1. ¹Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA
2. ²Department of Hematology/Oncology, St Jude Children's Research Hospital and the University of Tennessee, Health Science Center, Memphis, TN, USA
3. ³Section of Hematology/Oncology, University of Chicago, Pritzker School of Medicine, Chicago, IL, USA
4. ⁴Experimental Transplantation and Immunology Branch, National Cancer Institute, Bethesda, MD, USA
5. ⁵Oncology Business Unit, Sanofi-Synthelabo, SA, Paris, France
6. ⁶Departments of Pediatrics, Medicine, and Pathology, Columbia University, New York, NY, USA
7. ⁷North Texas Hospital for Children at Medical City, Dallas, TX, USA
8. ⁸Division of Pediatrics, University of Texas, MD Anderson Cancer Center, Houston, TX, USA
9. ⁹Department of Medicine, Division of Hematology and Medical Oncology, University of Maryland, School of Medicine, Baltimore, MD, USA
10. ¹⁰Division of Hematology/Oncology, Weill Medical College of Cornell University, New York, NY, USA
11. ¹¹Leo Jenkins Cancer Center, Brody School of Medicine, East Carolina University, Greenville, NC, USA

Correspondence: JA McCubrey, Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Brody Building 5N98C, Greenville, NC 27858, USA. Fax: 1 252 816 3104

Received 4 September 2002; Accepted 6 November 2002.

Abstract

Renal precipitation of uric acid associated with tumor lysis syndrome (TLS) is a major complication in the management of leukemia, lymphoma, and other drug-sensitive cancers. Management of hyperuricema has historically consisted of administration of allopurinol, hydration, alkalinization to maintain pH between 7.0 and 7.3, and in some cases diuresis. Allopurinol, a xanthine analogue, blocks xanthine oxidase and formation of uric acid. Urate oxidase converts uric acid to allantoin, which is 5–10 times more soluble than uric acid. Homo sapiens cannot express urate oxidase because of a nonsense mutation. Urate oxidase was initially purified from Aspergillus flavus fungus. Treatment with this nonrecombinant product had been effective in preventing renal precipitation of uric acid in cancer patients, but was associated with a relatively high frequency of allergic reactions. This enzyme was recently cloned from A. flavus and is now manufactured as a recombinant protein. Clinical trials have shown this drug to be more effective than allopurinol for prevention and treatment of hyperuricemia in leukemia and lymphoma patients. This drug has been approved in Europe as well as the US and several clinical trials are in progress to further determine its clinical utility in other patient subsets. The purpose of this meeting was to discuss usefulness of recombinant urate oxidase, also known as rasburicase, Fasturtec^®, and Elitek™, for the management of TLS in certain cancer patients.