Bullous pemphigoid possibly induced by psoralen plus ultraviolet A therapy

A 65-year-old woman had a history of deep vein thrombosis and depression. Psoriasis was diagnosed in 1986 and various topical and systemic therapies, singly or in combination, were prescribed: tar, topical corticosteroids, cyclosporine, etretinate, and methotrexate. Two courses of oral and one course of bath psoralen plus UVA (PUVA) therapy (cumulative dose, 467 J/cm(2)) and UVB (2.96 J/cm(2)) had been given. In January 1999, she developed a flare of generalized psoriasis. In May 1999, therapy with PUVA (8-methoxypsoralen) plus topical acetonide triamcinolone 0.1% was initiated. At the time, she was taking acenocoumarol, lorazepam, and hydroxyzine chlorhydrate. In August 1999, at session 30, when the dose of UVA was 9 J/cm(2), and the total dose was 205 J/cm(2), a bulla appeared on the dorsum of the toe and was controlled with topical antibiotics. Five further sessions of PUVA were given and a generalized itching bullous eruption appeared all over the body. PUVA was stopped and the patient was hospitalized. On physical examination, extensive psoriatic plaques plus vesicles and bullae on the normal skin and on psoriatic lesions were observed all over the body (Fig. 1). Histopathologic study of a lesion showed a subepidermal vesicle containing fibrin, neutrophils, and a few eosinophils. No sunburn cells were observed (Fig. 2). The direct immunofluorescence (DIF) test of perilesional uninvolved skin revealed immunoglobulin G (IgG) (Fig. 3) and C3 at the dermal-epidermal junction. The DIF study using the patient's skin, previously treated with 1 m NaCl, localized the IgG at both the epidermal and dermal sides of the basement membrane zone (Fig. 4). Bullous pemphigoid (BP) was diagnosed and therapy with prednisone (60 mg/day) was started. The disease was well controlled in 3 weeks. The dose of prednisone was tapered and stopped 20 months later, without any recurrence. Study of the antibodies by the indirect immunofluorescence (IIF) test, using monkey esophagus and guinea pig as substrate, was positive at a titer of 1/160 in September 1999. The titer decreased to 1/10 in January 2000, and was negative in July 2000. An enzyme-linked immunosorbent assay (ELISA) test, performed using the commercial kit MBL, which identifies antibodies directed against epitopes of the extracellular fragment NC16 of antigen 2 of BP, was positive at 15 U/mL (normal value, < 9 U/mL) in September 1999, and negative in July 2000 (Table 1).

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“…BP has been previously reported in psoriatic patients 2–5 . Furthermore, psoralen plus UVA (PUVA) therapy may trigger the development of BP 6–13 …”

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confidence: 99%

Bullous pemphigoid in a patient with psoriasis during the course of PUVA therapy: study by ELISA test

Barnadas¹,

Gilaberte²,

Pujol³

et al. 2006

Int J Dermatology

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“…Medications, 2 ultraviolet A and B phototherapy, 3 trauma, surgery, and radiotherapy 4 have been reported as potential triggering factors of BP. We report here a case of BP in an elderly patient that developed after PDT.…”

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confidence: 99%

Categorization of and comments on isomorphic and isotopic skin reactions

Caccavale

Kannangara²,

Ruocco

2017

Clinics in Dermatology

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“…Psoralen ultraviolet A (PUVA) can induce blister formation acrally and in areas with friction or trauma . While this is generally distinct from BP, these blisters represent the initial manifestation of BP in some patients, and are thus considered PUVA‐induced BP …”

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confidence: 99%