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)

After World War II the incidence of urolithiasis increased consistently among the general population in this country. Nearly 25% of all examined renal calculi contain uric acid, sodium acid urate or ammonium acid urate as constituents. There are two peaks in lifespan of occurring urate stones: in the adolescence and in the age between 40 and 60 years. The following conditions are due to the formation of uric acid-containing stones: 1. Gout and primary hyperuricemia; 2. secondary hyperuricemia; 3. idiopathic cases with normal renal excretion of uric acid and normouricemia, but with a higher degree of acidity of the urine than normal considering the total renal excretion of acid products; 4. iatrogenic hyperuricemia during insufficient uricosuric therapy. Up to more than 30% of all the patients with recurrent formation of oxalate stones show a clear association with hyperuricemia, hyperuricosuria and increased renal excretion of calcium. In the presence of sodium urate a considerable promotion of precipitation of crystals consisting of calcium oxalate from a meta-stable solution may occur (so-called epitaxy). Frequently the existence of uric acid stones is without any symptoms. Modern views with regard to prophylactic procedures, diet, general and specific medical management including surgical intervention are presented.
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PMID:[Urate nephrolithiasis. Cause of consequence?]. 95 52

Acute uric acid nephropathy has been described almost uniformly in patients with massive uric acid overload (malignancies with rapid cell destruction, epileptic seizures). Severe hyperuricosuria and intratubular uric acid precipitation result. Here we present two patients with gout, normal uric acid production, and moderate hyperuricemia, both of whom developed acute uric acid nephropathy. Because of pronounced urine acidity (pH values of 4.6 and 5.0 in morning fasting urines), supersaturation with respect to undissociated uric acid exceeded solubility (0.54 mmol/l), despite basal urate secretions of less than 2.2 mmol/24 hours. Additional predisposing factors, such as uricosuric treatment, heavy beer-drinking, over-consumption of purine-rich foods, and hot environment, were superimposed in both cases.
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PMID:Acute uric acid nephropathy in two gouty patients with moderate hyperuricemia and high urine acidity. 221 14

Uric acid is the end-product of purine nucleotide metabolism in man. The renal handling of urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically the most stable uric acid crystal. Uric acid is a weak acid that ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid solubility is strongly increased by urinary pH. The prevalence of uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for uric acid stone formation correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. Hyperuricosuria is the major risk factor, the most common cause being increased purine intake in the diet. Acquired and hereditary diseases accompanied by hyperuricosuria and stone disease include: gout, in strong correlation with the amount of uric acid excreted, myelo- and lymphoproliferative disorders, multiple myeloma, secondary polycythemia, pernicious anemia and hemolytic disorders, hemoglobinopathies and thalassemia, the complete or partial deficiency of HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH. Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uric acid nephrolithiasis. 778 6

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

The structural study of monosodium urate monohydrate, as the principal component in gout stones, reveals that a simple and biocompatible way to break down the crystals into polymerised molecules at pH 7.4 (the acidity of normal human blood) is to peel them off along the [001] direction by sonication.
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PMID:Structure and cleavage of monosodium urate monohydrate crystals. 3069 21