Introduction
Rheumatoid arthritis (RA) affects approximately 1% of the population, leading to significant morbidity and even increased mortality. There are treatments available; however, they have adverse effects, they are financially costly, and they do not work for everyone. Therefore, ideally RA would be prevented, rather than just treated once it develops. An attractive approach to the prevention of RA would be to identify and remove the triggers for disease, or intervene with factors that protect against RA development. Unfortunately, while there are some possible triggers of RA noted, much more specific knowledge is needed regarding risk as well as protective factors for disease before these factors can be used to prevent disease. Fortunately, the rheumatology community is getting closer to understanding the role of environmental and genetic factors that influence RA development. In particular, these 3 studies discussed here have utilized unique resources to evaluate the role of a variety of environmental factors and genetic interactions on the development of RA.
Study Summary
Smoking and HLA-DRB1. In this study, using 439 cases with incident RA (all female cases, with 1:1 matched controls) identified from the prospective US-based Nurses' Health Study, the authors demonstrated a high risk for future RA in subjects who were heavy smokers (> 10 pack-years) and positive for 2 copies of HLA-DRB1 alleles containing the shared epitope (odds ratio for RA 7.47, 95% confidence interval [CI] 2.77-20.11). Of note, stratifying degree of tobacco smoke use (ie, pack-years) allowed for the identification of a stronger gene-environment interaction than when smoking was analyzed only as a never-ever variable, suggesting that the dose of tobacco smoke exposure is an important factor in RA risk.
Statins. In this study, using a large Israeli computerized medical database of 211,627 subjects with 2578 cases of incident RA, these authors demonstrated that patients with the greatest duration of statin use (multiple types of statins) had a significantly decreased risk for future RA compared with those with lesser statin use (hazard ratio for incident RA: 0.58, 95% CI 0.52-0.65). Of note, persistent statin use was determined by evaluating the mean proportion of days covered (PDC) by statin use, with PDC calculated by dividing the quantity of statin pills distributed by the total time interval from first prescription of statin to predetermined endpoints (diagnosis of RA, etc).
Alcohol. Using data regarding current and prior alcohol consumption from patients with established RA from Sweden and Denmark (total RA cases = 1648, with 1404 controls), these authors determined that subjects in the highest category of alcohol consumption had a decreased risk for RA (statistically significant odds ratios of 0.5 and 0.6 in the Swedish and Danish cohorts, respectively). Of note, the category of highest alcohol consumption included subjects who had weekly alcohol consumption that was > 75% above the median intake, or about 5 drinks/weekly (with 1 drink = 16 g of alcohol) (for reference, 12 ounces of beer that is approximately 5% alcohol contains approximately 14 grams of alcohol). The highest reduction in risk for RA was seen in smokers who were positive for HLA DRB1 and shared epitope-containing alleles.
http://www.medscape.com/viewarticle/729300
Copyright ArthritisInsight.com