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The concept of a fungal/mycotoxin etiology of gout/hyperuricemia in humans was first reported by Costantini in 1989. Gout and/or hyperuricemia have been induced in animals by the fungal species Ustilago maydis, Chaetomium trilaterale, Saccharomyces cerevisiae, and by the mycotoxins, aflatoxin, ochratoxin, oosporein, oxalic acid. Gout and/or hyperuricemia have been induced in humans by the yeast Candida utilis and by the fungal metabolites cyclosporin, ergotamine and penicillin. Gout is documented to be etiologically linked to beer, a Saccharomyces fermented beverage. Beers contain significant amounts of ochratoxin and large amounts (7 to 9 mg/dl of uric acid, a metabolite produced by the brewer's yeast Saccharomyces cerevisiae. Consistent with the fungal etiology of gout and hyperuricemia, the mode of action of colchicine in the treatment of gout is antifungal. Colchicine shares antitubulin activity with griseofulvin, a potent antifungal antibiotic. Griseofulvin is as equally effective in the treatment of gout as colchicine. Similarly, another antitubulin drug, vinblastine is also antifungal and effective in the treatment of gout. All of the other drugs used to treat gout and/or hyperuricemia possess antifungal activity. Biomedical Reviews 1992; 1: 47-52.

The fungal etiology of gout and hyperuricemia: the antifungal mode of action of colchicine