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Retrospective cohort study.
The Eastern Cooperative Oncology Group (ECOG) studied 29 patients with advanced measurable colon cancer who were treated with Aminothiadiazole (NSC #4728) 125 mg/m2 intravenously. Allopurinol 300 mg daily was taken by all patients during treatment. Three patients (12%) demonstrated partial responses on this regimen. Hematologic toxicity did not occur. Gastrointestinal toxicity was severe in 16% of patients and consisted primarily of vomiting and diarrhea. No life-threatening toxicity was encountered. A lack of appreciable toxicity together with the few responses seen suggest that further studies at higher dose may be indicated.
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In an isolated perfused rat liver model, hepatocellular damage and liver function were assessed during reperfusion with Krebs-Henseleit buffer after 24 hours hypothermic MP using Polysol-HES, Polysol-dextran, or Polysol-PEG. Control livers were preserved by MP using UW-G.
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Our results suggest the addition of 10% allogenic serum to University of Wisconsin solution enhances viability of osteochondral tissue samples.
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Age, gender, lipid profile, eGFR, hemoglobin, glucose, and level of proteinuria were similar in hyperuricemic subjects and controls at baseline. As expected, hyperuricemic patients had higher levels of highly sensitive C-reactive protein and lower FMD compared with normouricemic patients. Allopurinol treatment resulted in a decrease in serum uric acid, a decrease in systolic BP, an increase in FMD, and an increase in eGFR compared with baseline. No significant difference was observed in the control hyperuricemic and normouricemic groups. In a multiple regression analysis, FMD levels were independently related to uric acid both before (beta = -0.55) and after (beta = -0.40) treatment.
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All 5 animals in Group 1 survived up to 7 days, the survey endpoint. In Group 2, only 2 animals survived to the same survey endpoint. All animals in Group 3 died within 12 hours. The 1-week survival rate of Group 1 was significantly higher than those of the other 2 groups. Group 1 showed a lower level of alanine aminotransferase (ALT) or aspartate aminotransferase (AST) after LTx, less pathological damage, higher concentration of adenosine triphosphate (ATP), and higher microcirculation blood flux in the grafted liver tissue at 1 hour after reperfusion than the other 2 groups.
The role of superoxide and lipid peroxidation in liver injury induced by ischemia-reperfusion was investigated in rats. Ischemic condition of the liver was created by applying small clamps to the right branch of portal vein and the right hepatic artery for 15 min. Clamping of hepatic artery and portal vein could decrease the hepatic blood flow to about 30% of that measured before the clamping. Levels of serum GPT and thiobarbituric acid (TBA) reactive substances in the liver tissue were significantly increased 30 min after the reperfusion following 15 min of ischemia. The increase in serum GPT and TBA reactants in the liver tissue was significantly inhibited by the treatment with superoxide dismutase combined with catalase. The treatment with allopurinol significantly inhibited the elevation of serum GPT levels and showed a tendency to inhibit the increase in TBA reactants in liver tissue. These results suggest that active oxygen species and lipid peroxidation may play an important role in the pathogenesis of ischemia-reperfusion injury in the liver, and hypoxanthine-xanthine oxidase system may be one of the main sources of active oxygen species.
In experiment 1, hind limb IR rats were treated intraperitoneally with one of following agents at 30 min before reperfusion: allopurinol (4, 40 mg/kg), superoxide dismutase (SOD, 4000 U/kg), N-nitro-l-arginine methyl ester (l-NAME, 10 mg/kg), or SOD (4000 U/kg) + l-NAME (10 mg/kg). In experiment 2, 5,10,15,20-tetrakis (N-methyl-4'-pyridyl) porphyrinato iron (III) (FeTMPyP) was administered intraperitoneally (1, 3, or 10 mg/kg) 30 min before reperfusion. After 3 d reperfusion period, the spinal cord (L4-6) was harvested to investigate MAPK signaling activity.
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Rats were subjected to sham laparotomy (SL), portal hypertension (PH) by calibrated stenosis of the portal vein, and common bile duct ligation (CBDL). Animals of each group were either treated with allopurinol (50 mg/kg twice a week), glutamine (1 g/kg/d), and allopurinol and glutamine.
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A patient with acute oliguric uric acid nephropathy was treated with hemodialysis. Recovery in this disorder is based on treatment of both the uremic state and the intrarenal crystal obstruction. Hemodialysis with high uric acid clearance is much more efficient than other forms of therapy in this disorder.
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Diabetic nephropathy is the most prevalent cause of end-stage renal disease. Besides factors such as angiotensin II, cytokines, and vascular endothelial growth factor, uric acid may play a role as the underlying cause of diabetic nephropathy. We evaluated allopurinol effects on proteinuria in diabetic patients with nephropathy.
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Eurocollins has almost been abandoned because of the glucose disadvantage. UW is certainly the most used preservation solution for livers, kidneys, and pancreases with excellent clinical and experimental preservation data. UW can certainly be considered the current golden standard solution. However, the disadvantage of high viscosity, high price, uneasy handling of many 1-L bags, and the fact that the radical scavenger glutathion cannot be detected in the bags by chemical analysis (presumably due to diffusion) encourage competitors to produce new compounds with better cost to effect ratios. HTK has a firm place in cardiac preservation; by demonstration of equal safety and efficacy in preserving livers and kidneys, at least in the middle and lower range of cold ischemia time, HTK will be sued more frequently, particularly with the consideration of lower price and more easy handling aspects. The suggested high volume perfusion is not really necessary, calculation based on a total volume of 10 L for a multiorgan donor show significant cost reductions. Celsior is current only used for cardiac preservation. Beyond all aspects of conservation and preservation potencies of all these fluids, it must not be forgotten that cold ischemia itself is a risk factor for organ function. Therefore, cold ischemia time should be kept as short as possible. People are willing to accept 24 hours or more cold ischemia time in kidney transplantation because organ failure can be treated by dialysis. In other organs, where immediate organ function is essential, like in clinical heart transplantation, cold ischemia is hardly ever extended beyond 6 hours. Why are hearts and kidneys so different? Very likely, there is no difference, and the outstanding results in living unrelated kidney transplants is mostly due to short cold ischemia time.
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Allopurinol decreases C-reactive protein and slows down the progression of renal disease in patients with chronic kidney disease. In addition, allopurinol reduces cardiovascular and hospitalization risk in these subjects.
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Liver ischemia/reperfusion injury is a severe problem in transplantation, and preservation solutions could be critical for liver viability. The aim of our study was to evaluate the cytosolic and mitochondrial glutathione levels, the glyoxalase II activity, and the mitochondrial hydroperoxide contents of livers stored in different preservation solutions for 7 or 24 h and after transplantation.
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Many quantitative studies globally have identified suboptimal management of gout.
This report is first case of rhabdomyolysis associated with initiation of febuxostat. Febuxostat should be withdrawn when rhabdomyolysis is confirmed.
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Most of the primates, unlike other mammals, have mutations in urate oxidase gene and cannot catabolize urate in the bodies. In addition to the genetic defects, some human subjects have various abnormalities in urate metabolism. Urate metabolism abnormalities are classified into two categories, hyperuricemia and hypouricemia. Usually, the urate pool size of an adult male is about 1,200 mg, and 700 mg urate is produced daily. The production is balanced by the excretion of urate into urine (500 mg) and intestine (200 mg). If this balance is disturbed, either hyperuricemia or hypouricemia occurs. According to the mechanisms, hyperuricemia is classified into overproduction and underexcretion, and hypouricemia into underproduction and overexcretion. Overproduction of ruate is caused by PRPP synthetase superactivity, HPRT deficiency, leukemia and alcohol ingestion. Underexcretion of urate is caused by renal insufficiency and treatment by diuretics. Underproduction of urate is caused by xanthine dehydrogenase deficiency, purine nucleoside deficiency and allopurinol treatment. Overexcretion of urine is caused by familial renal hypouricemia, Fanconi's syndrome, diabetes mellitus and treatments with benzbromarone and probenecid. All of these conditions are classified, according to other aspects, into primary and secondary, and genetic and non-genetic abnormalities.
Study design and sample size calculations were based on previously published experience of our group with low protein diet. The primary outcome of the study was the modification of serum urea nitrogen concentration. From 423 patients randomly assigned to the two diets 392 were analysed: 200 for the 0.55-Group and 192 for the 0.8-Group. The follow-up ranged 6-18 months.
1. Community workers who speak Pacific languages may assist GPs in communicating to non-English speaking patients. 2. Alternative diagnoses should be considered in symptomatic patients with prolonged normouricaemia. 3. GPs should gradually introduce allopurinol after acute gout attacks, emphasising importance of prophylaxis. 4. A campaign to inform patients about benefits of allopurinol should be considered. 5. A simple one keystroke audit is needed for gout audit and benchmarking. 6. GP guidelines for gout diagnosis and management should be available.
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To characterize the clinical characteristics of drug hypersensitivity syndrome (DHS).
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The Eurocollins (EC) and University of Wisconsin (UW) preservation solutions were compared in a rat liver transplant model. After hepatectomy, 48 rat livers were flushed with either EC or UW preservation solution and were randomly assigned to 1, 12, 24, and 30 h of preservation at 4 degrees C, resulting in eight groups each containing six livers. Following preservation, orthotopic liver transplantation with reconstruction of the hepatic artery was performed. The efficacy of the preservation solution was assessed at 48 h post-transplantation by survival histological features and aspartate transaminase assay (AST) values. None of the rats survived 30 h of liver preservation with EC whereas five out of six rats did with UW preservation. After 24 h of liver preservation, three of the six rats in the EC group survived, compared to all six rats in the UW group. Histological evidence of severe ischemia was found in both groups in all but one survivor (UW, 24 h). After 12 h of EC preservation, one rat died within 48 h and severe ischemic changes were found in the remaining five rats. Among the rats with 12 h of UW preservation, only two out of six showed ischemic changes, and all six rats survived beyond 48 h. Without preservation (1 h), ischemic damage was found in two out of six rats in each group and all rats survived. The median AST values were higher in the EC groups than in the UW groups; the difference became significant after 12-h preservation (EC 900 IU/l versus UW 465 IU/l) and 24-h preservation (EC 5220 IU/l versus UW 631 IU/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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The alanine aminotransferase level in perfusate in RMP during perfusion preservation was maintained at less than that of HMP. The levels of aspartate aminotransferase and lactate dehydrogenase in the 2 hours after reperfusion were significantly lower in group 3. Histologically, the necrosis of hepatocytes was less severe in group 3. The survival rate in group 3 was 2/4, but 0/4 in the other group.
These results indicate that superoxide mediates cerebral endothelial dysfunction after hypoxia/reoxygenation largely via activation of NADPH oxidase and possibly activation of NF-kappaB pathway.
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To evaluate the efficacy of University of Wisconsin solution for clinical heart transplantation, load-independent parameters were used to assess left ventricular function after transplantation. Donor hearts were arrested with and stored in buffered cold cardioplegic solution for control (n = 5) and University of Wisconsin solution for the experimental group (n = 5). Orthotopic transplantations were performed in a routine manner. Mean donor age (cardioplegic solution, 28 +/- 5.2 years; University of Wisconsin solution, 28 +/- 5.1 years) and ischemic times (cardioplegic solution, 181 +/- 27 minutes; University of Wisconsin solution, 224 +/- 23 minutes) were similar. Two hours after reperfusion of the heart, transesophageal echocardiography was used to image the left ventricle at the mid-papillary muscle level, and a high-fidelity catheter-tipped manometer was placed in the left ventricle to record left ventricular pressure simultaneously. These images were digitized during apneic baseline conditions and during an acute reduction in preload from inferior vena caval occlusion. The left ventricular cross-sectional areas were measured and matched with left ventricular pressure from the catheter-tipped manometer to reveal pressure-area relationships. The baseline parameters fractional area change and stroke force were calculated. End-systolic elastance, the slope of end-systolic pressure-area relationship and preload recruitable stroke force, the slope of stroke force versus end-diastolic area were calculated from the inferior vena cava occlusion measurements.(ABSTRACT TRUNCATED AT 250 WORDS)
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Celsior solution was compared with the clinical standard University of Wisconsin solution (UW) in a porcine allogenic heart transplantation model with accurate isovolumic measurement of right ventricular (RV) function.
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We used the isolated perfused rat lung to test how two preservation solutions (low potassium dextran and University of Wisconsin solution) affected quality of lungs after 6, 12, and 24 hours of preservation. Also, we tested modifications of the University of Wisconsin solution, including reversing the ratio of Na/K, the addition of 1.5 mmol/L calcium, and the combination of calcium and butanedione monoxime, agents that improve cardiac preservation. After preservation at 4 degrees C, lungs were reperfused at 37 degrees C with a physiologically balanced solution. Pulmonary artery flow rate, airway peak inspiratory pressure, and tissue edema were used to assess degree of preservation and reperfusion injury.
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The effect of different pH of resuspension media on the viability of hepatocytes preserved (for 96 h at 4 degrees C) in University of Wisconsin solution (UW solution) was analyzed. After this cold resuspension media storage, we evaluated the rewarming step (incubation time 120 min at 37 degrees C) using different pH levels (6.80, 7.00, 7.20, and 7.40). Cell viability assessed by trypan blue exclusion (TBE) showed a significant difference (p < 0.05) for cells incubated at pH = 7.20. For instance, TBE expressed as percent of change was 78.1 +/- 1.4 compared with cells tested at other pH (pH = 6.80, TBE = 44.2 +/- 9.5; pH = 7.00, TBE = 66.5 +/- 1.1 and pH = 7.40, TBE = 62.0 +/- 1.4). We also evaluated the capacity of these cells both to maintain potassium content (0.509 +/- 0.230 microEq. K+/10(6) cells) and to synthesize urea (5.36 +/- 1.81 mumol Urea/10(6) cells). These results were compared with those obtained from freshly isolated non preserved hepatocytes (0.518 +/- 0.060 microEq. K+/10(6) cells and 5.91 +/- 0.43 mumol Urea/10(6) cells). The results show that viability is pH dependent and suggest that when resuspension media were used, the viability of hepatocytes was improved after 96 h of cold storage.
To review indications for HTx, current immunosuppressive therapy, posttransplant morbidities, and outcome in Chagas' heart transplant recipients. Review of articles linking HTx and Chagas' disease at PubMed and Scielo database from 1966 onward. HTx can reasonably be indicated in patients with an annual probability of death of 70%. HTx has been associated with a similar incidence of rejection episodes in Chagas' and non-Chagas' heart transplant recipients. A lower incidence of infection episodes has been observed in Chagas' in comparison to non-Chagas' heart transplant recipients. T. cruzi infection reactivation is easily treated with either benznidazole or allopurinol and portends a very low mortality rate. Other posttransplant morbidities have a similar incidence in Chagas' and in non-Chagas' patients. Survival probability for Chagas' HTx recipients at 1 month, 1 year, 4 years, and 10 years follow-up is 83%, 71%, 57%, and 46%, respectively. Such an outcome is better than that seen in non-Chagas' heart transplant recipients.
A rapid method is described for benzbromarone assay in human serum. Protein precipitation is followed by extraction of the active substance. After centrifugation the clear organic layer is evaporated to dryness, redissolved in methanol and injected on a HPLC-column. Detection limits for this method of assay are 0.1 microgram benzbromarone/ml serum. The blood level for therapeutic concentrations lies between 1 and 2.5 microgram/ml. Some pharmacokinetic data were presented. The half-life of benzbromarone is 2.6 h.
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To ensure reproducibility of measurements of xanthine concentration in urine samples collected from dogs that are affected with urate uroliths and receiving allopurinol, urine should be diluted 1:20 with deionized water. These measurements may be useful for monitoring dogs that are receiving allopurinol for dissolution or prevention of urate uroliths.
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A reversed-phase high-performance liquid chromatographic method was developed for the simultaneous determination of pyrazinamide and its metabolites in urine. Study of the metabolism of pyrazinamide by this method demonstrated that 5-hydroxypyrazinamide excretion was compatible with pyrazinoic acid excretion and allopurinol decreased in vivo conversion of pyrazinamide to 5-hydroxypyrazinamide and blocked that of pyrazinoic acid to 5-hydroxypyrazinoic acid.
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Gout is one of the most common forms of arthritis and the prevalence is increasing. Management comprises rapid and effective control of the inflammation in acute gout and sustained urate lowering in the long term. Improving the outcomes for cheaper old drugs and for the increasing number of new, more expensive agents is an important clinical goal. The role of pharmacogenetics in predicting response and adverse events to gout therapies is of considerable interest. Currently, prospective screening is employed to detect HLA-B*5801 carriage and glucose-6-phosphate dehydrogenase deficiency, to minimize occurrence of allopurinol hypersensitivity and pegloticase-related hemolytic anemia. In the future it is likely that other genetic markers of drug response will make the transition to clinical practice to further improve the efficacy and safety of gout therapies. In this review, we will examine the potential clinical relevance of specific genetic variants in the management of gout.
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Allopurinol is often prescribed for the treatment of hyperuricemia. It inhibits the uric acid production binding tightly to xanthine oxidase. Although it is generally well tolerated, an almost 10% prevalence of adverse reactions has been reported, particularly gastrointestinal and neurological effects. Some hypersensitivity syndromes have also been described (rash, vasculitis or exfoliative dermatitis). In these cases, if a substitute treatment is not available, a desensitization procedure to the drug must be considered. We present three patients with cutaneous hypersensitivity to allopurinol, two who developed urticaria and other one who had a fixed drug eruption. Skin test were all negatives with positive oral challenge test. An out- patient desensitization procedure to allopurinol was initiated, repeating the last tolerated doses for 4 or 5 days, and reaching maintenance therapeutic drug doses without any significant adverse effect (only one case of cutaneous pruritus). These experiences and the previously reported in the literature, show that the desensitization to allopurinol is a good therapeutic alternative in hypersensitivity reactions to the drug.