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TLS was characterized by hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. Three cases had renal dysfunction and the other died of acute renal failure. After allopurinol therapy and alkalinization of urine, the blood biochemical parameter became normalization in all the three cases.
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To determine the prevalence, the clinical patterns of drug eruptions, and the common drugs implicated, particularly in severe cADR such as Stevens-Johnson Syndrome/Toxic epidermal necrolysis (SJS/TEN) and drug rash with eosinophilia and systemic symptoms (DRESS) in our population.
Computerised searches of Cochrane Oral Health Group Specialised Register, CCTR, MEDLINE and EMBASE were undertaken. Reference lists from relevant articles were searched. Authors of eligible trials were contacted to identify trials and obtain additional information. Date of most recent searches: May 2001 (CCTR 2001, issue 3)
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In the isolated rat liver perfused in situ stimulation of the nerve bundles around the portal vein and the hepatic artery caused an increase of urate formation that was inhibited by the alpha 1-blocker prazosine and the xanthine oxidase inhibitor allopurinol. Moreover, nerve stimulation increased glucose and lactate output and decreased perfusion flow. Infusion of noradrenaline had similar effects. Compared to nerve stimulation infusion of glucagon led to a less pronounced increase of urate formation and a twice as large increase in glucose output but a decrease in lactate release without affecting the flow rate. Insulin had no effect on any of the parameters studied.
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Effective preservation of liver grafts is the first essential step for successful liver transplantation. Insufficient perfusion leads to ischemic-type biliary lesions after transplantation. Perfusion of the graft can be performed either in situ or ex situ, with gravity flow or pressure-controlled. Mainly University of Wisconsin (UW) and histidine-tryptophan-ketoglutarate (HTK) solutions are used widespread in clinical liver transplantation. Due to a persistent lack of data, we performed this systematic investigation of in situ and ex situ perfusion of liver grafts with HTK (low-viscous) and UW (high-viscous) solutions at different pressure steps on the perfusion solution (gravity flow, 50, 100, 150, and 200 mm Hg). End points were perfusion flow and pressure in the hepatic artery. A pig model was used with n = 8 pigs randomized to each (HTK and UW) group. In situ perfusion was ineffective for both solutions at any pressure on the perfusate bag. Ex situ perfusion showed significantly improved flow and pressure in the hepatic artery and, therefore, was highly effective. No major differences between HTK and UW solutions could be detected. Therefore, an additional ex situ perfusion of the hepatic artery should be mandatory in every liver procurement.
We studied 51 pulmonary tuberculosis patients who were initially treated with pyrazinamide (PZA) at our hospital between April 1996 and December 1997. PZA dosage was less than 1.5 g per day, and the chemotherapy course lasted 2 months. Uric acid levels of higher than 8 mg/dl were observed in 44 patients (86%). Arthralgia was observed in 9 patients. Acute gout was observed in only 1 patient who had hyperuricemia prior to PZA treatment and a predisposition for gout. The other 8 patients with arthralgia had symptoms in the shoulders and knees, but no gouty pain. Arthralgia was not related to serum uric acid level and disappeared after PZA treatment was stopped. We concluded that PZA can be used for up to 2 months without the combined administration of allopurinol or benzbromarone even if hyperuricemia or arthralgia develops.
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Identification of facilitators and barriers to high ULT adherence in African-Americans with gout in this study lays the foundation for designing interventions to improve ULT adherence in racial minorities.
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In this prospective, randomized study we have looked at the influence of a multiantioxidant supplementation regime, using allopurinol, vitamins E and C, mannitol and N-acetylcysteine, perioperatively. Twenty-two patients received standard treatment and 20 patients received supplementation. Gut permeability was determined using a double sugar test with lactulose and rhamnose.
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To investigate the protective effect of two anti-reactive oxygen species (ROS) substances, copper-zinc superoxide dismutase (CuZn-SOD) and allopurinol, in impulse noise-exposed guinea pigs.
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We identified 328 patients with hyperuricaemia treated with NSAIDs at Seoul National University Hospital between December 1998 and January 2008 to investigate risk factors for NSAID-induced AKI. The risk factors evaluated included age, sex, BMI, comorbidity, NSAID COX-2 selectivity, baseline glomerular filtration rate (GFR), serum uric acid, serum albumin, haemoglobin level, ratio of blood urea nitrogen and serum creatinine and the use of allopurinol. After extracting possible risk factors through univariate analysis, multivariate logistic regression analysis was performed with backward selection to derive a risk model for NSAID-induced AKI in patients with hyperuricaemia.
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Drug-induced hypersensitivity syndrome (DIHS) is a multi-system syndrome resulting from an idiosyncratic reaction to medication. While it commonly results in multi-organ involvement, particularly the liver, there are few reports of DIHS causing cerebral vasculitis and neurological deficits. We report the case of a 63-year old woman with DIHS secondary to allopurinol leading to multiple neurological deficits with magnetic resonance imaging findings consistent with a cerebral vasculitis.
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As part of a prospective cohort study, a baseline questionnaire was sent to 1805 participants with gout aged≥18 years from UK primary care. Participants had a gout diagnosis or prescriptions for allopurinol or colchicine in their medical records 2 years prior to baseline. Prevalence of anxiety was defined using the Generalised Anxiety Disorder questionnaire and depression using the Patient Health Questionnaire. Logistic regression was used to examine any association between gout characteristics (12-month attack frequency, oligo/polyarticular gout and gout duration) and the presence of anxiety or depression. Crude and adjusted associations were reported as odds ratios (OR) and 95% confidence intervals (CI). Adjusted gout characteristics were stratified by allopurinol use.
Hyperuricemia is a biochemical hallmark of gout, renal urate lithiasis, and inherited purine disorders, and may be a result of enormous ATP breakdown or purine release as a result of cardiovascular disease, hypertension, kidney disease, eclampsia, obesity, metabolic syndrome, psoriasis, tumor lysis syndrome, or intense physical training. The beneficial role of dairy products on hyperuricemia management and prevention is well documented in the literature. The primary aim of our experimental study was to examine the effect of milk dietary regimen (commercial 1.5% fat UHT milk or patented depurinized milk) compared with allopurinol therapy on experimental hyperuricemia induced by oxonic acid in rats. Principal component analysis was applied on a data set consisting of 11 variables for 8 different experimental groups. Among the 11 parameters measured (plasma uric acid and the liver parameters NFκB-p65, Akt kinase/phospho-Akt kinase, ERK kinase/phospho-ERK kinase, IRAK kinase/phospho IRAK kinase, p38/phospho-p38, and DNase), Akt/phospho Akt and ERK/phospho-ERK signaling were extracted as the most discriminating. We also compared the content of various potentially toxic compounds (sulfur compounds, ketones, aldehydes, alcohols, esters, carboxylic acids, and phthalates) in untreated commercial milk and depurinized milk. Of all the compounds investigated in this study that were observed in commercial milk (24 volatile organic compounds and 4 phthalates), 6 volatile organic compounds were not detected in depurinized milk. For almost all of the other compounds, significant decreases in concentration were observed in depurinized milk compared with commercial milk. In conclusion, a depurinized milk diet may be recommended in nutritional treatment of primary and secondary hyperuricemia to avoid uric acid and other volatile, potentially toxic compounds that may slow down liver regeneration and may induce chronic liver diseases.