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 double-blind study of hydrochlorothiazide and spironolactone, alone and in combination, was conducted in 49 patients with mild-to-moderate essential hypertension after a 4-wk placebo washout period. In the whole group mean arterial blood pressure fell to levels of less than or equal to 107 mm Hg or declined by more than 15 mm Hg in 78% of the patients after twelve weeks of treatment. Sixty-nine percent of patients receiving hydrochlorothiazide alone developed serum potassium levels lower than 3.5 mEq/L; serum potassium levels were above 5.5 mEq/L in 2 patients (5.5%) receiving spironolactone 400 mg/day. Uric acid levels rose in all patients, more in those on hydrochlorothiazide, but clinical gout did not develop in any subject. Hydrochlorothiazide, spironolactone, and the combination of the two are effective antihypertensives. Spironolactone in doses of 200 and 400 mg/day was associated with side effects but did not induce a greater antihypertensive effect than doses of 100 mg/day. Our data suggest that when hydrochlorothiazide is associated with potassium loss, when gout or elevated uric acid levels are of concern, or when carbohydrate tolerance is abnormal, supplementation or replacement with spironolactone (up to 100 mg/day) may be useful in controlling blood pressure while reducing side effects.
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PMID:Hydrochlorothiazide and spironolactone in hypertension. 36 34

Protein binding of urate may have some pertinence to the pathogenesis of gout. However, binding studies have been hampered by problems with in vitro methodology and by the problem of relating the results of in vitro studies to the physiological situation. In the present study urate binding was determined by an ultrafiltration procedure. All manipulations were performed anaerobically and at 37 degrees in order to maintain the sample under physiological conditions. Normal urate bound was 15 +/- 7.5% in males and 10 +/- 6.6% in females. Urate binding did not correlate significantly with either the albumin or total urate concentration. It is suggested that the interaction between protein and urate is influenced by a number of factors other than the concentrations of free urate and binding protein. Some possible ones are discussed. The techniques described might usefully be applied to a study of urate binding in various pathological states.
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PMID:The binding of urate by plasma proteins. 47 69

The effect of feeding on plasma-uric acid concentrations of the snake was studied. The values were monitored in 2 gopher snakes and 2 black rat snakes which were fed mice. Plasma uric acid values in snakes increased after eating and gradually returned to base line with the digestion of the mice. Uric acid concentrations were greater in snakes eating 2 mice than in those eating only 1 mouse. The base-line plasma uric acid concentration in snakes was approximately 2 to 5 mg/dl. Plasma uric acid concentrations may be useful in making a diagnosis of gout. Presence of gout is usually indicated by increased uric acid concentrations; however, interpretation of these concentrations should be based on information about the feeding schedule.
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PMID:Effect of feeding on plasma uric acid levels in snakes. 69 68

The release of human platelet constituents by the etiologic agent of gout, the monosodium urate crystal, is described here. In suspensions of washed platelets, response to urate crystals proceeded in two phases: A secretory phase involved the rapid active release of serotonin, ATP, and ADP with little loss of lactic dehydrogenase or beta-glucuronidase. A lytic phase involved the slower loss of all platelet constituents. Both phases were inhibited by iodoacetate plus dinitrophenol, suggesting an energy requirement. In ultrastructural studies, lysis of washed platelets which appeared to contain crystals was seen. Urate crystals were also shown to induce serotonin release and platelet lysis in citrated platelet-rich plasma. Since urate crystals are deposited at a variety of sites, urate crystal-platelet interaction in vivo is a possibility. Such interactions, leading to release of platelet constituents, might contribute to gouty inflammation or to enhanced atherogenesis.
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PMID:Release of platelet constituents by monosodium urate crystals. 90 64

The antihypertensive effect and side-effects during 12 months' treatment with bendroflumethiazide and propranolol have been compared in two randomly selected, equally large groups (n= 53) of previously untreated male hypertensives. Systolic BP above 170 or diastolic BP above 105 mmHg on two occasions were defined as hypertension. The same BP reduction was achieved in both groups. During the 12 months' treatment one subject on bendroflumethiazide developed diabetes mellitus and one on propranolol developed cardiac decompensation. None developed gout. Contrary to what had been presumed, glucose tolerance improved during 12 months' treatment with both agents, while there were no changes in fasting blood sugar, insulin or triglyceride concentrations. No changes were found in serum potassium or total body potassium during 12 months' bendroflumethiazide treatment, while serum potassium increased during treatment with propranolol. Uric acid increased slightly during treatment with both agents. Prolongation of the follow-up to 24 months did not change any of the findings regarding metabolic changes during treatment. The frequency of subjective side-effects decreased to the same extent during treatment with both drugs. It is concluded that bendroflumethiazide and propranolol are equally useful as antihypertensive agents and that the risk of impariment of glucose metabolism and potassium balance seems to be very slight during treatment with bendroflumethiazide in mild hypertension.
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PMID:Antihypertensive effect and side-effects of bendroflumethiazide and propranolol. 93 76

In addition to uricosuric agents and purine synthesis inhibitors, Urate Oxydase may be used in the treatment of hyperuricaemia. This substance breaks down uric acid to allantoin which is soluble and easily excreted. Use of the medication in 14 cases of major gout with tophi and 9 cases of hyperuricaemia secondary to renal insufficiency showed the good tolerance of the substance and it's clinical and biological effectiveness.
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PMID:[Uricolytic therapy. Value of urate oxidase in the treatment of hyperuricemias]. 109 13

Seven young adults with uric acid overproduction due to sickle cell anemia were normouricemic with a mean serum uric acid level of 4.9 mg/100 ml. Urate clearance was greater in these patients than in normal subjects or in patients with primary hyperuricemia due to uric acid overproduction. The increase in urate clearance was entirely accounted for by increased pyrazinamide suppressible urate clearance. Pyrazinamide administration abolished the uricosuric response to ribonucleic acid (RNA) feeding in these patients with sickle cell anemia, and maximal uricosuric response to the administration of probenecid was similar in the patients with sickle cell anemia and in normal subjects suggesting that reabsorption of both filtered and secreted urate was not impaired in sickle cell disease. Pyrazinamide suppressible urate clearance at maximal uricosuric response to probenecid was increased in patients with sickle cell disease suggesting increased tubular secretion of urate. This increase in urate secretion permits most young adults with urate overproduction due to sickle cell anemia to remain normouricemic and may account for the low frequency of secondary gout in this disease.
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PMID:Hyperuricosuria and increased tubular secretion of urate in sickle cell anemia. 110 19

The etiology of hyperuricemia following myocardial infarction was investigated by uric acid kinetic studies carried out on seven male patients following myocardial infarction and on two control subjects. The patients selected had uncomplicated myocardial infarction and were maintained on a low-purine diet. Measurements of uric acid pool size and turnover rates using 2-C14 uric acid were made, commencing on days 2-5 following myocardial infarction. Initial concentration of serum uric acid ranged from 2.9 to 9.8 mg/100 ml. Uric acid pool size was elevated in six of seven patients. Five had a pool size of from 36.9 to 79.6 mg/kg, while the single gouty subject demonstrated 104 mg/kg compared with 12.6 and 16.8 mg/kg for the control subjects. Turnover rates were also increased, ranging from 1036 to 2772 mg/day (controls, 612 and 872 mg/day). Twenty-four-hour urine uric acid excretions ranged from 358 to 623 mg/24 hr. Serum lactic acid concentration was normal (1.03 plus or minus 0.17 muM/ml), and endogenous creatinine clearance in all cases was 77.9 ml/min or greater. These data suggest that following myocardial infarction there is an expansion of the uric acid pool with an increased uric acid turnover rate. Only the patient with a previous history of gout had uric acid excretion outside the normal range.
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PMID:Uric acid kinetic studies in the immediate post-myocardial-infarction period. 111 39

Gout may be associated with renal disease in two situations: (i) when the abnormal urate metabolism is the primary phenomenon and renal disease occurs secondary to this; or (ii) when the intrinsic renal disease is primary, and results in secondary abnormalities of renal function. Kidney damage secondary to gout is associated with urate deposits either in the intersitium as microtophi or as uric acid crystals within tubules, and vascular disease and infection are superimposed. Hyperuricaemia is a frequent sequel to parenchymal renal disease, but gouty arthritis develops only when the hyperuricaemia is unusually severe. Urate metabolism alters when renal excretion of urate is reduced. The management of these problems is discussed.
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PMID:Gout, uric acid and renal disease. 127 25

Urate crystal formation, and subsequent gout, occurs in only a minority of hyperuricaemic subjects indicating that factors other than hyperuricaemia are involved. Biological substances (especially proteins) alter crystal growth in vitro independently of uric acid concentration. Physiological crystal formation, known to be under biological control, is characterised morphologically by uniformity of size and constraint of crystal shape. To determine whether pathological urate crystal formation is influenced by the surrounding biological milieu we examined, using scanning electron microscopy, the morphology of urate crystals formed either in vivo or in vitro. We found morphological evidence of biological control of in vivo urate crystal formation and demonstrated that those characteristics could be induced in vitro by the addition of serum, synovial fluid and certain serum proteins to the growth medium during crystal formation. Urate crystal formation is dependent, not only on the degree of hyperuricaemia, but also on the surrounding biological milieu.
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PMID:Morphological evidence for biological control of urate crystal formation in vivo and in vitro. 143 29


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