allopurinol and Vitamin-D-Deficiency

It has been shown that serum concentrations of 1,25(OH)2D3 are decreased in patients with gout. A short-term administration of allopurinol increases plasma concentrations of 1,25(OH)2D3 in mild to moderate renal failure, with or without hyperuricemia. It has been reported that subjects who perform regular vigorous and/ or moderate physical activities have higher plasma and serum 25(OH)D3 levels. However, little is known about the influence of allopurinol and/or physical exercise on serum 25(OH)D3 concentrations in humans.. We investigated the effect of allopurinol administration and/or physical activity on vitamin D metabolism by measuring serum uric acid, 25(OH)D3, and calcium levels in twelve professional soccer players.. The athletes supplemented with allopurinol, but not those who received placebo, exhibited a significant decrease in uric acid serum concentrations after the match. We also found a significant increase in serum calcium and 25(OH)D3 concentrations in the supplemented group.. We conclude that allopurinol administration might be an effective drug to lower hyperuricemia and treat hypovitaminosis D.

Topics: Adult; Allopurinol; Athletes; Calcifediol; Calcium; Cellulose; Double-Blind Method; Enzyme Inhibitors; Exercise; Humans; Hyperuricemia; Male; Soccer; Treatment Outcome; Uric Acid; Vitamin D Deficiency; Xanthine Oxidase; Young Adult

Hyperuricemia is common among patients with chronic kidney disease (CKD). In the general population, hyperuricemia is associated with secondary hyperparathyroidism (SHPT), in a mechanism that involves vitamin D metabolism. Data for patients with CKD, however, are scarce. We aimed to evaluate the relationship between hyperuricemia and mineral and bone metabolism, particularly hyperparathyroidism.. This is a retrospective study that included 922 adult patients with stages 3, 4, or 5 CKD, not on dialysis. Clinical, demographic, and biochemical data were collected from charts and included uric acid, parathyroid hormone (PTH), 25(OH)-vitamin D, calcium, phosphate, renal function (estimated glomerular filtration rate-eGFR), and medications such as allopurinol, furosemide, and cholecalciferol. SHPT was defined as PTH > 65 pg/ml.. Our patients were mostly Caucasian women, with a mean age of 64 ± 16 years. SHPT and hyperuricemia were observed in 70% and 62.4% of patients, respectively. Patients with SHPT presented higher levels of uric acid (7.2 ± 1.8 vs. 6.6 ± 1.7 mg/dL, p = 0.0001) and a higher frequency of hyperuricemia (66% vs. 33%, p = 0.0001). Patients with hyperuricemia were mostly female, with lower eGFR, higher phosphate, and higher PTH. The risk of hypovitaminosis D was higher among patients with SHPT (69.7% vs. 53.1%, p = 0.0001). Hyperuricemia remained independently associated with hyperparathyroidism, (p = 0.033) even after adjustments for eGFR, calcium, phosphate, hypovitaminosis D, and use of allopurinol, calcitriol, furosemide, and cholecalciferol.. Hyperuricemia seems to be a contributing factor for SHPT in patients with CKD. The mechanisms behind this finding have yet to be elucidated.

Topics: Adult; Aged; Aged, 80 and over; Allopurinol; Calcium; Cholecalciferol; Female; Furosemide; Humans; Hyperparathyroidism, Secondary; Hyperuricemia; Male; Middle Aged; Parathyroid Hormone; Phosphates; Renal Insufficiency, Chronic; Retrospective Studies; Uric Acid; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency and polypharmacy is a common problem over chronic kidney disease (CKD) population.. To assess the clinical and analytical characteristics of CKD patients with 25-OH-D3 deficiency (<15 ng/mL), including the possible role of associated drugs.. A single center observational review of 137 incident patients referred to our outpatient clinic with different stages of CKD and 25-OH-D3<15ng/mL (male gender 53.3%, mean age 70.8 [±16.1] years, mean GFR (MDRD-4) 43.6 [±25.5] ml/min/1.73 m²). 25-OH-D3 levels were collected in spring. Clinical and biochemical data and associated medications were recorded.. Mean 25-OH-D3 levels were 8.23 [±4.03] ng/ml. Eighty-eight patients (64.7%) had 3 or more concomitant drugs. Only 7 patients (5.1%) were not receiving any medication. Patients were divided in three groups according the therapies into none (n=26), RAS inhibitors or allopurinol (n=81), and RAS inhibitors plus allopurinol (n=30); with the aim to study the influence of statin therapy. Patients under renin angiotensin (RAS) inhibitors or Allopurinol treatment presented significantly higher 25-OH-D3 levels (p=0.001 and p=0.01 respectively), however patients with Statins treatment had lower 25-OH-D3 level (p=0.039). Personal history of diabetes, cardiovascular events or other therapies did not modify 25-OH-D3 levels, adjusted by age and eGFR.. CKD patients with vitamin D deficiency who received RAS inhibitors or Allopurinol treatment had higher 25-OH-D3 levels, however those with statins treatment had lower vitamin D levels. Randomized controlled trials are required to confirm these findings.

Topics: Aged; Aged, 80 and over; Allopurinol; Antihypertensive Agents; Calcifediol; Cross-Sectional Studies; Drug Interactions; Female; Glomerular Filtration Rate; Hematinics; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemic Agents; Male; Middle Aged; Parathyroid Hormone; Phosphates; Renal Insufficiency, Chronic; Renin-Angiotensin System; Vitamin D; Vitamin D Deficiency

This study was investigated to clarify the role of intracellular Ca2+ following endotoxin treatment (1 mg/kg, intraperitoneally) to D-galactosamine-sensitized mice (400 mg/kg, intraperitoneally), and to observe lipid peroxide levels, an index of hepatotoxicity, in endotoxin/galactosamine (Ga1N)-challenged mice under activation of macrophages, especially Kupffer cells, by zymosan. The liver lipid peroxide level and serum glutamic pyruvic transminase activity in mice 18 hr after administration of endotoxin/Ga1N were markedly higher than those in mice treated only with endotoxin. In spite of an increase in lipid peroxide formation, there was little or no effect of Ga1N administration on xanthine oxidase and superoxide dismutase activities in mice given endotoxin. However, the injection of verapamil (10 mg/kg, subcutaneously) markedly decreased lipid peroxide levels in liver of endotoxin/Ga1N-injected mice. In the mice given a Ca(2+)-deficient diet, lipid peroxide level in liver after endotoxin/Ga1N injection was markedly decreased compared to that in mice fed a normal diet. Administration of dexamethasone (200 micrograms/kg, intraperitoneally) in mice 1 hr before treatment with endotoxin/Ga1N did not induce lipid peroxide formation. Administration of endotoxin to Ga1N-treated mice resulted in a higher level of liver cytosolic free Ca2+ ([Ca2+]i) than that in endotoxin-treated mice. On the other hand, Ca(2+)-ATPase activity in liver plasma membrane in the endotoxin/Ga1N-treated mice was markedly decreased as compared with endotoxin alone. On the contrary, the Ca(2+)-ATPase activity in liver mitochondria was higher in endotoxaemic mice treated with GA1N than in mice given endotoxin alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Alanine Transaminase; Animals; Calcium; Calcium-Transporting ATPases; Cell Membrane; Cell Respiration; Cytosol; Endotoxins; Galactosamine; Injections, Intraperitoneal; Kupffer Cells; Lipid Peroxidation; Liver; Macrophages; Male; Mice; Mitochondria, Liver; Superoxide Dismutase; Superoxides; Vitamin D Deficiency; Xanthine Oxidase; Zymosan

Topics: Amino Acids; Animals; Autoanalysis; Caseins; Depression, Chemical; Diet; Dietary Proteins; Ergocalciferols; Histidine; Isoleucine; Leucine; Liver; Lysine; Male; Methionine; Phenylalanine; Rats; Stimulation, Chemical; Threonine; Vitamin D Deficiency; Xanthine Oxidase; Zinc