Total and free-plasma tryptophan concentrations in rheumatoid disease

Abstract

Abstract It has been proposed (McArthur, Dawkins & others, 1971) that human connective tissue diseases may arise from modifications in the binding characteristics of the plasma proteins. McArthur, Smith & Freeman (1972) presented evidence that human serum contains a substance that possesses anti-inflammatory activity and is bound to circulating proteins. Furthermore, it has been suggested that, in patients with active rheumatoid arthritis, the anti-inflammatory substance is bound to an abnormal extent to the plasma proteins and that the clinically useful antirheumatic drugs act by re-establishing the bound: free ratio to that in the normal subject (Smith & Dawkins, 1971). There is evidence that the behaviour of L-tryptophan mimics that of the hypothetical substance which protects susceptible tissues against chronic inflammatory insults. All the clinically useful antirheumatic agents were found to displace L-tryptophan from human plasma in vitro (McArthur, Dawkins & Smith, 1971) but not so other drugs which bind to plasma proteins to an equivalent extent but have no demonstrable antirheumatic effects (Smith, Dawkins & McArthur, 1971). In patients with rheumatoid arthritis receiving drug therapy the percentage of L-tryptophan bound to plasma proteins is significantly reduced but increases when drug administration is stopped (McArthur, Dawkins & others, 1971).