American Journal of Cancer

, Volume 1, Issue 6, pp 409–422 | Cite as

Hyperuricemia in Patients with Cancer

Review Article

Abstract

Hyperuricemia is a common early complication in patients with hematological malignancies treated with intensive chemotherapy. It results from the breakdown of nuclear proteins leading to increased blood levels of hypoxanthine and xanthine. These compounds are degraded into uric acid by the enzyme xanthine oxidase. Because the mechanisms of excretion of uric acid are limited in humans and blood levels are near saturation level, a common complication of hyperuricemia is renal failure resulting from the deposition of uric acid in renal tubules.

When renal insufficiency occurs in conjunction with other metabolic aberrations, such as hyperkalemia, hyperphosphatemia, and hypocalcemia, this process is termed tumor lysis syndrome. Patients with acute lymphoblastic leukemia and non-Hodgkin’s lymphoma, particularly Burkitt’s lymphoma, are at greatest risk because of the high sensitivity of the cells to chemotherapy. Other factors associated with increased risk of hyperuricemia and tumor lysis syndrome include hyperleukocytosis, massive organomegaly, renal enlargement, extrinsic compression of the genitourinary tract, and elevated serum lactate dehydrogenase activity. Conventionally, patients at risk of developing hyperuricemia receive alkalinized fluids and allopurinol, an inhibitor of the enzyme xanthine oxidase. These measures have been effective in reducing mortality associated with metabolic complications during tumor lysis in the majority of the cases. However, as many as 25% of patients at high-risk of developing tumor lysis syndrome require dialysis, and some of them have the treatment course altered because of these complications.

Recently, a synthetic recombinant form of the enzyme urate oxidase, rasburicase has become available in the US. This enzyme acts directly on urate and degrades it to allantoin, a much more soluble compound.

Keywords

Uric Acid Allopurinol Hyperuricemia Tumor Lysis Syndrome Hyperphosphatemia 

Notes

Acknowledgements

Supported in part by grant CA-21765 from the National Institutes of Health (US Department of Health and Human Services), a grant from Sanofi-Synthelabo, a Center for Excellence grant from the State of Tennessee, and the American Lebanese Syrian Associated Charities (ALSAC). C-H Pui is the American Cancer Society - FM Kirby Clinical Research Professor.

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Copyright information

© Adis International Limited 2002

Authors and Affiliations

  1. 1.Department of Hematology-OncologySt Jude Children’s Research HospitalMemphisUSA
  2. 2.Department of PediatricsUniversity of Tennessee College of MedicineMemphisUSA

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