Bullous pemphigoid associated with scabies: coincidence or causality?

Abstract

Bullous pemphigoid (BP) is the most common autoimmune blistering disease, predominantly occurring in the 6th decade of life. The pathogenesis of the disease involves a dysregulated immune response of T lymphocytes, the synthesis of IgG and IgE autoantibodies against hemidesmosomal proteins (BP180 and BP230), and neutrophil chemotaxis, ultimately leading to the degradation of the epidermal basement membrane. Triggering factors include medications, trauma, neurological pathologies, tumors, and skin infections. Clinical cases of the association of BP with human scabies are described in the literature. Data indicate a higher incidence of BP in patients with a history of scabies compared to those who have not suffered this skin infestation. The objective was to examine and document the association between Bullous pemphigoid and Sarcoptes scabiei infection, to identify a possible causal relationship in the triggering of the autoimmune skin disease. Materials and Methods We present a clinical case study. Case report A 73-year-old man presented with bullous lesions on an erythematous background, disseminated on the trunk and limbs, with the diameter of the bullae ranging from 1 to 5 cm, accompanied by moderate, intermittent pruritus. From the anamnesis: three weeks before the appearance of the bullous lesions, the patient was diagnosed with scabies, confirmed by direct microscopic examination, and treated with topical sulfur ointment 33%. Examination of the content of the bullae revealed 25% eosinophils, with no acantholytic cells. Serological examination for Anti-BP180 antibodies was highly positive (226 U/ml), and anti-epidermal basement membrane antibodies were weakly positive. The diagnosis of BP was established, and treatment was initiated with prednisolone tablets at 0.7 mg/kg/day, with gradual dose reduction. The skin lesions were treated with topical antiseptics. By the 5th day of treatment, the first signs of regression of the lesions were observed, with subsequent epithelialization. After 4 weeks, most of the lesions had reepithelialized, with some secondary hyperpigmented macules. Discussion The particularity of this BP case lies in the presence of cutaneous Sarcoptes scabiei infection in the anamnesis. Retrospective studies of scabies in the history of patients with bullous pemphigoid are encouraged to certify the presence of a causal relationship. As the incidence of BP is increasing, studying the triggering factors is of clinical interest. Conclusions BP is a disease with a complex pathogenesis involving altered immune reactivity and triggering factors. Cutaneous infestation with Sarcoptes scabiei could be a triggering factor for the onset of bullous pemphigoid.