The natural history of hyperuricemia among asymptomatic relatives of patients with gout.

Abstract

1. Hyperuricemia is common among the gouty relatives as reported by others (8-11). It is of interest to note that serum urate fluctuates periodically. Hyperuricemia is not necessarily maintained in a steady state throughout the years. Thus a single determination of serum uric acid can be misleading. 2. Development of gout from asymptomatic hyperuricemia is often correlated with the degree of hyperuricemia as observed from population or family studies (12-14). The data presented indicate that unequivocal hyperuricemia is more often accompanied by excessive excretion of uric acid, diminished excretion of ammonia and abnormally high plasma glutamic acid. All are undoubtedly important risk factors for gout. 3. The elevated glutamate could be due to a deficiency of glutamic dehydrogenase, as postulated by Pagliara and Goodman (15). In presence of intracellular accumulation of glutamate in glutamic dehydrogenase deficiency, renal production of ammonium may be reduced due to its inhibitory action on glutaminase 1. As a result of a renal block of ammonia formation, the glutamine in surplus may be diverted for uric acid synthesis. 4. Long-term studies indicate serum urate in most hyperuricemia relatives of gout can be modified by environmental factors, such as diet, weight and changes of life style. When hyperuricemia is under better control, the potential hazard of developing symptomatic gout may be circumvented.