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At least 289 records · Page 16Linked to original sources
PubMed2002

Endotoxin-lipoprotein complex formation as a factor in atherogenesis: associations with hyperlipidemia and with lecithin:cholesterol acyltransferase activity.

A potential role of endotoxin-lipoprotein (bacterial lipopolysaccharide-lipoprotein, LPS-LP) complex formation as a pathogenic factor for atherosclerosis has not been studied yet. The aim of this study was to test the hypothesis that in endotoxinemia in humans hyperlipidemia associated with atherosclerosis development can favor an excessive LPS-LP complex formation, and endotoxin presented in blood can inhibit lecithin:cholesterol acyltransferase (LCAT), one of the key enzymes of reverse cholesterol transport. Endotoxin-binding capacity of lipoproteins (LP) in patients with normolipidemia and hyperlipidemia types IIa and IV was estimated from label incorporation into different LP fractions isolated by means of sequential ultracentrifugation following serum preincubation with Salmonella minnesota R595 125I-labeled LPS. The effect of varied concentrations of S. minnesota R595 LPS on LCAT activity was evaluated from the overall esterifying activity of serum using [1,2-3H2]cholesterol-labeled substrate. The elevation of low density LP (LDL) and very low density LP (VLDL) contents in blood serum in hyperlipidemia types IIa and IV, respectively, resulted in significant elevation of LPS binding to these fractions. LPS added to the blood serum leads to the dose-dependent decrease in LCAT activity. The revealed phenomena of elevated LPS binding to atherogenic LP fractions in hypercholesterolemia and endotoxin-induced LCAT inhibition suggest the pathogenic role of LPS-LP complexes in atherogenesis.

Arteriosclerosis↗
PubMed2002

Adenoviral insulin gene therapy prolongs survival of IDDM model BB rats by improving hyperlipidemia.

Diabetes is frequently associated with hyperlipidemia, which results in atherogenic complications. Insulin-dependent diabetes mellitus (IDDM) model BB/Wor//Tky (BB) rats exhibit both hyperglycemia and hyperlipidemia and die within 3 weeks after the onset of diabetes unless insulin therapy is given. We performed insulin gene therapy in BB rats with adenovirus vectors through the tail vein. After infusion, plasma triglyceride levels dropped quickly and maintained low levels for 1 week, whereas blood glucose levels showed a slight decrease. The survival period of diabetic BB rats was prolonged to up to 75 days by infusing insulin gene-expressing adenoviral vectors. We suggest that the control of hyperlipidemia can be a life-saving measure when combined with hyperglycemia control in the treatment of diabetes.

Adenoviridae↗
PubMed2002

[Hyperlipidemia--side-effect of the treatment with an atypical antipsychotic (zotepine)?].

In the last few years some studies and case reports has been published that suggest a frequent occurrence of metabolic disorders like hyperglycemia and hyperlipidemia during the treatment with atypical antipsychotics. However, regarding the high prevalence rates of these disorders in the general population, a possible causative relationship should be substantiated, i.e. occurrence of elevated blood levels within a short time interval after the starting of the medication. In the presented case a hyperlipidemia (triglycerides up to 1247 mg/dl) was observed soon after the beginning of zotepine medication. After the reduction of zotepine lipid levels in serum decreased and normalised after switching to classical antipsychotics. Therefore a causative relationship between the occurrence of the hyperlipidemia and the zotepine medication is very likely.

Adult↗
PubMed2004

Familial combined hyperlipidemia: controversial aspects of its diagnosis and pathogenesis.

Familial combined hyperlipidemia is the most frequent cause of primary dyslipidemia in Mexico. Its manifestations include hypercholesterolemia, hypertriglyceridemia, or a combination of both. Despite its high frequency, a proper diagnosis is rarely made. Assessment of the lipid profiles of at least three first-degree relatives is necessary. The diagnosis of familial combined hyperlipidemia in a family not only leads to the identification of other affected family members but, more important, allows cardiovascular risk stratification of those affected. Prospective studies have confirmed the atherogenicity of the disease. A critical review of the current literature in this field is presented in this article. Although three screenings of the genome have been completed, the genes responsible for this disorder have not been identified. Limitations with respect to the characterization of affected subjects and the heterogeneity of the disease are among possible explanations. However, familial combined hyperlipidemia, because of its high prevalence, must be given greater priority. It represents a great challenge for physicians involved in the treatment of dyslipidemic patients.

Apolipoproteins B↗
PubMed1988

Hyperlipidemia and in vivo hemostatic system activation.

Coagulation system activity in vivo is a well-recognized consequence of advanced atherosclerotic disease, the association of coagulation system activity with atherogenesis is much less clear. The data reviewed here argue against ongoing increased coagulation system activity in persons with hyperlipidemia. The possibility remains that episodic activity could easily be missed with available tests, such bursts of activity might well require new agents and strategies for effective control. Failure to find evidence of increased coagulation activity in patients with hyperlipidemia does not refute models of atherogenesis based on thrombosis. Rather, the data reviewed here should cause us to focus attention on the time scale of such events. On the other hand, the findings do allow for a simpler interpretation of data showing evidence of activation of coagulation in patients with concurrent hyperlipidemia.

Arteriosclerosis↗
PubMed1998

Influence of hyperlipidemia and smoking on age-related changes in caloric response and pure-tone hearing.

To examine the influence of hyperlipidemia and smoking on age-related changes in caloric response and pure-tone hearing, a caloric test and pure-tone audiometry were performed in 14 healthy volunteers and in 78 tinnitus patients without subjective hearing loss. The patients were from 24 to 84 years of age, and were divided into 4 groups: the no-risk group (N group), the smoking alone group (S group), the hyperlipidemia alone group (L group), and the smoking plus hyperlipidemia group (S-L group). Slow phase eye velocity of the caloric nystagmus (SPEV) and average hearing level at high frequencies were compared between the N groups and the other groups. There was a significant difference in SPEV only between the N and S-L groups, but not in the hearing level. This suggests that age-related changes in the caloric response be promoted by atherosclerosis, unlike presbycusis.

Adult↗
PubMed1976

Therapy of the hyperlipidemias.

Although the diagnosis of hyperlipidemia is somewhat arbitrary, in that the upper limits of normal are not universally agreed upon, it is clear that the risk of atherosclerosis increases with plasma cholesterol concentration; it may also increase in hyperglyceridemia. We take 220 mg/100 ml as the upper limit of normal for plasma cholesterol and 140 mg/100 ml as the upper limit for triglycerides. Treatment of hyperlipidemia is aimed at reducing the risk of atherosclerosis or arresting its course. Alteration of diet is the first step. If maximal diet therapy does not lower plasma lipids to acceptable levels, drug therapy is added. The decision to treat hyperlipidemia with drugs should be based on a careful weighing of risk vs. benefit for each patient. Because of the rapid change in our knowledge of both the risks and the benefits of therapy, that decision must be reviewed and updated at regular intervals.

Anticoagulants↗
PubMedDate not supplied

The effect of ciprofibrate on flow-mediated dilation and inflammatory markers in patients with combined hyperlipidemia.

Impairment of flow-mediated dilation (FMD) has been shown to be associated with hypercholesterolemia and hypertriglyceridemia and reduction of cholesterol and/or triglyceride levels can improve FMD. In hyperlipidemia the role of inflammatory substances on endothelial function requires further clarification. In patients with combined hyperlipidemia (n = 29), the capacity of FMD was weaker whereas the levels of interleukin (IL)-lalpha, tumor necrosis factor alpha (TNFalpha), soluble intercellular adhesion molecule (sICAM), and fibrinogen were higher compared to normolipemic controls with normal FMD adjusted for age and sex. Patients were randomized to a diet-only or to a ciprofibrate treatment group. After 8 weeks FMD levels rose significantly both in the diet-only (10.2%) and the ciprofibrate treatment (79.4%) groups. In the diet-only group improvement of FMD was significantly associated with the reduction of triglyceride (by 15.9%) and cholesterol (6.9%) levels. The much larger improvement of FMD due to ciprofibrate therapy was accompanied by significant reductions of cholesterol (by 14.4%), fibrinogen, IL-1alpha, and sICAM levels and by significant increase of high-density lipoprotein (HDL) cholesterol concentration, but the change in FMD correlated only with the reduction of the cholesterol level. In line with previous data the authors emphasize that improvement of FMD in patients with combined hyperlipidemia treated with diet and/or ciprofibrate is linked directly to the reduction of cholesterol and triglyceride concentrations rather than to changes in the level of the investigated inflammatory markers.

Adult↗
PubMed1986

Sterol excretion and cholesterol absorption in diabetics and nondiabetics with and without hyperlipidemia.

Fecal neutral and acidic sterols and cholesterol absorption were measured in 12 normal control subjects, 40 diabetic subjects with and without hyperlipidemia, and 27 subjects with hyperlipidemia but without diabetes mellitus. All subjects were on a low-cholesterol diet (less than 300 mg cholesterol/day). Fecal excretion of neutral and acidic sterols was increased in patients with hypertriglyceridemia and was more marked in diabetic patients with hypertriglyceridemia. Cholesterol absorption was decreased in diabetic patients with hypertriglyceridemia. Otherwise, there were no significant differences in sterol excretion or cholesterol absorption in diabetic and nondiabetic subjects compared with control groups with similar lipid levels. The best predictors of fecal neutral- and acidic-sterol excretion and of estimated cholesterol synthesis were very low [corrected]-density lipoprotein triglycerides and high-density lipoprotein cholesterol. Correction of hyperlipidemia may be beneficial in decreasing cholesterol synthesis and, thereby, in decreasing the risk of atherogenesis.

Adult↗
PubMed1995

Reduction of hyperlipidemia and proteinuria without growth retardation in nephritic rats by a methionine-supplemented, low-soy-protein diet.

Effect of a low-soy-protein-isolate (SPI) diet supplemented with methionine on hyperlipidemia, proteinuria, and hypoalbuminemia was studied in rats with nephrotoxic serum nephritis (NSN). Rats were fed experimental diets for 14 d after an injection of nephrotoxic serum. An 8.5%-SPI diet (8.5S), as compared with a basal 20%-SPI diet (20S), improved the hyperlipidemia, proteinura, and hypoalbuminemia secondary to NSN but retarded the growth of rats. The addition of 0.3% methionine to 8.5S (8.5SM) alleviated the growth retardation without loss of the above-mentioned beneficial effects. 8.5SM was found to suppress hepatic cholesterol synthesis compared with 20S. These results suggest that the methionine-supplemented low-SPI diet has a beneficial effect on hyperlipidemia, proteinuria, and hypoalbuminemia without inducing either growth retardation or severe fatty liver in nephritis. They also suggest that the hypocholesterolemic effect of 8.5SM in nephritic rats may be partly attributable to reduced hepatic cholesterol synthesis.

Animals↗
PubMed2006

Possible involvement of hyperlipidemia in increasing risk of colorectal tumor development in human familial adenomatous polyposis.

BACKGROUND: Familial adenomatous polyposis (FAP) results from germline adenomatous polyposis coli (APC) gene mutations and many affected patients die from colorectal cancers which arise from colorectal polyps. We previously reported that two strains of Apc gene-deficient mice developing multiple intestinal polyps exhibit a hyperlipidemic state. The triglyceride (TG) levels were approximately 10-fold higher than the levels observed in wild-type mice. METHODS: To examine whether a positive relationship might exist between hyperlipidemia and colorectal tumor development in FAP patients, as with Apc gene-deficient mice, a pilot experiment was performed using readily available clinical data such as ages, serum lipid levels, number of colorectal polyps and cancer development in 28 FAP patients from the National Cancer Center Hospital, Japan. RESULTS: The overall prevalence of hyperlipidemia in FAP cases was 58%. Average TG levels in the 40-60 year age groups of FAP patients were > or =150 mg/dl (the defined threshold level of hyperlipidemia). Moreover, there was a tendency for higher serum TG levels in patients who developed colorectal cancer, as compared with those without colorectal cancer. CONCLUSIONS: These results show that a hyperlipidemic state occurs in FAP patients. Although it is weaker than that in Apc gene-deficient mice, it may be linked to colon tumor development. These data warrant further studies for wider populations of FAP patients.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Hyperlipidemia and myocardial infarction among 118 patients with polycythemia vera.

Hyperlipidemia was reported among 46 of 118 polycythemia vera patients as compared to a control group of 115 healthy subjects in whom hyperlipidemia was reported in 20. Among the 46 hyperlipidemic patients with polycythemia vera 14 had a myocardial infarction, while among the other 72 nonhyperlipidemic polycythemia vera patients myocardial infarction occurred amont 17. Since repeated phlebotomies may induce hyperlipidemia, this form of treatment of polycythemia vera may be potentially dangerous in already hyperlipidemic polycythemia vera patients.

Female↗
PubMed1985

Familial combined hyperlipidemia and otosclerosis--the occurrence in a large kindred.

The occurrence of otosclerosis and hyperlipidemia in four generations of a single family is described. The lipid abnormality fulfilled the characteristics of combined familial hyperlipidemia. Whereas a genetic linkage between combined hyperlipidemia and otosclerosis is feasible, our study indicates that both conditions are inherited through autosomal but unlinked genes.

Adolescent↗
PubMed1987

Reversal of severe diabetic hyperlipidemia by prandial insulinization.

Severe hyperlipidemia was nearly completely corrected in 16 diabetic patients who were treated with regular insulin at breakfast and supper. Serum cholesterol levels fell from 572 +/- 52 mg/dl to 247 +/- 10 mg/dl, and serum triglycerides fell from 6,330 +/- 820 mg/dl to 354 +/- 40 mg/dl over a 4-month period of treatment. Establishment of comparable degrees of control of the fasting blood glucose and hemoglobin A1C levels by NPH insulin did not correct the hyperlipidemia. Regular insulin timed to act for the disposal of ingested substrates appears to provide physiologic actions important in the treatment of diabetic hyperlipidemia.

Adult↗
PubMed1979

Intimal thickening and hyperlipidemia in experimental primate vascular autografts.

Intimal thickening is a significant cause of late failure of aorto-coronary vein grafts. The microscopic appearance of this thickening has some similarities to the microscopic appearance of arterial atherosclerosis, and it has been suggested that hyperlipidemia may play a role in its pathogenesis. This study examines the morphology and lipid composition of autologous vein and artery grafts in normal and hyperlipidemic rhesus monkeys. Grafts were examined six months after insertion by light and electron microscopy and tissue lipids were determined quantitatively. Intimal thickening occurred in all grafts. Specific morphological and lipid compositional features of the grafts were influenced by the type of tissue used for grafting and the presence or absence of hyperlipidemia. However, the degree of intimal thickening per se could not be related to either of these two factors. It is concluded that surgical transplantation in this model provides the most powerful stimulus for intimal thickening and any additional effect on this process by hyperlipidemia is small.

Animals↗
PubMed1995

Alpha-tocopherol ameliorates cyclophosphamide-induced hyperlipidemia in fibrosarcoma-bearing rats.

Cyclophosphamide, an alkylating agent, is currently being used for the treatment of various types of cancer, either alone or in combination with other cytostatic drugs. However, cyclophosphamide has a detrimental effect on lipid metabolism and causes hyperlipidemia in patients. Since alpha-tocopherol is known to reduce hyperlipidemia, we have investigated the effects of adding alpha-tocopherol to the cyclophosphamide treatment. Our study, carried out on fibrosarcoma-bearing rats, shows that alpha-tocopherol markedly reduces cyclophosphamide-induced hyperlipidemia and brings lipid metabolism down to values observed in untreated controls.

Animals↗
PubMedDate not supplied

Long-term use of low molecular weight heparin ameliorates hyperlipidemia in patients on hemodialysis.

Hyperlipidemia is one of the major risk factors for cardiovascular death in long-term hemodialysis (HD) patients. To clarify whether unfractionated heparin (UFH) contributes to the pathogenesis of hyperlipidemia, nine Type IIb, seven Type IV, and 10 normolipidemic patients, who had been dialyzed with 80.7 IU/Kg heparin, were dialyzed with 40 anti-Xa U/kg of low molecular weight heparin (LMWH) (Logiparin, Novo-Nordisk, Gentfe, Denmark) for 6 months. Seven normolipidemic patients were also dialyzed with heparin as controls. Decreases in triglyceride (TG) during HD with LMWH were significantly less than those with heparin. However, lipoprotein lipase activities (LPL) during HD with LMWH and heparin, and those before and after 6 months on LMWH, were no different. During the 6 months on LMWH, serum total cholesterol, TG, and alpha lipoprotein significantly decreased in Type IIb patients but did not change in Type IV. In contrast, beta lipoprotein slightly increased in Types IIb, IV, and normolipidemic patients who were dialyzed with LMWH but was unchanged in the controls. These observations suggest that UFH aggravates hyperlipidemia in patients, but these effects cannot be attributed to depletion of endothelial LPL liberated by UFH.

Adult↗
PubMed1997

Physician education in hyperlipidemia management: the impact on collaboration.

Collaboration of health care professionals is likely beneficial in modifying patient behavior in the treatment of hyperlipidemia. The purpose of this study was to determine whether limited instruction and demonstration of collaborative management of hyperlipidemia in a continuing medical education (CME) would change physicians' office practices, as determined 1 year later by questionnaire. Collaborative practice was defined as physicians working with other allied health care professionals as a team to increase patients' medication compliance and other behavioral outcomes. A 19-credit hour CME Lipid Disorders Training Program (LDTP) was offered emphasizing the collaborative approach to hyperlipidemia patient management. Physicians (n = 196) were surveyed 1 year after LDTP. The response rate was 52.5%, nonrespondents were similar in locations. About 51% of respondents reported increased collaborative practice; of these respondents, 68% reported saving time, 78% reported improved patient outcomes, 76% improved office efficiency, and 90% increased patient satisfaction. According to self-reporting by these physicians, increased collaboration practices after attending the LDTP course led to improved patient outcomes.

Education, Medical, Continuing↗