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Risk of C1q variation in systemic lupus erythematosus: a meta-analysis with Trial Sequential Analysis

INTRODUCTION: 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. AIM: The primary aim of this meta-analys...

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Detalles Bibliográficos
Autores principales: Wang, Hong, Wang, Tingrui, Wang, Haili, Wu, Yue, Wu, Lingling, Ling, Huayun, Ye, Dong-Qing, Wang, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9131952/
https://www.ncbi.nlm.nih.gov/pubmed/35645665
http://dx.doi.org/10.5114/ada.2022.115965
Descripción
Sumario:INTRODUCTION: 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. AIM: The primary aim of this meta-analysis was to examine the association between C1q polymorphisms and the risk of SLE. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.