The fungal etiology of gout and hyperuricemia: the antifungal mode of action of colchicine
Th e concept of a fungalImycotoxin etiology of gout/ hyperuricemia in humans was first reported by Costantini (1989) (1). Gout and/or hyperuricemia have been induced in animals by the fungal species Ustilago maydis, Chaetomium trilaterale, Saccharomyces cerversiae, and by the mycotoxins, aflatox’m, 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 beveage. Beers contain significant amounts of ochratoxin and large amounts (7 to 9 mg/dl of uric acid, a metabolite produced by the brewers’s yeast Saccharomyces cen’ersiae. Consistent with the fungal etiology of gout and hyperuricemia, the mode of action of colchicine in the treatment of gout is antifimgal. Colchicine shares antitubulin activity with griseofulvin, a potent antifimgal antibiotic. Griseofiilvin is as equally effective in the treatment of gout as colchicine. Similarly, another antitubulin drug, vinblastine is also antifimgal and effective in the treatment of gout. All of the other drugs used to treat gout and/or hyperuricemia possess antifimgal activity (Costantini 1989).
Biomed Rev 1992; 1: 47-52