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No genetic evidence found for causal relation between RA, CAD
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There was no evidence that rheumatoid arthritis-associated single nucleotide polymorphisms as a group were associated with coronary artery disease, according to results of a genetic analysis.
“The underlying concept is that if [rheumatoid arthritis] RA is causally related to [coronary artery disease] CAD, RA-related alleles would also translate into observable increases in CAD risk,” Henning Jansen, MD, at Technische Universität München in Germany, and colleagues wrote. “However, in our large dataset including 22,233 CAD cases and 64,762 controls, we found no such evidence.”
To assess whether RA and CAD share a common cause, Jansen and colleagues assessed 61 single nucleotide polymorphisms (SNPs) associated with RA and determined whether these were also associated with CAD. For the control group, the researchers used SNPs associated with low-density lipoprotein cholesterol (LDL-C). They published their results as a part of the CARDIoGRAM meta-analysis.
The researchers found 29 SNPs were associated with CAD, while 32 SNPs were not. However, this 48% proportion of SNPs is equal to that expected by chance (50%), suggesting the associations do not carry any significance. To show this genomic analysis worked, 74% of LDL-C SNPs were associated with CAD. There was one SNP (rs10774624, locus SH2B3) showed a study-wide significance in its association with CAD. While the researchers noted the SH2B3 locus has been previously found to increase inflammation, they also wrote this association is possibly due to pleiotropic effects on high blood pressure or type 1 diabetes.
“Together with a shared inflammatory background of CAD and RA, traditional risk factors might explain the increased prevalence of CAD in patients with RA more than a common genetic architecture,” the researchers wrote. – by Will Offit
Disclosure: Healio Rheumatology could not confirm relevant financial disclosures at the time of publication.
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