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American Journal of Physiology. Renal... Oct 2018
Topics: Allopurinol; Heat-Shock Response; Humans; Hyperuricemia; Liver; Uric Acid
PubMed: 29897286
DOI: 10.1152/ajprenal.00244.2018 -
The Israel Medical Association Journal... Oct 2005Hyperuricemia is present in approximately 5% of the population, the vast majority of whom are asymptomatic and at no clinical risk. Complications, including renal... (Review)
Review
Hyperuricemia is present in approximately 5% of the population, the vast majority of whom are asymptomatic and at no clinical risk. Complications, including renal calculi, uric acid nephropathy and gout, occur in a small proportion of patients. Allopurinol, an analog of hypoxanthine, has been widely used in clinical practice for over 30 years for the treatment of hyperuricemia and gout. Two percent of patients taking this medication develop a mild exanthema. A syndrome characterized by exfoliative dermatitis, hepatitis, interstitial nephritis and eosinophilia has been described previously. Termed allopurinol hypersensitivity syndrome, its etiology is related to the accumulation of one of the allopurinol metabolites, oxypurinol; clearance of oxypurinol is decreased in the setting of renal insufficiency and the use of thiazide diuretics. The term DRESS syndrome (Drug Rash with Eosinophilia and Systemic Symptoms) was recently introduced to describe a disorder associated with various drugs or viral infections and characterized by similar features. The pathophysiology of allopurinol-induced hypersensitivity, clinical presentation and treatment are reviewed.
Topics: Allopurinol; Drug Hypersensitivity; Gout; Gout Suppressants; Humans
PubMed: 16259349
DOI: No ID Found -
The Journal of Thoracic and... Jan 2018
Topics: Allopurinol; Data Interpretation, Statistical; Humans; Postoperative Period; Research Design; Tetralogy of Fallot
PubMed: 28942973
DOI: 10.1016/j.jtcvs.2017.08.108 -
British Medical Journal Feb 1967
Topics: Allopurinol; Animals; Enzyme Therapy; Gout; Humans
PubMed: 6017531
DOI: No ID Found -
Cardiovascular Therapeutics Aug 2018Oxidative stress and endothelial dysfunction are two inter-related conditions commonly seen in patients with cardiovascular risk factors. The enzyme, xanthine oxidase,... (Meta-Analysis)
Meta-Analysis Review
AIM
Oxidative stress and endothelial dysfunction are two inter-related conditions commonly seen in patients with cardiovascular risk factors. The enzyme, xanthine oxidase, is an important contributor to these phenomena but to a variable degree in different patient populations. This meta-analysis will summarize the effect of allopurinol, an established xanthine oxidase inhibitor, on endothelial function among patients with different comorbidities.
METHODS
Medline Complete, PubMed, ProQuest, ClinicalKey, Wiley Online Library, and Cochrane Central Register of Controlled Trials were searched till July 29, 2017. Meta-analysis was planned for randomized controlled trials (RCTs) that investigated allopurinol effects on endothelial function. A random effect model was used to calculate the standardized mean difference (with 95% confidence intervals: CI) as an estimate of effect size. Heterogeneity was quantified by four types of information: Q statistics, I statistic, Tau-squared (T ), and Tau (T).
RESULTS
Thirty eligible studies were identified; 12 were included in the final analysis and subdivided among 3 patient's groups: patients with chronic heart failure (CHF; 197 patients), patients with chronic kidney disease (CKD; 183 patients), and patients with type 2 diabetes mellitus (DM; 170 patients). Allopurinol was found to have a statistically significant benefit on endothelial function in patients with CHF and CKD but not in type 2 DM. The standardized mean differences and CI in the three patient's groups were 0.776 (0.429, 1.122), 0.350 (0.009, 0.690), and 1.331 (-0.781, 3.444), respectively.
CONCLUSION
Allopurinol has an antioxidant property that might partially reverse endothelial dysfunction in patients with certain comorbidities. The importance of this property and the magnitude of the beneficial effect are likely to be related to the relative contribution of xanthine oxidase into the oxidative stress associated with different underlying pathologies.
Topics: Aged; Allopurinol; Antioxidants; Cardiovascular Diseases; Comorbidity; Endothelium, Vascular; Enzyme Inhibitors; Female; Humans; Male; Middle Aged; Oxidative Stress; Randomized Controlled Trials as Topic; Risk Factors; Treatment Outcome; Xanthine Oxidase
PubMed: 29673103
DOI: 10.1111/1755-5922.12432 -
Indian Journal of Pharmacology 2013Allopurinol, a widely prescribed urate lowering agent is responsible for various adverse drug reactions, including erythroderma. A 45-year-old male patient was admitted...
Allopurinol, a widely prescribed urate lowering agent is responsible for various adverse drug reactions, including erythroderma. A 45-year-old male patient was admitted with the complaints of fever, redness and scaling all over the body after 3-4 weeks of allopurinol treatment for asymptomatic hyperuricemia. Elevated liver enzymes were detected in his blood analysis. Skin biopsy was consistent with drug induced erythroderma. Allopurinol was stopped and steroids were started. Patient improved over a period of 2 weeks.
Topics: Allopurinol; Dermatitis, Exfoliative; Humans; Male; Middle Aged; Treatment Outcome; Uric Acid
PubMed: 24347776
DOI: 10.4103/0253-7613.121381 -
PloS One 2022The benefits of xanthine oxidase inhibitors to chronic heart failure (CHF) patients is controversial. We investigated the beneficial effects of a novel xanthine... (Comparative Study)
Comparative Study Randomized Controlled Trial
Topiroxostat versus allopurinol in patients with chronic heart failure complicated by hyperuricemia: A prospective, randomized, open-label, blinded-end-point clinical trial.
BACKGROUND
The benefits of xanthine oxidase inhibitors to chronic heart failure (CHF) patients is controversial. We investigated the beneficial effects of a novel xanthine oxidoreductase inhibitor, topiroxostat, in patients with CHF and hyperuricemia (HU), in comparison to allopurinol.
METHODS AND RESULTS
The prospective, randomized open-label, blinded-end-point study was performed in 141 patients with CHF and HU at 4 centers. Patients were randomly assigned to either topiroxostat or allopurinol group to achieve target uric acid level ≤6.0 mg/dL. According to the protocol, 140 patients were followed up for 24 weeks. Percent change in ln (N-terminal-proB-type natriuretic peptide) at week 24 (primary endpoint) was comparable between topiroxostat and allopurinol groups (1.6±8.2 versus -0.4±8.0%; P = 0.17). In the limited number of patients with heart failure with reduced ejection fraction (HFrEF) (left ventricle ejection fraction <45%), ratio of peak early diastolic flow velocity at mitral valve leaflet to early diastolic mitral annular motion velocity (E/e') decreased in topiroxostat group, but not in allopurinol group. Urinary 8-hydroxy-2'-deoxyguanosine and L-type fatty acid-binding protein levels increased and osmolality decreased significantly in allopurinol group, while these changes were less or absent in topiroxostat group. In allopurinol group HFrEF patients, additional to the increases in these urinary marker levels, urinary creatinine levels decreased, with no change in clearance, but not in topiroxostat group.
CONCLUSIONS
Compared with allopurinol, topiroxostat did not show great benefits in patients with CHF and HU. However, topiroxostat might have potential advantages of reducing left ventricular end-diastolic pressure, not worsening oxidative stress in proximal renal tubule, and renoprotection over allopurinol in HFrEF patients.
Topics: Aged; Aged, 80 and over; Allopurinol; Biomarkers; Female; Heart Failure; Humans; Hyperuricemia; Male; Middle Aged; Natriuretic Peptide, Brain; Nitriles; Peptide Fragments; Prospective Studies; Pyridines; Stroke Volume; Treatment Outcome
PubMed: 35077456
DOI: 10.1371/journal.pone.0261445 -
Tidsskrift For Den Norske Laegeforening... Nov 2012Perinatal asphyxia can cause serious illness or death. By taking steps in the «latent phase», which occurs 6-24 hours after the hypoxic event, the neurological damage... (Review)
Review
BACKGROUND
Perinatal asphyxia can cause serious illness or death. By taking steps in the «latent phase», which occurs 6-24 hours after the hypoxic event, the neurological damage caused by perinatal asphyxia can be limited. We wish to present a selection of such measures that are either established treatment today or that appear promising.
METHOD
We searched in the Medline and Cochrane Library databases for options for treating perinatal asphyxia.
RESULTS
An overwhelming number of potential treatments were identified. From among them we selected 44 indexed, peer-reviewed original articles in English on strategies for neuroprotective treatment after perinatal asphyxia. The treatments target different cellular mechanisms that cause neurological damage following perinatal asphyxia. In randomised clinical trials, only hypothermia treatment has improved the long-term outcome for newborns with perinatal asphyxia. Xenon gas, erythropoeitin and allopurinol are undergoing clinical testing.
INTERPRETATION
The efficacy of xenon gas, erythropoeitin and allopurinol in combination with the established treatment form of hypothermia must be studied more closely. Antioxidants, stem cell treatment and DNA repair mechanisms can pave the way for new opportunities in the future.
Topics: Allopurinol; Anesthetics, Inhalation; Asphyxia Neonatorum; Combined Modality Therapy; Erythropoietin; Free Radical Scavengers; Humans; Hypothermia, Induced; Infant, Newborn; Neuroprotective Agents; Time Factors; Xenon
PubMed: 23160590
DOI: 10.4045/tidsskr.12.0120 -
Clinical and Translational Science Aug 2022ABCG2 is a gene that codes for the human breast cancer resistance protein (BCRP). It is established that rs2231142 G>T, a single nucleotide polymorphism of the ABCG2...
ABCG2 is a gene that codes for the human breast cancer resistance protein (BCRP). It is established that rs2231142 G>T, a single nucleotide polymorphism of the ABCG2 gene, is associated with gout and poor response to allopurinol, a uric acid-lowering agent used to treat this condition. It has also been suggested that oxypurinol, the primary active metabolite of allopurinol, is a substrate of the BCRP. We thus hypothesized that carrying the rs2231142 variant would be associated with decreased oxypurinol concentrations, which would explain the lower reduction in uric acid. We performed a cross-sectional study to investigate the association between the ABCG2 rs2231142 variant and oxypurinol, allopurinol, and allopurinol riboside concentrations in 459 participants from the Montreal Heart Institute Hospital Cohort. Age, sex, weight, use of diuretics, and estimated glomerular filtration rate were all significantly associated with oxypurinol plasma concentration. No association was found between rs2231142 and oxypurinol, allopurinol and allopurinol riboside plasma concentrations. Rs2231142 was not significantly associated with daily allopurinol dose in the overall population, but an association was observed in men, with T carriers receiving higher doses. Our results do not support a major role of ABCG2 in the pharmacokinetics of allopurinol or its metabolites. The underlying mechanism of the association between rs2231142 and allopurinol efficacy requires further investigation.
Topics: ATP Binding Cassette Transporter, Subfamily G, Member 2; Allopurinol; Cross-Sectional Studies; Humans; Oxypurinol; Ribonucleosides; Uric Acid
PubMed: 35689378
DOI: 10.1111/cts.13318 -
Journal Der Deutschen Dermatologischen... Aug 2013Acquired reactive perforating dermatosis is characterized by umbilicated erythematous papules and plaques with firmly adherent crusts. Histopathological examination... (Review)
Review
Acquired reactive perforating dermatosis is characterized by umbilicated erythematous papules and plaques with firmly adherent crusts. Histopathological examination shows a typical cup-shaped ulceration in the epidermis containing cellular debris and collagen. There is transepidermal elimination of degenerated material with basophilic collagen bundles. The etiology and pathogenesis of acquired reactive perforating dermatosis are unclear. Metabolic disorders and malignancies are associated with this dermatosis. Associated pruritus is regarded as a key pathogenic factor. Constant scratching may cause a repetitive trauma to the skin. This pathogenesis may involve a genetic predisposition. The trauma may lead to degeneration of the collagen bundles. Treatment of acquired reactive perforating dermatosis follows a multimodal approach. Apart from the treating any underlying disease, treatment of pruritus is a major goal. Systemic steroids and retinoids, as well as UVB phototherapy are well-established treatment options. Some patients may also benefit from oral allopurinol.
Topics: Allopurinol; Collagen Diseases; Combined Modality Therapy; Diagnosis, Differential; Humans; Immunosuppressive Agents; Retinoids; Skin Diseases, Genetic; Steroids; Ultraviolet Therapy
PubMed: 23718268
DOI: 10.1111/ddg.12131