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Gene Linked to Inflammatory Arthritis Also Raises Heart Risks
Date:2/7/2008

British study found HLA-DRB1 increased chances of dying from cardiovascular causes

THURSDAY, Feb. 7 (HealthDay News) -- A gene called HLA-DRB1 that's associated with an increased risk of developing inflammatory arthritis may also increase the chances of premature death from cardiovascular disease (CVD), a British study finds.

People with rheumatoid arthritis (an autoimmune disease) tend to die younger, and largely from CVD, according to background information in the study, which looked at 1,022 people with inflammatory polyarthritis, including 751 people with rheumatoid arthritis (RA).

During the study period, 242 (24 percent) of the patients died, and CVD was the cause of death in 76 (31.4 percent) of those patients.

The researchers, led by Dr. Tracey M. Farragher at the University of Manchester, investigated whether genetic variants associated with increased risk of RA might also increase the risk of death from CVD. Their report was published in the February issue of Arthritis & Rheumatism.

They found evidence that implicates HLA-DRB1 genotypes, already associated with RA susceptibility and severity, as a predictor of premature death from CVD in patients with inflammatory arthritis.

The researchers said that, for RA patients in particular, having the shared epitope (SE) -- a group of HLA-DRB1 alleles with kindred amino acid traits -- plus anti-cyclic citrullinated peptide (anti-CCP) antibodies and being a current smoker is an especially lethal combination.

This is the first study to link the HLA-DRB1 genotypes with premature death, particularly from CVD, among people with inflammatory arthritis. Farragher said the findings "raise the possibility of a targeted strategy to prevent CVD in these patients" and reinforces the danger of smoking for people with a genetic predisposition for arthritis.

More information

The Arthritis Foundation has more about rheumatoid arthritis.



-- Robert Preidt



SOURCE: Arthritis & Rheumatism, news release, Jan. 31, 2008


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