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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of endogenous cholesterol synthesis in blood lymphocytes and skin fibroblasts from patients with type IIa hyperlipidemia was found to be increased in comparison with healthy donors. The cells of hyperlipidemic patients had lowered levels of glucocorticoid receptors concomitantly with a partial loss of their sensitivity to glucocorticoids. In fibroblasts from patients with hereditary hypercholesteremia of homozygous type the number of glucocorticoid receptors did not exceed 10% of their content in normal cells. The decrease of the number of glucocorticoid receptors in patients with type IIa hyperlipidemia seems to be a compensatory response of cells culminating in activation of endogenous cholesterol synthesis.
Biokhimiia 1991 Dec
PMID:[Regulation of intracellular cholesterol synthesis in hypercholesterolemia by glucocorticoids]. 180 4

High blood cholesterol levels are associated with an increased risk of coronary heart disease. Guidelines for the detection and treatment of patients with hypercholesterolaemia have been developed in the United States and in Europe. The causes of secondary hyperlipidaemia are generally well known, but not always diagnosed. A wide variety of drugs cause secondary hyperlipidaemia but the incidence of this event is infrequently recognised. This article focuses on those drugs that are known to have an adverse effect on the serum lipid profile and the clinical significance of this effect.
Minerva Cardioangiol 1991 Dec
PMID:[Adverse effects of drugs on serum lipids. Clinical implications]. 181 8

The major risk factors for cardiovascular disease include hypertension, hyperlipidemia, hyperinsulinemia and smoking. They promote the development of atherosclerosis and thromboembolic complications, i.e. strokes and heart attacks. There are diverse interactions between these factors, the outstanding common denominator being alterations in serum lipoproteins, mainly elevated low-density lipoprotein (LDL)-cholesterol and reduced high-density lipoprotein (HDL)-cholesterol concentrations, which results in disturbed cholesterol homeostasis (transport and metabolism) and eventually in perturbations of cellular integrity/function. In addition to their roles as cholesterol-transporting molecules, LDL and HDL directly influence inter- and intracellular communication via stimulation of pivotal signal transduction processes. The 'hormonal' effects of LDL on platelets, endothelial cells and vascular smooth muscle cells are potentially harmful, whereas the effects of HDL may be protective in as much as HDL can antagonize LDL-mediated stimulation of cells. Therapy aimed at reducing serum LDL-cholesterol levels and increasing HDL-cholesterol levels will have multifactorial beneficial effects on cardiovascular disease.
J Hypertens Suppl 1991 Dec
PMID:Low- and high-density lipoproteins as hormonal regulators of platelet, vascular endothelial and smooth muscle cell interactions: relevance to hypertension. 181 68

Atherosclerosis is a degenerative disease responsible for the majority of deaths in the western populations. According to the idea of the reaction to injury the endothelial cells lining the vascular wall are exposed to repeated insults to their integrity. The injury results in a loss of functional attributes of endothelium and leads to a sequence of events including platelet adherence and aggregation, release of platelet granular components, migration and proliferation of medial smooth muscle cells into the intima. Examples of types of injury include chemical injury, as in hyperlipidemia, or mechanical stress associated with critical changes in vascular flow. Atherosclerosis has been considered a disease primarily concerned with lipid metabolism by regarding the intramural caseous material of atheromatous arteries as the sine qua non of the disease. The limitation of the lipid theory is that the conventional cholesterol-fed animal does not exactly reproduces the pathology of atherosclerosis. An alternative theory suggests that atherosclerosis is induced by mechanical fatigue which produces the progressive change in structure and mechanical properties of the vessel wall. In this view the lipid accumulation is a secondary phenomenon, the consequence of concomitant biochemical alterations of mural constituents. The hypothesis of reaction to injury provides a plausible explanation for the lesion formation and the different theories of atherogenesis are not mutually exclusive.
Cardiologia 1991 Dec
PMID:[The vascular and metabolic mechanisms of the development of the atherosclerotic plaque]. 184 83

In the last years, a plasmatic fibrinogen increase, a fibrinolytic system activity reduction and platelet activation, seemed to play a significant role on the genesis and progression of atheromatous plaques, especially when combined to a plasmatic lipoprotein increase. The results obtained in normolipidaemic patients (2000 asymptomatic subjects, 364 non-insulin diabetic patients randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 69 nifedipine-30 mg/daily-treated subjects, and 38 patients submitted to nifedipine-30 mg/daily-combined to indobufen-400 mg/daily-therapy), are reported. The results obtained in hyperlipidaemics (blood cholesterol level > 240 mg/dl; 356 patients, randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 56 patients with simvastatin 40 mg/daily and 85 with low saturated fat and low cholesterol diet), are also reported. Follow-up of all the patients was 4 years, but the simvastatin group followed-up only 1 year. An ultrasound examination of carotid and femoral arteries was performed in all the patients by means of a Duplex Scanner ATL Ultramark 5, with a high resolution probe (10 MHz). Subjects were graded into I-VI classes, according to the vessel progressive atherosclerotic impairment. In normolipidaemics, wall atheromatous changes were seen with increasing frequency with age, and a significant relationship among plaque progression rate and developed cerebrovascular symptoms, developed symptomatic peripheral symptoms, increased cardiovascular events and mortality rate, was evidenced. Non-insulin dependent diabetes, combined to normal levels of blood lipoproteins, appears an independent risk factor, superimposable to hyperlipidaemia. In this group of patients, bezafibrate therapy significantly reduced plaque progression, acting on blood coagulation factors and similar results were obtained in nifedipine and nifedipine plus indobufen groups. Also in hyperlipidaemics treated with diet, simvastatin and bezafibrate, the plaque progression was significantly reduced with respect to control group, especially when blood lipoproteins and coagulation were normalized. In conclusion, hyperlipidaemia, Ca++ and blood coagulation disorders, appear to be the main factors affecting the plaque progression, and the prevalence of each factor in the atheroma development must be well evaluated in the single patients to establish an adequate therapeutic strategies.
Cardiologia 1991 Dec
PMID:[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]. 184 88

Factors contributing to deep vein thrombosis (DVT) were studied in 51 patients (62 knees) who had a cementless total knee arthroplasty (TKA) and in 51 patients (69 knees) who had a cemented TKA. All patients were treated with a primary TKA using a porous-coated anatomic prosthesis with a porous-coated central tibial stem. Deep vein thrombosis was diagnosed by roentgenographic venography, and pulmonary embolism was diagnosed by perfusion lung scanning. Incidence of DVT was 32%, and there was no pulmonary embolism. The factors that do not seem to have much relevancy to DVT were advanced age, orthopedic disease, one- or two-staged bilateral TKA, venous anatomic variations, number of venous valves, coagulation assay data, hypertension, tourniquet time, choice of cementless or cemented TKA, severity or duration of operation, amount of blood loss, and amount of blood transfused. Conversely, more immediate relevant factors were obesity, postoperative prolonged immobilization, earlier venous disease, and hyperlipidemia.
Clin Orthop Relat Res 1991 Dec
PMID:Factors leading to low incidence of deep vein thrombosis after cementless and cemented total knee arthroplasty. 195 58

Disorders of lipid metabolism during chronic renal failure (CRF) play a crucial role in the pathogenesis of early cardiovascular complication of this syndrome. In addition, some experimental evidence suggests that hyperlipidemia may accelerate progression of renal disease. We have studied 65 patients with CRF (S-creatinine 1.5-9.0 mg/dl), 52.3% of whom were hypertensive. Patients were divided in 2 groups matched for age, sex and degree of renal failure: group 1 was kept for 36 +/- 8 months on a free diet; group 2 was kept for 39 +/- 6 months on a low-protein diet with an elevated polyunsaturated/saturated fatty acid (PUFA/SFA) ratio. We found significantly higher levels of triglycerides (TG) and lower levels of esterified cholesterol in high density lipoprotein (HDL-C) in group 1 than in group 2. Patients on the diet had a lower percentage of membrane SFA and a higher percentage of PUFA than patients on free diet. Only in group 1 a direct correlation between cholesterol/phospholipid (Chol/P) ratio and age was observed; in group 2, a negative correlation between levels of PUFA and TG and between linoleic/oleic (Lin/Ol) ratio and serum Chol was shown. S-creatinine levels were directly correlated with Chol/P ratio in group 1 and indirectly with Lin/Ol ratio and PUFA in group 2. These data show that a low-protein diet, containing an elevated PUFA/SFA ratio, is able to counteract lipid abnormalities in patients with CRF and the normalization of this pattern is associated with significant improvement of membrane lipid composition and, presumably, of "functional" activity of cell membranes with a better control of supposed "renal lipoprotein toxicity".
Clin Nephrol 1990 Dec
PMID:Modification of serum and membrane lipid composition induced by diet in patients with chronic renal failure. 207 70

Short term hypolipidemic effects of oral L. sporogenes therapy (360 million spores/day in tablet form) were studied in 17 patients with type II hyperlipidemia in an open label fixed dose trial. Total serum cholesterol (330 +/- 55 mg/dl vs 226 +/- 46 mg/dl, P less than 0.001), LDL-cholesterol (267 +/- 58 mg/dl vs 173 +/- 54 mg/dl, P less than 0.001) and total cholesterol to HDL cholesterol and LDL-cholesterol to HDL-cholesterol ratios (P less than 0.001) were reduced significantly over a period of three months. HDL-cholesterol was marginally increased (43.6 +/- 7 mg/dl vs 46.8 +/- 8.9 mg/dl, P less than 0.05); however there was no change in serum triglyceride levels.
Indian J Med Res 1990 Dec
PMID:Preliminary observations on effect of Lactobacillus sporogenes on serum lipid levels in hypercholesterolemic patients. 207 58

Hepatic diseases differ from most other causes of secondary dyslipidaemia in that the circulating lipoproteins are not only present in abnormal amounts but they frequently also have abnormal composition, electrophoretic mobility and appearance. Pre-beta and alpha bands can be absent on electrophoresis in all types of liver disease although material in the VLDL and HDL ranges can be isolated in the ultracentrifuge. Cholestatic liver disease has been the most extensively studied and the hyperlipidaemia can be extreme with marked elevations of free cholesterol and phospholipids. This results largely from the presence of LP-X, an abnormal LDL, with a vesicular structure that appears in rouleaux formation under the electron microscope. It is virtually specific for cholestasis and familial LCAT deficiency. The LDL, however, is heterogeneous and may also contain a large triglyceride-rich particle (LP-Y) as well as more normal-looking particles, which are none the less depleted in cholesteryl esters and rich in triglycerides. Indeed, when patients with cholestasis are hypertriglyceridaemic the excess triglyceride is to be found predominantly in these two LDL fractions rather than in VLDL. HDL in cholestasis may contain disc-like particles, similar to those newly secreted by the liver and intestine, as well as more normal-looking spherical particles. In extrahepatic obstruction concentrations of HDL and its major apolipoproteins, apoAI and apoAII, are frequently reduced, although a subfraction rich in apoE is often found. In all but the latest stages of chronic intrahepatic cholestasis due to primary biliary cirrhosis, however, HDL, especially HDL2, concentrations are increased, probably due to the presence of a circulating inhibitor of HL. Many of these lipoprotein changes found in cholestasis resemble those of familial LCAT deficiency, although the hyperlipidaemia is not usually so severe in the latter condition. Indeed, in patients with cholestasis but well-preserved LCAT activity many of the characteristic lipoprotein changes, such as LP-X, LP-Y and discoidal HDL, may not be seen. In acute hepatocellular disease, such as alcoholic or viral hepatitis, it is not unusual for the patient to go through a cholestatic phase and many of the same lipoprotein changes may be seen. In cirrhosis without cholestasis the patients are not usually significantly hyperlipidaemic and in advanced cases cholesterol and apoB levels may be reduced. Although LCAT activity and the proportion of plasma cholesterol esterified may also be markedly reduced, LP-X is not usually seen, possibly because the flux of free cholesterol and phospholipid (lecithin), the LCAT substrates, is relatively low. Discoidal HDLs are often present.(ABSTRACT TRUNCATED AT 400 WORDS)
Baillieres Clin Endocrinol Metab 1990 Dec
PMID:Dyslipoproteinaemia of liver disease. 208 7

Hyperlipidaemia and hypertension are commonly found in the population and are independent risk factors for cardiovascular complications. The combined presence of hypertension and hypercholesterolaemia increases considerably the risk for cardiovascular complications. These high-risk patients have to be identified early and treated appropriately in order to avoid complications. The goal of antihypertensive therapy is to reduce the average levels of diastolic pressure to below 90 mm Hg and the systolic pressure to below 140 mm Hg. The goals set for lipid levels in these patients are total cholesterol less than or equal to 200 mg/dl, LDL cholesterol less than or equal to 135 mg/dl and triglycerides less than or equal to 200 mg/dl. The first step in the treatment of patients with both hyperlipidaemia and hypertension is to seek underlying causes and to take appropriate therapeutic measures for both diseases. Non-pharmacological treatment of these high-risk patients includes weight reduction, appropriate dietary measures including alcohol and salt restriction, cessation of smoking and increasing physical activity. If pharmacological antihypertensive treatment is needed, drugs without adverse effects on lipid and lipoprotein levels should be preferred. If, in addition to dietary measures, drug treatment is necessary to reduce high cholesterol levels, bile acid sequestrants are the drug of first choice at present. If long-term safety can be established for HMG CoA reductase inhibitors, these drugs will represent a major advance in the therapy of hypercholesterolaemia.
Baillieres Clin Endocrinol Metab 1990 Dec
PMID:Hyperlipidaemia and hypertension. 208 8


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