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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is not solely a phenomenon of elevation of systemic blood pressure. It frequently occurs in association with a great deal of metabolic derangement's and should never be regarded as coincidental only. Furthermore, a knowledge of these metabolic derangements may provide a clue to unveil the underlying mechanisms how essential hypertension and its associated complications arise. Therefore we devoted our attention to platelet dysfunction and dyslipidemia which are closely associated with atherosclerosis-the commonest complication of hypertension. We found there exists enhanced platelet aggregation in essential hypertension and a variety of its associated atherosclerotic diseases. Such an aberration in platelet function may be modified after administration of antihypertensive medications such as angiotensin converting enzyme (ACE) inhibitors, calcium channel blockades, beta blockades and dietary manipulation. We also demonstrated the close association between hypertension and its associated atherosclerotic complications and abnormal lipids profile. Hypertriglyceridemia which was initially regarded unimportant in the pathogenesis of atherosclerosis is found to be closely related to hypertension. In an intensive review, we found that people in Taiwan has experienced a huge increase in dietary calories and total fat consumption. In order to solve this emerging problem, a national guideline for diagnosis and management of lipid disorders in Taiwan was developed and announced. Through these efforts, we hope we can reduce the cardiovascular morbidity and mortality in Taiwan and even extend our experience to other countries.
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PMID:Thrombogenic and lipid risk factors in hypertension and coronary artery disease. 868 58

Disorders in lipoprotein metabolism (dyslipidemia) can result in premature atherosclerosis or pancreatitis. Dyslipidemias can be classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low density lipoprotein cholesterol and decreased levels of HDL cholesterol predispose to premature atherosclerosis. Triglyceride levels greater than 1,000 mg/dL increase the risk for pancreatitis. In the appraisal of the dyslipidemias, measurement of serum cholesterol, triglycerides, HDL-cholesterol and obtaining the LDL cholesterol by Friedewald equation is usually sufficient in the majority of patients. However, in some cases, such as the diagnosis of the Type III dyslipidemia and when triglycerides are > or = 400 mg/dL, ultracentrifugation is required to determine the VLDL or LDL cholesterol. Lipoprotein electrophoresis can be useful in the diagnosis of Type III dyslipidemia (broad beta band) and also to detect chylomicrons. In young subjects with coronary artery disease with a normal LDL cholesterol an apolipoprotein B-100 level may be a useful test. In children and young adults with severe hypertriglyceridemia, measurement of lipoprotein lipase activity or assaying apolipoprotein C-II levels can be useful in elucidating the cause. Also, laboratory tests are useful in excluding a secondary cause of dyslipidemia (urinalysis, plasma creatinine, TSH, glucose, protein electrophoresis, alkaline phosphatase and transaminases). Thus, laboratory investigations play an important role in the management of dyslipidemia.
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PMID:A practical approach to the laboratory diagnosis of dyslipidemia. 870 23

Advances in our understanding of the pathology, epidemiology, genetics (particularly the recent research on transgenic animals) and the results of randomized prospective clinical trials all contribute to the formation of public health policy on serum cholesterol and other lipids. This article outlines the scientific background of these policies. There remains little doubt that dyslipidemia contributes to the development of coronary atherosclerosis and that effective treatment can prevent or retard its development.
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PMID:Cholesterol and atherosclerotic vascular disease: from science to public health policy. 871 14

Patients with renal disease have an increased cardiovascular mortality. Hyperlipidemia, a hallmark of renal disease, is recognized as a principal cause of atherosclerosis. However, it is difficult to prove a pathogenetic role of renal dyslipidemia per se in this increased cardiovascular risk since multiple risk factors are often present in patients with progressive renal insufficiency, e.g. hypertension, diabetes and hypercoagulability. However, evidence is accumulating demonstrating detrimental effects of hyperlipidemia during both initiation and progression of the atherosclerotic process. The present review discusses this evidence in patients with renal disease, and the possible implications for treatment.
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PMID:Mechanisms of cardiovascular injury in renal disease. 871 68

In the process of screening apolipoprotein (apo) E genotypes in a population of subjects with lipid abnormalities, we have identified five subjects (one homozygote and four heterozygotes) with an abnormal 109 base pairs band following apo E restriction isotyping of amplified DNA with the restriction endonuclease CfoI. The polymerase chain reaction (PCR) products were cloned and their sequencing revealed a C-->A substitution at the first nucleotide of codon 136. This mutation resulted in an amino acid substitution Arg to Ser, previously described as apo E2 Christchurch. Family studies were carried out for four of the probands. In these kindreds, stepwise multiple regression analyses indicated that 78% of the cholesterol variability in men was predicted by body mass index, age and the rare apo E2 (Arg136-->Ser) variant. In women, age and the apo E2 (Arg136-->Ser variant predicted 54.9% of the variability in cholesterol levels. Linkage analysis suggested that the presence of the apo E2 (Arg136-->Ser) variant was linked with the occurrence of cholesterol enriched triglyceride rich lipoproteins and with an incomplete dominance of type III hyperlipoproteinemia. Our data indicates that this mutation may be a relatively common cause of dyslipidemia in the Spanish population.
Atherosclerosis 1996 Apr 26
PMID:Incomplete dominance of type III hyperlipoproteinemia is associated with the rare apolipoprotein E2 (Arg136-->Ser) variant in multigenerational pedigree studies. 872 10

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.
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PMID:Dyslipidemia in renal disease. 873 63

Platelets (PLT) play an important role in hemostasis, modulation of immunological and inflammatory processes. There is also evidence that PLT takes part in the development of atherosclerosis and glomerulosclerosis. The aim of presented study was to determine morphological and functional changes of platelets and their relation to the lipid, protein and coagulation factors disturbances in patients with chronic glomerulonephritis (CGN). The studies were carried out in 60 patients with CGN diagnosed by renal biopsy: 30 patients without nephrotic syndrome (NS)-CGN and 30 patients with NS-CGN+NS. Protein and lipid disturbances, coagulation factors were estimated using routine laboratory methods. Platelet count (PLT), mean platelet volume (MPV) and modal platelet volume (PLT-Mode) were measured using Technicon H1 hematological autoanalyser. Platelet function was assessed by aggregometry using turbidimetric method (inductors: ADP 1-3 microM, collagen 50g/ml, epinephrine 0.25-5 microM). Spontaneous platelet aggregation (SPA) was measured in platelet rich plasma (PRP) without inductors for 15 min, in 1-2 hours after venesection. SPA was observed in 9 of 30 patients with CGN and in 19 of 30 patients with CGN+NS. MPV and PLT Mode were significantly higher in patient showing SPA compared with those without. Significant correlations between SPA and the concentration of plasma albumin (r = -0,70; p < 0.02) TG and CH-LDL (r = 0,61; p < 0.05) were found in CGN+NS patients. APTT was significantly shorter in patients showing SPA compared with those without and negative significant correlation between SPA and APTT was found. Platelet aggregation to inductors in CGN and CGN+NS patients was diminished compared with control group. Lack of second phase aggregation in response to aggregation inducers was observed in patients with SPA. Conclusions. 1. Platelet hyperaggregation play an important role in hypercoagulation state in CGN patients. 2. SPA in vitro was observed in majority of CGN+NS patients and in some without NS. 3. Pathomechanism of SPA is probably multifactorial (hypoalbuminemia, dyslipidemia, changes in concentration of coagulation parameters).
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PMID:[Evaluation of factors influencing platelet aggregation in patients with chronic glomerulonephritis (CGN)]. 875 9

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.
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PMID:[Strategies for the detection of dyslipemias in primary care in La Rioja]. 876 69

Recent trends in the American lifestyle, such as a high-fat diet and inactivity, have promoted the emergence of a metabolic disorder titled syndrome X. Although originally linked to non-insulin-dependent diabetes mellitus (NIDDM) and characterized by insulin resistance, syndrome X is now better described as a cascade of disorders encompassing not only NIDDM, but also hypertension, atherosclerosis, centrally distributed obesity, and dyslipidemia. Further pathology has been linked to syndrome X, such as polycystic ovary disease, microvascular angin, and the presence of acanthosis nigricans. Recognition and appropriate management of syndrome X will prevent deleterious patient outcomes that might occur without continuity of care in treating associated disorders. Pharmacological management of syndrome X includes the use of insulin-sparing antihyperglycemic agents and/or combination therapy and avoidance of several frequently prescribed medications. Clinicians need to initiate renewed efforts to provide lifestyle counselling to promote ideal body weight, since interpretation of research data concerning syndrome X reinforces that serious health consequences will result from obesity and inactivity.
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PMID:Syndrome X. Recognition and management of this metabolic disorder in primary care. 878 76

Increased concentration of cholesteryl ester transfer protein (CETP) in plasma favours a lipoprotein profile characterized by a reduced high density lipoprotein (HDL) cholesterol. Previous studies have demonstrated that a diet high in cholesterol and saturated fat (HCSF) is associated with elevated plasma CETP and increased release of cholesterol ester transfer activity (CETA) from hamster adipose tissue incubated in vitro. The present study investigated the effects of vitamin E (Vit.E) ingestion on plasma CETP activity and adipose tissue CETA in Syrian Golden hamsters. A regular diet supplemented by the addition of 1% cholesterol and 10% coconut oil (w/w) was associated with a time-dependent increase in plasma CETP activity and increased release of adipose CETA following incubation of fragments of perirenal adipose tissue. Vit.E ingestion (100 mg/kg body weight per day for 8 weeks) suppressed 85% of the increase of CETA released from cultured hamster adipose tissue and 70% of the increase of plasma CETP activity induced by the HCSF diet. Significant decreases in plasma total and LDL cholesterol and an increase in HDL cholesterol were found in hamsters receiving the HCSF diet plus Vit.E compared to the animals on the HCSF diet alone. In the hamsters on regular chow, Vit.E ingestion alone did not significantly alter adipose tissue CETA, plasma CETP activity or plasma lipoproteins. The results indicate that Vit.E prevents the HCSF diet-induced increase in plasma CETP activity, probably via a reduction of CETA secretion from hamster adipose tissue. This suggests that Vit.E supplementation may help to ameliorate the dyslipidemia caused by a HCSF diet through its inhibitory influence on CETP production in adipose tissue.
Atherosclerosis 1996 Aug 02
PMID:Effect of dietary vitamin E supplements on cholesteryl ester transfer activity in hamster adipose tissue. 883 Sep 34


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