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)

We investigated the prognosis of 153 hypertensive patients, whose initial concentration of serum uric acid had been evaluated. One hundred and seventeen subjects could be followed up after 4 years and 16 of them died during the follow-up period. Cerebrovascular disease was seen in 6 subjects, 4 of whom died from the disease. Myocardial infarction and heart failure occurred in 9 and 7 of them died as a result. The frequency of these diseases was greater among the hyperuricemic group and 8 of the 11 who died belonged to this group. Four men were struck by gouty attacks. They were all hyperuricemic and had been proven to have at least one family member with asymptomatic hyperuricemia and/or gout. It is reasonable to regard the presence of hyperuricemia as one of the poor risk factors for vascular diseases. I addition, we must investigate more closely personal and family histories of gout when we see hyperuricemic subjects, regardless of absence of gouty symptoms.
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PMID:Hyperuricemia associated with hypertension. A 4-year follow-up study of hyperuricemic hypertensives. 71 25

A nearly 72-old black male with sickle cell anemia suffered from heart failure, hypertension, chronic impaired kidney function with hyperuricemia and gout. Anoxemia due to refractory anemia of the sideroachrestic type most probably precipitated the sudden heart failure.
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PMID:Long survival in sickle cell anemia. 113 54

The authors revealed heart failure in 7 of 216 patients with gout. Two of them showed isolated mitral valve insufficiency and two patients aortal insufficiency while combined aortal disease, combination of mitral and aortal insufficiency and combined mitral valve disease with aortal insufficiency occurred each in 1 patient. One could not find distinct dependence between the clinical variant of the course of gout and development of a definite heart failure. Clinical and electrocardiographic signs of the revealed kinds of cardiac abnormalities are described. The morphological changes of the valves are described on the basis of 2 autopsy cases. The possible mechanism of development of podagric heart failures is discussed.
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PMID:[Gouty heart defects]. 208 May 68

The atoll community of Fenuafala was surveyed during July-August, 1987. A disproportionate demographic structure was found: There was a large, young population with an uneven sex distribution in the adolescent cohorts. Adoption of relatives was frequent. Employment varied according to sex, with women restricted from horticulture, fisheries, and hard labour. The use of alcohol and tobacco was common. Causes of mortality included cancer, heart failure, meningitis, alcoholism, and accidents. Bacterial and fungal skin infections were prevalent. There were several cases of congenital disorders. Malaria, leprosy, and most other tropical diseases were absent. However, there was a single case of filariasis. Musculoskeletal disorders were numerous and more common among women. Falls from trees have resulted in serious sequelae including epilepsy and death. Hypertension, diabetes, and gout appear to be on the increase, but angina and myocardial infarction were not reported. There were also cases of epilepsy and Parkinson's disease.
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PMID:Fenuafala health survey: the ecology of health and disease on a coral atoll village. 280 43

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

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

Bumetanide and furosemide were compared for efficacy in reducing edema due to congestive heart failure in 28 patients (21 receiving bumetanide and seven receiving furosemide) in a long-term study for periods from one week to 18 months. In both groups the patients showed decreases in body weight, abdominal girth, edema, hepatomegaly, blood pressure, and heart rate. Commonly observed decreases frequently achieved statistical significance, more often with bumetanide, but the differences between treatments were rarely statistically significant. Both drugs were generally well tolerated. A breast nodule and gynecomastia were each reported once in the bumetanide group as was gynecomastia in one patient who had been on furosemide, all remotely related to test drugs. Soft stools, flatulence, mild constipation, and diminished vision each reported once in the bumetanide group were judged to be unrelated or remotely related to the drug therapy. Tendencies toward hypokalemia, hypochloremia, alkalosis, and hyperuricemia without clinical gout were deemed the result of the pharmacologic action of the diuretics. Others were attributable to the underlying disease state of these patients. Both diuretics proved to be effective in the treatment of cardiac edema and other manifestations of heart failure. Bumetanide treatment beyond six months in 11 patients indicated continued safety as well as efficacy.
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PMID:Comparative efficacy and safety of bumetanide and furosemide in long-term treatment of edema due to congestive heart failure. 733 79

During the history taking and physical examination, several important diseases should be searched for before diagnosing essential hypertension. A critical investigation is repetitive abdominal auscultation for a bruit. In young patients with significant hypertension, coarctation of the aorta must be excluded by clinical examination. Investigations will especially be aimed at uncovering renal artery disease (relatively common) or a phaechromocytoma (relatively rare). The initial assessment must also diagnose associated diseases which will influence the type of therapy chose. Thus asthma and heart failure contraindicate beta-blockers, liver disease contraindicates methyldopa, severe depression contraindicates reserpine, methyldopa and beta-blockade, while diabetes or gout may be precipitated or aggravated by thiazide diuretics.
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PMID:Hypertension in general practice. Part I. Examination and investigation of a patient with hypertension. 744 97

Hypokalaemia, hyperuricaemia, hypomagnesaemia and alterations to lipid and glucose metabolism undoubtedly occur with loop and thiazide diuretic treatment. Many of the metabolic effects induced by thiazide diuretics, however, can be limited by the use of low doses. Apart from precipitation of gout and worsening control of diabetes the clinical importance of these changes is slight. In hypertensive patients treated with diuretics, long-term outcome trials have shown significant benefit in terms of reduction in stroke and coronary events. Diuretics should therefore remain first-line treatment for all patients with heart failure, and in patients with hypertension except those with diabetes or gout.
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PMID:Metabolic effects of diuretics. 795 46

Heart transplantation is an effective means of treating irreversible heart failure in selected patients. Preventing organ rejection requires immunosuppressor treatment with corticosteroids, azathioprine and/or cyclosporine. Bone and joint complications are frequent and increase overall morbidity directly related to anti-rejection therapy. Corticosteroids favour osteopenia which can be detected by measurement of bone density. The risks include spontaneous wedge fractures of the spine and aseptic necrosis. The frequency of complications has been reduced with the use of cyclosporine allowing a reduction in corticosteroids. Raised serum urate levels and increased risk of gout can be induced by cyclosporine. The gout in these patients has a particular course since it appears rapidly after only a few months of hyperuricaemia. Several joints may be involved with production of tophi. Treatment is particularly difficult. Its frequency increases after heart transplantation compared with other organs which can be explained by the more prevalent prescription of diuretics which further aggravate urate secretion. These complications cause further discomfort in transplant recipients.
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PMID:[Osteo-articular complications of heart transplantation]. 854 32


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