Between July 1992 and September 1997, 350 infants were enrolled and 348 subsequently randomized. A total of 318 infants (131 HLHS and 187 non-HLHS) underwent heart surgery using DHCA. There was a nonsignificant treatment effect for the primary efficacy endpoint analysis (death, seizures, and coma), which was consistent over the 2 strata. The addition of cardiac events to the primary endpoint resulted in a lack of consistency of treatment effect over strata, with the allopurinol treatment group experiencing fewer events (38% vs 60%) in the entire HLHS stratum, compared with the non-HLHS stratum (30% vs 27%). In HLHS surgical survivors, 40 of 47 (85%) allopurinol-treated infants did not experience any endpoint event, compared with 27 of 49 (55%) controls. There were fewer seizures-only and cardiac-only events in the allopurinol versus placebo groups. Allopurinol did not reduce efficacy endpoint events in non-HLHS infants. Treated and control infants did not differ in adverse events.
The effects of oxygen partial pressure on cryopreservation of the cells with organ preservation solution were explored. Hypoxic UW solution was made by purging the UW solution with argon. The pig proximal tubule epithelial cells (LLC-PK1 cells) were cryopreserved in hypoxic UW solution (Ar-UW group) or standard UW solution (UW group) at 4 degrees C for 48 h. Trypan blue staining and LDH detection were performed to evaluate the injury of the cells. The results showed that the oxygen partial pressure in Ar-UW group was significantly declined from 242+/-6 mmHg to 83+/-10 mmHg. After cryopreservation at 4 degrees C for 48 h, LDH leakage rate and Trypan blue-stained rate in Ar-UW group were (11.3+/-3.4)% and (10.5+/-4.7)%, respectively, which were significantly lower than in UW group [(49.5+/-6.9)% and (47.6+/-9.3)% respectively, both P<0.01]. It was concluded that lower oxygen partial pressure of UW solution was more beneficial to the cryopreservation of LLC.
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Hypoxia-reoxygenation leads to an increase in ICAM mRNA levels that peaks at 4 hours in human brain microvascular endothelial cells. Pretreatment with N-acetyl-L-cysteine can completely block the increase in ICAM-1 mRNA levels.
The University of Wisconsin solution differs from other types of solutions used for organ preservation because it contains high-energy phosphate precursors (adenosine and phosphate), impermeants (lactobionate and raffinose), an oncotic agent (pentafraction), and antioxidants (allopurinol and glutathione). These components have the potential to enhance the preservation of ATP, reduce intracellular and extracellular edema, and attenuate free-radical-mediated injury. The University of Wisconsin solution has been demonstrated to enhance and extend the preservation of the liver, pancreas, and kidney, but its potential role in the heart remains unproven. We have evaluated the University of Wisconsin solution (Du Pont) by comparing it with the St. Thomas' Hospital cardioplegic solutions No. 1 and No. 2 (Plegisol), which are used in Europe and the United States for routine cardiac surgery and transplantation. For each solution, 10 isolated working rat hearts were arrested by 10 ml of the solution (at 4 degrees C) and then maintained immersed in the same solution for 4 hours at 4 degrees C. Mean recovery of functional indexes (expressed as a percentage of their preischemic control values) after use of the University of Wisconsin solution were as follows: peak aortic pressure, 90.6 +/- 1.0; dP/dt, 71.5 +/- 5.5; aortic flow, 81.6 +/- 4.7; coronary flow, 87.5 +/- 3.5; and cardiac output, 82.6 +/- 3.5. In contrast, the mean recoveries after St. Thomas' Hospital solution No. 1 were as follows: peak aortic pressure, 82.8 +/- 1.3; dP/dt, 49.7 +/- 3.0; aortic flow, 58.4 +/- 5.3; coronary flow, 79.6 +/- 5.9; and cardiac output, 63.0 +/- 4.9. In contrast still, mean recoveries after St. Thomas' Hospital solution No. 2 were as follows: peak aortic pressure, 83.1 +/- 1.2; dP/dt, 40.7 +/- 6.1; aortic flow, 37.0 +/- 5.1; coronary flow, 65.8 +/- 3.6; and cardiac output, 43.1 +/- 5.6. The recovery of all indexes were significantly superior (p less than 0.005) after preservation with University of Wisconsin solution compared with either of the St. Thomas' Hospital solutions.(ABSTRACT TRUNCATED AT 250 WORDS)
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A decision analytical model over a time period of 12 months was employed to compare the cost and outcomes of treatment informed by HLA-B5801 genotyping with that of a conventional treatment strategy using a hypothetical cohort of gout patients with chronic renal insufficiency. Direct medical costs were obtained from real patients with SCARs from 2 tertiary hospitals. Outcomes were measured as a total expected cost and an incremental cost-effectiveness ratio.
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In this work, pure solvent solubilities of drugs, such as paracetamol, allopurinol, furosemide and budesonide, measured in the temperature range between 298.2-315.2K are presented. The solvents under study were water, ethanol, acetone, ethyl acetate, carbon tetrachloride and n-hexane. Measurements were performed using the shake-flask method for generating the saturated solutions followed by compositional analysis by HPLC. Previous literature values on the solubilities of paracetamol were used to assess the experimental methodology employed in this work. No literature data was found for any of the other drugs studied in this assay. Melting properties of the pure drugs were also determined by differential scanning calorimetry (DSC) to provide a broader knowledge about the solubilization process and also for modeling purposes. The solubility data as a function of temperature were used to determine the thermodynamic properties of dissolution like, Gibbs energy, enthalpy and entropy. Theoretical work was essentially focused on the evaluation of the Nonrandom Two-Liquid Segment Activity Coefficient (NRTL-SAC) model, which has been referred as a simple and practical thermodynamic framework for drug solubility estimation. A satisfactory agreement was found between experimental and calculated values: the absolute average deviation was 68% for the correlation in the organic solvents and 38% for the prediction in water, where the best results in prediction could be related to the selected solvents.
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Authors present a 10 year old boy with Lesch-Nyhan syndrome with self-inflicted mutilations to the lips, tongue and interior cheek wall, partially avoided by tooth extraction. Hand lesions were prevented by arm restriction. Born with anoxia and in spite of seizures for several years and a marked muscle stiffness, he is relatively aware of his surroundings. HGPRT activity in blood and hair was nil, while the APRT activity was increased. The mother, a maternal aunt and grandmother are not carriers. Hyperuricemia measured several times and treated with allopurinol is kept between 3 and 4 mg/dl and lastly under 3 mg after increasing dosage. Some years ago, elimination of acid uric stones in urine was observed without hematuria. It seems that recently stone elimination produced pain difficult to evaluate in this patient.
Trials were searched in computerized general and specialized databases (MEDLINE, Cochrane Library, Cochrane Prostate Group database), bibliographies of obtained articles, and direct contact with authors.
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In clinical transplantation, exposure of donors to gut-derived endotoxin occurs frequently and may adversely affect liver transplantation therapy. The aim of this study was to investigate: 1) whether brief exposure of rats to endotoxin before liver procurement aggravates the early phase of reperfusion injury of hepatic explants; and if so 2) whether Kupffer cell activation is a contributing factor to liver injury; and 3) whether heparin and pentoxifylline could minimize this effect.
Wild-type and ACE8/8 mice with and without 2 weeks of treatment with L-NIO (NO synthase inhibitor), sepiapterin (precursor of tetrahydrobiopterin), MitoTEMPO (mitochondria-targeted antioxidant), TEMPOL (a general antioxidant), apocynin (nicotinamide adenine dinucleotide phosphate oxidase inhibitor), allopurinol (xanthine oxidase inhibitor), and ACE8/8 crossed with P67 dominant negative mice to inhibit the nicotinamide adenine dinucleotide phosphate oxidase were studied. Western blotting, detection of mitochondrial ROS by MitoSOX Red, electron microscopy, immunohistochemistry, fluorescent dye diffusion technique for functional assessment of connexin43, telemetry monitoring, and in vivo electrophysiology studies were performed. Treatment with MitoTEMPO reduced sudden cardiac death in ACE8/8 mice (from 74% to 18%; P<0.005), decreased spontaneous ventricular premature beats, decreased ventricular tachycardia inducibility (from 90% to 17%; P<0.05), diminished elevated mitochondrial ROS to the control level, prevented structural damage to mitochondria, resulted in 2.6-fold increase in connexin43 level at the gap junctions, and corrected gap junction conduction. None of the other antioxidant therapies prevented ventricular tachycardia and sudden cardiac death in ACE8/8 mice.
A 43-year-old man developed fever, systemic erythema, and hepatic dysfunction approximately 1 month after initiating treatment with oral allopurinol and anti-TB drugs. The high fever, skin rash, headache, vomiting, and general malaise aggravated even after discontinuation of the anti-TB drugs and allopurinol, and they continued for more than 2 weeks. Hence, the patient was diagnosed with atypical drug-induced hypersensitivity syndrome. Oral prednisolone was introduced at a dosage of 65 mg, and the systemic symptoms rapidly subsided. Drug lymphocyte stimulation test was positive for isoniazid and oxypurinol, a metabolite of allopurinol. The prednisolone dosage was gradually reduced with 3-7 day intervals, and the patient was discharged on day 31 without any recurrence of the symptoms. Although high fever and erythema occurred again upon resumption of isoniazid, the symptoms gradually improved with oral prednisolone. Finally, the patient was diagnosed with atypical drug-induced hypersensitivity syndrome caused by isoniazid.
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Thrombolysis is a promising therapy for acute ischemic stroke. However, there is evidence that neutrophils may physically plug cerebral microvessels on reperfusion, preventing the full benefit of thrombolysis. We undertook this study to determine whether there was increased endothelial expression of the intercellular adhesion molecule-1 (ICAM-1) gene during hypoxia-reoxygenation.
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In this study, HLA-B alleles did not deviate from Hardy-Weinberg equilibrium (P > 0.05). The most common HLA-B alleles observed in this population were HLA-B (*) 46:01 (11.51%), HLA-B (*) 58:01 (8.62%), HLA-B (*) 40:01 (8.22%), HLA-B (*) 15:02 (8.16%) and HLA-B (*) 13:01 (6.95%). This finding revealed that HLA-B allele frequency in the Thai population was consistent with the Chinese population (p > 0.05), however, differed from the Malaysian population (p < 0.05). The top five HLA-B genotypes were HLA-B (*) 40:01/46:01 (2.13%), HLA-B (*) 46:01/46:01 (2.03%), HLA-B (*) 40:01/58:01 (2.03%), HLA-B (*) 46:01/58:01 (1.93%) and HLA-B (*) 15:02/46:01 (1.83%). This study found that 15.92% of Thai subjects carry HLA-B (*) 15:02, which has been associated with carbamazepine-induced severe cutaneous adverse drug reactions (SCARs). Moreover, 16.33% of Thai subjects carry the HLA-B (*) 58:01 allele, which has been associated with allopurinol-induced SCARs.
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Of 1380 patients, 139 (10%) had a diagnosis of gout or were prescribed allopurinol. They had more co-morbidities (7.0 vs 5.6; P<0.0001) and consumed more drugs (6.8 vs 5.0; P<0.0001). The CIRS (co-morbidity index) was worse in these patients (OR 1.28 95% CI 1.15-1.41). Multivariable regression analysis showed that only renal and heart failures were independently associated with gout/allopurinol intake. Moreover, this combined event was associated with an increased risk of adverse events during hospitalization (OR 1.66, 95% CI 1.16-2.36), but not with the risk of re-hospitalization, length of hospital stay or death.
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Drug Rash Eosinophilia Systemic Symptoms (DRESS) syndrome is a systemic hypersensitivity reaction characterized by exfoliative dermatitis and maculopapular rash, lymphadenopathy, fever, eosinophilia, leukocytosis, and involvement of internal organs as liver, lung, heart, and kidney; the disorder starts within 2-6 weeks after taking a drug with an incidence that ranges from 1/1000 to 1/10000 exposures. Fatal cases are reported. The exact pathogenesis of DRESS syndrome is not completely understood, while it is reported that amoxicillin could trigger it in patients who are taking allopurinol, sulfasalazine, NSAIDs, carbamazepine, strontium ranelate, lisinopril, lansoprazole, and minocycline. Amoxicillin could act directly, inducing the reactivation of a viral infection (HHV 6 and EBV) with symptoms similar to DRESS syndrome or by reducing the patients' ability to detoxify the body from substances chronically taken. We describe a case of a patient admitted to our hospital for a DRESS syndrome flared after amoxicilline intake during treatment with sulfasalazine; this combination can activate severe reactions often with an insidious onset that can mimic an infectious disease.
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The ethanol extracts from Dioscoreae Nipponicae Rhizoma have certain hypouricemic effect in hyperuricemic mice induced by hypoxanthine and potassium oxonate or by uric acid.
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Data provide consistent evidences linking uric acid with the acute renal failure induced by C. d. terrificus venom, as well as that this envenoming in mice constitutes an attractive animal model suitable for studying the hyperuricemia and that the allopurinol deserves to be clinically evaluated as an approach complementary to anti-snake venom serotherapy.
The oxidative injury of a pancreatic graft preserved for 18 or 24 hours occurs during reperfusion, with an extraordinary intensity, but similarly with CS and UW, an observation that may help to explain graft pancreatitis.
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rhPRL supplementation to islet culture media improved human beta-cell-specific survival without altering islet quality. Addition of rhPRL to cultured islets may grant a more viable beta-cell mass in culture. The development of beta-cell cytoprotective strategies will be of assistance in improving islet transplantation outcomes.
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Sinusoidal endothelial cells (SEC) are significantly more vulnerable to cold storage and reperfusion than hepatocytes. Swelling and disruption of the sinusoidal lining induce the microcirculatory disturbances seen after reperfusion. In this article, the investigation of a method to assess the adhesion and morphology of SEC in vitro during reperfusion after preservation is described.
The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart.
An approximately 10-yr-old, captive-born female toco toucan ( Ramphastos toco ) was presented due to an acute onset of depression and apathy. On visual and physical examination, it showed an abnormal posture and dehydration, respectively. Serum biochemistry revealed hyperuricemia (39.4 mg/dl) and elevated glutamic oxaloacetic transaminase (GOT; 1,050 U/L). Radiographs demonstrated an enlargement of the cardiac silhouette. The bird died 7 days after presentation, despite treatment with enrofloxacin, allopurinol, a preparation of hepatorenal protectors, and complex B vitamins with dextrose. Necropsy revealed severe fibrinohemorrhagic pericarditis with a 15 mm long and 2.5 mm diameter, rigid foreign body in the pericardial exudate. Microscopically, this foreign body was of vegetal origin.
Allopurinol ameliorates endothelial dysfunction and arterial stiffness among patients without chronic kidney disease (CKD), but it is unknown if it has similar effects among patients with CKD. Furthermore, because arterial stiffness increases left ventricular afterload, any allopurinol-induced improvement in arterial compliance might also regress left ventricular hypertrophy (LVH). We conducted a randomized, double-blind, placebo-controlled, parallel-group study in patients with stage 3 CKD and LVH. We randomly assigned 67 subjects to allopurinol at 300 mg/d or placebo for 9 months; 53 patients completed the study. We measured left ventricular mass index (LVMI) with cardiac magnetic resonance imaging (MRI), assessed endothelial function by flow-mediated dilation (FMD) of the brachial artery, and evaluated central arterial stiffness by pulse-wave analysis. Allopurinol significantly reduced LVH (P=0.036), improved endothelial function (P=0.009), and improved the central augmentation index (P=0.015). This study demonstrates that allopurinol can regress left ventricular mass and improve endothelial function among patients with CKD. Because LVH and endothelial dysfunction associate with prognosis, these results call for further trials to examine whether allopurinol reduces cardiovascular events in patients with CKD and LVH.
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Reactive oxygen species (ROS) are important mediators in vascular biology. Venous function, although relevant to cardiovascular disease, is still understudied. We compared aspects of ROS metabolism between a major artery (the aorta) and a major vein (the vena cava, VC) of the rat, with the hypothesis that venous ROS metabolism would be overall increased compared with its arterial counterpart. Superoxide and hydrogen peroxide (H2O2) release in basal conditions was higher in VC compared with aorta. The antioxidant capacity for H2O2 was also higher in VC than in aorta. Exogenous superoxide induced a higher contraction in VC compared with aorta. Protein expression of three major ROS metabolizing enzymes, xanthine oxidase (XO), CuZn-SOD, and catalase, was higher in VC compared with aorta. Because XO seemed a likely source of the higher VC ROS levels, we examined it further and found higher mRNA expression and activity of XO in VC compared with aorta. We also investigated the impact of XO inhibition by allopurinol on aorta and VC functional responses to norepinephrine, ANG II, ET-1, and ACh. Maximal ET-1-mediated contraction was decreased by allopurinol in VC but not in the aorta. Our results suggest that there are overall differences in ROS metabolism between aorta and VC, with the latter operating normally at a higher set point, releasing but also being able to handle, higher ROS levels. We propose XO to be an important source for these differences. The result of this particular comparison may be reflective of a general arteriovenous contrast.
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Hypertension is a major cardiovascular risk factor. Of the many processes involved in the pathophysiology of hypertension, vascular damage due to oxidative stress (excess bioavailability of reactive oxygen species [ROS]) is particularly important. Physiologically, ROS regulate vascular function through redox-sensitive signalling pathways. In hypertension, oxidative stress promotes endothelial dysfunction, vascular remodelling, and inflammation, leading to vascular damage. Vascular ROS are derived primarily by nicotinamide adenine dinucleotide phosphate oxidases, which are prime targets for therapeutic development. Although experimental evidence indicates a causative role for oxidative stress in hypertension, human data are less convincing. This might relate, in part, to suboptimal methods to accurately assess the redox state. Herein we review current knowledge on oxidative stress in vascular pathobiology and implications in human hypertension. We also discuss biomarkers to assess the redox state in the clinic, highlight novel strategies to inhibit ROS production, and summarize how lifestyle modifications promote vascular health by reducing oxidative stress.