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)

During a study of clinical and laboratory features in 83 patients with sickle cell disease in the Netherlands, serum creatinine, sodium, potassium, uric acid and osmolality were determined and reported for 65: 39 with homozygous sickle cell (SS) disease, 5 with beta degrees thalassaemia (S beta degrees thal), with sickle cell beta + thalassaemia (S beta degrees + thal) and 17 with sickle cell haemoglobin C (SC) disease. Data on history of hyposthenuria was unreliable. Haematuria was reported in 6 (7%) of the 83 patients. Four of the six patients with a history of haematuria, two of whom had elevated creatinine levels, had SS disease. Lower mean levels of serum sodium and higher levels of serum potassium were observed in SS's than in the other genotypes (p less than 0.001). Hyperkalaemia of greater than 5 mmol/l was seen in 50% of SS disease cases and in 33% of paediatric SC disease cases. Some high potassium levels must be ascribed to in vitro haemolysis. The rate of hyperuricaemia ranged from 24% to 40% among the various genotypes. Clinical gout was not observed.
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PMID:Renal and electrolyte profile in steady state sickle cell disease: observations in patients with sickle cell disease in The Netherlands. 276 58

The activity of the plasma membrane Na+/K+-ATPase and cellular sodium (Nai) and potassium (Ki) content were analysed in RBCs from 15 rheumatoid arthritis (RA) and 30 reference subjects (11 healthy controls, 12 osteoarthritis and 7 gouty patients). Na+/K+-ATPase activity was determined by measuring the inorganic phosphate (Pi) released by incubation in a reaction medium in the presence and absence of K ions or ouabain. Nai and Ki were measured with an ion-selective electrode analyser on the hemolysates, after washing the RBCs in 110 mM MgCl2. The Na/K-ATPase activity was significantly lower in RA patients than in both healthy controls and patients with osteoarthritis or gout. A slight but significant increase in Nai was observed in rheumatoid subjects. It is hypothesized that the decrease in the Na+/K+-ATPase activity in RA may be the result of a defective expression of membrane proteins, which is probably related to the altered cell sensitivity observed.
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PMID:Decreased NA+, K+-ATPase activity in erythrocyte membrane from rheumatoid arthritis patients. 282 52

The influence of a once daily dose of 200 mg celiprolol alone and in combination with 12.5 mg chlorthalidone on uric acid and electrolyte metabolism was investigated in 22 hypertensive patients with gout in a randomized trial. All patients were treated with allopurinol and diet. A four weeks treatment with celiprolol (11 patients) showed no influence on uric acid metabolism, electrolytes, blood glucose, cholesterol and triglycerides. Under treatment with celiprolol plus chlorthalidone (11 patients) only a small rise in serum uric acid was observed after four weeks but at the same time uric acid clearance and excretion increased significantly. There was no obvious change in serum electrolytes but an increase in sodium, potassium and chloride urine excretion. Serum uric acid, uric acid clearance and excretion decreased during a 6 months treatment period. A small decrease in cholesterol and triglycerides was observed. Blood pressure decreased in both treatment groups but there was only a small change in heart rate.
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PMID:[Uricosuric action of a new beta receptor blocker-diuretic drug combination]. 287 73

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

1. The renal and metabolic effects of the sulphamoylbenzoic acid diuretic, piretanide, have been studied, under controlled dietary conditions, in 39 patients with congestive cardiac failure. 2. In acute studies, peak saluresis occurred within 4 h of oral piretanide administration; saluresis was complete within 6 h, after which a significant antidiuretic effect was observed. Addition of triamterene, 50 mg, blunted the 0-6 h kaliuretic effect of piretanide. Over 24 h, piretanide, alone, caused insignificant urinary losses of potassium when compared with control. 3. In comparative studies, the piretanide dose-response curve was found to be parallel to that of frusemide over the dose range studied. The 0-6 h saluretic responses of piretanide, 6, 12 and 18 mg, were found to be equivalent to frusemide, 40, 80 and 120 mg respectively. The collective mean ratios of all the saluretic responses to each dose of piretanide with the corresponding dose of frusemide was observed to be 0.99 +/- 0.12, over 0-6 h period, and 0.86 +/- 0.09 over the 24 h period. The relative potency of piretanide, when compared with frusemide was found to be 6.18 (95% confidence limits 4.87-8.33), over the 0-6 h period, and 4.73 (95% confidence limits 3.65-6.14), over 24 h period. 4. In 15 patients in severe cardiac failure, urinary recovery of piretanide, over first 6 h, at the start of treatment was 21.2 +/- 2.1% while efficiency of the diuretic (mmol Na/mg drug) was 47.3 +/- 4.1. Long-term piretanide therapy was continued in the same group for up to and in some cases over 3 years. No other diuretics or potassium supplements were given. Piretanide dosage ranged from 6 to 24 mg day-1 according to clinical need. Plasma potassium fell significantly at 12 and 24 months, though remaining within the normal range. At these same times, significant elevations in both plasma urate and total fasting cholesterol were observed. Two patients developed overt gout on high dose piretanide therapy (24 mg day-1). Piretanide was well tolerated, and effective in the management of congestive cardiac failure without any other recognized metabolic or electrolyte changes.
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PMID:Acute and long-term renal and metabolic effects of piretanide in congestive cardiac failure. 320 51

Thiazide diuretics have been in use for over 30 years in the treatment of hypertension. Their action results in a reduction in peripheral resistance without a significant decrease in cardiac output or a major shift in plasma volume. They are as or more effective than any of the other antihypertensive agents when used as monotherapy and can serve as baseline therapy in combination with any of the available adrenergic, converting enzyme-inhibiting agents, or calcium-entry blockers. There is a high degree of patient acceptance; titration to an effective dosage is relatively easy; and cost, relatively low. Although certain undesirable metabolic changes may occur following the use of these agents, most of them are controllable, and there is no evidence to date that they offset the benefits achieved by blood pressure lowering. Asymptomatic elevated uric acids have not been shown to be of great significance. If gout occurs, it can be managed. Alterations in glucose metabolism may occur, and in some patients, it appears that blood glucose levels are elevated over time. This is not a desirable metabolic change, but is one of doubtful prognostic significance. Changes in lipids are generally short-term, and in the major clinical trials, lipid levels have not remained elevated with a continuation of diuretic therapy. Although diuretics produce hypokalemia in a fairly high percentage of patients, this is not generally severe (less than 3.3 mEq per liter) and usually does not produce symptoms. There is no firm evidence that the hypokalemia produced by diuretics predisposes the patient to severe arrhythmias or sudden death, although this point has been emphasized repeatedly in recent publications. Diuretics can usually be given without potassium-maintenance therapy. However, hypokalemia should be prevented in the elderly, in patients with ischemic heart disease, left ventricular hypertrophy and those on digitalis, or with diabetes. We prefer potassium-sparing agents along with a diuretic over supplements to prevent hypokalemia; the number of pills is kept at a reasonable level, and cost is minimized. Physicians should continue to prescribe diuretics as first-step therapy in the majority of patients to maximize therapeutic outcome.
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PMID:Diuretics in the management of hypertension. 330 12

Blood pressure (BP) and metabolic variables were determined initially and after 1, 2, 4, 6 and 10 years' treatment in two groups of hypertensive men (n = 53 each) randomized to bendroflumethiazide 2.5-5 mg/day or propranolol 160-320 mg daily. There was no significant differences in BP or metabolic variables between the two groups at entry. BP was reduced to the same degree by both treatments. Five men in the propranolol group and one man in the thiazide group developed clinically overt diabetes during follow-up. Fasting blood sugar increased slightly but significantly though equally in both groups. Oral glucose tolerance was initially impaired to the same degree in both groups but improved significantly during treatment with both drugs. Fasting insulin increased slightly but to the same degree. While serum potassium decreased significantly in the thiazide group, the total body potassium was unchanged in this group. In the propranolol group, serum potassium rose, while total body potassium decreased significantly. Serum urate increased in both groups, though slightly more during thiazide treatment. One case of gout was found in each group. There was no difference in serum lipids between the two groups. The finding in this long-term trial indicate that in middle-aged men with mild to moderate hypertension a low-dose thiazide diuretic like bendroflumethiazide is as effective and safe an antihypertensive agent as the beta-blocker propranolol is and that it does not induce diabetes. The total clinical picture favors the retention of thiazide diuretics as a first choice drug in hypertension.
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PMID:Low-dose antihypertensive treatment with a thiazide diuretic is not diabetogenic. A 10-year controlled trial with bendroflumethiazide. 354 90

High dose furosemide is commonly used in renal failure to induce diuresis but rarely employed in cardiac failure. As furosemide elimination depends largely on renal excretion, drug accumulation with attendant side-effects would be expected to occur more commonly with renal failure than with cardiac failure. Response to a combination of thiazide diuretics and lower doses of furosemide is often unpredictable, ineffective and sometimes hazardous. High dose furosemide (greater than or equal to 0.5 g day-1) was administered for at least four weeks in 24 patients with severe cardiac failure refractory to a lower dose and to other conventional therapy. Mean maintenance dose of furosemide was 0.7 g day-1 and the maximum dose of furosemide averaged 1.3 g day-1. A peak dose of 8 g day-1 was used successfully in one patient. Improvement was observed in all patients when dosage was increased to and above 0.5 g day-1. There were no major side-effects although new-onset gout (4) and tinnitus (1) were reported; hypokalaemia was readily controlled with spironolactone or potassium supplements. Average duration of therapy was 12 months with a maximum of 33 months. High dose furosemide is logical and effective therapy (with other measures) for severe cardiac failure and relatively safe when administered cautiously. The maximum safe dose is probably no less than that used in renal failure.
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PMID:High dose furosemide in refractory cardiac failure. 407 5

Significant alterations in the structure and functions of the kidney are caused by a number of metabolic disturbances and deficiencies of physiological substances. These include intercapillary glomerulosclerosis, gout, hypercalcemia, hereditary cystinuria, potassium depletion, pyrophosphates deficiency, vitamin D deficiency and liver disorders. Some of these metabolic disorders are secondary to drug ingestion.
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PMID:Renal disease secondary to metabolic disorders or physiological deficiency states. 604 89

The antihypertensive effect and metabolic side effects of bendroflumethiazide have been compared with those of propranolol in two randomly selected groups, of 53 previously untreated middle-aged men during 6 years' treatment for mild to moderately severe essential hypertension. The blood pressure-reduction was the same in the two groups. During the follow-up 1 man in the bendroflumethiazide group and 3 in the propranolol group died while 2, 1 on each treatment, became diabetic. None had gout but serum urate increased in both groups. Glucose tolerance improved significantly in both groups during the first year and this improvement was sustained for the follow-up period. Serum potassium did not differ in the two groups during the first 5 years but during the sixth year it decreased in the diuretic group. Total potassium was, however, unchanged in both groups. These results indicate that the frequency of metabolic side effects during diuretic treatment of mild to moderately severe essential hypertension is low and has been grossly exaggerated. Since the antihypertensive effect and side effects were equal with both drugs, and since the diuretics are cheaper, they should be the drug of first choice in this type of hypertension.
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PMID:beta-blockers or diuretics in hypertension? A six year follow-up of blood pressure and metabolic side effects. 611 Sep 54


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