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Association between complement gene polymorphisms and systemic lupus erythematosus: a systematic review and meta-analysis.
- Source :
-
Clinical and experimental medicine [Clin Exp Med] 2022 Aug; Vol. 22 (3), pp. 427-438. Date of Electronic Publication: 2021 Sep 14. - Publication Year :
- 2022
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Abstract
- Complement dysfunction results in impaired ability in clearing apoptotic cell debris that may stimulate autoantibody production in systemic lupus erythematosus (SLE). Herein, we provided a comprehensive search to find and meta-analyze any complement gene polymorphisms associated with SLE. The ITGAM, C1q, and MBL gene polymorphisms were included in this meta-analysis to reveal the exact association with SLE risk. Electronic databases, including Scopus, PubMed, and Google Scholar, were searched to find studies investigating the ITGAM, C1q, and MBL gene polymorphisms and SLE risk in different populations. The pooled odds ratio (OR) and its corresponding 95% confidence interval (CI) were used to analyze the association between ITGAM, C1q, and MBL gene polymorphisms and susceptibility to SLE. According to inclusion criteria, a total of 24 studies, comprising 4 studies for C1QA rs292001, 5 studies for C1QA rs172378, 9 studies for ITGAM rs1143679, 8 studies for MBL rs1800450, 3 studies for MBL2 rs1800451, and 3 studies for MBL2 rs5030737, were included in the final meta-analysis. A significant positive association was found between rs1143679 and SLE risk, while rs1800451 significantly associated with decreased SLE susceptibility. In summary, ITGAM gene rs1143679 SNP and MBL gene rs1800451 SNP were positively and negatively associated with SLE risk, respectively.<br /> (© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)
Details
- Language :
- English
- ISSN :
- 1591-9528
- Volume :
- 22
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Clinical and experimental medicine
- Publication Type :
- Academic Journal
- Accession number :
- 34519938
- Full Text :
- https://doi.org/10.1007/s10238-021-00758-0