Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
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Chronic hemodialysis, using acetate-containing dialysate, may accelerate the development of atherosclerosis in uremic patients. To assess the effect of acetate on plasma lipid levels and development of atherosclerosis, rabbits and rats were fed cholesterol-free semipurified atherogenic, Zn++-supplemented diets containing either 10% sodium acetate or sodium bicarbonate. Rabbit plasma cholesterol gradually increased during the 8-month study (58--485 mg/100 ml) but there was no significant difference between the acetate-fed and control groups. After 8 months, all rabbits had some degree of aortic intimal change. The changes involved a mean of 10% of the total aortic area. This involvement is much smaller than those previously reported and there was no significant difference between the acetate-fed rabbits and the control groups. Rabbit mortality was low (25%) and the mean weight increased from 1.7 to 2.7 kg. It is concluded that dietary acetate does not affect the rate and degree of development of hyperlipidemia and atherosclerosis. Furthermore, supplemental dietary Zn++ may have been responsible for the low rabbit mortality rate, weight gain and possibly the retarded development of atherosclerosis.
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PMID:Effects of dietary acetate and bicarbonate on experimental atherosclerosis in rabbits. 735 53

In spite of the nearly total effectiveness of classic estrogen-progestogen oral contraception and its good overall tolerance, in a not inconsiderable number of situations yet, it is not possible to resort to it. These situations are the following: high blood pressure, hyperlipemia, diabetes, minor mastopathy, premenstrual tension either spontaneous or under estroprogestogen therapy. Macroprogestational contraception using either pregnanes (chlormadinone acetate) or nor-pregnanes, promegestone, nomegestrol acetate, can be then the right solution. Clinical and metabolic tolerance is excellent. In the occurrence of hypoestrogeny symptoms, a combination of nomegestrol acetate-estradiol 17 beta, transdermally administered, has given top results in a preliminary study.
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PMID:[High-dose progestational contraception: advantages]. 752 30

A rapid method is described for measuring the antioxidant activity of low density lipoproteins. Studies were undertaken on individuals attending a hyperlipidaemia clinic, an unsupplemented group and a group after supplementation with 300 mg dl-alpha-tocopherol acetate for nine weeks. The results show a positive correlation between the antioxidant activity and alpha-tocopherol content of LDL in the supplemented group.
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PMID:Total antioxidant activity of low density lipoproteins and the relationship with alpha-tocopherol status. 778 72

Patients with diabetes mellitus are more frequently hypertensive than age-matched non-diabetic subjects. They are confronted with a markedly increased risk of coronary vascular disease, of progressive nephropathy and renal end-stage diseases. The most common type of hypertension in type I and type II diabetics is essential hypertension, probably as a consequence of insulin resistance and hyperinsulinemia. Hyperglycemia and hypertension are both significantly involved in the progression of diabetic nephropathy. Hence, the modern therapeutic concept consists of optimal blood glucose control and strict blood pressure control. Progression of the nephropathy may be halted in most of the cases by adhering to set limits in mean arterial blood pressure, glycated hemoglobin and urinary albumin excretion rate. Furthermore, a significant decrease in cardiovascular mortality may be achieved. In case the blood pressure targets cannot be met by non-drug therapies and life-style modifications, antihypertensive drug therapy has to be initiated. The selection of antihypertensives should be based on the concomitant diabetes mellitus with its additional cardiovascular risk factors hyperlipidemia and hyperinsulinemia. In general, preference should be given to so-called metabolic neutral substances such as ACE inhibitors or calcium antagonists or to alpha-blockers which may have positive metabolic effects. Meanwhile, data from several prospective studies claim that ACE inhibitors and calcium antagonists exert nephroprotective effects beyond their beneficial blood pressure lowering effects, thereby preventing the progression of diabetic nephropathy. However, these drugs should not be uncritically used and we should be aware of their potential adverse effects. The differential therapy of hypertension in diabetes mellitus requires mature consideration before initiation of therapy, an individualized concept of therapy, and careful monitoring during treatment.
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PMID:[Hypertension, microalbuminuria and insulin resistance in diabetes mellitus]. 784 97

The metabolic syndrome is characterized by cluster-like occurrence of various risk-factors for vascular disease: overweight, hypertension, hyperlipidemia, hyperproteinuria. In the pathogenesis of this syndrome the peripheral resistance to insulin leading to hyperinsulinemia plays most likely a central role, as the development of individual components of the metabolic syndrome may causally be explained in this way. Various possible explanations exist for the development of insulin resistance: on the receptor level, as a result of changes in the capillary bed or in muscle fiber composition, or resulting from disturbed circulation of muscles. Clinical symptoms of hyperinsulinemia are hypertension, lipodystrophy, and type II diabetes. Patients with metabolic syndrome represent a group at high risk for arteriosclerotic vascular disease. Therapy aims primarily at reduction of hyperinsulinemia as the underlying factor. In particular non-medical intervention plays an important role (reduction of body weight, exercise). In drug therapy of hypertension only such antihypertensives which remain neutral to metabolism should be applied, i.e., ACE-inhibitors which even improve the metabolic condition.
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PMID:[ACE inhibitor in metabolic syndrome]. 785 77

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria. 805 29

After a brief synopsis of the classical antihypertensive drugs a survey is given of the newer therapeutics, such as calcium antagonists, ACE-inhibitors and alpha 1-adrenoceptor antagonists. Experimental drugs, such as imidazoline receptor agonists, renin inhibitors, angiotensin II receptor antagonists, alpha 2-adrenoceptor antagonists, potassium channel openers, ketanserin, endopeptidase inhibitors, and hybrid (multifactorial) drugs are discussed, with special attention for their modes of action. In spite of the ever increasing number of antihypertensive drugs and principles, the large scale of clinical evidence for a beneficial effect of long-term treatment (in particular with respect to protection against stroke) remains limited to diuretics and beta-blockers. In spite of this limitation it seems worthwhile to consider the newer antihypertensive drugs as well, especially for optimal treatment of the individual patient. The newer drugs may in particular offer special advantages in the presence of concomitant diseases, such as diabetes mellitus, hyperlipidaemia, angina pectoris or congestive heart failure.
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PMID:New avenues in antihypertensive drug treatment. 826 86

Thiazide diuretics have been the mainstay of antihypertensive therapy for over 30 years. Their precise mechanism of antihypertensive action is still incompletely understood. They reduce arterial pressure initially through a fall in plasma volume and cardiac output. However, with chronic administration cardiac output tends to return toward pretreatment levels, suggesting that the long-term pressure reduction is mediated through a reduction in vascular resistance. Although multiple lines of evidence suggest that salt and water loss is an essential part of the mechanism, at least in some cases an indirect vasodilator effect may play a role as well. The antihypertensive efficacy of diuretics is proven; they are at least as effective as other classes of antihypertensive drugs. They have been shown to protect against stroke, but not against mortality from myocardial infarction. There is some concern about the metabolic side effects, such as hypokalemia, hyperglycemia, and hyperlipidemia. In order to minimize these side effects the lowest effective dose should be used. Diuretics are likely to remain first-line antihypertensive agents, but they should be considered as one of several possible choices for the initial therapy among other classes, such as beta-blockers, ACE inhibitors, or calcium entry blockers.
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PMID:The place of diuretics in the treatment of hypertension: a historical review of classical experience over 30 years. 843 77

Risk factors are associated with disease and are not necessarily causative; as they are additive they should not be judged in isolation. Thus, 'mild blood pressure' does not imply a 'mild' risk in a cigarette-smoking, hypertensive diabetic. Cardiologists are usually fortunate, in that they see patients when there is already evidence of disease (ie, when secondary prevention is the issue, which is much less contentious than primary prevention). In the 'whizz-bang' specialty of cardiology, a balloon can remove in a matter of seconds what a lipidologist has toiled over for years. Attention to detail may not come easily in a stressful world: it is the detail of prevention that is likely to slow the progression of disease and induce regression rather than angioplasty or bypass surgery. In the presence of coronary artery disease, the essence of management is the team approach, the patient being the most important member of the team. Furthermore, the factors that need the most concentrated effort include cigarette smoking, hypertension, and hyperlipidaemia. As risk factors are additive, treatment of one should not make another one worse. Some drugs for hypertension can exacerbate hyperlipidaemia or impair glucose tolerance (eg thiazides), while ACE inhibitors can beneficially decrease insulin resistance in diabetes. Therapy must be tailored to the individual, but the overall prognostic benefits of drugs that might have slightly adverse metabolic profiles (such as beta-blockers) must not be ignored. Science is often a loser when faced with the power of marketing. When one risk factor (eg hypertension) is present, it is important to be vigorous in treating other factors (eg hyperlipidaemia) with general advice and support, as well as with specific drug therapy if indicated. There are two individuals that tend to lack education in risk factors--the patient and the cardiologist. The patient is a victim of poor investment in prevention, while the cardiologist is put off by a perceived lack of balance from the medical protagonists.
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PMID:Risk factor management: the cardiologist's perspective. 1949 71

The kidneys play an important role in the development of cardiovascular risk factors. It is well known that heavy proteinuria can induce hyperlipidemia, the uric acid is elevated in some renal deficiencies and that hypertension develops in most end stage renal diseases. In prehypertensive states, specially in subjects with a family history of hypertension, some hemodynamic changes take place, characterized by an increase in renal vasoconstriction with a reduction in renal plasma flow and an elevation of sodium reabsorption. The mechanisms for these alterations are not well understood, but an increase in intracytosolic calcium in vascular smooth muscle cells, a reduction in vasodilatory substances such as nitric oxide and an increased sympathetic nervous activity have been proposed. In normotensive subjects with two hypertensive parents a reduction in sodium diet, an increase in protein intake or in arginine diet could prevent established essential hypertension from developing. In borderline hypertension an early therapy with low doses of calcium antagonists, ACE inhibition or diuretics could be indicated.
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PMID:Can the kidney prevent cardiovascular diseases? 874 38


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