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April 1962

The Pathogenesis of Gout

Author Affiliations


From the Argonne Cancer Research Hospital, operated by the University of Chicago for the United States Atomic Energy Commission, and the Department of Medicine, The University of Chicago.

Arch Intern Med. 1962;109(4):379-390. doi:10.1001/archinte.1962.03620160005002

Since Garrod's original observation1 in 1848 that excessive amounts of serum uric acid were present in gouty patients, there has been widespread agreement that gout is attributable to a sustained accumulation of uric acid in the body. I believe that if a patient has a sufficient degree of hyperuricemia for a long enough period he will eventually develop gout, irrespective of the nature of the hyperuricemia. This, then, implies that the clinical syndrome of gout comprises several distinct entities. The accumulation of uric acid must result from a disturbance in the normal equilibrium between the production of uric acid on one hand and the elimination of urate on the other. As a consequence, hyperuricemia will occur in the following circumstances:

  1. When the production of urate is so great that, even though the routes of elimination are of normal capacity, they are inadequate to handle the excessive load.

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