Children with acute lymphoblastic leukemia (ALL) can experience a decrease in their white blood count (WBC) prior to chemotherapy, a phenomenon commonly attributed to the administration of allopurinol and hydration. We reviewed the records of 20 children with newly diagnosed ALL prior to the administration of allopurinol and found that 80% of patients experienced a decrease in their WBC (median decrease 14,000/mm(3)) in the less than 24-hr interval between evaluation at the referring center and admission to our hospital (P = 0.002). The basis for this often-observed phenomenon appears to be that leukemic cells rapidly lyse in response to the stress-induced release of endogenous corticosteroids.
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In a rat liver tumour system with a nitrosoguanidine-induced carcinoma and in an in vitro system with the same tumour, the effect of allopurinol on the toxicity and antitumour effect of 5-fluorouracil (5-FU) was explored. Two doses of 5-FU, 30 and 60 mg/kg b.w. intraperitoneally (i.p.), were tested with a large dose of allopurinol subcutaneously (s.c.( (300 mg) in rats. The drugs were given for three consecutive days. The lethal toxicity of 60 mg 5-FU i.p. could not be counteracted by allopurinol. Allopurinol and 30 mg 5-FU reduced the tumour growth rate more than 5-FU alone. The spleen was smaller, as a sign of increased toxicity, without allopurinol. The concentration of allopurinol and its metabolites in the general circulation was high. In vitro, there was no additive or specific effect of allopurinol. These results indicate some in vivo metabolic modulation of 5-FU efficacy by allopurinol if 5-FU is administered intraperitoneally and allopurinol systemically.
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Patients with a crystal proven gout diagnosis, who newly started allopurinol treatment, were included in this prospective cohort study. After evaluation at baseline for cardiovascular diseases, tophi, uric acid, CRP and CXCL8 serum levels, patients were followed for changes in uric acid and CXCL8 levels. A subgroup analysis was performed in 10 patients with the longest follow-up period and at least 4 assessments of serum uric acid and CXCL8.
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We report here the effect of oxygen free radicals, OFR (superoxide, O2-; hydroxy, OH; t-butylhydroperoxide, H2O2) lipid peroxides (malondialdehyde, MDA), free radical scavengers (superoxide dismutase, catalase, allopurinol) and generator (ferrous chloride) antioxidants (ascorbate, glutathione) spin traps (5,5-dimethyl-1-pyroline-N-oxide, N-t-butyl-L-pheny nitrone) on the cardiac isoenzyme (CK, CK-MB, LDH, LD1) concentrations in the sera of patients with acute myocardial infarction. CK-MB and LD1 were rapidly and completely inactivated by O2- (50 nmol/ml), OH (1 nmol/ml) and MDA (0.6 microM). Butylhydroperoxide (600 microM), and ferrous chloride (200 microM) selectively inhibited CK-MB. The free radical scavengers, antioxidants and spin traps all had minimal effects, and H2O2 had none.
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Karapxa decoction (KD) is a Traditional Uighur Medicine used for hepatitis, cholecystitis, gastralgia, oedema, gout and arthralgia. Because of its purported effect in gout, its effects were tested in hyperuricemic mice models induced by yeast extract paste or potassium oxonate, as well as its capacity to scavenge free radicals in vitro.
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Surgical stress can lead to bacterial translocation from the intestine into systemic circulation. Adherence of bacteria onto the glycoconjugates of the brush border membrane (BBM) and surfactant coat (SLP) of the mucosal cells is the first step in the translocation of luminal bacteria. Our earlier study showed that surgical manipulation of the intestine results in oxidative stress leading to structural and functional alterations in the mucosa. This study looks at the effect of surgical manipulation on the glycoconjugate alterations of SLP and BBM.
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Organ preservation is one of the important steps that predicts the patient outcome. However, after revascularization, the high concentration of potassium that influxes into the circulation might cause immediate postreperfusion hyperkalemia. To prevent this complication, the portal vein has been washed out with flush fluid to remove preservation fluid before reperfusion. Up to now, it has not been established what exact amount volume of albumin provides washout of the UW solution.
ROS, probably derived from NADPH oxidase and mitochondria, partially regulate alpha1-adrenoceptor-activated smooth muscle contraction by altering myosin phosphatase-mediated MLC20 phosphorylation through both RhoA/Rho kinase- and CPI-17-dependent pathways.
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We have investigated the possible protective effect of superoxide dismutase and allopurinol in a rat model of mild and severe hepatic necrosis produced by Corynebacterium parvum with or without endotoxin. Histology showed a sinusoidal mononuclear cell infiltrate with multiple granulomata but variable degrees of hepatic necrosis. In the severe hepatic injury model there was a reduction in mortality, associated with a decrease in histologic and biochemical evidence of hepatic necrosis, after treatment with superoxide dismutase. This protective effect was not demonstrated with partially heat-inactivated superoxide dismutase. In the mild hepatic injury model similar trends in reduction of serum levels of hepatic enzymes were observed after treatment with both superoxide dismutase and allopurinol. These results indicate that oxygen-derived free radicals may play an important role in the pathogenesis of hepatic injury in the rat.
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Thirty-three children ranging from 2 weeks to 12 years of age were selected for allopurinol loading, 16 on the basis of an increased urinary ourotate excretion detected by routine organic acid analysis (group A), and 17 for clinical reasons suggesting a urea cycle defect (group B). The allopurinol load test proved positive in 13 of 16 patients from group A, mean peak orotate 64.0 mumol/mmol creatinine (upper limit of reference range, 13.2) and 11 of 17 patients from group B, mean peak orotate 41.0 mumol/mmol creatinine (upper limit of reference range, 13.2). Thorough investigation of these patients including urinary and plasma amino acid analysis and, in 17 cases, liver biopsy for histology and measurement of ornithine carbamyltransferase (OCT) and carbamyl-phosphate synthetase (CPS) activity failed to identify any evidence of a urea cycle disorder. However, muscle biopsies performed in 11 patients showed some evidence of mitochondrial disease in four cases, two defined on the basis of reduced respiratory chain enzyme activity and two on the basis of mtDNA abnormalities. These findings indicate that an increased excretion of orotate in sick children may not be uncommon and that a positive allopurinol load test result may not indicate a specific inherited urea cycle defect. In addition, these results raise the interesting possibility that defective ureagenesis may be a feature of mitochondrial disease in some individuals.
A 54-year-old man was receiving allopurinol therapy to treat hyperuricemia that followed an inferior wall, myocardial infarction. After three weeks of allopurinol therapy, the patient developed signs and symptoms of toxic epidermal necrolysis that included pseudomembranous conjunctivitis with ulcerative lesions on the lids and conjunctiva, and punctate corneal staining with subsequent corneal abrasions. Treatment with topical antibiotics and artificial tears relieved the symptoms somewhat, but punctate staining and dry eyes persisted after 14 months of follow-up. Bilateral corneal ulcers developed and necessitated conjunctival flaps in each eye. Visual acuity in each eye was 20/40.
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We investigated the metabolism of high dose 6 mercaptopurine (HD-6MP) infusions and its influence on the metabolism by allopurinol, an inhibitor of xanthine oxidase, the enzyme that catabolizes 6MP into thioxanthine and thiouric acid.
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A retrospective review of 154 PTx performed over a 61-month period included 77 grafts preserved with UW and 77 with C. The two groups were comparable for both donor and recipient characteristics.
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The past decade has witnessed an exponential increase of novel therapeutic modalities for a variety of rheumatic disorders, including gout. During the past few years two novel therapeutic agents have been approved by the US Food and Drug Administration for the treatment of hyperuricemia in patients with gout, one of them being febuxostat, a nonpurine selective inhibitor of xanthine oxidase. Review of its pharmacokinetics and pharmacodynamics, efficacy and safety profile, and use in gout patients with comorbid conditions reveals that age and gender have no clinically significant effect and dose adjustments based on age or gender are not required. In addition, febuxostat can be used in patients with mild-to-moderate renal or hepatic involvement. Its overall efficacy and safety profile is comparable and, in certain subsets such as gout patients with mild and moderate renal insufficiency, is superior to allopurinol.
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Allopurinol hypersensitivity was identified within 3 months since the first prescription. The period for measuring related hospitalizations was 1 month since the episode, and the period for measuring renal complications or mortality was 2 months since the episode. Poisson regression test and multivariable logistic regression analysis were performed, and P < .01 was considered statistically significant.
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In the differential diagnosis of hepatic fibrin-ring granulomas, serologic titers remain the determining factor, since an infective agent is the most common cause. When hepatic fibrin-ring granulomas are present, other histopathological features may be helpful in making the differential diagnosis.
Serum xanthine concentrations as high as 148 mg/L were noted after treatment of a patient with Burkitt's lymphoma who was receiving allopurinol. These markedly above-normal values for xanthine led to spuriously low values for serum uric acid as measured by the uricase method. Rapid tumor lysis in patients who are receiving allopurinol may lead to marked hyperxanthinemia, which in turn may obscure hyperuricemia in such patients when the uricase method is used for uric acid analysis. In such situations, uric acid concentrations should be measured by the phosphotungstate colorimetric assay.
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Homocysteine inhibits endothelium-dependent NO-mediated dilation in the retinal arterioles by producing superoxide from NAD(P)H oxidase, which appears to be linked with p38 kinase. By impairing endothelium-dependent NO-mediated vasoreactivity, homocysteine potentially facilitates development of retinal vascular diseases. In addition, pioglitazone can prevent homocysteine-induced endothelial dysfunction possibly by activating PPAR-γ.
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The irreversible loss of adenine nucleotides and the formation of free radicals have both been suggested as causes of irreversibility following prolonged hemorrhagic shock. This study was performed to assess the effect of xanthine oxidase inhibition (allopurinol 50 mg/kg/day), free radical scavenging (superoxide dismutase 15,000 u/kg, catalase 15,000 u/kg, dimethylsulfoxide 20 mg/kg, and alpha tocopherol 100 mg/kg/day) or both, on the 24-hr survival of dogs subjected to irreversible haemorrhagic shock. Twenty anesthetized dogs were bled to a mean arterial pressure of 30 mm Hg for 4 hr. The dogs were allocated to a control, an allopurinol pretreated, a free radical scavenger, or a combined treatment group. Both groups pretreated with allopurinol had significantly improved survival (P < 0.05) over that seen in the control group, but the free radical scavenger treated group was not significantly different from the control group. This study demonstrates the beneficial effect of xanthine oxidase inhibition on survival, and suggests that it may be due to preservation of adenine nucleotides rather than prevention of free radical formation.
The failure of allopurinol users to achieve target SUA levels of <6.0 mg/dL may be attributed to lack of awareness of optimal SUA, allopurinol dosing, compliance, and efficacy. Patients who did not achieve target SUA were at increased flare risk.
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A brief period of liver ischemia decreases sinusoidal endothelial cell killing after cold liver storage and improves graft survival after liver transplantation, a phenomenon called ischemic preconditioning. In this study, we investigated the mechanism of sinusoidal endothelial cell protection after ischemic preconditioning. Livers were preconditioned by 5 minutes of ischemia and 5 minutes of reperfusion. Subsequently, livers were stored for 30 hours in cold University of Wisconsin (UW) solution and reperfused briefly with physiological buffer containing Trypan blue. Ischemic preconditioning decreased sinusoidal endothelial cell killing after storage/reperfusion, as assessed by Trypan blue staining of nonparenchymal cells. Adenosine A(2) receptor blockade prevented the protective effect of ischemic preconditioning. By contrast, adenosine A(1) receptor blockade did not prevent protective ischemic preconditioning. Other rat livers were treated with adenosine A(1) and A(2) receptor agonists or dibutyryl-cyclic adenosine monophosphate (DB-cAMP) before storage. The adenosine A(2) receptor agonist, CGS-21680, and DB-cAMP decreased sinusoidal endothelial cell killing to the same extent as ischemic preconditioning, but the adenosine A(1) receptor agonist, 2-chloro-N(6)-cyclopentyladenosine (CCPA), had no effect. The adenosine A(2) agonist and prostaglandin E(2), another agent that preconditions sinusoidal endothelial cells against storage/reperfusion injury, but not the adenosine A(1) agonist, increased cAMP levels in cultured sinusoidal endothelial cells. In conclusion, an adenosine A(2) receptor pathway coupled to increased cAMP mediates sinusoidal endothelial cell protection by ischemic preconditioning.
Applying algorithms to national administrative data sets provides a readily available method for estimating the prevalence of a chronic condition such as gout, where diagnosis and drug treatment are relatively specific for this disease. We have demonstrated high gout prevalence in the entire Aotearoa New Zealand population, particularly among Māori and Pacific people.
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The luminol-dependent chemiluminescence (CL) response in vitro of guinea-pig C. parvum-activated peritoneal macrophages to platelet activating factor (PAF) has been compared with that to opsonized zymosan (OpZ). The response to PAF (5 X 10(-6) mol/l.) reached a peak within 1 min, that to OpZ (0.17 mg/ml) within 10-20 min. Peak responses to both stimuli were dose-dependently inhibited in a similar manner by p-hydroxymercuribenzoate (10(-5) - 10(-3) mol/l), sodium benzoate (10(-5) - 10(-3) mol/l.) and quinacrine (10(-6) - 10(-3) mol/l.). In contrast, the xanthine oxidase inhibitor allopurinol (IC50 vs OpZ, 220 mumol/l.; vs PAF greater than 1000 mumol/l.), the methylation-inhibiting combination homocysteine + 3-deazaadenosine (IC50 vs OpZ, 22 mumol/l.; vs PAF greater than 100 mumol/l.), the phospholipase A2 inhibitor and alkylating agent p-bromophenacylbromide (pBPB; IC50 vs OpZ, 2.6 mumol/l.; vs PAF 15 mumol/l.) and the beta-adrenoceptor agonist isoprenaline (IC50 vs OpZ, 0.1 mumol/l.; PAF greater than 10 mumol/l.) all exerted differential inhibitory effects on the CL responses to the two stimuli, though colour quenching by adrenochrome cannot be ruled out in the differential effect of isoprenaline. In screening studies, carried out with CL responses measured 2 or 5 min after PAF and OpZ, respectively, verapamil (less than or equal to 10(-4) mol/l.), trifluoperazine (less than or equal to 10(5) mol/l.) EDTA (less than or equal to 10(6) mol/l.), mannitol (less than or equal to 10(-2) mol/l.), metyrapone (less than or equal to 10(-5) mol/l.), SQ 22536 (less than or equal to 10 micrograms/ml.), iso-butyl methylxanthine (less than or equal to 10(-5) mol/l.).(ABSTRACT TRUNCATED AT 250 WORDS)
Randomised, double-blind, placebo controlled trial.