Development of a system, which can pre-avoid anti-platelet agents-induced severe hepatic disfunction that is difficult to predict

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We have developed a simple genotyping method to detect HLA-A^*3303, which appeared to be responsible for severe hepatic disfunction induced by ticlopidine. In this study, we have confirmed that another candidate gene polymorphism, which may be involved in ticlopidine-induced hepatotoxicity. We found that either or both HLA-A^*0206 and HLA-B^*3901 may be responsible for clopidogrel-induced hepatic disfunction in our preliminary studies. Thus, simple genotyping methods to detect these specific HLA alleles were developed. Then, we applied these genotyping methods to confirm whether either or both HLA alleles were truly related to the clopidogrel-induced hepatic disfunction in the second population. However, reproducible results were not obtained, possibly due to a small number of patients with clopidogrel-induced hepatic disfunction. It was suggested that different genetic factors may be involved in hepatic disfunction induced by ticlopidine and clopidogrel, although we have not identify the causal HLA allele responsible for clopidogrel-induced hepatic disfunction. These results indicate that ticlopidine and clopidogrel could be used safely as alternative drug each other.