Erlotinib binds to intracellular domain of the epidermal growth factor receptor (EGFR), causing several cutaneous and mucous membrane reactions. However no cases of erlotinib-induced bullous pemphigoid where previously reported. A 77-year-old man came to us with multiple pruritic annular lilac-reddish patches with peripheral vesicles and bullae, target-shaped erythematous plaques and erythematous small tense blisters on the trunk and limbs. He had been taking erlotinib (150 mg daily) for 1 month for metastatic lung adenocarcinoma. Laboratory analyses revealed eosinophilia and increased serum IgE levels. Skin biopsy showed subepidermal blister with many eosinophilic granulocytes. Direct immunofluorescence revealed linear and homogenous deposits of C3 along the basement membrane zone. Enzyme-linked immunosorbent assay identified serum antibodies to the NC16a protein of BP180. Erlotinib was withdrawn and the eruption resolved completely in 1 month. Two months later erlotinib was restarted (100 mg daily) because of cancer progression. After 4 days widespread blistering eruption with target-like lesions of the palms and soles appeared. The diagnosis of drug-induced bullous pemphigoid (DBP) from erlotinib was made. The drug was discontinued and oral prednisone (25 mg daily) was started. All of the lesions resolved in 2 months and no relapse over the 5-month follow-up was observed. The implicated pathogenic mechanism is not easy to postulate, but DBP may be explained by the EGFR expression with basal keratinocytes. The immunological findings rule out an altered hemidesmosome cohesion, as recommended for drugs releasing thiol groups. Therefore it is possible that erlotinib binds a protein in the lamina lucida, thus rendering it antigenic or induced ‘‘derepression’’ of CD8 suppressor/cytotoxic cells.

Erlotinib-induced bullous pemphigoid

STINGENI, LUCA
Conceptualization
;
BIANCHI, LEONARDO
Conceptualization
;
LISI, Paolo
2012

Abstract

Erlotinib binds to intracellular domain of the epidermal growth factor receptor (EGFR), causing several cutaneous and mucous membrane reactions. However no cases of erlotinib-induced bullous pemphigoid where previously reported. A 77-year-old man came to us with multiple pruritic annular lilac-reddish patches with peripheral vesicles and bullae, target-shaped erythematous plaques and erythematous small tense blisters on the trunk and limbs. He had been taking erlotinib (150 mg daily) for 1 month for metastatic lung adenocarcinoma. Laboratory analyses revealed eosinophilia and increased serum IgE levels. Skin biopsy showed subepidermal blister with many eosinophilic granulocytes. Direct immunofluorescence revealed linear and homogenous deposits of C3 along the basement membrane zone. Enzyme-linked immunosorbent assay identified serum antibodies to the NC16a protein of BP180. Erlotinib was withdrawn and the eruption resolved completely in 1 month. Two months later erlotinib was restarted (100 mg daily) because of cancer progression. After 4 days widespread blistering eruption with target-like lesions of the palms and soles appeared. The diagnosis of drug-induced bullous pemphigoid (DBP) from erlotinib was made. The drug was discontinued and oral prednisone (25 mg daily) was started. All of the lesions resolved in 2 months and no relapse over the 5-month follow-up was observed. The implicated pathogenic mechanism is not easy to postulate, but DBP may be explained by the EGFR expression with basal keratinocytes. The immunological findings rule out an altered hemidesmosome cohesion, as recommended for drugs releasing thiol groups. Therefore it is possible that erlotinib binds a protein in the lamina lucida, thus rendering it antigenic or induced ‘‘derepression’’ of CD8 suppressor/cytotoxic cells.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/1069270
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