Purine excretion during tumor lysis in children with acute lymphocytic leukemia receiving allopurinol: Relationship to acute renal failure

Andreoli, Sharon P.; Clark, Joseph H.; McGuire, Warren A.; Bergstein, Jerry M.

doi:10.1016/s0022-3476(86)80387-0

Cited by 98 publications

(58 citation statements)

References 18 publications

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“…excretion of the uric acid precursors hypoxanthine and xanthine. 8 Unlike hypoxanthine, xanthine is actually less soluble than uric acid in urine. 9 In fact, occasional case reports of Chemotherapy xanthine nephropathy and calculi suggest that allopurinol treatment is detrimental to some patients.…”

mentioning

confidence: 99%

Urate oxidase in prevention and treatment of hyperuricemia associated with lymphoid malignancies

et al. 1997

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Standard prophylaxis and treatment of malignancy-associatedily excretable metabolite with 5-to 10-fold higher solubility hyperuricemia in the USA has been allopurinol with vigorous than uric acid -offers a potentially useful alternative for the hydration, urinary alkalinization and osmotic diuresis. Urate prophylaxis and treatment of hyperuricemia. 14 However, the oxidase, the enzyme that converts uric acid to allantoin (a readnon-recombinant product (Uricozyme; Sanofi Winthrop, ily excreted metabolite that has 5-to 10-fold higher solubility Paris, France) Of 176 patients with non-B cell ALL, five with B cell ALL and Keywords: acute lymphoblastic leukemia; urate oxidase; uric acid; six with stage III or IV B cell NHL who were consecutively hyperuricemia; tumor lysis syndrome admitted to St Jude Children's Research Hospital from February 1994 to December 1996, 126, five and three, respectively, were treated with non-recombinant urate oxidase (Uricozyme, Introduction provided free of charge by Sanofi Winthrop). The enzyme was not given to 43 patients because of a history of allergy (atopic Hyperuricemia, a well-recognized complication of lymphoid allergy, glucose-6-phosphate dehydrogenase deficiency and malignant diseases and their treatment, has been associated pregnancy are listed as contraindications in the Uricozyme with high morbidity rates and delays in the delivery of chemopackage insert), six because they received the new recombitherapy, especially in patients with B cell or T cell acute lymnant urate oxidase (which recently became available for cliniphoblastic leukemia (ALL) and advanced-stage B cell noncal testing in a multicenter clinial trial), and four because they Hodgkin lymphoma (NHL). 1-6 The standard prophylaxis or did not receive methotrexate or 6-mercaptopurine as preintreatment of hyperuricemia in patients with neoplastic disduction therapy. Children with newly diagnosed non-B cell orders consists of allopurinol, vigorous hydration, urinary alk-ALL who were consecutively treated with allopurinol between alinization and osmotic diuresis. [2][3][4][5]7 By inhibiting the enzyme December 1991 and February 1994 served as historical conxanthine oxidase, hence uric acid formation, allopurinol thertrols. Informed consent was obtained from the parents or legal apy reduces the renal load of uric acid but increases the renal guardians of all patients. excretion of the uric acid precursors hypoxanthine and xanthine. 8 Unlike hypoxanthine, xanthine is actually less soluble than uric acid in urine. 9 In fact, occasional case reports of Chemotherapy xanthine nephropathy and calculi suggest that allopurinol treatment is detrimental to some patients. [10][11][12][13] Patients with non-B cell ALL receiving non-recombinant urate Urate oxidase, by converting uric acid to allantoin -a readoxidase and historical controls were the subjects of two consecutive Total Therapy studies (XIIIA and XIIIB). and randomized patients to receive either high-dose metho-

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confidence: 99%

Urate oxidase in prevention and treatment of hyperuricemia associated with lymphoid malignancies

et al. 1997

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“…Hydration and diuresis Treatment is based on strong hydration and diuresis unless acute renal failure and oliguria develop. Increased hydration and accompanying increase in the amount of urine increase the intracellular volume, renal blood flow and glomerular filtration and renal excretion of uric acid and phosphorus (12,21). Patients should be given 2-4-fold of their daily maintenance fluid (approximately 3000 mL/m 2 /day or 200 mL/kg/day, if the child weighs below 10 kg) and 100 mL/m 2 /h (3 mL/kg/h, if below 10 kg) urine output should be provided.…”

Section: Tiraje Et Al Tumour Lysis Syndromementioning

confidence: 99%

“…Urate is mostly dissolved at a pH level of 7.5. However, the solubility of xanthine and hypoxanthine strongly decreases at a pH level of 6,5 and xanthine crystals are formed during or after allopurinol treatment (21,22). In addition, urinary alkalinization decreases calcium-phosphate solubility and leads to agglutination of calcium phosphate crystals in the renal tubules.…”

Section: Alkalinization Of Urinementioning

confidence: 99%

Tumour lysis syndrome; new approaches at diagnose, follow up and treatment

Çelkan¹,

Tüysüz²

2013

Turk Pediatri Ars

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SummaryTumor lysis syndrome is a clinical picture which occurs with the lysis of malignant cells and causes metabolic abnormalities that threatens life. These metabolic abnormalities are caused by the release of intracellular ions, nucleic acids, proteins and their metabolites from the instantly degraded tumor cells. These rapidly released metabolites can impair the body's normal homeostatic mechanism and cause uremia, hyperuricemia, hyperkalemia and hyperphosphatemia. Hypocalcemia which is commonly seen in tumor lysis syndrome is secondary to hyperphosphatemia. Generally, tumor lysis syndrome occurs after the initiation of chemotherapy, but it is rarely observed in fast growing tumours before the treatment due to spontaneous lysis of malignant cells. The possibility of tumor lysis syndrome is higher in tumours with high proliferative rates and high tumour burden including Burkitt's lymphoma and acute lymphoblastic leukemia. The principle of prophylaxis/treatment of tumour lysis syndrome includes virgous hydration, adequate diuresis, control of hyperuricemia with rasburicase or allopurinol, regulation of serum electrolytes and dialysis, if necessary. If the necessary measures are not taken or the clinal situation is not treated properly, metabolic abnormalities can cause renal insufficiency, cardiac arrhythmia, neurologic complications and propably sudden death in patients with cancer. Alkalization of urine used to be applied to all patients previously, but it is not recommended any longer and this issue is still open to debate. In this paper, new approaches and innovations in the treatment of tumor lysis syndrome are discussed. (Turk Arch Ped 2013; 48: 188-194)

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“…et al, 1995;Rundles, 1966;Watts, 1966). Through blocking uric acid formation, allopurinol can effectively lower the serum uric acid level, but it increases the renal load of hypoxanthine and xanthine (both are uric acid precursors) (Andreoli et al, 1986;DeConti and Calabresi, 1966). Allopurinol treatment has been associated with xanthine nephropathy and calculi because xanthine is actually less soluble than uric acid in urine (Band et al, 1970;Wyngaarden, 1970).…”

Section: Supportive Care 71 Tumor Lysis Syndromementioning

confidence: 99%