Immunologic mechanism of selective anaphylaxis to aceclofenac

초록

The pathogenic mechanism of cyclooxygenase(COX)-1 inhibition in NSAIDs hypersensitivity results in multiple cross-reactive intolerance to aspirin and NSAIDs. However, selective reaction to single NSAID resembling type I hypersensitivity has been sporadically reported. Aceclofenac and diclofenac are widely used NSAID derivative of phenylacetic acid. Selective hypersensitivity reaction to aceclofenac has been rarely reported, and there is no report about cross-reactivity between aceclofenac and diclofenac. This study was performed to investigate pathogenic mechanism of selective anaphylactic reaction to aceclofenac, and to evaluate cross-reactivity between aceclofenac and diclofenac. Three female patients with aceclofenac-induced anaphylaxis were enrolled. All 3 patients had definite history of anaphylactic shock to aceclofenac, and two patients also had episode of anaphylaxis to diclofenac. However, all were tolerable to aspirin or other NSAIDs. Skin test with aceclofenac, diclofenac, aspirin and other NSAIDs were performed. One patient showed positive response to aceclofenac and diclofenac both in prick and intradermal tests. Another patient showed positive intradermal response to aceclofenac and diclofenac, but the other patient showed negative skin reactivity to all test drugs. Oral provocation test with aspirin and other NSAIDs showed no specific response in all patients, even though the challenge tests with aceclofenac or diclofenac could not be performed because of the risk. To detect serum-specific IgE, we prepared aceclofenac- and diclofenac-human serum albumin (HSA) conjugates respectively. ELISA result showed high level of specific IgE to aceclofenac- and diclofenac-HSA conjugates in sera from 2 patients with positive skin response to the drug. ELISA inhibition tests showed significant inhibitions of specific IgE responses with additions of aceclofenac- and diclofenac-HSA conjugate in dose-dependent manners in these two sera. In conclusion, we demonstr