Clinical and laboratory measures of disease expression were compared within and between 33 families with two or more affected siblings with rheumatoid arthritis (RA). None of the variables studied--age and calendar year of disease onset, pattern of joint involvement, the presence of rheumatoid nodules, Sjögren's syndrome, a positive latex or antinuclear antibody (ANA) titre--showed a greater concordance within the families than between them. The families were then divided into those in which the affected sibling pairs were and were not HLA identical. Such a division did not alter the conclusion, with the possible exception of a positive latex titre. These results suggest that genetic or unique environmental factors within families may have only a limited role in explaining disease heterogeneity in RA. Conversely, the absence of homogeneity within the families justifies their use in genetic linkage studies and the extrapolation of results obtained from affected siblings to the commoner sporadic disease.
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