and had a completely normal skin in the past. Family history included longstanding history of psoriasis in mother. The clinical presentation and the genetic history suggested a diagnosis of psoriasis. She was initially treated with topical clobetasol 0.05% [clobetasol propionate] ointment once daily for several weeks, with no clinical improvement. She was then treated with topical betamethasone in combination with calcipotriol ointment once daily for several weeks. Even the last topical treatment did not improve the her lesions. Subsequently, it was decided to treat her with UVB-phototherapy while the use of topical steroids with creams containing 10% urea was also continued. There were still no clinical improvements. So, the topical dermocorticosteroids were discontinued and oral acitretin was administered for 8 weeks combined with a keratolytic cream. There was no clinical improvement of the lesions, and she was switched to a biotherapy. She was treated with two injections of risankizumab, administered with a 15-day interval between injections [route not stated]. In the weeks after the last injection, her skin condition progressively deteriorated. A new profuse crusted lesions developed on previously non-involved skin areas, and she again presented to ED. On admission, the entire tegument was hyperkeratotic with an ichtyosiform appearance. There was involvement of the scalp and the extension regions of the limbs. There were multiple painful skin fissures in the flexural region. No systemic signs, fever and lymphadenopathies were noted. A skin biopsy revealed an epidermal infiltration of a large number of Sarcoptes scabiei, suggesting a final diagnosis of CS. A blood test showed hyperleukocytosis with significant increase of neutrophils and a severe inflammatory syndrome with C-reactive protein at 124 mg/L, which was probably linked to a bacterial superinfection of the fissured lesions. Her mother and uncle who were living in the same house, also presented with signs of pruritic scabies infestation. Considering the severity of the dermatosis and the Down’s syndrome, she was hospitalised. The woman was started on anti-parasitic treatment scheme. A tube of permethrin cream was applied for a du