Cyclosporine-Induced Hyperuricemia and Gout
- 1 February 1990
- journal article
- letter
- Published by Massachusetts Medical Society in New England Journal of Medicine
- Vol. 322 (5) , 334-336
- https://doi.org/10.1056/nejm199002013220514
Abstract
Could Lin et al. (Aug. 3 issue)1 give their recommendations on how to treat transplant recipients with gouty arthritis? The care of these patients is complicated by the existence of a potentially serious drug interaction between allopurinol and azathioprine. Allopurinol is a xanthine oxidase inhibitor and an important part of the armamentarium for the treatment of gout. Azathioprine is an immunosuppressive agent used primarily with cyclosporine and prednisone for the prevention of organ rejection in transplant recipients. The pathway responsible for the metabolism of azathioprine is xanthine oxidase. The inhibition of this pathway may therefore result in severe neutropenia that could be life-threatening. Current recommendations are that doses of azathioprine be reduced by 50 to 75 percent when administered concomitantly with allopurinol.2Keywords
This publication has 5 references indexed in Scilit:
- Gout in the heart transplant recipient: Physiologic puzzle and therapeutic challengeThe American Journal of Medicine, 1989
- Cyclosporine-Induced Hyperuricemia and GoutNew England Journal of Medicine, 1989
- Use of Polyethylene Glycol-Modified Uricase (PEG-Uricase) to Treat Hyperuricemia in a Patient with Non-Hodgkin LymphomaAnnals of Internal Medicine, 1988
- Bone lead in dialysis patientsKidney International, 1988