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December 17, 1898


JAMA. 1898;XXXI(25):1445-1446. doi:10.1001/jama.1898.92450250003001a

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The great Fothergill and Garrod taught us that uric acid was the causative factor in gout; that it was formed by the metabolism of nitrogenous waste; that it represents a lower degree of oxidation than urea; that uric acid and its salts, being insoluble, are much less easily eliminated, and hence they accumulate in the system; that it is in the liver the splitting up of peptones into glycogen and waste, azotized substance takes place, and its insufficiency causes the diminished oxidation that produces uric acid instead of urea. Haig, in his masterly treatise on uric acid, accepts this theory. This tracing of gout to an excess of nitrogenous ingesta results in the exclusion of this important group of alimentary principles from this class of patients.

This origin of uric acid, as the exclusive one, can not be maintained today, for we know that much, if not all, of this

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