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At least 199 records · Page 11Linked to original sources
PubMed2000

Age-related increases in plasma phosphatidylcholine hydroperoxide concentrations in control subjects and patients with hyperlipidemia.

BACKGROUND: The basal lipid peroxide concentration in the plasma of patients with hyperlipidemia may be related to atherosclerosis. Quantitative determination of lipid peroxides in the plasma is an important step in the overall evaluation of the biochemical processes leading to oxidative injury. Unfortunately, the currently available methods for lipid peroxidation lack specificity and sensitivity. METHODS: Hyperlipidemic patients (44 males and 50 females), ages 12-82 years (mean +/- SE, 53 +/- 2.3 years for males, 58 +/- 2.0 years for females, and 56 +/- 14 years for total cases), and normolipidemic volunteers (controls, 32 males and 15 females), ages 13-90 years (49 +/- 4 years for males, 65 +/- 4 years for females, and 55 +/- 24 years for total cases), were recruited in the present study. Plasma phosphatidylcholine hydroperoxide (PCOOH) was determined by chemiluminescence-HPLC (CL-HPLC). RESULTS: Plasma PCOOH concentrations increased with age in both controls and hyperlipidemic patients. However, the mean plasma PCOOH concentration in patients with hyperlipidemia (331 +/- 19 nmol/L; n = 94) was significantly (P <0.001) higher than in the controls (160 +/- 65 nmol/L; n = 47). Plasma PCOOH concentrations were similar in three hyperlipidemic phenotypes: hypercholesterolemia (IIa), hypertriglyceridemia (IV), and combined hyperlipidemia (IIb). The mean plasma PCOOH in patients with treatment-induced normalized plasma lipids was 202 +/- 17 nmol/L. There was no significant correlation between plasma PCOOH concentration and total cholesterol, triglycerides, or phospholipids in hyperlipidemic patients. For all subjects, there was a significantly positive correlation between plasma PCOOH and each lipid (total cholesterol, P = 0.0002; triglycerides, P = 0.0137; and phospholipids, P <0.0001). Analysis of fatty acids composition of plasma phosphatidylcholine showed significantly low concentrations of n-6 fatty acids moieties (linoleic acid and arachidonic acid) in patients compared with controls. CONCLUSIONS: Our results suggest that an increase in plasma PCOOH in patients with hyperlipidemia may be related to the development and progression of atherosclerosis, particularly in the elderly. Measurement of plasma PCOOH is useful for in vivo evaluation of oxidative stress.

Adolescent↗
PubMed2000

Impact and management of hyperlipidemia posttransplantation.

CVD morbidity and mortality is a major cause of premature death and allograft loss in recipients of renal and cardiac transplants, and hyperlipidemia--a major risk factor for CVD in the general population--may be a significant risk factor for CVD in transplant recipients. Hyperlipidemia is common after transplantation, and immunosuppression with corticosteroids, cyclosporine, or sirolimus causes posttransplantation hyperlipidemia. Posttransplantation hyperlipidemia can be treated in various ways, but statin therapy has thus far proved to be the most effective in lowering lipid levels in the transplant population. However, to date, no large solid end-point studies have demonstrated that lipid-lowering therapy with statins (or any other class of agents) significantly reduces CVD morbidity or mortality and improves allograft survival in transplant recipients, although some smaller studies point in that direction. The ongoing ALERT trial is currently studying whether early and later intervention with a statin (fluvastatin) can reduce chronic allograft dysfunction, decrease CVD, and improve patient survival in transplant recipients.

Heart Transplantation↗
PubMedDate not supplied

Association between obesity and hyperlipidemia among children.

BACKGROUND: This study was undertaken to show the association between obesity and hyperlipidemia among the children. METHODS: In March 2000, while conducting a comprehensive health examination, we analyzed 2011 children from the first grade of primary schools in Taichung City in Taiwan. To study the association between obesity and hyperlipidemia, the t test, chi-square analysis, and multivariate logistic regression were used. RESULTS: There were 1057 boys (52.56 percent) and 954 girls (47.44 percent). The mean age was 7.27 +/- 0.46 years. The proportion of overweight was 11.07 percent in boys and 11.64 percent in girls. The proportion of obesity was 14.19 percent in boys and 12.89 percent in girls. After controlling the other covariates, the multivariate logistic regression analysis showed that overweight was associated with a low level of high density lipoprotein cholesterol. Obesity was associated with hypertriglyceridemia, a high level of low density lipoprotein cholesterol, and a low level of high density lipoprotein cholesterol. CONCLUSIONS: Our findings disclosed that the prevalence of overweight and obesity was high in childhood. Early intervention to control and prevent childhood obesity might be warranted. Obesity was associated with hyperlipidemia in children. A wide-scale survey will be suggested in the future to establish causal-effect issues between obesiyy and hyperlipidemia.

Body Weight↗
PubMed1975

Hyperlipidemia in peripheral atherosclerotic arterial disease.

One hundred and ten patients with radiologically established peripheral atherosclerotic arterial disease were studied. None of them suffered from diabetes, endocrine disorders or renal disease. Their serum cholesterol and triglyceride values were compared with those of a reference group consisting of 548 individuals. When the 95th percentile of the reference values was used for cut-off, the frequency of hyperlipidemias in the patients with peripheral arterial atherosclerosis was about 52%. Combined hyperlipidemia was slightly more common (21%) than isolated increase of either cholesterol (17.9%) or triglycerides (12.6%). Using other cut-off limits for the definition of hyperlipidemia, a striking change in the distribution between these three types of hyperlipidemia occurred. In our patients, the frequencies of different blood groups were not significantly different from those of a comparable population. The serum lipids were at the same level in the different blood groups.

ABO Blood-Group System↗
PubMed2002

[Medical therapy corresponding to the morbid state of hyperlipidemia].

An appearance of statin did not only cause fall of onset rate and the death rate of coronary arteries disease, but also a fall of the total death rate. These results are restraint of cardiovascular event, development and regression restraint of plaque, function improvement of plaque constitution cells, resulting in the decrease of the total death. However, most of the clinical lipid intervention trial were European and USA results, and there was a difference of a quantity of dosage, too, and results in a Japanese were waited for. Results of a clinical lipid intervention trials in a Japanese appeared by degrees, too though a little too late. From those results, it is proposed that hyperlipidemia is managed whether there are several risk factors of atherosclerosis except hyperlipidemia. Needless to say, it is for the greatest purpose of hyperlipidemia treatment to prevent the development and progression of atherosclerosis. Therefore, it is necessary to treat hyperlipidemia after having fully understood the function mechanism of lipid-lowering agents and after having thought about the morbid state of a patient. In addition, on the occasion of a combination treatment it is necessary to administer it after having understood the each other's function mechanism.

Arteriosclerosis↗
PubMed2002

[Effects of fluvastatin on the levels of C-reactive protein and lipids in patients with hyperlipidemia].

OBJECTIVE: To observe the changes of C-reactive protein (CRP) level and its relationship with blood lipids, and the effects of fluvastatin on CRP and the lipids in patients with hyperlipidemia. METHODS: Serum levels of cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C) and lipoprotein(a)[Lp(a)] were measured by enzyme assay, and plasma CRP level by immunonephelometry before and after fluvastatin treatment (20 mg/d for 4 weeks) in patients with hyperlipidemia. RESULTS: CRP levels were above normal in 90.3% hyperlipidemia cases in spite of the various accompanying diseases. Fluvastatin treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL (-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01), and also brought down Lp(a) concentration (-13.81%). CRP levels was very effectively reduced after the treatment (-15.92%, P<0.001). No association between basal CRP levels and basal lipids and Lp(a) concentrations was observed. Positive correlation of CRP, however, was observed after fluvastatin treatment with TC/HDL (r=0.62, P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations were noted between CRP and HDL (r=-0.288, P=0.023). CONCLUSION: CRP levels increases markedly in patients with hyperlipidemia, a fact that is independent of the accompanying diseases. In addition to modulating blood lipid levels, fluvastatin also reduces CRP level, the latter possibly serving as an independent predictive factor for atherosclerotic cardiovascular diseases and also as an indicator for estimating the effectiveness of the treatment.

Adult↗
PubMed2002

[Correction of atherogenic exogenously-induced postprandial hyperlipidemia with pravastatin].

Effect of an HMG-CoA reductase inhibitor pravastatin on atherogenic changes in the lipid transport system during postprandial hyperlipidemia immediately after ingestion of fatty meal was studied in patients with coronary heart disease and fasting hyperlipidemia. Treatment with pravastatin (20-40 mg/day for 3 months) resulted in normalization of fasting levels of blood lipids and decreased postprandial hyperlipidemia due to of enhanced removal of triglyceride-rich atherogenic lipoproteins from blood and their diminished secretion in response to fat load. Moreover pravastatin increased tolerance of the lipid-transport system to exogenous saturated fats. KEY WORDS. coronary heart disease; postprandial hyperlipidemia; pravastatin; lipoproteins, metabolism.

Anticholesteremic Agents↗
PubMedDate not supplied

Comparative pharmacokinetics of propranolol and atenolol in primary hyperlipidemia.

The study was aimed to examine the effects of different types of hyperlipidemia on the pharmacokinetics of lipophilic propranolol and hydrophilic atenolol. Thirty subjects were divided into four study groups: normolipemics, hypercholesterolemics, hypertriglyceridemics, and patients with mixed form of hyperlipidemia. The drugs were administered orally at a single dose of 80 mg for propranolol and 100 mg for atenolol, using a cross-over study design. Pharmacokinetic parameters of the drugs were calculated using a noncompartmental open model. The results of the present study demonstrated a possible influence of dyslipidemia on pharmacokinetics of both the lipophilic and hydrophilic drugs. As for the lipophilic drug propranolol, a significant decrease in elimination rate constant was found (from 0.24 +/- 0.08 h(-1) to 0.16 +/- 0.04 h(-1), p < 0.03) in comparison to normolipemic subjects. In the case of the hydrophilic atenolol, the most marked alterations were also seen in subjects with mixed form of hyperlipidemia, especially significantly lower values of area under the concentration-time curve (8950.8 +/- 2060.5 ng/ml x h and 6715.4 +/- 1813.8 ng/ml x h, p < 0.05) as well as higher elimination rate constant (0.08 +/- 0.03 h(-1) and 0.13 +/- 0.05 h(-1), p < 0.05) in comparison with the controls, respectively. Total body clearance per kg of body weight of propranolol as well as atenolol was not influenced by dyslipidemias. The results of the study indicate that lipid metabolism disturbances might to some extent influence the pharmacokinetics of propranolol and atenolol, with the most significant alterations seen in the patients with mixed form of hyperlipidemia.

Adult↗
PubMedDate not supplied

[Effect of low glycemic index diets in hyperlipidemia].

INTRODUCTION: After consuming a low-glycemic-index (GI) diet, patients with diabetes and hyperlipidemia showed reduced biochemical markers of dyslipidemia. Despite Mexican food habits include low-GI foods; there have not been published results on the effect of low-GI diet on hyperlipidemia. The aim of this study was to compare the effects of a low and high glycemic index (GI), using cultural based foods to Mexicans on LDL, HDL, total cholesterol, and triacylglycerol. METHODS: Eight volunter's individuals with hyperlipidemia participated in the study. Six diets were designed, three with low-GI and three with High-GI. The study design included 2 times 3-week treatment periods with a 4-week washout period between treatments. Biochemical data was obtained at the start and finish of each dietary period. Subjects completed 1-day dietary diaries during the first and third weeks of each of the treatment periods. Paired t-test was used to compare biochemical data at the baseline and after the dietary treatment periods. RESULTS: At the end of the study periods, total cholesterol (P < 0.05) and LDL (< 0.02) were improved significantly by 10 and 13% respectively. A low GI diet containing Mexican foods during three week period may help to improve LDL and total cholesterol in individuals with hyperlipidemia.

Adult↗
PubMed2003

[Study on the relationship between smoking, alcohol intake and hyperlipidemia in fishermen].

OBJECTIVE: To identify the relationship between smoking, alcohol intake and hyperlipidemia in fishermen. METHODS: 115 fishermen were randomly recruited and divided into case and control groups according to the result of blood lipoprotein. A questionnaire was used to record general information and the history of smoking and alcohol intake. Statistics were gathered to compare the difference of lipoprotein and apolipoprotein level between exposure and control groups and to calculate the OR value of smoking and alcohol intake. RESULTS: The OR of smoking was 3.417 (95% CI: 1.132 - 10.308), with significant dosage-effect relationship between smoking index and hyperlipidemia. The serum low density lipoprotein-cholesterol (LDL-C) and apolipoprotein (apo) B levels in smoking group was higher than that of control group. The OR value of alcohol intake at early age (early than 20) were 3.275 (95% CI: 1.249 - 8.580) and 4.016 (95% CI: 1.475 - 10.952) respectively. The LDL-C, apoB, the serum total cholesterol (TC)/high density lipoprotein-cholesterol (HDL-C) levels in alcohol abuse group were higher than that of control group. CONCLUSION: Smoking and alcohol abuse were important risk factors of hyperlipidemia, through changing the level of LDL-C and apoB. There was synergistic action between smoking and alcohol abuse in the development of hyperlipidemia.

Adolescent↗
PubMed2004

[Effect of hyperlipidemia on pharmacodynamics of propranolol and atenolol].

The study was aimed to examine the effects of different presentations of hyperlipidemia on the pharmacodynamics of lipophilic propranolol and hydrophilic atenolol. Thirty subjects were divided into four study groups: the normolipemic subjects, patients with hypercholesterolemia, hypertriglyceridemia and patients with mixed form of hyperlipidemia. The drugs were administered orally at a single dose of 80 mg propranolol and 100 mg atenolol, using a cross-over study design. The plasma concentrations of propranolol and atenolol were determined using high-performance liquid chromatography (HPLC). Heart rate as well as systolic and diastolic blood pressure were evaluated in relation to the serum drug concentrations. In the light of the results obtained, the following conclusions were drawn: 1) hyperlipidemia affects pharmacodynamic properties of lipophilic propranolol and hydrophilic atenolol, 2) a modification of the drug dosage in hyperlipidemia is warranted.

Administration, Oral↗
PubMedDate not supplied

[Hyperlipidemia with disseminated eruptive xanthomas and hyperglycemia caused by mental stress--a case report].

This article presents the case of a 36-year-old man who developed disseminated eruptive xanthomas, hyperlipidemia and hyperglycemia. The patient was exposed to strong mental stress. He was previously healthy and close family members did not show metabolic and cardiovascular diseases. After a short period of time, when the intensity of stress weakened, generalised eruptive xanthomas and metabolic disturbances completely resolved. Numerous studies have shown that psychosocial stresses lead to the disturbance of the metabolism of lipids, insulin resistance and eventually to cardiovascular diseases. The clinical signs of hyperlipidemia and especially eruptive xanthomas are rare but characteristic features of primary hyperlipidemias. Among secondary causes of hyperlipidemia, eruptive xanthomas are most often described in diabetics, usually localised on extensor surfaces, but generalised eruptive xanthomatosis is rarely the presenting feature of diabetes. The presenting case is most probably a very rare phenomenon of disseminated eruptive xanthomas and serious metabolic disturbances provoked by mental stress.

Adult↗
PubMed2006

[Effects of cholesterol ester transfer protein Taq1B polymorphism on response of serum HDL-C to dietary factors in hyperlipidemia patients].

OBJECTIVE: To analyze the effects of cholesterol ester transfer protein (CETP) Taq1B polymorphism on the response of serum HDL-C to dietary factors in hyperlipidemia patients. METHODS: All 141 hyperlipidemia residents in a community in Shanghai were investigated by a 3-day diet questionnaire. The serum lipids were analyzed, and the polymorphism of CETP gene was detected by PCR-RFLP method. The correlation between dietary factors and serum HDL-C in different genotype was analyzed when considering the effects of sex, age and body mass index. RESULT: The HDL-C of hyperlipidemia patients was affected by dietary factors and CETP gene Taq1B polymorphism. The strength of the correlation between dietary factors and serum HDL-C was different among the genotype groups. The relation was shown closer in B(2)B(2) subjects than in B(1)B(1). CONCLUSION: The Taq1B CETP gene polymorphism should be a strong determinant of HDL-C in hyperlipidemia patients, and might contribute to the heterogeneity in HDL-C response to dietary intervention.

Cholesterol Ester Transfer Proteins↗
PubMed1991

Beclobrate:pharmacodynamic properties and therapeutic use in hyperlipidemia.

Beclobrat is a new fibric acid derivative with potent cholesterol- and triglyceride-lowering effects. Pharmacodynamic and pharmacokinetic investigations suggest that once-daily administration in a dosage of 100 mg is admissible. In comparison with other lipid-lowering drugs such as dose, even when calculated on a molar basis, is as effective as 300 mg fenofibrate, 600 mg bezafibrate or 900 mg gemfibrozil. The effectiveness of the drug has been investigated in a variety of studies including patients with hyperlipidemia types IIa, IIb and IV and patients suffering from secondary hyperlipidemia attributable to diabetes mellitus, liver disease, end-stage renal failure requiring hemodialysis, and kidney transplantation. According to the type of hyperlipidemia studied, the mean reduction of LDL-cholesterol ranges from -10% to -28% and that of triglycerides from -20% to -58%. Mean serum HDL-cholesterol increase has been reported to be 8.5-23.9%. In general, side-effects of beclobrate therapy are comparable with those of other fibric acid derivatives, but have to be investigated carefully in a greater number of patients. Advantages in clinical use are administration of a small capsule in a single daily dose. This has been shown to increase patient compliance and is especially useful for treatment of hyperlipidemia in those patients requiring antihyperlipidemic combination therapy or additional medication for further diseases.

Benzhydryl Compounds↗
PubMed1990

Acquired hyperlipidemia (secondary dyslipoproteinemias).

Acquired hyperlipidemia (secondary dyslipoproteinemias) results from underlying disorders that lead to alterations in plasma lipid and lipoprotein metabolism. Secondary dyslipoproteinemias may mimic primary forms of hyperlipidemia and can have similar consequences. They may result in increased predisposition to premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to the development of pancreatitis and other features of the chylomicronemia syndrome. Diabetes mellitus and use of drugs such as diuretics, beta blockers, and estrogens are commonly encountered causes of secondary dyslipoproteinemia. Other conditions leading to acquired hyperlipidemia include hypothyroidism, renal failure, nephrotic syndrome, alcohol usage, and some rare endocrine and metabolic disorders. When secondary and familial forms of hypertriglyceridemia coexist, triglyceride removal mechanisms may be saturated and marked hypertriglyceridemia with fasting chylomicronemia might ensue. Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.

Diabetes Complications↗
PubMed1986

Contemporary recommendations for evaluating and treating hyperlipidemia.

The biochemistry, etiology, and evaluation of hyperlipidemia and its management, including dietary and drug therapies, are discussed. Strong evidence supports the role of increased cholesterol concentrations as an independent risk factor for coronary artery disease (CAD); however, evidence that elevated triglyceride concentrations are also an independent risk factor remains questionable. The cornerstone of the laboratory diagnosis of hyperlipidemia involves repeated measurement of serum or plasma cholesterol and triglyceride concentrations. The goals of therapy should be to reduce cholesterol or triglyceride concentrations or both to below the 75th percentile, modify co-existing risk factors, individualize the treatment, and minimize any adverse effects. Specific interventions must be determined on the basis of patient age, gender, etiology of hyperlipidemia, presence of other risk factors, and degree of lipid abnormality. The majority of patients may be managed with dietary therapy alone. The three-phase diet developed by the American Heart Association emphasizes a gradual reduction in cholesterol and fats with the substitution of polyunsaturated for saturated fats. Patients at risk for CAD with sustained elevations in plasma cholesterol concentrations above the 95th percentile or a triglyceride concentration above 500 mg/dL after an adequate dietary trial should be considered for drug therapy. The effects of cholestyramine and colestipol hydrochloride, niacin, dextrothyroxine, clofibrate, neomycin sulfate, probucol, gemfibrozil, and mevinolin and compactin on lipids and lipoproteins are reviewed. Hyperlipidemia should be managed systematically using information about the association between increased lipid concentrations and CAD, patient risk factors, and limitations of both diet and drug therapy.

Clofibrate↗
PubMedDate not supplied

[Blood lipids and the incidence of hyperlipidemia in pilots].

The content of cholesterol and triglycerides was measured in healthy pilots. Over 1500 subjects were examined and age-related norms of the parameter were established. They were compared with published data. Physiological variations of cholesterol and triglycerides were related to age, height and body weight. The authors developed a method for diagnosing hyperlipidemia based on the agreement or disagreement between experimentally measured and theoretically calculated values. The authors maintain that hyperlipidemia can be diagnosed if the difference between the real and expected values is over 10%. The authors calculated the incidence of hyperlipidemia in all subjects examined (over 2100) and found that it was high: even in pilots of the age group 20-29 years hyperlipidemia occurred in 30% of subjects.

Adolescent↗
PubMed1979

[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)].

A serie of 12 cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general), is reported. It is suggested that: 1--Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a manifesting hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2--Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3--The hyperlipidemia can be familial or can result from growth hormone deficiency alone.

Adult↗