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)

A 62 year-old man had suffered from gout and mild renal insufficiency since he was 40 years old. He was admitted to our hospital complicated by a productive cough, high fever and a right swollen knee joint. The chest radiographs demonstrated a left upper lobe infiltration shadow. Streptococci pneumoniae were found in the sputum, arterial blood and synovial fluid of the right knee joint, suggesting a severe pneumonia followed by pneumococcal septicemia which led to purulent arthritis. He was treated with cefamandole (CMD) and penicillin G (PC-G) for one week, but the chest X-ray findings were not improved. After treatment with cefbuperazone (CBPZ) and latamoxef (LMOX), his fever and other symptoms gradually resolved. Streptococcus pneumoniae is an uncommon organism of septic arthritis. Pneumococcal arthritis in a patient without immunodeficiency such as this case is very rare, and has not been reported in Japan.
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PMID:[A case of pneumococcal arthritis in a patient with gout]. 261 92

Superactive phosphoribosylpyrophosphate (PRPP) synthetases were characterized in fibroblasts and erythrocytes from 5 unrelated men with gout and/or hyperuricemia and uric acid overproduction. The kinetic basis of enzyme superactivity in all patients was increased maximal reaction velocity. Affinities of the enzymes for substrates and activators and responsiveness to inhibitors were normal, and levels of immunoreactive enzyme in patient and control fibroblast and erythrocyte extracts were comparable. Enzymes purified to homogeneity from 2 patients confirmed the presence of isolated catalytic defects. Altered physical properties of certain of the superactive enzymes suggested the presence of several distinctive structural defects among the aberrant forms. Fibroblasts from each affected patient showed increased PRPP concentration and generation, as well as accelerated rates of all PRPP-requiring purine nucleotide synthetic pathways. These findings support the concept that enzyme superactivity results in uric acid overproduction as a consequence of increased rates of PRPP and purine nucleotide synthesis. Cultured cells from female relatives of 2 patients showed evidence for the heterozygous carrier state, as measured both by enzyme activities and by rates of PRPP and purine synthesis. The clinical phenotype in 4 patients was limited to early adult-onset gout and its consequences, whereas the fifth patient expressed a familial constellation of hyperuricemia, sensorineural deafness, ataxia, and renal insufficiency. The severity of the derangements in PRPP synthetase and in PRPP and purine synthesis in cells from the 5 patients, however, was comparable. The neurologic accompaniments of enzyme superactivity found in 1 family described here, and in 2 others described previously, thus may not necessarily be consequences of primary defects in PRPP synthetase.
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PMID:Phosphoribosylpyrophosphate synthetase superactivity. A study of five patients with catalytic defects in the enzyme. 301 68

Numerous trials have shown the efficacy of ACE-inhibitors in moderate and severe essential hypertension. Their use must be regarded as very promising. They lower peripheral vascular resistance without influencing cardiac index and heart rate. Additionally, they maintain serum potassium and do not effect plasma lipids or provoke diabetes mellitus or gout. In 20-30% of hypertensive patients ACE-inhibitors have to be combined with diuretics and/or calcium antagonists. The addition of beta-blockers is useful in patients with resting tachycardia. In mild hypertension the use of ACE-inhibitors as first-line drugs is indicated in patients with adverse reactions to beta-blockers or diuretics. In bilateral renovascular hypertension, ACE-inhibitors may induce a strong blood pressure fall; in bilateral stenosis they contribute to a deterioration of renal function with reversible renal insufficiency. In renoparenchymal hypertension, ACE-inhibitors may attenuate the progression of renal insufficiency; in addition, proteinuria is lowered. In systolic hypertension in the elderly, one must be aware of a marked first-dose hypotensive effect. ACE-inhibitors decrease exaggerated exercise-induced elevation of blood pressure and heart rate and therefore lower myocardial oxygen consumption. In patients with hypertension and diabetes mellitus, antihypertensive treatment should be initiated for blood pressure levels above 140/90 mmHg, to attenuate the progression of vascular damage in the kidney. In patients with severe left ventricular hypertrophy, ACE-inhibitors reduce left ventricular mass within three months by about 30%. In hypertension and coronary heart disease, recent studies report benefits of ACE-inhibitors on coronary circulation. Presently available ACE-inhibitors and those in preparation do not differ in pharmacodynamic, but in pharmacokinetic properties, concerning the beginning and duration of blood pressure lowering. A hypotensive first-dose effect can be observed in diuretic pretreated patients, in severe (malignant) and renovascular hypertension. ACE-inhibitors should not be used during pregnancy or in patients with autoimmune diseases or those undergoing treatment with immunosuppressive drugs, due to the side effects of neutropenia and proteinuria, which are more often seen under these conditions. Results from long-term studies on the influence of ACE-inhibitor treatment on cardiovascular risk in mild hypertension have not been available until now. In the decision to treat mild hypertension with ACE-inhibitors as first-line drug therapy, the costs of therapy in comparison to cheaper antihypertensives must be taken into account.
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PMID:[The value of angiotensin-converting enzyme inhibitors in the treatment of hypertension]. 306 60

We reviewed crystal-proved gouty arthritis in 23 women. Twenty-one (91%) developed gout after menopause onset. Tophaceous gout occurred in six (26%), polyarticular involvement in 13 (57%); 70% manifested an underlying arthropathy, usually osteoarthritis. We studied 75 men with crystal-proved gout for comparison. Women developed gout significantly later compared with men, more often were receiving diuretics before gout onset, and more frequently manifested renal insufficiency and monoarticular involvement. These differences were significant when controlled for the women's later age at onset. Significantly more men than women had alcoholism and an identifiable precipitating event for acute attacks. There were no significant differences in race, age, family history of gout, disease duration, hypertension, distribution of joint involvement, tophi, or mean serum urate concentration. Gout in women is overwhelmingly postmenopausal, apparently associated with diuretic therapy and renal insufficiency independent of the effects of age. Articular characteristics in men and women are remarkably similar.
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PMID:The clinical spectrum of gouty arthritis in women. 377 53

The authors observed 10 patients from 4 families with hereditarily determined gout and detected some specific features in its course. The familial disease was sex-unrelated, its first signs manifested themselves early acquiring a subsequent severe course; purine metabolic derangement was of a metabolic type, a urolithic form of nephropathy was seldom observed. A morphological picture was characterized by a glomerular lesion looking like focal segmental mesangiocapillary or mesangioproliferative glomerulonephritis with noticeable changes in the tubules, stroma and vessels causing early renal insufficiency. Pathogenetic therapy with uricodepressants made it possible to improve the course of nephropathy. The authors described a pedigree of 3 generations of a family in which gout developed in its 10 out of 17 members, in 6 with chronic renal insufficiency.
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PMID:[Familial gout]. 396 78

A family is described many of whose members suffered from renal insufficiency, hypertension, gout, and hyperuricaemia in conjunction. Adequate information was obtained on 72 subjects from five generations. In 17, one or more of the above mentioned abnormalities was or had been present. The hereditary distribution suggested an autosomal dominant disease entity. The renal disease was characterized by an early loss of urinary concentrating power, minimal proteinuria, and death at a relatively early age dominating the clinical picture. The histological picture in three biopsies and one necropsy showed predominant tubular atrophy and interstitial fibrosis, with striking tubular basement membrane thickening. It is suggested that these patients suffered from a hereditary degenerative renal disease. The question whether hyperuricaemia was primary or secondary in these cases is discussed.
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PMID:An unusual form of renal disease associated with gout and hypertension. 555 22

Ten patients with gout, hypertension, and mild to moderate renal insufficiency were studied for possible lead nephropathy by measuring stimulated urinary lead excretion. Seven had a history of lead exposure, 5 from illegal alcohol and 2 from industrial sources. Occult lead was assessed by 24 h urine collection measurements over a 72 h period after intramuscular administration of calcium disodium EDTA. Two patients with a history of lead exposure excreted 707 and 687 micrograms Pb/72 h, respectively, and a 3rd excreted 506 micrograms Pb/72 h. The remainder had a normal response, with mean urinary lead excretion of 251 +/- 42 micrograms Pb/72 h. Since we were unable to demonstrate that lead was important to the pathogenesis of the renal we were unable to demonstrate that lead was important to the pathogenesis of the renal failure in 7 patients despite a positive history of lead exposure in 2, we suggest that factors other than lead may be the cause of renal failure in most patients with gout and renal disease.
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PMID:Occult lead intoxication in patients with gout and kidney disease. 643 39

A patient with lead nephropathy and gout was treated with three months of edetic acid chelation. The therapy resulted in normalization of a previously abnormal result of edetic acid lead mobilization test. Nevertheless, progressive renal insufficiency occurred. At autopsy, an increased bone lead content was documented, suggesting that the edetic acid lead mobilization test may underestimate total body lead stores and that chelation therapy may not be effective in reversing advanced lead nephropathy. Alternatively, a longer period of therapy may be necessary to remove lead stores. More studies are needed to determine the relationship between the results of the edetic acid test and bone lead stores. Methods other than the edetic acid lead mobilization test should be considered to monitor the adequacy of treatment in lead nephropathy.
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PMID:Failure of chelation therapy in lead nephropathy. 643 41

Two patients had onset of juvenile gouty arthritis at ages 16 and 1 1/2 years, respectively. Both had mild renal insufficiency, with creatinine clearances of 46 and 54 mL/min/1.73 sq m, respectively. Their presenting hyperuricemia (13.8 and 11 mg/dL, respectively) was out of proportion to the degree of renal insufficiency. Clinical and laboratory studies did not suggest an inborn error of purine metabolism, glycogen storage disease type I, or any myeloproliferative disorder. Neither patient had a family history of gout or inherited renal disease. Although juvenile gouty arthritis is rare, it must be considered in the differential diagnosis of episodic arthritis in children, especially if renal impairment, even mild, is present.
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PMID:Juvenile gouty arthritis. Two cases associated with mild renal insufficiency. 647 56

In order to elucidate the influence of the parathyroid function on the uric acid metabolism, 24 patients (14 males, 10 females) with primary hyperparathyroidism (PHP) and 17 patients (9 males, 8 females) with idiopathic hypoparathyroidism (IHP) were extensively studied. The mean age was not significantly different between these groups, being 40.3 +/- 2.8 and 39.0 +/- 3.5 respectively. Hyperuricemia was found in 4 patients with PHP, but none of the patients had experienced gout. The serum uric acid levels were significantly higher and uric acid clearances were significantly lower in PHP than in IHP. There was no difference in daily urinary excretion of uric acid and in creatinine clearance between the two groups. In PHP, a positive correlation was observed between the levels of serum uric acid and calcium, both of which negatively correlated to renal uric acid clearance. Although the serum uric acid levels did not correlate to serum PTH levels in PHP, the removal of parathyroid adenoma resulted in a significant fall of serum uric acid levels. In IHP, the administration of PTH induced a small but significant decrease in serum uric acid levels with a coincidental increase in urinary uric acid excretion. Four hours of calcium infusion had no effect on the serum uric acid levels and urinary uric acid excretion. Treatment of IHP with 1 alpha-OH D3 to restore normal serum calcium levels caused significant increase in serum uric acid levels. These data indicate that the parathyroid function influences uric acid metabolism, even in the absence of renal insufficiency, mainly through changes of uric acid clearance. Levels of active vitamin D or chronically abnormal calcium levels in the circulation may be major determinant for uric acid metabolism in parathyroid disorders.
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PMID:[Parathyroid function and uric acid metabolism]. 666 55


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