24 FUNGALBIONICS-A NEW CONCEPT OF THE ETIOLOGY OF GOUT AND HYPERURICEMIA

Fungalbionics implicates fungi and fungal metabolites as the cause of gout/hyperuricemia. The mechanisms are not the usual patterns of invasive-type mycoses nor of mycotoxicoses, but rather

incorporate occult features of both mechanisms. Gout and/or hyperuricemia can be induced in fowl by the mycotoxins oosporein, ochratoxin and by oosporein-produclng fungi. Gouty tophi have

been induced in primates by aflatoxin. Fungi produce preformed uric acid, preformed urate crystals, lipoproteins, glycosaminoglycans and glutamates, excess of which are found in gout. Gouty

tophi are granulomatous and possess all of the features of delayed hypersensitivity. Giant cells in avian and human gouty tophi contain asteroid bodies which are fungal in origin.

Fungal-like spherules have been found in avian gouty lesions; cultural and immunological electron microscopy studies are in progress. The findings in acute gout are those of an acute

infection. All drugs used in treating gout/hyperuricemia are antifungal. Griseofulvin, an antifungal antibiotic, is as effective as colchicine in gout. Both are antitubulins and arrest

fungal cell division. Probenecid, allopurinol, corticosteroids, NSAIDS, possess antifungal activity. The fungalbionic concept gives a unitarian explanation of gout, hyperuricemia and related

diseases and findings.

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