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-
The effect of food intake on the pharmacokinetics of DEPAKINE CHRONO 500 mg (Sanofi, France), a sustained release formulation containing 333 mg sodium valproate and 145 mg valproic acid, was studied in 12 young healthy female volunteers. Relative to fasting conditions (F), when the tablet was given at the midpoint of the breakfast (NF), the maximum concentration (F: 34.6 +/- 8.9 micrograms ml-1 and NF: 40.9 +/- 7.3 micrograms ml-1; p = 0.014) and the mean cumulative amount absorbed up to time 6 h (F: 76.3 +/- 11.8% and NF: 90 +/- 10.4%; p = 0.0099) were significantly increased. Nevertheless, the extent of absorption (F: 46.7 +/- 9.9 mg l-1; NF: 48.7 +/- 7 mg l-1) was not significantly affected. There was no change in the area under the curve (1129 micrograms.h ml-1), in the mean residence time (28 h), or in the elimination half-life (16 h). On the basis of this study, the question as to whether DEPAKINE CHRONO should be administered to subjects in the fasting or non-fasting state would not appear to be a major consideration when deciding on the regimen.
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