Association between gene polymorphism of inflammatory factors, thrombogenic factors, and stress-related proteins and abdominal aortic aneurysm: A meta-analysis and systematic review

Abstract

Background Abdominal aortic aneurysm (AAA) is a deadly disease in the elderly population. Currently, the association between single nucleotide polymorphisms (SNPs) and the presence of AAAs has become a hot topic and is a concern for many researchers. Method We performed a document retrieval in PubMed, EMBASE, and the Cochrane Library (to January 2020). A total of 17 case-control reports on SNPs of AAAs and eight SNPs of correlation factors were selected. All essential data, including race, age, country, criteria of AAA diagnosis, method of AAA measurement, method of genotype detection, name of SNPs, minor allele frequency (MAF), Hardy Weinberg equilibrium (HWE) of the control group, and number of cases and control groups were extracted by two reviewers independently. The fixed-effect model and random-effect model were used to calculate the overall odds ratios (ORs) and 95% confidence intervals (CIs). The association between selected SNPs and the presence of AAAs was evaluated under different genetic models (dominant, codominant, recessive, overdominant, and allele models). Results A total of 17 articles (sample size ranging from to 42–665 AAA cases and 49–2,297 controls) and 23 SNPs of related factors were identified. Eight SNPs were assessed in at least two studies and were selected for further meta-analysis. We found that the A allele of interleukin (IL)-10 (−1082 G/A) (OR: 1.35, 95% CI: 1.18–1.54, p < 0.0001) was a risk factor for AAAs under random and fixed-effect models. In addition, partial genetic models of these SNPs were confirmed to be related to the presence of AAA. Subgroup analysis revealed that haptoglobin (HP)-1 was a risk factor for AAAs (OR: 1.30, 95% CI: 1.04–1.63, p = 0.02) in the European population. No association was found between the occurrence of AAA and the other SNPs. Conclusion In our current meta-analysis, we speculated that the genotype distribution of IL-10 (−1082 G/A) may be associated with the emergence of AAA.