A study of the incidence and prevalence of rheumatoid arthritis conducted in Rochester, MN, during the period 1950 through 1974 revealed an average annual incidence rate of 28.1 per 100,000 population for males and of 65.7 per 100,000 for females. These rates include classic, definite, and probable cases. Age-specific rates generally increased with age. The secular trend of the incidence in males and females differed. Rates for males, although fluctuating, remained relatively stable throughout the entire 25-year period, whereas rates for females declined dramatically during the last 10 years of the study. The decline was present both in cases presenting as definite at the time of earliest diagnosis and in the probable cases. No explanation was found for the observed decline, but the authors believe that a factor introduced in the 1960s and acting selectively on females has affected the incidence rates. From recent evidence, it could be inferred that oral contraceptives and postmenopausal estrogens are likely causes. Prevalence rates for January 1, 1975, were 4.0 per 1000 for males and 10 per 1000 for females. Among adults, prevalence rates were 5.8 per 1000 for males and 13.4 for females. Mortality among the patients with rheumatoid arthritis was not different from that for the total Olmsted County population.
This investigation of the familial aggregation of rheumatoid arthritis in Rochester, Minnesota, was prompted by the considerable variability in previous reports and the need to interpret findings in light of the recently established human lymphocyte antigen (HLA)-DR4 association. The historical cohort methodology was applied to determine the incidence of adult-onset rheumatoid arthritis in 1631 biologic relatives of 78 probands compared with the Rochester population incidence. The ratio of the age- and sex-adjusted rates in first-degree relatives compared with the general population was 1.7 (95% confidence interval 1.0-2.9). The increase was concentrated in the 16- to 40-year-old age group, suggesting some disease heterogeneity. However, the level of familial risk was not significantly affected by the proband's sex, seropositivity, age, or parental disease status. Integrating these findings with prior research in which case ascertainment was complete led to the conclusion that familial aggregation of rheumatoid arthritis is weak. The apparent discrepancy between weak familial aggregation and the known strong HLA-DR4 association with rheumatoid arthritis was resolved by examining the mathematical relationship between the measures of association in the two different types of studies. Results show that to be consistent with weak familial clustering, any putative susceptibility gene must have very low penetrance, and/or there must be a large residual of sporadic cases.
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