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Following the demonstration in Peters' laboratory (1, 2) of the specific inability of the thiamindeficient pigeon brain to metabolize pyruvic acid, attempts have been made to utilize methods of demonstrating this biochemical dysfunction as a laboratory test for detecting thiamin deficiencies. Thompson and Johnson (3) in 1935 showed an accumulation of pyruvic acid in the blood of thiamin-deficient animals, and a similar accumulation was demonstrated in human beriberi (4). The pyruvic acid values were obtained by estimating the bisulphite-binding capacity of the blood and expressing the results in terms of pyruvic acid. In a later paper Platt and Lu (5) showed that, although in animals the large increase in bisulphite-binding substances (B.B.S.) in the blood was probably due entirely to pyruvic acid, only a fraction of the B.B.S. in human cases could be accounted for as pyruvic acid when the latter was determined by the specific hydrazone method of Peters and Thompson (1). The elevated B.B.S. values have been observed to return to normal soon after the administration of thiamin (3, 4, 5). Subsequently, Taylor and associates (6, 7) reported that the elevation of blood B.B.S. was not specific for thiamin deficiency but occurred in other diseased conditions. This finding was supported by studies from the same laboratory (8) on the rate of removal of pyruvic acid administered both intravenously and orally. In these studies clinical findings were the sole criteria of thiamin deficiency. A specific chemical method for the determination of thiamin in the urine (9) and the application of this procedure (10, 11) to the diagnosis of thiamin deficiency have been reported by us.

CORRELATION BETWEEN THE CONCENTRATION OF BISULPHITE BINDING SUBSTANCES IN THE BLOOD AND THE URINARY THIAMIN EXCRETION 1