Heavy coffee drinking was associated with progression of undifferentiated arthritis to rheumatoid arthritis.
The study included 280 patients aged 18–75 years with arthritis of at least one joint. A total of 55% were women, mean age was 45.7 years, and median disease duration was 23 days, Dr. Maria D. Mjaavatten reported at the annual European Congress of Rheumatology. Data were collected from patient history, and exams included swollen and tender joint counts, measurement of C-reactive protein and erythrocyte sedimentation rate, and patient-reported health status. At baseline, 130 patients had monoarthritis, 96 had oligoarthritis, and 54 had polyarthritis. At 1 year, 30 of these patients (10.7%) had developed RA. Multivariate analysis revealed that the strongest predictor of RA development was a positive titer of anti-cyclic citrullinated peptide (CCP) at presentation, with an odds ratio of 73.23. But drinking 10 or more cups of coffee daily also was tied to an elevated risk, with an odds ratio of 22.50, according to Dr. Mjaavatten of the department of rheumatology, Diakonhjemmet Hospital, Oslo. In one report from the Mini-Finland Health Survey, carried out between 1978 and 1980, the odds ratio for RA was 14.80 in subjects whose daily coffee intake was 11 or more cups. After adjustment for age, sex, smoking, alcohol intake, body mass index, and serum cholesterol, the relative risk was 2.20 for subjects who drank four or more cups of coffee daily (Ann. Rheum. Dis. 2000;59:631–5). Another study implicated decaffeinated coffee, determining that subjects who drank four or more cups per day had a relative risk of 2.58 for RA. The investigators suggested that exposure to the industrial solvents used for extracting caffeine before the mid-1970s might have played a role (Arthritis Rheum. 2002;46:83–91). More recently, a case-control study in Denmark between 2002 and 2004 found that subjects who were shared epitope carriers and smoked, drank more than five cups of coffee each day, or used oral contraceptives were at high risk for anti-CCP-positive RA. One hypothesis says that exposure to environmental stimuli might be a primary triggering event for RA, with tobacco smoke being the prototype. Long-term exposure to smoke can induce the presentation of citrullinated autoantigens in the lungs in genetically predisposed persons, resulting in an activation of the adaptive immune response. The Danish investigators suggested that other environmental exposures like coffee also might somehow operate in this citrullination process, contributing to anti-CCP-positive RA (Arthritis Rheum. 2007;56:1446–53).