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)

Participants in the Medical Research Council treatment trial for mild hypertension are randomly allocated to one of four treatment groups: bendrofluazide, propranolol, or a placebo for either of these drugs. The trial is single-blind. 23 582 patient-years of observation have been completed so far, 10 684 on active drugs and 12 898 on placebos. The results show an association between bendrofluazide treatment and impotence, and impotence also occurred more frequently in patients taking propranolol than in those taking placebos. Other adverse reactions significantly linked with active drugs include impaired glucose tolerance in men and women and gout in men, associated with bendrofluazide treatment, and Raynaud's phenomenon and dyspnoea in men and women taking propranolol. No corneal disease is known to have occurred in the propranolol group. Mean serum potassium level fell, and urea and uric acid levels rose, in men and women taking bendrofluazide. In the propranolol group, serum potassium and uric acid levels rose in both sexes, but the urea level rose significantly in women only.
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PMID:Adverse reactions to bendrofluazide and propranolol for the treatment of mild hypertension. Report of Medical Research Council Working Party on Mild to Moderate Hypertension. 611 99

A randomized, double-blind, parallel treatment trial was carried out in 24 patients with moderate to severe hypertension to compare the effectiveness and tolerance of two treatment regimens in reducing and maintaining supine diastolic blood pressure below 90 mmHg. Patients in Group I received 10 to 40 mg enalapril maleate per day with the addition of 50 mg hydrochlorothiazide per day and then 250 to 1000 mg alpha-methyldopa per day, if necessary. Patients in Group II received 50 mg hydrochlorothiazide per day with the addition of 80 to 240 mg propranolol and then 100 to 200 mg hydralazine per day, if necessary. Apart from the hydrochlorothiazide dosage which was fixed, the dosage of the other active drugs was titrated incrementally until the target blood pressure level was achieved. Blood pressures, heart rate and body weight were monitored at 2-weekly intervals during 26 weeks of active therapy. In Group I, blood pressure control was achieved and maintained with enalapril alone in 9 patients, 2 patients required double therapy and 1 patient triple therapy. In Group II, 9 patients required double therapy, 2 triple therapy, and only 1 patient received monotherapy. Supine and erect blood pressure control was comparable in both groups. There was, however, a significant decrease in supine heart rate in patients in Group II. More importantly, 8 of the 12 patients in Group II experienced non-life threatening adverse reactions (4 were hypokalaemic and required supplementary potassium, 2 had cold hands and feet, 1 man had sexual dysfunction and 1 acute gout) and no adverse reactions were reported by Group I patients.
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PMID:An appraisal of antihypertensive efficacy and adverse reactions with two drug regimens: enalapril maleate as part of triple therapy compared to conventional triple therapy in moderate to severe hypertension. 632 7

Thiazide induced metabolic effects reflected in serum and 24 h urine excretions were investigated in general practice in 48 recurrent urinary calcium stone formers on prophylaxis with 50 mg hydrochlorthiazide or placebo (average duration of treatment 3 years). After 10 months of treatment, there was a significantly greater decrease in urinary calcium excretion among patients receiving thiazide than in patients given placebo (p less than 0.05). There was a significant increase in urinary magnesium in the thiazide group (p = 0.02), while there was no significant alteration in urinary uric acid. An increase was observed in the 24 h urine volume of 400 ml in the placebo group in contrast to a decrease in the thiazide group. The effects on serum calcium, potassium and uric acid were in accordance with previous reports. Few and only mild side effects were observed except for one attack of gout. The necessity of having adequate control groups in such studies is emphasized.
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PMID:Metabolic effects of thiazide versus placebo in patients under long-term treatment for recurrent urolithiasis. 646 98

A fixed combination tablet containing 5 mg of timolol, 25 mg of hydralazine, 25 mg of hydrochlorothiazide and 37.5 mg of triamterene was prepared and its antihypertensive effect compared with placebo in a randomized double-blind cross-over study lasting 16-20 weeks. 37 patients entered the study and 32 of them completed it. The trial drug caused a highly significant drop in blood pressure in both the supine and standing positions (from 172/112 to 142/91 mm Hg supine and from 168/17 to 136/100 mm Hg standing). There was also a highly significant fall in heart rate. Three patients were nonresponders with maximal dose used (4 tablets daily) and two patients had to withdraw from the trial because of complications. In general the side effects recorded were mild and equally common both on placebo and the trial drug. The serum potassium level was well maintained. The serum urate concentration was increased, but no signs of gout were observed. The conclusion was that this fixed combination of timolol, hydralazine, hydrochlorothiazide and triamterene is effective and well tolerated in the treatment of mild to moderate hypertension.
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PMID:Antihypertensive action of drug combination: Timolol, hydralazine, hydrochlorothiazide and triamterene. 701 63

We present a patient in whom indomethacin treatment for acute gouty arthritis induced reversible azotaemia and hyperkalaemia. Re-introduction of the drug under controlled conditions of metabolic balance resulted in recurrence of hyperkalaemia and azotaemia, and was associated with a fall in plasma renin activity, but no change was observed in plasma aldosterone. Since potassium retention and hyperkalaemia occurred in the absence of hypoaldosteronism, other factors must be invoked to explain the observed upset in potassium homeostasis. This, and other recent case reports suggest that prostaglandin synthetase inhibitors such as indomethacin should be used with caution, especially in patients with pre-existing azotaemia, congestive heart failure, or gout.
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PMID:Indomethacin-induced azotaemia and hyperkalaemia: a case study. 703 49

Turkey poults were fed diets containing oosporein at concentrations of 0, 500, 1,000, and 1,500 micrograms/g from hatching until three weeks of age. Low feed consumption resulted in poor growth rates at every dietary level of oosporein; however, a dose-related increase in water consumption was observed. The most significant effect of dietary oosporein was severe visceral and articular gout, with death ensuing in 24 and 52% of the poults at the 1,000 and 1,500 micrograms/g levels, respectively. Gout and mortality were absent at 0 and 500 micrograms/g. In addition to tissue urate deposition, necropsies revealed dehydration, swollen pale kidneys, hemorrhagic proventriculitis with mucosal necrosis, gizzard enlargement and lining discoloration, an increase in gall bladder size, and focal hepatic necrosis. The relative weights of the kidney, liver, proventriculus, gizzard, and pancreas were increased in a dose-related fashion; spleen and bursa weights were unaffected. Among plasma constituents, uric acid, urea, and the activities of glutamic-oxalacetic transaminase and lactic dehydrogenase were elevated in response to dietary oosporein; albumin, potassium, phosphorus, and calcium were decreased. The toxin had no effect on plasma total protein, sodium, glucose, cholesterol, triglycerides, alkaline phosphatase, or creatine phosphokinase. These data substantiate the original classification of oosporein as a nephrotoxin and etiologic agent of gout in avian species.
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PMID:Oosporein-toxicosis in the turkey poult. 709 45

Forty-nine patients with gout, many with hypertension and/or renal calculi, were given hydrochlorothiazide, furosemide, or ticrynafen. Diuresis and increased clearances of sodium (Na), potassium (K), chloride (Cl), and calcium (Ca) occurred after a single dose of hydrochlorothiazide, 100 mg, or furosemide, 40 mg, orally. There was very slight change in urate and phosphorus clearances. With prolonged use of hydrochloride or furosemide, diuresis and increased electrolyte excretion disappeared. Urate and Ca excretion fell with hydrochlorothiazide. With long-term use of furosemide, urate excretion was suppressed, but Ca excretion was sustained. Ticrynafen produced diuresis and increased clearances of Na, K, and Cl. Calcium excretion was increased after a single dose and minimally decreased after long-term use. Most striking was the severe and rather sustained uricosuria. Though ticrynafen is an effective uricosuric, natriuretic, and antihypertensive agent, its hepatotoxicity and nephrotoxicity mitigate against its clinical use.
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PMID:Effects of diuretics on urate and calcium excretion. 723 11

Fifty-two middle-aged patients with essential hypertension were treated for five months with 25 mg mefruside as the only antihypertensive drug. Blood pressure, heart rate, fasting blood glucose, cholesterol, triglycerides, uric acid, electrolytes and weight were controlled regularly before and during treatment. Blood pressure normalized in 43 cases (82.7%). The decrease was more marked in the females and their maximal response appeared later. No significant changes were seen in cholesterol and triglycerides. Serum uric acid levels increased significantly in both sexes (p < 0.001) but no patient developed gout. A significant decrease (p < 0.001) in serum potassium was seen; only one male, with heredity for diabetes mellitus, showed a decreased glucose tolerance.
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PMID:Effects of mefruside treatment in hypertension. 744 7

The effect of intracellular and extracellular pH on potassium conductance (GK) was examined in isolated amphibian (Rana pipiens) proximal tubule cells under whole cell voltage clamp conditions. Internal perfusion of the patch pipette was used to precisely control intracellular pH. In the region of normal resting potential (-51 +/- 3 mV), raising cell pH from 6.5 to 8.0 did not significantly increase GK (1.1 +/- 0.3 vs. 1.3 +/- 0.3 nS; P > 0.08, n = 8). Similar elevations in external (bath) pH had even less of an effect on GK. In contrast, when cells were voltage clamped to 30 mV more negative than the resting potential, raising internal pH from 6.5 to 8.0 did increase GK from 1.05 +/- 0.3 to 1.8 +/- 0.5 nS (P < 0.04; n = 8). These results suggest that modest changes in pH have little effect on GK, except at large negative potentials. In the process of examining the pH dependence of GK, a slowly activating, voltage-dependent conductance of 7.5 +/- 1 nS (n = 20; for 20 microns cells) was observed during cell depolarization. Although the instantaneous current-voltage relation of this conductance was linear, its marked voltage dependence produced an apparent steady-state rectification, with Gm = 0.5 +/- 0.2 nS and Gout = 9.0 +/- 1 nS (n = 11). Outward current was reversibly blocked by 3 mM Cu, Cd, or Co. In the absence of Na, K, and Ca (and only trace amounts of Cl), rapid changes in bath pH from 6.5 to 8.0 shifted the steady-state reversal potential (Erev) by -37 +/- 4 mV (n = 9) and the instantaneous Erev by -56 +/- 4 mV (n = 9). These shifts in Erev were consistent with a hydrogen ion conductance (GH), similar to what has been reported for snail neuron, neutrophils, alveolar epithelial cells, and phagocytes. Since the magnitude of this GH would be insignificant at resting cell pH and membrane potential, its role in renal proximal tubule under normal conditions is somewhat obscure. Nonetheless, in pathological situations, GH could function to prevent acid overload during any process that depolarizes the cell, such as low temperature or metabolic inhibition.
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PMID:Effect of pH on potassium and proton conductance in renal proximal tubule. 757 77

High blood pressure (BP) in the elderly must not be ignored as a normal consequence of aging. The criteria for the diagnosis of hypertension and the necessity to treat it are the same in elderly and younger patients. The aim of treatment of elderly hypertensive patients is to decrease BP safely and to reduce risk factors associated with cerebrovascular, cardiovascular and renal morbidity and mortality. The treatment of elderly hypertensive patients should be adjusted according to the needs of the individual, based upon age, race, severity of hypertension, co-existing medical problems, other cardiovascular risk factors, target-organ damage, risk-benefit considerations and costs. In addition to the elevated BP, other cardiovascular risk factors include smoking, glucose intolerance, hyperinsulinaemia, dyslipidaemia, hypercreatininaemia, peripheral vascular disease, left ventricular hypertrophy, and microalbuminuria (or albuminuria). Thus, the choice of initial antihypertensive therapy in elderly hypertensive patients should be based not only on the expected response, but also on the effects of therapy on lipid, potassium, glucose and uric acid levels, and left ventricular anatomy and function. Co-existing medical conditions (such as asthma, diabetes mellitus, heart failure, renal failure, gout, coronary artery disease, hyperlipidaemia and peripheral vascular disease) are major determinants for the selection of antihypertensive medications. With previous therapies (diuretics, beta-blockers, etc.), good BP control in the elderly was associated with clear and statistically significant reductions in stroke-related morbidity and mortality, but the overall effects on cardiovascular and renal complications of hypertension was either more variable or less obvious. Angiotensin converting enzyme (ACE) inhibitors are not only efficacious antihypertensive agents in the elderly, but also appear promising in counteracting some of the cardiovascular and renal consequences of hypertension. They are well tolerated and have a relatively low incidence of adverse effects. ACE inhibitors possess ancillary characteristics that are potentially beneficial for many elderly patients, including reduction of left ventricular mass, lack of metabolic and lipid disturbances, no adverse CNS effects, no risk of induction of heart failure, and a low risk of orthostatic hypotension. Since ACE inhibitors may improve perfusion to the heart, kidney and brain, they are well worth considering for the treatment of elderly patients with hypertensive target organ damage, especially in patients with heart failure, and diabetic patients with early nephropathy.
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PMID:ACE inhibitors. Differential use in elderly patients with hypertension. 857 91


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