Hypertaurinuria in rheumatoid arthritis.

Patients with rheumatoid arthritis show several metabolic abnormalities, including abnormal tryptophan metabolism (Bett, 1962a, b; Flinn, Price, Yess, and Brown, 1964). This was postulated as due to a functional deficiency in vitamin B6 (Flinn and others, 1964), and McKusick, Sherwin, Jones, and Hsu (1964) did in fact demonstrate low urinary B6 in patients with rheumatoid arthritis. An alternative hypothesis, that the abnormality of tryptophan metabolism was the result of increased tryptophan pyrrolase activity due to the induction of this enzyme by increased fibrinogen breakdown, has also been proposed (editorial comment, Arthritis and Rheumatism, 1966). The formation of taurine from cysteine in the body is another metabolic pathway which maydepend on vitamin B6 (Wiss and Weber, 1964) deficiency resulting in low urinary output of taurine. The main product from the metabolism of cysteine is sulphate and the relevant pathways, as established in the rat, are shown in Fig. 1. The decarboxylation stages involve pyridoxal phosphate as co-enzyme and are said to be particularly sensitive to B6 deficiency (Wiss and Weber, 1964; S6rbo, 1965; and Berlow, 1967). It seemed of interest to examine the urinary taurine and sulphate levels in patients with rheumatoid arthritis in view of the possible deficiency of vitamin B6 in such patients.