Gout has an increased prevalence in some populations but is rare in others. For example, the frequency of gout is higher in populations such as the Chamorros and Maori and in the Blackfoot and Pima tribes. Many Maori and other Polynesian women have a genetic defect in renal urate handling that increases their risk for hyperuricemia and gout. However, racial differences may at least in part reflect differences in diet. Black Americans have an increased risk for incident gout compared with white Americans; these differences are demonstrable beyond known racial differences in serum urate level.
In the United States, attacks of gout have been noted to occur more frequently in the spring and less frequently in the winter. Acute pseudogout attacks have not shown the same seasonal variation.
Gout also has a male predominance. This difference is largely a consequence of age at onset; estrogenic hormones have a mild uricosuric effect, and gout is unusual in premenopausal women. For pseudogout, the male-to-female ratio is more even.
Earlier onset of gout occurs in patients with renal insufficiency or a genetic abnormality of purine metabolism (eg, hypoxanthine-guanine phosphoribosyltransferase deficiency or phosphoribosylpyrophosphate synthetase superactivity). Cyclosporine A can cause an accelerated form of gout, even in premenopausal women. Gout can present after only a few years of hyperuricemia, particularly if the patient is also receiving diuretics.
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Cite this: Herbert S. Diamond. Fast Five Quiz: Gout and Pseudogout - Medscape - Dec 04, 2019.