Pharmacogenomic Advances in the Prediction and Prevention of Cutaneous Idiosyncratic Drug Reactions

被引:35
作者
Pan, R-Y [1 ,2 ,3 ,4 ]
Dao, R-L [1 ]
Hung, S-I [4 ]
Chung, W-H [1 ,2 ,3 ,5 ,6 ,7 ]
机构
[1] Chang Gung Mem Hosp, Dept Dermatol, Drug Hypersensit Clin & Res Ctr, Taipei, Linkou, Taiwan
[2] Chang Gung Mem Hosp, Chang Gung Immunol Consortium, Taoyuan, Taiwan
[3] Chang Gung Univ, Taoyuan, Taiwan
[4] Natl Yang Ming Univ, Inst Pharmacol, Taipei, Taiwan
[5] Chang Gung Mem Hosp, Whole Genome Res Core Lab Human Dis, Keelung, Taiwan
[6] Xiamen Chang Gung Hosp, Dept Dermatol, Xiamen, Peoples R China
[7] Chang Gung Univ, Coll Med, Taoyuan, Taiwan
关键词
STEVENS-JOHNSON-SYNDROME; TOXIC EPIDERMAL NECROLYSIS; HLA CLASS-I; ADVERSE-REACTIONS; HLA-B-ASTERISK-1502; ALLELE; T-CELLS; HYPERSENSITIVITY REACTIONS; JAPANESE PATIENTS; INDUCED SKIN; RISK-FACTOR;
D O I
10.1002/cpt.683
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cutaneous idiosyncratic drug reactions (CIDRs) are usually unpredictable, ranging from mild maculopapular exanthema (MPE) to severe cutaneous adverse drug reactions (SCARs) such as drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). Increasing evidence suggests that HLA alleles are strongly associated with drug-induced-CIDRs. The pathomechanisms for CIDRs include genetic polymorphisms affecting complex immune-specific HLA/drug antigen/T-cell receptor interactions and drug metabolism. Pharmacogenomic tests to prevent CIDRs have been widely implemented in clinical practice in recent years.
引用
收藏
页码:86 / 97
页数:12
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