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Serum amyloid-A protein (SAA) is the putative precursor of amyloid-A (AA) protein which forms the fibrils in reactive systemic or secondary amyloidosis. By means of a novel immunoradiometric assay, the concentration of SAA was found to be greatly elevated in patients with rheumatoid arthritis and juvenile chronic arthritis and correlated with activity of their primary disease. However, in patients with systemic lupus erythematosus SAA levels were only modestly raised, even in those with severe active disease, unless significant intercurrent microbial infection was also present. In Crohn's disease SAA levels showed a pattern similar to that seen in rheumatoid arthritis, whereas in ulcerative colitis it resembled that of systemic lupus erythematosus. The level of SAA response in these different disorders corresponds with the incidence of reactive systemic amyloidosis in them. These observations support the view that major increases in SAA levels are a necessary condition for the deposition of this form of amyloid and suggest that prospective monitoring of the SAA concentration in predisposing diseases may help to identify those individuals who are most at risk for amyloidosis.