Progress in research on correlation between allopurinol-induced severe cutaneous adverse reactions and HLA-B*58∶01 allele

Abstract

Allopurinol is an inhibitor of xanthine oxidase, which is used for the treatment of gout and hyperuricemia by inhibiting uric acid synthesis thereby reducing uric acid. Allopurinol can cause severe cutaneous adverse reactions (SCAR), including drug hypersensitivity syndrome, Stevens-Johnson syn-drome (SJS), and toxic epidermal necrolysis (TEN). The study on the correlation between HLA-B*58∶01 alleles and allopurinol-induced SCAR in different racial groups showed that there was a strong correlation between HLA-B*58∶01 alleles and allopurinol-induced SCAR in Taiwan, Hong Kong, and the mainland of China, as well as in Thailand, Korea with high frequency of HLA-B*58∶01, while there was also an significant correlation between them in Japan and Europe with low frequency of HLA-B*58∶01. Presently, there have been few studies on the specific mechanism of HLA-B*58∶01 alleles in the process of the allopurinol-induced SCAR. Representative research found that allopurinol and its metabolite oxypurinol directly and immediately activates the drug-specific T cells by bounding to HLA-B*58∶01 through the mechanism of pharmacological interaction with immune receptors, afterwards leading to SCAR. Key words: Stevens-Johnson syndrome; Epidermal necrolysis, toxic; Alleles; Allopurinol