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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.

Background ITGAM is one of the major non-human leucocyte antigen that has been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The association of ITGAM polymorphism with SLE has been reported in several studies, but with inconclusive results. Objectives The aim of this study was to assess whether combined evidence shows the association between ITGAM polymorphism and SLE. Methods A meta-analysis was performed to survey studies on the ITGAM polymorphism and SLE using comprehensive Medline search and review of the references. A total of five published studies including 12 123 patients with SLE and 17 016 controls were involved. Meta-odds ratios (ORs) and 95% confidence intervals (CIs) based on fixed effects models or random effects models were depended on Cochran’s Q-statistic and I2 values. Results The overall ORs for the minor A-allele (OR 1.795; 95%CI 1.676–1.921), AA vs. GG (OR 3.540; 95%CI 2.771–4.522), AG vs. GG (OR 1.750; 95%CI 1.617–1.895), dominant model (OR 1.857;95%CI 1.719–2.005), recessive model (OR 3.041; 95%CI 2.384–3.878) of ITGAM rs1143679 were significantly increased in SLE and fixed effects models were conducted. All controls were in Hardy–Weinberg (HW) proportion. Although this meta-analysis showed significant association of rs1143683 (A vs. G, OR 1.534;95%CI 1.312–1.792), rs9888739 (T vs. C,OR 1.627;95%CI 1.380–1.918), rs1143678 (T vs. C, OR 1.543; 95%CI 1.330–1.790), rs9937837 (A vs. G, OR 0.466; 95%CI 0.227–0.957) with SLE; all of these were conducted in random effects model as heterogeneity was detected. No significant association was detected in the analysis between rs11574637 and SLE. No publication bias was presented. Conclusions This meta-analysis demonstrates a significant association between ITGAM gene polymorphism and SLE in multiple ethnic populations.

Objective. To investigate whether a functional integrin alpha M (ITGAM) variant is involved in susceptibility to and clinical manifestations of giant cell arteritis (GCA). Methods. A Spanish cohort of 437 white patients with biopsy-proven GCA and 1388 healthy controls were genotyped using the TaqMan allele discrimination technology. Results. No association was observed between ITGAM rs1143679 and GCA (p = 0.80, OR 0.97). Similarly, subphenotype analyses did not yield significant differences between the case subgroups and the control set or between GCA patients with or without the main specific features of GCA. Conclusion. Our results suggest that the ITGAM rs1143679 variant does not play an important role in the pathophysiology of GCA. The Journal of Rheumatology Copyright © 2011. All rights reserved.