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SLCO1A2 基因变异与人类类风湿关节炎治疗中甲氨蝶呤毒性的关联。

Association between SLCO1A2 genetic variation and methotrexate toxicity in human rheumatoid arthritis treatment.

机构信息

Department of Rheumatology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Department of Nephrology, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu, China.

出版信息

J Biochem Mol Toxicol. 2020 Aug;34(8):e22513. doi: 10.1002/jbt.22513. Epub 2020 Apr 18.

Abstract

Methotrexate (MTX), one of the important disease-modifying anti-rheumatic drugs, is the first-line drug for rheumatoid arthritis (RA) treatment. However, its adverse drug effects (ADEs) often lead to the abortion of MTX therapy. Human organic anion-transporting polypeptide 1A2 (OATP1A2, also referred as OATP-A or OATP1) encoded by SLCO1A2 gene is an important isoform of the solute carrier transporter (SLC) family. It is known to participate in the cellular uptake of MTX. In our previous study, we identified four OATP1A2 natural variants (E184K, D185N, T259P, and D288N) with impaired MTX uptake activity. This study aimed to evaluate the association of the SLCO1A2 genetic variations encoding these OATP1A2 variants and MTX-related toxicity in RA patients. A total of 60 RA patients were genotyped for these four polymorphisms (G550A, G553A, A775C, and G862A). The association between SLCO1A2 genetic variations and MTX toxicity was analyzed by binary logistic regression analysis. Single nucleotide polymorphisms (SNPs) analysis revealed that A775C and G862A SNPs were not detected in RA patients enrolled in this study, and the presence of 550AA genotype was associated with a high risk of MTX ADEs. Haplotype analysis revealed that H3 (H3 = AG) showed a high risk of MTX ADEs. Furthermore, there was a significant association of 550AA genotype and impaired MTX disposition, which might be the cause of the increased incidence of MTX ADEs in RA patients. Therefore, genetic variations in SLCO1A2 gene are risk factors for MTX toxicity and its information contributes to the prediction of MTX-related toxicity in RA treatment.

摘要

甲氨蝶呤(MTX)是一种重要的疾病修饰抗风湿药物,是类风湿关节炎(RA)治疗的一线药物。然而,其药物不良反应(ADEs)常导致 MTX 治疗中断。人有机阴离子转运多肽 1A2(OATP1A2,也称为 OATP-A 或 OATP1)由 SLCO1A2 基因编码,是溶质载体转运蛋白(SLC)家族的重要亚型。已知它参与 MTX 的细胞摄取。在我们之前的研究中,我们鉴定了四种 OATP1A2 天然变体(E184K、D185N、T259P 和 D288N),它们具有受损的 MTX 摄取活性。本研究旨在评估编码这些 OATP1A2 变体的 SLCO1A2 基因变异与 RA 患者 MTX 相关毒性的关系。共对 60 例 RA 患者进行了这四种多态性(G550A、G553A、A775C 和 G862A)的基因分型。采用二元逻辑回归分析方法分析 SLCO1A2 基因变异与 MTX 毒性的关系。单核苷酸多态性(SNP)分析显示,本研究纳入的 RA 患者未检测到 A775C 和 G862A SNP,550AA 基因型与 MTX ADE 风险增加相关。单体型分析显示 H3(H3=AG)具有较高的 MTX ADE 风险。此外,550AA 基因型与 MTX 处置受损显著相关,这可能是 RA 患者 MTX ADE 发生率增加的原因。因此,SLCO1A2 基因的遗传变异是 MTX 毒性的危险因素,其信息有助于预测 RA 治疗中 MTX 相关毒性。

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