Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The safety and tolerability of antihypertensive therapies are an important clinical concern, because the demonstrated benefits of successful blood pressure-lowering depend on long-term compliance with pharmacologic treatments. Thiazide diuretics and beta blockers have been specifically recommended as preferred initial drug therapy by the Fifth Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC-V), unless their use is contraindicated by concomitant disease, there is intolerance to these agents, or there is a specific indication for another drug class. These recommendations are a result of the lengthy clinical experience with these drugs and the results of long-term clinical trials that have demonstrated significant reductions in cardiovascular morbidity and mortality. However, data from these same clinical studies have also shown that diuretics (and beta blockers) can cause abnormalities in carbohydrate, electrolyte, and lipid metabolism and also may influence quality of life. The safety of diuretics was evaluated with regard to effects on carbohydrate, electrolyte, and lipid metabolism by seeking references from a MEDLINE search of documents published from 1966 to 1994 based on the search terms "hypertension," "human," and "hydrochlorothiazide" (HCTZ) dosed in a range of 12.5-25 mg daily. Two long-term clinical trials using low-dose (12.5-15 mg/day) chlorthalidone-the Systolic Hypertension in the Elderly Program (SHEP) and the Treatment of Mild Hypertension Study (TOMHS)-were also included. During the course of treatment with HCTZ in these studies, serum potassium was reduced and uric acid was increased in a dose-dependent manner. Although low doses of HCTZ elevated serum glucose, cholesterol, and triglycerides, the magnitude of effect was small in most cases and was probably of no clinical significance. Other laboratory parameters were not adversely affected, and subjective reporting of clinical adverse events was generally lower with low-dose HCTZ than with placebo or standard HCTZ dosing. The literature on the effects of low-dose diuretic therapy on quality of life is not large, although the results from the SHEP and TOMHS studies support the concept that diuretics either do not interfere with, or may actually improve, quality of life in hypertensive patients. Low-dose thiazide treatment is a well-tolerated, excellent first-line choice for hypertensive patients, especially older patients. However, diuretics should probably be avoided, whenever possible, in patients with preexisting diabetes, gout, and in men with erectile dysfunction.
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PMID:Tolerability, safety, and quality of life and hypertensive therapy: the case for low-dose diuretics. 887 78

The uric acid concentration in blood has been widely accepted as a diagnostic indicator of hyperuricemia and gout, and its assay method is well established. In the present study, we developed a simple and rapid method for the determination of uric acid in hair, which can be obtained non-invasively. The concentration (nmol/mg hair) of uric acid extracted from 10-20 mg hair with 0.1 M potassium hydroxide was determined by an enzymatic method using uricase. The concentration of uric acid (nmol/mg hair, mean+/-S.D.: 0.49+/-0.157, n=16) in hair from hyperuricemic patients was significantly higher than that (0.26+/-0.107, n=8) in healthy volunteers (p<0.01). The within-run and between-day precision (CVs) of the assay was 9.6-10.3% (n=10 each) and 11.6-16.3% (n=7 each), respectively. The concentration (nmol/mg hair, y) of uric acid in hair correlated well with that in serum (mg/l, x): y=0.09x-0.12 (r=0.75, Syx=0.122, n=23). Changes in the concentration of uric acid in the hair of antihyperuricemic drug-treated patient paralleled that in serum, suggesting that the concentration of uric acid in hair is a reliable indicator of the metabolic control in hyperuricemia.
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PMID:Determination of uric acid in scalp hair for non-invasive evaluation of uricemic controls in hyperuricemia. 958 80

A 79-year-old man with atrial fibrillation and coronary heart disease who was taking warfarin (Coumadin) was converted to fenofibrate from gemfibrozil therapy for persistently elevated triglyceride levels. The patient took fenofibrate for 1 month and subsequently experienced rectal bleeding that required a visit to the emergency room. Before starting fenofibrate therapy, his coagulation values were within therapeutic range, but when measured in the emergency room the international normalized ratio (INR) was grossly elevated. The patient denied any changes in diet, alcohol ingestion, compliance with therapy, or use of other new drugs except for fenofibrate. His drug therapy profile consisted of digoxin, fosinopril, and furosemide for chronic heart failure, allopurinol for gout, and potassium supplementation. To minimize the risk of supratherapeutic INR values and/or hemorrhagic events, clinicians should perform serial monitoring of INR when initiating fenofibrate therapy in a patient previously stabilized on a coumarin anticoagulant.
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PMID:Fenofibrate and warfarin interaction. 1144 87

Uric acid (UA) is a purine metabolite that selectively inhibits peroxynitrite-mediated reactions implicated in the pathogenesis of multiple sclerosis (MS) and other neurodegenerative diseases. Serum UA levels are inversely associated with the incidence of MS in humans because MS patients have low serum UA levels and individuals with hyperuricemia (gout) rarely develop the disease. Moreover, the administration of UA is therapeutic in experimental allergic encephalomyelitis (EAE), an animal model of MS. Thus, raising serum UA levels in MS patients, by oral administration of a UA precursor such as inosine, may have therapeutic value. We have assessed the effects of inosine, as well as inosinic acid, on parameters relevant to the chemical reactivity of peroxynitrite and the pathogenesis of EAE. Both had no effect on chemical reactions associated with peroxynitrite, such as tyrosine nitration, or on the activation of inflammatory cells in vitro. Moreover, when mice treated with the urate oxidase inhibitor potassium oxonate were fed inosine or inosinic acid, serum UA levels were elevated markedly for a period of hours, whereas only a minor, transient increase in serum inosine was detected. Administration of inosinic acid suppressed the appearance of clinical signs of EAE and promoted recovery from ongoing disease. The therapeutic effect on animals with active EAE was associated with increased UA, but not inosine, levels in CNS tissue. We, therefore, conclude that the mode of action of inosine and inosinic acid in EAE is via their metabolism to UA.
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PMID:Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors. 1245 Nov 83

About one-half million adults in the United States experience a renal stone each year, about two hundred thousand of whom are hospitalized; the lifetime incidence of renal stones in men is about ten percent. Risk factors for stone formation include a positive family history, nutritional factors (excessive intake of animal protein, fat, sugar, oxalates, colas, alcohol, caffeine, salt, and vitamin D), nutritional deficiencies (water, magnesium, calcium, potassium, and vitamin B6), lifestyle factors (physical inactivity and problematic pharmaceuticals), and associated disease states (osteoporosis, parathyroid problems, osteoporosis, gout and recurrent urinary tract infections). The chemical makeup of the stone is important since prevention of recurrences varies somewhat depending on the type of stone involved. The outline of preventive steps holds the potential for preventing recurrence in the vast majority of cases.
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PMID:A complementary approach to urolithiasis prevention. 1252 85

The chief dangers reported with some common drugs are reviewed. Hazards of antibiotic therapy include: the increasing incidence of sensitization to penicillin with occasional anaphylactic reactions; aplastic anemia with chloramphenicol, and the poor tolerance of infants for chloramphenicol; staphylococcal enterocolitis; unnecessary "prophylactic" use of antibiotics. Thiazide diuretics may precipitate potassium depletion, skin reactions, pancreatitis, blood dyscrasias, gout, diabetes mellitus and hepatic coma. Reserpine can increase gastric acidity, induce mental depression, and when used with digitalis lead to ventricular premature beats. Hydralazine may aggravate angina pectoris, cause tachycardia, and bring about a syndrome resembling disseminated lupus erythematosus. Guanethidine may result in loose stools, impotence, and postural hypotension. Hazards of phenothiazines include jaundice, parkinsonian states and tremors, convulsions, hypotension, and blood dyscrasias. The butanediols have numerous side effects including gastrointestinal, cutaneous and hypotensive reactions. Prolonged corticosteroid therapy introduces a new danger in surgical treatment. The progesterone-like drugs may induce masculinization of the female fetus.
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PMID:Dangers in the use of some potent drugs. 1398 37

Uric acid stones occur in 10% of all kidney stones and are the second most-common cause of urinary stones after calcium oxalate and calcium phosphate calculi. The most important risk factor for uric acid crystallization and stone formation is a low urine pH (below 5.5) rather than an increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrhea or severe dehydration. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. The treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml daily), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary alkalization with potassium citrate or sodium bicarbonate is a highly effective treatment, resulting in dissolution of existing stones. Urinary uric acid excretion can be reduced by a low-purine diet. Potassium citrate is the treatment of choice for the prevention of recurrence of uric acid calculi. Allopurinol reduces the frequency of stone formation in hyperuricosuric patients with recurrent uric acid stones and/or gout.
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PMID:[Diagnosis and prevention of uric acid stones]. 1549 18

Kidney disease has not been considered a frequent complication in Down syndrome (DS) patients; a variety of urological abnormalities and glomerulopathies have been reported in this population, and some DS patients develop chronic renal failure (CRF). The aim of this study was to improve the understanding of renal disease in patients with DS, focusing on the incidence and range of kidney and urological abnormalities in a population of DS patients. A cross-sectional study was carried out in DS patients referred from a pediatric genetics unit of a tertiary care center. Medical records were reviewed. A 24-h urine specimen and a blood sample were obtained. Fractional excretion of sodium and potassium, tubular reabsorption of phosphate, urinary excretion of calcium, magnesium, uric acid, creatinine clearance and proteinuria were determined. Ultrasound was performed to evaluate the kidneys and the urinary tract. Laboratory data were reviewed for any possible renal disorder. Sixty-nine patients, aged 12 months to 24 years, were recruited. Pathological findings included three cases of voiding disturbances and a case of hypertension in a 7-year old girl. Eight patients (11.6%) had hyperuricemia without gout. Eighteen patients (24.2%) had hyperuricosuria. Urinalysis revealed three cases of mild proteinuria and two patients with microscopic hematuria. Minor radiological abnormalities were found in five patients (7.3%). Three patients (4.5%) had CRF. Renal disease in patients with DS is not as rare as previously thought, although the majority of findings are of minor relevance. According to the variety of pathologies, and in order to detect early irreversible renal injury, it seems quite reasonable to perform regular monitoring of renal function in these patients.
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PMID:Renal involvement in Down syndrome. 1578 39

1. An experiment was conducted to test the independent and combined effects of high dietary calcium and protein concentrations on the induction of visceral gout in growing birds of a layer strain. 2. One hundred and sixty healthy birds were randomly divided into 4 groups at 35 d of age. The different groups were given 4 diets containing normal or high concentrations of dietary calcium or crude protein in a 2 x 2 factorial experiment for 30 d. The diets contained normal calcium (Ca) and crude protein (CP) (NCNP, 8.5 g Ca/kg and 175g CP/kg), high calcium and normal protein (HC, 36.3 g Ca/kg and 175 g CP/kg), normal calcium and high protein (HP, 8.8 g Ca/kg and 245 g CP/kg) or high calcium and high protein (HCHP, 36.8 g Ca/kg and 242 g CP/kg), respectively. 3. Typical visceral gout was induced by the HCHP diet. The HCHP and HC diet caused severe kidney damage. The HP diet did not cause kidney damage, but significantly increased plasma uric acid and inorganic phosphorus concentrations. 4. The HC diet significantly increased plasma uric acid, calcium and sodium, but significantly decreased plasma inorganic phosphorus, potassium and magnesium concentrations. The HCHP diet significantly increased plasma uric acid, calcium and sodium. 5. Urine volumes were significantly higher on the HCHP and HC diets than on the control. The growers raised on HC and HCHP diets had significantly higher total quantity of 24 h urinary excretion of uric acid, calcium, magnesium, inorganic phosphorus and potassium and a significantly lower 24 h urinary excretion of sodium. The growers fed on the HP diet had a higher 24 h urinary excretion of uric acid and inorganic phosphorus than the control. 6. It is concluded that growing layer birds should not be fed on layer rations.
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PMID:Clinicopathology of gout in growing layers induced by high calcium and high protein diets. 1635 21

The methanol extract from the leaves of Phyllanthus niruri L. showed oral antihyperuricemic activity in potassium oxonate- and uric acid-induced hyperuricemic rats. Fractionation of the extract by resin chromatography led to the isolation of a less polar fraction which exhibited the highest reduction of plasma uric acid. Further antihyperuricemic-guided purification of the fraction afforded three lignans, phyllanthin (1), hypophyllanthin (2) and phyltetralin (3), of which 1 significantly reversed the plasma uric acid level of hyperuricemic animals to its normal level in a dose-dependent manner, comparable to that of allopurinol, benzbromarone and probenecid which are used clinically for the treatment of hyperuricemia and gout. Thus, the lignans of P. niruri are potential antihyperuricemic agents worthy of further investigation.
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PMID:Antihyperuricemic lignans from the leaves of Phyllanthus niruri. 1695 66


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