Studies of blood lipid fractions of quiescent rheumatic fever patients and their siblings.

THE MATURATION of the rheumatic process in man requires a summation of several factors. As pointed out by McKusick (1), “presumably, genetic factors determine the qualitative and/or quantitative nature of the host response to repeated streptococcal infections. The mechanism of this gene action is, of course, of great interest but is unknown.” In studying the roles of the genes and nutrition on blood fat content in man, Osborne et at. (2) concluded: “By this method it has been possible to demonstrate that both genetic and environmental factors may produce measurable variations in the serum lipid levels of healthy adults.” The present study is designed to determine whether rheumatic fever is associated with abnormalities in serum lipids, which might be due to genetic or environmental factors. Todd, Coburn, and Hill (3) showed that rheumatic children, in contrast to their siblings, failed to develop the expected rise of antistreptolysin S following hemolytic streptococcal pharyngitis. Subsequently, antistreptolysin S was shown to be streptolysin inhibitor (SSI) by Stollerman et at. (4, 5), who demonstrated that the inhibitor was associated with alpha and beta lipoproteins. Later Stoller.. man et at. (6) pointed out that the fall in serum levels of streptolysin S inhibitor during the rheumatic attack indicates a disturbance of lipoprotein metabolism in rheumatic fever. They found in acute rheumatic fever that: (a) the SSI level falls, (b) there is a positive correlation between the serum SSI and phospholipid concentration, and (c) this relationship is best illustrated by the lecithin fraction.