HE best evidence to date suggests that in patients with familial gout the metabolic alterations are related in large part to an overproduction of uric acid. Furthermore, a considerable volume of experimental data has been accumulated which shows that patients with various blood dyscrasias develop a disturbance of uric acid metabolism that is clinically, histologically, and in some stages biochemically undifferentiable from that observed in patients with familial gout.1 Basically, however, the mechanism is different. The increased concentration of serum uric acid and the increased excretion in the urine follows an increased formation and destruction of red and white blood cells and an increased metabolism of nucleic acids in the bloodforming organs with the elaboration of intermediary products of purine metabolism. Such patients are susceptible to a sudden onset of acute distress associated with the cardinal signs of inflammation in one or more of the distal joints of an
GOUT AND BLOOD DYSCRASIAS. JAMA. 1960;172(2):168. doi:10.1001/jama.1960.03020020048011
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