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Fcγ受体ⅢB(FCGR3B)基因拷贝数缺失而非增加是系统性红斑狼疮和狼疮性肾炎的一个危险因素:一项荟萃分析。

FCGR3B copy number loss rather than gain is a risk factor for systemic lupus erythematous and lupus nephritis: a meta-analysis.

作者信息

Yuan Jin, Zhao Dongbao, Wu Lijun, Xu Xia, Pang Yafei, Zhang Jun, Ma Yanyun, Liu Jie, Wang Jiucun

机构信息

Department of Dermatology, Huashan Hospital affiliated to Fudan University, Shanghai, China.

Department of Rheumatology and Immunology, Changhai Hospital affiliated to Second Military Medical University, Shanghai, China.

出版信息

Int J Rheum Dis. 2015 May;18(4):392-7. doi: 10.1111/1756-185X.12342. Epub 2014 Mar 27.

DOI:10.1111/1756-185X.12342
PMID:24673810
Abstract

AIM

Some studies have been performed to elucidate the association between Fc gamma receptor 3B (FCGR3B) copy number (CN) and the risk of systemic lupus erythematosus (SLE) and/or lupus nephritis (LN), yet the results remain conflicting. Therefore, we have undertaken a systematic review of all the studies published and carried out a meta-analysis to obtain a better understanding of the role of FCGR3B CN in the susceptibility of SLE and LN.

METHOD

A computerized literature search was conducted in databases of PubMed, ISI Web of Knowledge for all studies investigating the association between FCGR3B CN and SLE and/or LN, published up to May 2013.

RESULTS

A total of six articles meeting all of the criteria were included in this study. There were five comparisons of SLE between 2490 patients and 4286 controls, and four comparisons of LN between 689 patients and 1924 controls. Our results showed that individuals with FCGR3B CN gain did not suffer an increased risk of SLE or LN as compared to the normal genotype in the total analysis (SLE: OR = 1.07, 95% CI = 0.79-1.45, P = 0.65; LN: OR = 0.83, 95% CI = 0.47-1.46, P = 0.52). However, individuals with FCGR3B CN loss exhibited an increased risk of SLE or LN (SLE: OR = 1.77, 95% CI = 1.51-2.06, P < 0.00001; LN: OR = 2.02, 95% CI = 1.59-2.57, P < 0.00001).

CONCLUSION

Our meta-analysis indicated that FCGR3B CN loss rather than CN gain was associated with susceptibility to SLE and LN.

摘要

目的

已有一些研究旨在阐明Fcγ受体3B(FCGR3B)拷贝数(CN)与系统性红斑狼疮(SLE)和/或狼疮性肾炎(LN)风险之间的关联,但结果仍存在冲突。因此,我们对所有已发表的研究进行了系统评价,并开展了一项荟萃分析,以更好地了解FCGR3B CN在SLE和LN易感性中的作用。

方法

在PubMed、ISI Web of Knowledge数据库中进行计算机化文献检索,查找截至2013年5月发表的所有研究FCGR3B CN与SLE和/或LN之间关联的研究。

结果

本研究共纳入6篇符合所有标准的文章。有5项对2490例患者和4286例对照进行的SLE比较,以及4项对689例患者和1924例对照进行的LN比较。我们的结果显示,在总体分析中,与正常基因型相比,FCGR3B CN增加的个体患SLE或LN风险并未增加(SLE:比值比[OR]=1.07,95%可信区间[CI]=0.79 - 1.45,P = 0.65;LN:OR = 0.83,95% CI = 0.47 - 1.46,P = 0.52)。然而,FCGR3B CN缺失的个体患SLE或LN的风险增加(SLE:OR = 1.77,95% CI = 1.51 - 2.06,P < 0.00001;LN:OR = 2.02,95% CI = (1.59 - 2.57),P < 0.00001)。

结论

我们的荟萃分析表明,与FCGR3B CN增加相比,CN缺失与SLE和LN的易感性相关。

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