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)

Felodipine is a dihydropyridine calcium antagonist which may be administered once daily in an extended release (ER) formulation. As monotherapy in older patients with mild to moderate essential hypertension, felodipine ER once daily provides effective control of blood pressure (BP). The drug has also been effective, either as monotherapy or in combination with other antihypertensive medications, in comparisons with other antihypertensive agents, and does not adversely affect lipid profiles or, in patients with diabetes mellitus, glycaemic control. Results in patients with angina pectoris and congestive heart failure indicate a potential role for felodipine ER in these indications and data also suggest the drug reduces left ventricular hypertrophy. In addition, felodipine ER appears suitable for use in patients with concomitant respiratory disease, renal or hepatic dysfunction, cerebrovascular or peripheral ischaemic disease, or gout, making it particularly useful in the elderly who often have more than one significant clinical condition. Felodipine ER has generally been well tolerated by older patients in clinical trials, although further confirmation in the long term is desirable. Thus, felodipine ER effectively lowers BP in older patients with essential hypertension with the added convenience of once daily administration. It may be used as monotherapy or in combination with other antihypertensive agents and is a practical advance in the treatment of hypertension in the elderly.
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PMID:Felodipine. A review of the pharmacology and therapeutic use of the extended release formulation in older patients. 139 20

Oral angiotensin converting enzyme inhibition was introduced eight years ago and is becoming increasingly popular for the treatment of hypertension and congestive heart failure. This treatment causes blood pressure lowering associated with suppression of angiotensin and aldosterone, lack of orthostatic hypotension or metabolic disturbances, redistribution of regional blood flows in favor of vital organs and, in the long term, decreased sympathetic drive and regression of left ventricular hypertrophy. It is effective as monotherapy in more than 50 percent of unselected patients; addition of a diuretic increases the percentage of responders to more than 80 percent. It is the treatment of choice for patients with concurrent diabetes, asthma, gout, depression, or very active life-style. Side effects, observed originally in patients with severe hypertension and renal failure treated with very high doses of captopril, are rare in otherwise healthy hypertensive patients receiving smaller doses of this drug and virtually absent with second-generation angiotensin converting enzyme inhibitors like enalapril.
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PMID:Clinical utility of angiotensin converting enzyme inhibitors in hypertension. 302 82

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

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

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256

Risk factors for cardiovascular disease include atherogenic personal attributes, living habits that promote them, signs of preclinical disease and host susceptibility. Atherogenic traits include the blood lipids, blood pressure and glucose tolerance. An increased low density lipoprotein cholesterol level is positively related, and an increased high density lipoprotein cholesterol level is inversely related, to cardiovascular disease incidence. Hypertension, whether systolic or diastolic, labile or fixed, casual or basal, at any age in either sex contributes greatly. The impact of diabetes is greater for women than men and varies depending on the level of the foregoing risk factors. An atherogenic lifestyle is typified by a diet excessive in calories, fat and salt, sedentary habits, unrestrained weight gain and smoking. Alcohol used in moderation may be beneficial. Oral contraceptives worsen atherogenic traits and, when used for long periods beyond age 35 and in conjunction with cigarettes, predispose to thromboembolism. Type A persons with an overdeveloped sense of time urgency, drive and competitiveness develop an excess of angina pectoris. Men married to more highly educated women are at increased risk as are men married to women in white collar jobs. Preclinical signs of compromised coronary circulation include silent myocardial infarction, left ventricular hypertrophy on the electrocardiogram, blocked intraventricular conduction and repolarization abnormalities. An electrocardiogram obtained during exercise may elicit still earlier evidence. Measures of innate susceptibility include a family history, history of premature cardiovascular disease, diabetes, hypertension and gout. Optimal prediction of risk requires a quantitative combination of risk factors in multiple logistic risk formulations to identify high risk persons with multiple marginal abnormalities.
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PMID:Status of risk factors and their consideration in antihypertensive therapy. 354 87

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

Several health hazards and social disabilities are associated with obesity. Increased mortality is associated with increased body weight. A high rate of mortality results from heart disease, diabetes mellitus, gallbladder disease, high blood pressure, and cancer. Physiologic cardiovascular changes occur, leading to left ventricular hypertrophy and lipid abnormalities. Hypertension, stroke, and venous stasis are increased. Pulmonary abnormalities include obstructive sleep apnea, which can be associated with secondary polycythemia and right ventricular hypertrophy. Gallstones, gallbladder disease, and accumulation of fat on the liver are significantly increased. Gout and reproductive abnormalities in women are common. Osteoarthritis of the knees and spine occur, although osteoporosis is rare. Risk for endometrial and breast cancer is increased, particularly in the presence of increased central fat. Changes in the skin include stretch marks, acanthosis negricans, hirsutism, intertrigo, and multiple papillomas. Impaired psychosocial function is manifested as social isolation, loss of job mobility, increased employee absenteeism, and economic and social discrimination.
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PMID:Health hazards of obesity. 897 52

The handwritten note of the post-mortem examination of Dr Samuel Johnson resides in the library of the Royal College of Physicians of London. Headed 'asthma' it suggests that he had only one functioning kidney, probably had hypertension, left ventricular hypertrophy and congestive heart failure. This article describes an imaginary presentation by Dr James Wilson, who did the autopsy, and alludes to Johnson's life, and medical history, including impaired vision and hearing, scrofula, abnormal limb movement, gout, abdominal cramps, melancholia and episodes of 'asthma' which were, more than likely to have been episodes of left ventricular failure. Johnson's personality as a demanding patient who took things into his own hands are described based upon reports from his physicians.
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PMID:Samuel Johnson's illnesses. 1687 22

During the last century, there has been an increasing prevalence of hyperuricaemia noted in many populations. While uric acid is usually discussed in the context of gout, hyperuricaemia is also associated with hypertension, chronic kidney disease, hypertriglyceridaemia, obesity, atherosclerotic heart disease, metabolic syndrome, and type 2 diabetes. Here we review the connection between hyperuricaemia and cardiovascular, kidney and metabolic diseases. Contrary to the popular view that uric acid is an inert metabolite of purine metabolism, recent studies suggest serum uric acid may have a variety of pro-inflammatory, pro-oxidative and vasoconstrictive actions that may contribute to cardiometabolic diseases. Hyperuricaemia is a predictive factor for the development of hypertension, metabolic syndrome, type 2 diabetes, coronary artery disease, left ventricular hypertrophy, atrial fibrillation, myocardial infarction, stroke, heart failure and chronic kidney disease. Treatment with uric acid-lowering therapies has also been found to improve outcomes in patients with hypertension and kidney disease, in some but not all studies. In conclusion, uric acid is emerging as a potentially treatable risk factor for cardiometabolic diseases, and more clinical trials investigating the potential benefit of lowering serum uric acid are recommended in individuals with hyperuricaemia with and without deposition and concomitant hypertension, metabolic syndrome or chronic kidney disease.
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PMID:Hyperuricaemia and gout in cardiovascular, metabolic and kidney disease. 3273 39


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