Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of Olbetam on serum lipid and lipoproteins was studied in 30 diabetic patients with hyperlipidemia in four weeks trial. The dose of Olbetram was 500 mg/d. The results showed serum concentrations of TC, TG, and VLDL-C were decreased while HDL-C especially HDL2-C increased significantly after treatment. There were no significant changes in FBG, blood creatinine and urine acid. This result suggests Olbetam can improve dyslipidemia in NIDDM and was well tolerated by all patients.
 ...
PMID:[Effect of olbetam on hyperlipidemia in NIDDM]. 873 67

In summary, dyslipidemia is a common feature of various renal syndromes. Whether this perturbed lipid metabolism results in accelerated atherosclerosis and increased cerebrovascular and cardiovascular morbidity and mortality remains a subject of inquiry. Also undefined is the role of dyslipidemia in the progression of renal injury. The malnutrition that becomes a dominant morbid feature in patients on maintenance renal replacement therapy provides a caveat against aggressive intervention for modest hyperlipidemia once dialysis is instituted. Individualized assessment of end organ atherosclerotic disease and cardiovascular risk factors should form the basis for modification of the treatment plan (ie, pharmacological intervention) should nonpharmacological means prove ineffective.
 ...
PMID:Dyslipidemia in renal disease. 873 63

Multiple cell membrane alterations have been described in humans and animals with various genetic forms of hypertension and/or dyslipidemia. The aim of our study was to characterize some properties of platelets and/or erythrocytes (cytosolic calcium handling, intracellular pH regulation and thrombin responsiveness) in a new model of genetic hypertension associated with hyperlipidemia-Prague hereditary hypertriglyceridemic (HTG) rats. There were no differences in basal cytosolic Ca2+ values in platelets or erythrocytes of HTG rats and control Wistar rats. Ca2+ influx into erythrocytes was also similar in HTG and control rats. In both strains Ca2+ influx correlated positively with plasma triglycerides. The slope of this relationship was less steep in HTG than in Wistar rats. Cytosolic Ca2+ response to thrombin stimulation was smaller in HTG platelets, which were also characterized by a major reduction of thrombin-induced Mn2+ entry through receptor-operated Ca2+ channels. Platelets of HTG rats had the same basal intracellular pHi values and similar buffering capacity as control rats but their pHi response to thrombin stimulation was substantially reduced. It can be concluded that reduced responsiveness to thrombin stimulation is a major alteration found in platelets of hypertensive hereditary hypertriglyceridemic rats.
 ...
PMID:Cell calcium handling and intracellular pH regulation in hereditary hypertriglyceridemic rats: reduced platelet response to thrombin stimulation. 876 14

We was carried out a survey between all primary care physicians (PCP) of La Rioja on their social and demographic data, anamnesis on their factors of cardiovascular risk and behavior in the strategies of hypercholesterolemia detection. The 65% of the PCP ask to their patient on knowledge of their cholesterol; this proportion increases between the physicians that know the recommendations of the Spanish Atherosclerosis Society (SAS) (p < 0.002). The 100% of the PCP determine some lipid parameter when they specify a blood sample for another reason or in presence of arterial hypertension, coronary heart disease, dyslipidemias or diabetes mellitus. In presence af smoking habit or oral contraceptive use, PCP that know the SAS or that they work in the rural environment, respectively, they solicit lipid parameters with a greater frequency (p < 0.04 and p < 0.03). Only a 23% of the PCP carry out electrocardiogram in case of a hyperlipidemia, percentage that is incremented between those that works in primary health centers ar in the urban medium (p < 0.03 and p < 0.03). A quarter af the PCP don't refer to the specialized attention to their patients with uncontrolled dyslipidemia and almost the 10% they would not send them under no circumstance. Although in general seem us adequate the behavior in opportunist detection of the PCP, this improves up on knowing the normative of national consensus.
 ...
PMID:[Strategies for the detection of dyslipemias in primary care in La Rioja]. 876 69

Hyperlipidemia occurs frequently after heart transplantation, and accelerated coronary artery disease remains the major cause of morbidity and mortality in patients who survive more than 1 year after heart transplantation. However, the risks and benefits of lipid-lowering therapy after heart transplantation remain poorly defined, and national guidelines for lipid-lowering drug therapy do not specifically address treatment of dyslipidemia in transplant recipients. Since the initial reports in the 1980s of rhabdomyolysis in heart transplant patients receiving high-dosage lovastatin, results of 11 post-transplantation series that used lovastatin, simvastatin, or pravastatin at lower dosages as drug monotherapy have been published. These studies have shown an overall 1% incidence of rhabdomyolysis, defined as creatine kinase > 10 times the upper limit of normal plus muscle symptoms. One randomized, controlled prospective trial has investigated the effects of lipid-lowering pharmacotherapy on patient outcome in cardiac transplant recipients. At 1-year follow-up in this nonblinded, single-center trial, patients treated with pravastatin (20 or 40 mg/day) initiated within 2 weeks of transplantation had a significant reduction in mortality rate and a significantly lower incidence of transplant arteriopathy. A number of important issues remain unanswered regarding treatment guidelines in patients with hyperlipidemia after heart transplantation. In January 1995 we began the Heart Transplant Lipid Registry, with 12 participant centers, to gather data prospectively on the efficacy and safety of lipid-lowering drugs in the treatment of dyslipidemia after heart transplantation.
 ...
PMID:Treatment of hyperlipidemia after heart transplantation and rationale for the Heart Transplant Lipid Registry. 880 37

During the last decade, our understanding of the role of nitric oxide for central renal functions has greatly been enhanced. We know now that nitric oxide is produced in renal arteries, macula densa, glomeruli, and tubules by different NO-synthases. Nitric oxide contributes to physiological regulation of renal blood flow, renal autoregulation, tubuloglomerular feedback, renin release, pressure natriuresis, and tubular function. The physiological role of nitric oxide can be modulated by a variety of pathophysiological influences, such as dyslipidemia, diabetes mellitus, hypertension, specific drugs, or radiocontrast agents. In this article, the possible interactions between nitric oxide and atherogenic lipoproteins with regard to important renal functions and development of glomerulosclerosis have been stressed. Atherogenic lipoproteins impair endothelium-dependent, nitric oxide-mediated dilations of renal arteries. The underlying mechanism involves formation of reactive oxygen species which inactivate nitric oxide. Lipoproteins induce formation of oxygen radicals not only in arteries, but also in glomeruli and juxtaglomerular cells, causing, e.g., stimulation of renin release. Although interactions between lipoprotein and nitric oxide take place at different levels, they finally may contribute to renovascular hypertension. Future studies will have to prove that treating hyperlipidemia has a positive influence on nitric oxide-mediated renal functions.
 ...
PMID:Impact of nitric oxide on renal hemodynamics and glomerular function: modulation by atherogenic lipoproteins? 881 12

Niacin has been used for many years to treat hyperlipidemia. It has been shown to reduce coronary death and non-fatal myocardial infarction and, in a separate analysis of long-term (15-year) follow-up, all cause mortality. It reduces total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglycerides and increases high density lipoprotein cholesterol (HDL-C). Sustained-release niacin may be associated with more dramatic changes in LDL-C and triglyceride, whereas the short acting preparation causes greater increases in HDL-C. The increase of HDL-C occurs at a lower dose (1500 mg/day) than the reduction of LDL-C (> 1500 mg/day). Niacin also favorably influences other lipid parameters including lipoprotein(a) [Lp(a)], alimentary lipemia, familial defective apolipoprotein B-100 and small dense LDL. Combination of niacin with a bile acid sequestrant or a reductase inhibitor represents a powerful lipid-altering regimen. Whereas the reductase inhibitors and bile acid binding resins primarily affect LDL-C, the combined therapy has a synergistic effect to reduce LDL-C and, in addition, the niacin reduces triglycerides and increases HDL-C. The major drawback in the use of niacin is associated side effects (flushing and palpitations) and toxicity (worsening of diabetes control, exacerbation of peptic ulcer disease, gout, hepatitis). Niacin has a long history of use as a lipid lowering agent and has several attractive features. Unfortunately, the side effect profile of this agent warrants its use only in patients with marked dyslipidemia in whom side effects and potential toxicity are closely monitored.
 ...
PMID:New developments in the use of niacin for treatment of hyperlipidemia: new considerations in the use of an old drug. 885 85

Patients with diabetes mellitus have a higher rate of mortality than the general population. This higher mortality may be attributed mainly to cardiovascular disease. A high prevalence of dyslipidemia in diabetics can be one of the reasons for this. The most commonly recognized lipid abnormality in non-insulin-dependent diabetics (NIDDM) is hypertriglyceridemia, which is known to be an independent risk factor for coronary heart disease in diabetics. Hypertriglyceridemia can be produced by two mechanisms, increased synthesis of very-low-density lipoprotein (VLDL) triglyceride and removal defect of plasma triglyceride. It has been a matter of debate whether insulin always stimulates hepatic VLDL secretion but it is generally accepted that insulin deficiency results in an impairment of plasma triglyceride clearance. Considerable attention has recently been focused on the atherogenecity of postprandial hyperlipidemia, remnant lipoproteins, small, dense LDL, lipoprotein (a) [Lp(a)] and isolated hypo-alphalipoproteinemia in NIDDM subjects. Several reports suggested that these atherogenic lipoprotein abnormalities are present in NIDDMs even if they are apparently normolipidemic. Association of visceral fat obesity, insulin resistance and nephropathy may aggravate the atherogenic lipoprotein profile. Therefore, we propose here that plasma lipid levels of diabetic subjects must be more strictly controlled than for the non-diabetic population in order to avoid an increased risk for coronary heart disease. If they are obese or associated with insulin resistance or nephropathy, these conditions should be carefully controlled.
 ...
PMID:Dyslipidemia in diabetes mellitus. 887 70

It is well known that hyperlipidemia is often present in patient with impaired glucose tolerance, obesity and/or hypertension. All of these are risk factors for coronary artery disease (CAD). The coexistence of these risk factors markedly increase the likelihood of CAD. Recently, it has been reported that the impaired glucose tolerance and insulin resistence are associated with the increased proinsulin, which is linked to the risk of CAD. We review that the impaired glucose tolerance is an important factor causing dyslipidemia. The characteristic of dyslipidemia associated with the impaired glucose tolerance include hypertriglyceridemia, high level of VLDL and low level of HDL cholesterol. They also associate with accumulation of remnant lipoproteins and appearance of small dense LDL. In addition, we pointed out that the increased number of risk factors is associated with elevated insulin and proinsulin level.
 ...
PMID:[The impaired glucose tolerance in the pathogenesis of dyslipidemia]. 891 26

Abdominal obesity has emerged as a strong and independent predictor for non-insulin dependent diabetes mellitus (NIDDM). Adiposity located centrally in the abdominal region, and particularly visceral as opposed to subcutaneous fat, is also distinctly associated with hyperlipidemia, compared with generalized distributions of body fat. These lipoprotein abnormalities are characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) levels, small dense LDL with elevated apolipoprotein B levels, and decreased high density lipoprotein2b (HDL2b) levels. This is the same pattern seen in both familial combined hyperlipidemia and NIDDM. The pronounced hyperinsulinemia of upper-body obesity supports the overproduction of VLDL and the increased LDL turnover. We have proposed that an increase in the size of the visceral fat depot is a precursor to the increased lipolysis and elevated free fatty acid (FFA) flux and metabolism and to subsequent overexposure of hepatic and extrahepatic tissues to FFA, which then, in part, promotes aberrations in insulin actions and dynamics. The resultant changes in glucose/insulin homeostasis, lipoprotein metabolism, and vascular events then lead to metabolic morbidities such as glucose intolerance, NIDDM, dyslipidemia, and increased risk for coronary heart disease.
 ...
PMID:Intra-abdominal fat: is it a major factor in developing diabetes and coronary artery disease? 896 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>