Pharmacogenomics of severe cutaneous adverse reactions and drug-induced liver injury

被引:53
作者
Kaniwa, Nahoko [1 ]
Saito, Yoshiro [1 ]
机构
[1] Natl Inst Hlth Sci, Div Med Safety Sci, Tokyo 1588501, Japan
关键词
drug-induced liver injury; genome-wide association study; human leukocyte antigen; pharmacogenomics; severe cutaneous adverse reactions; STEVENS-JOHNSON-SYNDROME; TOXIC EPIDERMAL NECROLYSIS; CLASS-II GENOTYPE; HLA CLASS-I; HLA-B-ASTERISK-1502; ALLELE; ABACAVIR HYPERSENSITIVITY; JAPANESE PATIENTS; GENOME-WIDE; RISK-FACTOR; GENETIC SUSCEPTIBILITY;
D O I
10.1038/jhg.2013.37
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Rare but severe adverse drug reactions (ADRs) are an important issue in drug development and in the proper usage of drugs during the post-approval phase. The ability to predict patient susceptibility to severe ADRs would prevent drug administration to high-risk patients. This would save lives and ensure the quality of life for these patients, but occurrence of idiosyncratic severe ADRs had been very difficult to predict for a long time. However, in this decade, genetic markers have been found for several ADRs, especially for severe cutaneous adverse reactions (SCARs) and drug-induced liver injury (DILI). In this review, we summarize recent progress in identifying genetic markers for SCARS and DILI, and discuss issues that remain unresolved. As for SCARs, associations of HLA-B*15:02 or HLA-A*31:01 and HLA-B*58:01 have been revealed for carbamazepine- and allopurinol-related Stevens-Johnson syndrome and toxic epidermal neclolysis, respectively. HLA-B*57:01 is strongly associated with abacavir-induced hypersensitivity syndrome. Several HLA alleles also demonstrate drug-specific associations with DILI, such as HLA-A*33:03 for ticlopidine, HLA-B*57:01 for flucloxacillin and HLA-DQA1*02:01 for lapatinib. Efforts should be continued to find other genetic markers to achieve high predictability for ADRs, with the goal being development of genetic tests for use in clinical settings.
引用
收藏
页码:317 / 326
页数:10
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