Department of Orthopedics, The Affiliated Changzhou No. 2 Hospital of Nanjing Medical University, Changzhou, Jiangsu Province, China.
Arch Med Res. 2011 Nov;42(8):698-702. doi: 10.1016/j.arcmed.2011.12.001. Epub 2011 Dec 30.
A single nucleotide polymorphism (SNP) of the protein tyrosine phosphatase nonreceptor gene (PTPN22) confers susceptibility to rheumatoid arthritis (RA) and certain other classical autoimmune diseases. The association between PTPN22 1858C/T polymorphism and the risk of RA is still controversial and ambiguous; therefore, we performed this meta-analysis to confirm some relationships.
We conducted a search in the PubMed database without a language limitation, covering all papers published until June 20, 2011. Overall, 19 case-control studies with 11,727 cases and 12,640 controls were retrieved based on the search criteria for RA susceptibility related to the 1858C/T polymorphism. Odds ratios (OR) and 95% confidence intervals (CI) were used to assess the strength of this association. Publication bias was assessed with Eggers test.
We found that PTPN22 1858C/T polymorphism could increase RA risk in overall genetic models in Europeans (T-allele vs. C-allele, OR = 1.54, 95% CI = 1.47-1.62, P(heterogeneity) = 0.143; TT vs. CC, OR = 2.86, 95% CI = 2.29-3.57, P(heterogeneity) = 0.302; TC vs. CC, OR = 1.45, 95% CI = 1.38-1.53, P(heterogeneity) = 0.273; TT + TC vs. CC, OR = 1.49, 95% CI = 1.42-1.56, P(heterogeneity) = 0.208; TT vs. TC + CC, OR = 2.52, 95% CI = 1.95-3.25, P(heterogeneity) = 0.296). Furthermore, significant relationships were detected among PTPN22 1858C/T polymorphism and RF(+) or RF(-) RA risk. No obvious evidence of publication bias was detected in the overall analysis.
Our study indicated that PTPN22 1858T allele was significantly associated with increased RA risk.
蛋白酪氨酸磷酸酶非受体基因(PTPN22)的单核苷酸多态性(SNP)可导致类风湿关节炎(RA)和某些其他经典自身免疫性疾病的易感性。PTPN22 1858C/T 多态性与 RA 风险之间的关联仍存在争议和不明确;因此,我们进行了这项荟萃分析以确认一些关系。
我们在 PubMed 数据库中进行了无语言限制的搜索,涵盖了截至 2011 年 6 月 20 日发表的所有论文。根据与 1858C/T 多态性相关的 RA 易感性搜索标准,共检索到 19 项病例对照研究,包括 11727 例病例和 12640 例对照。使用比值比(OR)和 95%置信区间(CI)来评估这种关联的强度。使用 Eggers 检验评估发表偏倚。
我们发现,在欧洲人群的总体遗传模型中,PTPN22 1858C/T 多态性可增加 RA 风险(T 等位基因与 C 等位基因相比,OR=1.54,95%CI=1.47-1.62,P(异质性)=0.143;TT 与 CC 相比,OR=2.86,95%CI=2.29-3.57,P(异质性)=0.302;TC 与 CC 相比,OR=1.45,95%CI=1.38-1.53,P(异质性)=0.273;TT+TC 与 CC 相比,OR=1.49,95%CI=1.42-1.56,P(异质性)=0.208;TT 与 TC+CC 相比,OR=2.52,95%CI=1.95-3.25,P(异质性)=0.296)。此外,还检测到 PTPN22 1858C/T 多态性与 RF(+)或 RF(-)RA 风险之间存在显著关系。在总体分析中未发现明显的发表偏倚证据。
我们的研究表明,PTPN22 1858T 等位基因与 RA 风险增加显著相关。