Wang Hong, Wang Tingrui, Wang Haili, Wu Yue, Wu Lingling, Ling Huayun, Ye Dong-Qing, Wang Bin
Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China.
Anhui Province Laboratory of Inflammation and Immune Mediated Diseases, Hefei, Anhui, China.
Postepy Dermatol Alergol. 2022 Apr;39(2):353-361. doi: 10.5114/ada.2022.115965. Epub 2022 May 9.
Systemic lupus erythematosus (SLE) is an autoimmune disease closely related to the immune system. C1q is an important component of complement system. However, the correlation between C1q gene polymorphism and SLE has not been completely unified.
The primary aim of this meta-analysis was to examine the association between C1q polymorphisms and the risk of SLE.
All relevant articles were retrieved from PubMed, Web of Science and CNKI until June 2020. Pooled OR and 95% CI with random model were used to evaluate the strength of the association between C1q polymorphisms and SLE. Considering the limited number of studies, Trial Sequential Analysis (TSA) was applied to estimate whether the information was sufficient to make reliable and conclusive evidence. Both Egg's test and trim and fill method were performed to assess the publication bias.
Eight articles were included in this meta-analysis. The pooled results showed that C1q rs631090 was associated with SLE only in the homozygous and recessive model (allelic model: 1.169 (0.632-2.162), homozygous model: 2.342 (1.239-4.427), heterozygous model: 0.983 (0.395-2.448), dominant model: 1.036 (0.418-2.567), recessive model: 2.281 (1.227-4.239)) and there was no association between C1q rs172378 and rs292001 and SLE (rs172378 (allelic model: 1.071 (0.949-1.210), homozygous model: 1.172 (0.868-1.584), heterozygous model: 1.080 (0.892-1.306), dominant model: 1.100 (0.918-1.317), recessive model: 1.112 (0.863-1.431)); rs292001 (allelic model: 0.877 (0.657-1.170), homozygous model: 0.713 (0.320-1.589), heterozygous model: 0.714 (0.448-1.138), dominant model: 0.703 (0.414-1.196), recessive model: 0.927 (0.601-1.430)). Nevertheless, TSA showed that more information was needed to get more accurate results. There is no publication bias.
This meta-analysis suggested that C1q rs631090 but not rs172378 and rs292001 may be a potential susceptible factor associated with SLE. Nevertheless, due to the limited sample size in this meta-analysis, more large-scale association studies are still needed to confirm the results.
系统性红斑狼疮（SLE）是一种与免疫系统密切相关的自身免疫性疾病。C1q是补体系统的重要组成部分。然而，C1q基因多态性与SLE之间的相关性尚未完全统一。
本荟萃分析的主要目的是研究C1q多态性与SLE风险之间的关联。
检索截至2020年6月PubMed、Web of Science和CNKI上的所有相关文章。采用随机模型的合并OR值和95%可信区间来评估C1q多态性与SLE之间关联的强度。考虑到研究数量有限，应用序贯试验分析（TSA）来估计信息是否足以得出可靠和确凿的证据。同时进行Egger检验和剪补法以评估发表偏倚。
本荟萃分析纳入了8篇文章。合并结果显示，C1q rs631090仅在纯合子和隐性模型中与SLE相关（等位基因模型：1.169（0.632 - 2.162），纯合子模型：2.342（1.239 - 4.427），杂合子模型：0.983（0.395 - 2.448），显性模型：1.036（0.418 - 2.567），隐性模型：2.281（1.227 - 4.239）），而C1q rs172378和rs292001与SLE之间无关联（rs172378（等位基因模型：1.071（0.949 - 1.210），纯合子模型：1.172（0.868 - 1.584），杂合子模型：1.080（0.892 - 1.306），显性模型：1.100（0.918 - 1.317），隐性模型：1.112（0.863 - 1.431））；rs292001（等位基因模型：0.877（0.657 - 1.170），纯合子模型：0.713（0.320 - 1.589），杂合子模型：0.714（0.448 - 1.138），显性模型：0.703（0.414 - 1.196），隐性模型：0.927（0.601 - 1.430））。然而，TSA显示需要更多信息才能获得更准确的结果。不存在发表偏倚。
本荟萃分析表明，C1q rs631090可能是与SLE相关的潜在易感因素，而rs172378和rs292001不是。然而，由于本荟萃分析中的样本量有限，仍需要更多大规模的关联研究来证实这些结果。
