Drugs online research references
Am J Kidney Dis. 1999 Nov;34(5):E20.
Hyperuricemia and renal insufficiency associated with malignant disease: urate oxidase as an efficient therapy?
Wolf G, Hegewisch-Becker S, Hossfeld DK, Stahl RA.
Department of Medicine, Division of Nephrology and Osteology, and the Division of Oncology and Hematology, University of Hamburg, Hamburg, Germany.
Hyperuricemia is a common finding in patients with malignant diseases. Chemotherapy can induce life-threatening tumor lysis syndrome with severe hyperuricemia, other metabolic abnormalities, and acute renal failure. Intrarenal precipitation of uric acid contributes to renal insufficiency in this situation. Allopurinol, by preventing the conversion of hypoxanthine and xanthine to uric acid, has been long considered the standard pharmacological approach to hyperuricemia and prevention of tumor lysis syndrome. However, allopurinol itself may facilitate precipitation of xanthine crystals and has little influence on already-formed uric acid crystals deposited in the kidney. Urate oxidase further oxidizes uric acid to the highly water-soluble allantoin in mammals, except humans, who lack this enzyme. We report four cases of hyperuricemia (initial serum uric acid concentrations, 14.0 to 25.0 mg/dL) associated with malignant diseases treated with exogenous urate oxidase. Two of the patients showed full-blown tumor lysis syndrome. A single urate oxidase infusion (1,000 U) readily reduced serum uric acid levels in all patients. Furthermore, renal insufficiency, determined by serum creatinine concentrations, improved in three of the four patients. No adverse effects were observed. Currently, a recombinant urate oxidase is undergoing clinical testing and may make this efficient therapy more widely available. We believe that treatment with urate oxidase is a safe and efficient therapy for patients with cancer-associated hyperuricemia and may be effective even in individuals with only moderately elevated serum uric acid concentrations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10561160&dopt=Abstract [PubMed - as supplied by publisher]
J Clin Invest. 1992 Sep;90(3):1007-15.
Synthesis and release of interleukin 1 by reoxygenated human mononuclear phagocytes.
Koga S, Ogawa S, Kuwabara K, Brett J, Leavy JA, Ryan J, Koga Y, Plocinski J, Benjamin W, Burns DK, et al.
Department of Physiology, Columbia University, College of Physicians and Surgeons, New York 10032.
To examine the possible involvement of cytokines in reperfusion injury, we have studied production of IL-1 by human vascular cells, including smooth muscle and mononuclear phagocytes. Exposure of cells to hypoxia (pO2 approximately 14 torr) followed by reoxygenation led to significant release of IL-1 only from the mononuclear phagocytes. Elaboration of IL-1 was dependent on the oxygen tension and duration of hypoxia (optimal at lower pO2s, approximately 14-20 torr, and after 9 h), as well as the time in reoxygenation (maximal IL-1 release at 6-9 h). Although a period of hypoxia was necessary for subsequent IL-1 production during reoxygenation of either peripheral blood monocytes or cultured monocyte-derived macrophages, no IL-1 release occurred during the hypoxic exposure. IL-1 released during reoxygenation was newly synthesized, and its production was triggered by the generation of oxygen free radicals, as it could be blocked by the addition of either allopurinol or free radical scavengers to cultures and could be stimulated in part by low concentrations of hydrogen peroxide or xanthine/xanthine oxidase. The potential pathophysiological effects of IL-1-containing supernatants from reoxygenated macrophages was shown by their induction of endothelial tissue factor and enhancement of endothelial adhesiveness for neutrophils, both of which could be blocked by anti-IL-1 antibody. The relevance of IL-1 to hypoxia/reoxygenation in vivo was suggested by the presence of circulating nanogram amounts of this cytokine in the plasma of mice during the reoxygenation period following a hypoxia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1325990&dopt=Abstract
Br J Pharmacol. 1986 Sep;89(1):149-55.
The protective action of allopurinol in an experimental model of haemorrhagic shock and reperfusion.
Allan G, Cambridge D, Lee-Tsang-Tan L, Van Way CW, Whiting MV.
Haemorrhagic shock was induced in anaesthetized, open-chest dogs by controlled arterial bleeding, sufficient to reduce and maintain mean arterial blood pressure at 40 mmHg for 30 min. The blood volume was then restored to the pre-shock level by rapid, intravenous reinfusion of the blood shed during the shock period. Haemorrhagic shock produced significant haemodynamic changes, characterized by a marked depression of myocardial function. Cardiac output (1226 +/- 57 ml min-1), peak aortic blood flow (6030 +/- 383 ml min-1) and maximum rate of rise of left ventricular pressure (2708 +/- 264 mmHg s-1) were all reduced by more than 50%. The haemodynamic profile was markedly improved by reinfusion of shed blood but this improvement was not sustained. There was a gradual decline such that 50% of the untreated animals suffered complete circulatory collapse and death between 60 and 120 min following reinfusion. Neither haemorrhagic shock, nor reinfusion of shed blood produced any consistent or significant changes in the myocardial adenine nucleotide pool. The ATP, ADP and AMP levels were, respectively, 25.9 +/- 4.2; 15.6 +/- 1.0; 4.3 +/- 1.9 nmol g-1 protein, before haemorrhagic shock; 21.6 +/- 3.4; 21.5 +/- 2.5; 10.2 +/- 2.7 nmol g-1 protein, after 30 min haemorrhagic shock; and 29.9 +/- 3.9; 16.5 +/- 1.2; 4.2 +/- 1.1 nmol g-1 protein, 60 min following reinfusion of shed blood. Pretreatment with allopurinol (50.0 mg kg-1 i.v.), 60 min before inducing haemorrhagic shock, had no significant effect upon the haemodynamic response to shock, but did prevent the gradual decline seen following reinfusion in the untreated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3801769&dopt=Abstract
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