Methotrexate pharmacogenetics in rheumatoid arthritis: a status report

被引：12

作者：

Malik, Fardina ^{[1
]}

Ranganathan, Prabha ^{[2
]}

机构：

[1] Alton Mem Hosp, Alton, IL 62002 USA

[2] Washington Univ, Sch Med, Dept Internal Med, Div Rheumatol, St Louis, MO 63110 USA

来源：

PHARMACOGENOMICS | 2013年 / 14卷 / 03期

关键词：

arthritis; methotrexate; pharmacogenetics; polymorphism; rheumatoid; METHYLENETETRAHYDROFOLATE REDUCTASE GENE; SINGLE-NUCLEOTIDE POLYMORPHISMS; REDUCED FOLATE CARRIER; C677T POLYMORPHISM; THYMIDYLATE-SYNTHASE; JAPANESE PATIENTS; RISK-FACTOR; MTHFR GENE; TOXICITY; EFFICACY;

D O I：

10.2217/PGS.12.214

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Methotrexate (MIX), an antifolate drug, is the first-line disease-modifying agent for the treatment of rheumatoid arthritis (RA) worldwide. MTX has excellent long-term efficacy, tolerability and safety. Early initiation of MTX in patients with RA controls joint destruction and slows progression of disease. However, the clinical response to MTX and frequency of adverse effects from the drug exhibit marked interpatient variability. Over the past decade, there has been a quest to identify genetic markers that reliably predict MTX efficacy and toxicity and help optimize MIX therapy in RA; that is, the field of MIX pharmacogenetics. This review will summarize key pharmacogenetic studies examining SNPs in the genes encoding enzymes in the MIX cellular pathway and their association with MIX response in RA. As evident from this review, MIX pharmacogenetics in RA remains a muddled field, mostly due to inconsistent results from several small underpowered studies.

引用

页码：305 / 314

页数：10

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