September 1966

The Effects of Allopurinol on Serum and Urinary Uric Acid

Author Affiliations


From the Rackham Arthritis Research Unit, Department of Internal Medicine, The University of Michigan Medical School, and the Department of Medicine, Wayne County General Hospital.

Arch Intern Med. 1966;118(3):224-228. doi:10.1001/archinte.1966.00290150038008

MODERN therapy of gout may be divided into two approaches: (1) control and prevention of the acute attack, and (2) control of hyperuricemia, the biochemical hallmark of gout. The former approach employs the use of colchicine, phenylbutazone, and antiinflammatory agents. Prior to the introduction of probenecid in 1951, little could be done to effectively correct the hyperuricemia. However with the advent of probenecid, practical uricosuric therapy became possible. Since then other uricosuric agents have become available, and the value of uricosuric therapy in gout has been established.1

Despite the general efficacy of uricosuric agents, still a number of patients are seen in whom it is impossible to adequately correct their hyperuricemia, usually because of impaired renal function. Thus, there exists a need for an agent that blocks the production of uric acid.

Allopurinol (4-hydroxypyrazolo [3, 4-d] pyrimidine) was initially developed as a potential cancer chemotherapeutic agent. As such allopurinol

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