Purine Metabolism in Man—II: Physiology, Pharmacology, and by Richard E. Rieselbach (auth.), Mathias M. Müller, Erich

By Richard E. Rieselbach (auth.), Mathias M. Müller, Erich Kaiser, J. Edwin Seegmiller (eds.)

The research of gouty arthritis has supplied a standard assembly floor for the learn pursuits of either the fundamental scientist and the clinician. The curiosity of the chemist in gout begun 1776 with the isolation of uric acid from a concretion of the urinary tract by way of the Swedish chemist SCHEELE. an identical substance used to be consequently extracted from a gouty tophus via the British chemist WOLLASTONE in 1797 and a part century later the reason for the deposits of sodium urate In such tophi was once traced to a hyperuricemia within the serum of gouty sufferers through the British surgeon Alfred Baring GARROD who had additionally bought education within the chemical laboratory and used to be for this reason a fore-runner of lots of contemporary clinician-investigators. the new surge of development in knowing of a few of the explanations of gout when it comes to particular enzyme defects marks the doorway of the biochemist into this box of research. The identity of the 1st basic illness of purine metabolism linked to over-production of uric acid, a critical or partial deficiency of the enzyme hypoxanthine-guanine phospho­ ribosyl transferase used to be completed below a decade in the past. the information of the mechanism of purine over-production that it generated led almost immediately to the id of households sporting a dominantly (possibly X-linked) inherited raise within the job of the enzyme phosphoribosylpyrophosphate synthetase as a reason behind purine over-production. but this can be just a begin as those different types of enzyme defects account for only 5 in line with cent of gouty patients.

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Purine Metabolism in Man—II: Physiology, Pharmacology, and Clinical Aspects

The examine of gouty arthritis has supplied a typical assembly flooring for the examine pursuits of either the fundamental scientist and the clinician. The curiosity of the chemist in gout begun 1776 with the isolation of uric acid from a concretion of the urinary tract by means of the Swedish chemist SCHEELE. an identical substance was once consequently extracted from a gouty tophus via the British chemist WOLLASTONE in 1797 and a part century later the reason for the deposits of sodium urate In such tophi was once traced to a hyperuricemia within the serum of gouty sufferers through the British healthcare professional Alfred Baring GARROD who had additionally obtained education within the chemical laboratory and was once hence a fore-runner of lots of modern day clinician-investigators.

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In the presence of a constant fractional excretion of secreted urate, it is proposed that major fluctuations in secretory load are masked by alterations in absolute reabsorptive rate which allow maintenance of a constant fractional excretion. "B" depicts a doubling of "secretory load" attained as the result of a doubling of plasma urate concentration. 01 mg/ml of plasma urate concentration (see text). RENAL HANDLING OF URIC ACID 11 tration were to be doubled, this would result in a doubling of the secretory load, as noted in Fig.

A quantitatively similar but more sustained diminution of Curate:Ccreatinine was observed after 3 g oral pyrazinamide in 3 patients. Four to 6 hours after oral ingestion, 1 g nicotinamide caused a minimal diminution in Curate:Ccreatinine in 3 patients. » -<=:::::t~ -1~~------~------~------~~------~-------T~ o 60 240 300 120. 180 mInutes Fig. 1. Effect of nicotinic acid, nicotinamide, and pyrazinamide on the renal handling of uric acid. The Curate:Ccreatinine was expressed as the percentage change from the control values 1 to 6 hours after drug ingestion.

12 During infusion of fructose, sorbitol and xylitol, but not during glucose or maltose, we found a considerable augmentation of uric acid levels in healthy young males (3-7). This increase of uric acid was dose- dependant. For fructose and sorbitol a dosage of 1,5 g/kg/h is needed, whereas xylitol augments uric acid after a dosage of only 0,25 g/kg/h BW (3-7). Now, we investigated the uric acid metabolism during infusion of a carbohydrate mixture containing fructose, glucose and xylitol at a rate of 2:1:1 (LGX = Triofusin E-1000, Pfrimmer).

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