A 66-year-old man with a history of hypertension and diabetes was diagnosed with bullous pemphigoid (BP) at an outside hospital in March 2023. He subsequently received long-term systemic corticosteroid therapy, with initial control of his skin lesions. Dupilumab was later added as a corticosteroid-sparing agent. After the sixth dupilumab injection, he developed severe generalized pruritus accompanied by worsening erythematous and vesiculobullous lesions. When he presented to our hospital in November 2023, he was receiving prednisone at 30 mg/day, but his symptoms remained poorly controlled. Examination revealed confluent dusky erythematous patches on the trunk and proximal lower extremities, with diffuse thick hyperkeratotic scaling and adherent crusts, most prominent on the buttocks (Fig. 1A and 1B). Scaling was also noted in the interdigital web spaces (Fig. 1C). Light microscopy of skin scrapings from a crusted plaque confirmed Sarcoptes scabiei eggs and mites (Fig. 1D and 1E). Biopsy of truncal erythema showed subepidermal blistering with eosinophilic infiltrates; direct immunofluorescence revealed linear immunoglobulin G (IgG) and complement component 3 (C3) deposits at the dermal-epidermal junction. Peripheral eosinophilia was noted at 8% (reference range, 1%–6%). He was diagnosed with BP complicated by crusted scabies (CS). Oral ivermectin was not administered because it was not available at our hospital. The patient received oral tinidazole 1 g once daily for 1 week, in combination with topical 10% sulfur ointment applied to the entire body. Dupilumab was discontinued, whereas the prednisone dose at presentation, 30 mg/day, was not reduced because of concern about active BP. Within 1 week, pruritus completely resolved, crusting markedly regressed, and no new bullous lesions developed.
CS is a highly contagious form of scabies characterized by hyperinfestation with
Sarcoptes scabiei[
1,
2]. BP is an autoimmune subepidermal blistering disorder[
3]. CS may present atypically in immunosuppressed patients, with diffuse hyperkeratotic scaling, adherent crusts, erythema, erosions, or vesiculobullous lesions, while classic burrows may be absent or difficult to identify[
1,
4]. In patients with BP, these findings may be misinterpreted as disease relapse or treatment resistance[
5]. Previous case reports have described CS in a patient with BP following systemic glucocorticoid therapy and in patients with atopic dermatitis during dupilumab treatment[
6,
7]. Susceptibility to CS in BP is likely multifactorial, involving advanced age, barrier disruption, excoriations, type 2 inflammation, and corticosteroid-related impairment of cell-mediated immunity. Although dupilumab may theoretically alter host responses to mite infestation through interleukin 4 (IL-4)/interleukin 13 (IL-13) blockade, it is not generally regarded as a potent immunosuppressant; therefore, a causal relationship with CS should be interpreted cautiously[
1,
7]. Persistent pruritus, crusting, or interdigital scaling in immunosuppressed patients with BP should prompt evaluation for concomitant scabies infestation. Prompt mite eradication with appropriate antiscabetic treatment should be prioritized.
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