Bullous pemphigoid occurring during efalizumab treatment for psoriasis: a paradoxical auto-immune reaction?

ELISA test (titer: 99 and 112 units, respectively). A side effect of efalizumab was suspected, and this medication was discontinued. The search for other auto-immune complications proved negative with absence of antinuclear antibodies, rheumatoid factor, other haematological disturbances and a negative Coombs’ test. The patient was initially treated with highly potent topical steroids (clobetasol dipropionate 40 g/day) with a poor clinical result on BP lesions and subsequently with systemic steroids with a significant improvement. Steroids were then rapidly tapered and eventually discontinued after 3 weeks, and methotrexate was introduced with an initial dosage of 12.5 mg/week. Psoriasis did not worsen after efalizumab discontinuation, even during systemic steroid treatment. Auto-immune phenomena represent serious, although infrequent, side effects of efalizumab therapy whereas unusual skin adverse effects have recently been reported [5, 6] . The main targets are the haematological cell lines and more specifically the platelets since immune-mediated thrombocytopenia has been oberved in 0.3% of patients [1] . However, other lineages can be affected and auto-immune hemolytic anemia [1, 2] or pancytopenia [3] have also been reported in 5 and 1 patients respectively during efalizumab treatment, whereas direct toxicity was probably the primary mechanism in another case of pancytopenia [7] . A lupuslike syndrome was finally observed in a patient with hepatitis, polyarthralgia, asthenia, pericarditis and presence of circulating antinuclear antibodies, with rapid resolution after discontinuation of the drug [4] . In all those cases, adverse effects appeared between 4 weeks and 6 months of treatment. The occurrence of auto-immunity during an immunomodulating therapy blocking T-cell activation is paradoxical and might be related to the disruption of immune balance rather than a specific drug-induced pathway requiring a simultaneous binding of the drug to the target molecule. It is of interest to underscore that such paradoxical phenomena have already been reported with other biotherapies of psorasis, the TNFblockers that can both treat and induce lupus syndrome and psoriasis. The coexistence of psoriasis vulgaris and auto-immune bullous diseases has already been described in the literature mainly with BP, and about 40 cases of BP have been reported in patients with psoriasis [8] . Moreover, the prevalence of psoriasis in patients with BP seems significantly higher than expected. However, this association remains relatively rare when compared to the frequency of both affections, and the pathogenic relationship between psoriasis and BP is unclear. It has been postulated that the auto-immune process responsible for BP lesions may be induced by ultraviolet light therapy or topical corticosteroids; the inflammation that occurs in psoriasis may also result in changes in the basement membrane zone possibly triggering the development of an auto-reactive antibody response. In our patient, BP appeared after an interval of time comparable with the delay observed in other efalizumab-induced auto