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PubMed1995

Overexpression of apolipoprotein E prevents development of diabetic hyperlipidemia in transgenic mice.

To determine the role of apolipoprotein E (apoE) in diabetic hyperlipidemia, we induced diabetes in transgenic mice overexpressing apoE by intravenous injection of streptozotocin (STZ) and examined plasma lipoprotein metabolism in these mice. In STZ-induced diabetic mice, blood glucose levels were > 19 mmol/l (350 mg/dl) and plasma insulin levels were reduced to < 5 pmol/l (1 microU/ml). The diabetic nontransgenic mice developed hypercholesterolemia (plasma total cholesterol level: 4.55 +/- 1.32 vs. 1.97 +/- 0.13 mmol/l [176 +/- 51 vs. 76 +/- 5 mg/dl]) and hypertriglyceridemia (plasma triglyceride level: 0.82 +/- 0.29 vx. 0.42 +/- 0.11 mmol/l [73 +/- 26 vs. 37 +/- 10 mg/dl]) compared with values before induction of diabetes. In the diabetic nontransgenic mice, enhanced intestinal acylCoA:cholesterol acyltransferase activity was demonstrated, a factor that may contribute to the development of diabetic hyperlipidemia. Induction of apoE remarkably reduced the development of hyperlipidemia in diabetic transgenic mice compared with diabetic nontransgenic mice (plasma cholesterol level: 4.55 +/- 1.32 vs. 3.31 +/- 0.47 mmol/l [176 +/- 51 vs. 128 +/- 18 mg/dl], P < 0.01, and plasma triglyceride level: 0.82 +/- 0.29 vs. 0.17 +/- 0.11 mmol/l [73 +/- 26 vs. 15 +/- 10 mg/dl], P < 0.01). Plasma lipoprotein analysis by gel filtration chromatography showed that the reduction of plasma cholesterol and triglyceride levels was due to the disappearance of lipoproteins containing apoB. In these studies, we demonstrated the usefulness of STZ-induced diabetes in mice as an animal model for diabetic hyperlipidemia and demonstrated that endogenous induction of apoE in transgenic mice improved diabetic hyperlipidemia.

Animals↗
PubMedDate not supplied

Family physician's knowledge, beliefs, and self-reported practice patterns regarding hyperlipidemia: a National Research Network (NRN) survey.

OBJECTIVE: Family physicians have the potential to make a major impact on reducing the burden of cardiovascular disease through the optimal assessment and management of hyperlipidemia. We were interested in assessing the knowledge, beliefs, and self-reported practice patterns of a representative sample of family physicians regarding the assessment and management of hyperlipidemia 2 years after the release of the evidence-based National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III guidelines. METHODS: A 33-item survey was mailed to a random sample (N = 1200) of members of the American Academy of Family Physicians in April of 2004, with 2 follow-up mailings to nonresponders. Physicians were queried about sociodemographic characteristics, their knowledge, attitudes, and self-reported practice patterns regarding the assessment and management of hyperlipidemia. Four case scenarios also were presented. RESULTS: Response rate was 58%. Over 90% of surveyed family physicians screened adults for hyperlipidemia as part of a cardiovascular disease prevention strategy. Most (89%) did this screening by themselves without the support of office staff, and 36% reported routine use of a flow sheet. Most had heard of the ATP III guidelines (85%), but only 13% had read them carefully. Only 17% of respondents used a coronary heart disease (CHD) risk calculator usually or always. Over 90% of those responding reported using low-density lipoprotein (LDL) as the treatment goal but only 76% reported using non-high-density lipoprotein (HDL) cholesterol as a secondary goal of therapy. CONCLUSION: We found a large variability in knowledge, beliefs, and practice patterns among practicing family physicians. We found general agreement on universal screening of adults for hyperlipidemia as part of cardiovascular disease prevention strategy and use of LDL cholesterol as a treatment goal. Many other aspects of the NCEP ATP III guidelines, such as use of a systematic, multidisciplinary approach, using non-HDL cholesterol as a secondary goal, routinely using a CHD risk calculator for risk assessment to guide cholesterol management, have not yet penetrated into self-reported clinical practice.

Adult↗
PubMed2004

Undertreatment of hyperlipidemia in a cohort of United States kidney dialysis patients.

BACKGROUND: Application of national guidelines regarding cardiovascular disease risk reduction to kidney dialysis patients is complicated by the conflicting observations that dialysis patients have a high risk of atherosclerotic cardiovascular disease (ASCVD), but dialysis patients with higher serum cholesterol have lower mortality rates. Actual treatment patterns of hyperlipidemia are not well studied. METHODS: We assessed the prevalence, treatment and control of hyperlipidemia in this high-risk patient population from 1995 - 1998. We measured low-density lipoprotein cholesterol, treatment with a lipid-lowering agent, and prevalence of hyperlipidemia as defined by the National Cholesterol Education Program (NCEP), Adult Treatment Panel (ATP) II guidelines in 812 incident hemodialysis (HD), and peritoneal dialysis (PD) patients from dialysis clinics in 19 states throughout the United States. RESULTS: Hyperlipidemia was present in 40% of HD and 62% of PD patients. Among subjects with hyperlipidemia, 67% of HD and 63% of PD patients were untreated and only 22% of HD and 14% of PD patients were treated and controlled. Those who entered the study in 1997 or 1998, those with diabetes, males and Caucasians were more likely to be treated and controlled, whereas subjects on PD and those with ASCVD were less likely to be treated and controlled. CONCLUSION: These data suggest that high rates of undertreatment exist in the United States ESRD dialysis population. Whether improved rates of treatment will result in decreased cardiovascular disease events needs to be tested in randomized clinical trials.

Cardiovascular Diseases↗
PubMed2003

Screening for familial combined hyperlipidemia in children using lipid phenotypes.

The purpose of this study was to screen for FCHL in children using serum lipid phenotypes. The subjects were 1190 (599 male, 591 female) children who participated in a screening and care program for life style-related diseases in school children. Total cholesterol, high-density lipoprotein cholesterol and triglyceride were determined, and information on the family history of parents was obtained by questionnaire. Candidates for FCHL were screened by the following criteria; type IIb hyperlipidemia, type IIa hyperlipidemia with positive family history of CHD, hyperlipidemia or both. We informed them of the results by mail. A second series of examinations to diagnose FCHL was performed on volunteer participants, including their parents. The candidates consisted of 9 children with type IIb and 27 with type IIa hyperlipidemia, 11 of whom participated, in the second series of examinations, in which 5 children were diagnosed with FCHL. The prevalence was 0.4%, suggesting that at least half of all individuals with FCHL already demonstrate hyperlipidemia in childhood.

Child↗
PubMed2001

Increasing plasma levels of soluble cell adhesion molecules (sE-Selectin, sP-Selectin and sICAM-1) in overweight adults with combined hyperlipidemia.

Combined hyperlipidemia (coincident present hypercholesterolemia and hypertriglyceridemia) may contribute to the development of atherosclerosis and coronary artery disease by increasing of cell adhesion molecules (CAMs). Although the cellular expression of CAMs is difficult to assess clinically, soluble forms of CAMs (sCAMs) are present in the circulation and may serve as marker of CAMs. The aim of this study was to determine whether combined hyperlipidemia in overweight adults without clinical evidence of cardiovascular disease, diabetes mellitus or hypertension is associated with increased expression of CAMs. We examined the levels of soluble cell adhesion molecules (sICAM-1, sE-Selectin and sP-Selectin) in blood plasma of overweight adults (n = 36), mean of BMI 27.08 +/- 4.12 kg/m2 with combined hyperlipidemia, with total cholesterol (TC) 7.27 +/- 1.50 mmol/l, LDL cholesterol 4.89 +/- 1.35 mmol/l, HDL cholesterol 1.27 +/- 0.51 mmol/l and triglycerides (TG) 4.08 +/- 2.22 mmol/l before lipid-lowering therapies, and in equal numbers of age, sex and BMI matched controls. Patients with combined hyperlipidemia had significantly higher plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) (298.13 +/- 41.24 ng/ml versus 241.35 +/- 37.48 ng/ml; P < 0.001), sE-Selectin (63.31 +/- 9.48 ng/ml versus 42.16 +/- 14.18 ng/ml; P < 0.001) and sP-Selectin (161.18 +/- 20.85 ng/ml versus 111.54 +/- 26.12 ng/ml; P < 0.001) compared with overweight, non-hyperlipidemic control subjects. Combined hyperlipidemia in adults with overweight is associated with elevated soluble plasma levels of CAMs. We suppose that levels of CAMs in these patients may be determined as a marker for appreciation of their potential atherosclerotic burden.

Arteriosclerosis↗
PubMed2003

Effects of gamichunggantang on hyperlipidemia.

AIM: To evaluate the therapeutic effects of gamichunggantang (GCT) on hyperlipidemia through high cholesterol diet model. GCT is an Oriental herbal medication, which has been used for the treatment of fatty liver, hyperlipidemia or alcoholic liver disease in Daejeon University Oriental Hospital, Korea since 1999. METHODS: Rats were fed with high cholesterol diet for 4 weeks and GCT was administrated for 2 weeks from 2 weeks later in experimental days. The levels of serum total cholesterol, HDL-cholesterol, and triglyceride were analyzed every week. Absolute and relative liver weight to body, and histopathological changes were determined at last day. And, lipid metabolism-related gene expressions (ACAT and DGAT) in liver tissue were analyzed by using RT-PCR. RESULTS: In GCT group, TG levels were reduced at 3 and 4 weeks after GCT administration (39.4 %, P < 0.05 and 36.3 %, P < 0.01 respectively). Total cholesterol levels also were reduced at 3 weeks (20.5 %, P < 0.05) and 4 weeks (35.86 %, P < 0.01) after GCT administration, but HDL-cholesterol levels were increased significantly (P < 0.05) at 3 weeks (14.7 %) and 4 weeks (25.5 %) compared with hyperlipidemia-induced group without GCT. In the GCT treated group, liver weight was lower and lipid accumulation was decreased in histological finding. ACAT gene expression was suppressed compared with hyperlipidemia-induced group but not DGAT. CONCLUSION: GCT possesses preventive or therapeutic effects on diet-induced hyperlipidemia by inhibiting the intestinal absorption and storage of exogenous and endogenous cholesterol.

Acyltransferases↗
PubMed2003

[Endothelial dysfunction in a family with familial combined hyperlipidemia].

Familial Combined Hyperlipidemia is the most frequent familial hyperlipidemia with a high risk a early manifestation of arteriosclerosis. Endothelial dysfunction is the first step in the development of arteriosclerosis. The aim of our investigation was to examine selected markers of endothelial dysfunction in hyperlipidemic members of families with familial combined hyperlipidemia and their normolipidemia first-line relatives and to compare them with healthy individuals. The study includes non-smoking members of the affected families (probands and first-line relatives), who have not suffered from clinical manifestations of arteriosclerosis and/or hypertension during the start of the study. The cohort was divided into hyperlipidemic individuals (N = 25) and normolipidemic individuals (N = 21). Both groups were compared with control groups of healthy individuals (two groups, N = 17 each), who were adjusted by age and sex. The following markers of endothelial dysfunction were examined: 1. ultrasound--flow mediated dilatation of brachial artery and 2. humoral--serum levels of von Willebrand factor, inhibitor of activator of plasminogen-1 and vasoadhesive molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). The members of families with familial combined hyperlipidemia displayed symptoms of endothelial dysfunction. In comparison with healthy controls the endothelial dysfunction was more expressed in hyperlipidemic individuals. They displayed a significantly lower flow-mediated dilatation of brachial artery (3.6 +/- 3.3% versus 6.6 +/- 2.8%, P < 0.01), higher levels of von Willebrand factor (152.8% +/- 79.1% versus 110.4% +/- 24.8%, P < 0.05), inhibitor of activator of plasminogen-1 (94.6 +/- 30.8 ng/ml versus 60.4 +/- 38.0 ng/ml, P < 0.01) and vasoadhesive molecules: vascular cell adhesion molecule-1 (927.0 +/- 167.7 ng/ml versus 814.7 +/- 171.1 ng/ml, P < 0.05), intercellular adhesion molecule-1 (601.7 +/- 89.5 ng/ml versus 544.8 +/- 59.8 ng/ml, P < 0.05). The normolipidemic individuals displayed only a significantly lower flow-mediated dilatation of brachial artery (5.6 +/- 2.6% versus 7.5 +/- 2.8%, P < 0.05) and higher levels of von Willebrand factor (136.8 +/- 40.32% versus 104.1 +/- 24.9%, P < 0.05). No significant difference was found in the levels of inhibitor of activator of plasminogen-1 and vasoadhesive molecules. The results indicated that members of families with familial combined hyperlipidemia represent a high-risk group from the standpoint of early manifestation of arteriosclerosis.

Adult↗
PubMed2003

Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands.

Epidemiological studies have shown a positive association of colon cancer with hyperlipidemia. Furthermore, signaling generated by peroxisome proliferator-activated receptor (PPAR) alpha and gamma ligands, suggested to be candidate tumor preventive agents, has been shown to lower serum triglyceride levels. In the present study, we assessed hyperlipidemia in Apc-deficient mice, model animals for human familial adenomatous polyposis, and examined the effects of pioglitazone and bezafibrate, respectively, PPARgamma and PPARalpha agonists, on both hyperlipidemia and intestinal polyposis. Serum lipid levels in Apc(1309) mice and Min mice from 6 to 15 weeks of age were measured. Although serum levels of triglyceride and cholesterol were low in both Apc(1309) and wild-type mice at 6 weeks, triglycerides were elevated 10-fold in Apc(1309) mice by the age of 12 weeks but not in their wild-type counterparts. Cholesterol was also increased significantly, and marked centrilobular-restricted steatosis was observed in the livers of aged Apc(1309) mice. Similar findings were observed for Min mice at 15 weeks of age. Moreover, lipoprotein lipase mRNA levels in the liver and small intestine of Apc(1309) and Min mice were demonstrated to be lower than those in wild-type mice. Treatment of Apc(1309) mice with 100 and 200 ppm pioglitazone or bezafibrate for 6 weeks from 6 weeks of age caused dose-dependent reduction in serum triglycerides and cholesterol, along with reduction in the numbers of intestinal polyps to 67% of the control value. The present study clearly demonstrated a hyperlipidemic state in Apc gene-deficient mice and a potential of PPARalpha and PPARgamma ligands to suppress both hyperlipidemia and polyp formation. Hyperlipidemia in these mice may thus be associated with their intestinal lesion development.

Age Factors↗
PubMed2007

Effects of phytosterols in diacylglycerol as part of diet therapy on hyperlipidemia in children.

BACKGROUND: The incidence of hyperlipidemia in children is increasing in Japan, but drug therapy for such children is limited. The ingestion of 4% phytosterols-containing diacylglycerol (PS/DAG) decreases serum total cholesterol and low density lipoprotein cholesterol (LDL-C) concentrations in adults. In the present study, we examined the effect of PS/DAG as part of a diet therapy in pediatric patients with hyperlipidemia. METHODS: Pediatric patients with hyperlipidemia with > or =5.18mmol (200 mg/dL) serum total cholesterol and/or >or =1.70mmol (150 mg/dL) triglycerides (N=22) ingested bread containing PS/DAG (total daily intake, 10g) for 6 months. Blood chemistry was examined prior to and 2, 4, 6 months after the initiation of ingestion, and 4 months after the ingestion period. RESULTS: No significant differences in energy intake or cholesterol intake during the study period were found. After 4 months of ingestion of PS/DAG, LDL-C, lipoprotein(a) [ Lp(a)], free fatty acids and total ketone bodies decreased significantly. In seven patients with familial hypercholesterolemia, total cholesterol and remnant-like lipoprotein particles (RLP)-cholesterol also significantly decreased in addition to LDL-C and Lp(a). CONCLUSIONS: PS/DAG improves serum lipid metabolism in pediatric patients with hyperlipidemia for whom drug therapy is limited, suggesting that PS/DAG may reduce the risk of developing various diseases induced by hyperlipidemia.

Adolescent↗
PubMedDate not supplied

[Lipid particles agglutinated in hyperlipidemias with opalescent sera (author's transl)].

During the last five years, we observed under the microscope all the hyperlipidemic sera received in our laboratory, to search a lipid particle agglutination. We have retained 24 sera with obvious agglutination (9 types V, 9 types IV and 6 types IIb), the lipidemia of which was compared, type to type, to 56 control sera (16 types V, 16 types IV and 24 types IIb), in which no agglutination has been found. We observed significant differences in the means of cholesterol (CT) triglycerides (TG), vitamin A (VA) and CT/TG, VA/TG and VA/CT ratios, comparing agglutinated and control sera. These differences suggest that the agglutination phenomenon is in relation with the nature of the lipid particles present in the hyperlipidemic sera, which could be "chylomicron remnants" in type V hyperlipidemias, and other forms of "remnants" in type IV and IIb hyperlipidemias. These "remnants" could result from a blockade of lipolysis. This blockade of lipolysis in the agglutinated sera might be related to what is known about the authentificated autoimmune hyperlipidemia (AIH). Thus we can suppose that hyperlipidemias with obvious serum lipid particle agglutination are autoimmune hyperlipidemias.

Agglutination Tests↗
PubMed1989

Limited effects of hyperlipidemia on the arterial smooth muscle response to mechanical stress.

Arteries respond to long-term changes in flow rate by alterations in caliber that tend to restore wall shear stress to normal baseline levels. Changes in radius, pressure, or geometric configuration elicit changes in structure and composition of the media in keeping with the altered level and distribution of tensile stresses. Similar stabilizing adaptations occur in the presence of conditions that induce the formation of atherosclerotic plaques, but the ultimate effectiveness of these reactions is variable. Several recent experiments provide information on the possible effects of hyperlipidemia on the smooth muscle cell (SMC) response to normal or increased levels of mechanical stress: (a) Normolipemic serum increases collagen synthesis by SMCs grown on purified elastin membranes compared to synthesis in serum-free medium, but synthesis is not further enhanced by cyclic stretching of the cells. Collagen production increase is less marked in hyperlipemic serum, but cyclic stretching raises synthesis to a degree comparable to that noted for serum-free medium. (b) The increase in artery diameter in response to increased flow rate and the elaboration of media components in relation to the increase in diameter are not hampered by hyperlipidemia. (c) The compensatory enlargement of arteries in response to plaque formation is not prevented by hyperlipidemia even in the presence of hypertension. (d) The healing of a transmural necrotizing injury of the media is, however, retarded and incomplete in the presence of hyperlipidemia. These findings indicate that hyperlipidemia per se does not necessarily interfere with the SMC response to mechanical stimuli. The usual adaptive reactions remain intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗
PubMed1978

[Lipid particles agglutinated in hyperlipidemias with opalescent sera (author's transl)].

During the five last years, we observed under the microscope all the hyperlipidemic sera received in our laboratory, to search a lipid particle agglutination. We have retained 24 sera with obvious agglutination (9 types V, 9 types IV and 6 types IIb), the lipidemia of which was compared, type to type, to 56 control sera (16 types V, 16 types IV and 24 types IIb), in which no agglutination has been found. We observed significant differences in the means of cholesterol (CT) triglycerids (TG), vitamin A (VA) and CT/TG, VA/TG and VA/CT ratios, comparing agglutinated and control sera. These differences suggest that the agglutination phenomenon is in relation with the nature of the lipid particles present in the hyperlipidemic sera, which could be "chylomicron remnants" in type V hyperlipidemias, and other forms of "remnants" in type IV and IIb hyperlipidemias. These "remnants" could result from a blockade of lipolysis. This blockade of lipolysis in the agglutinated sera might be related to what is known about the authentificated autoimmune hyperlipidemia (AIH). Thus we can suppose that hyperlipidemias with obvious serum lipid particle agglutination are autoimmune hyperlipidemias.

Agglutination↗
PubMed1972

Mechanisms of action of clofibrate on cholesterol metabolism in patients with hyperlipidemia.

The influence of clofibrate on cholesterol metabolism in patients with hyperlipidemia was studied by means of sterol balance and isotope kinetic techniques and by measurements of flow rates of cholesterol through the biliary tract. Long-term balance studies were carried out on a metabolic ward in 24 patients with all currently recognized types of hyperlipidemia; in five other patients with hypercholesterolemia, pool sizes and turnover rates of cholesterol were defined by compartmental analysis before and after three years' daily administration of the drug. Except in fat-induced hypertriglyceridemia (two patients), clofibrate caused reduced plasma levels of triglycerides and cholesterol in all categories of hyperlipidemia. As a general rule, excretion of cholesterol into bile and feces was significantly increased and fecal bile acid excretion was decreased, regardless of the type of lipoprotein abnormality. Despite a net increase in steroid excretion in most patients with hyperlipidemia, cholesterol synthesis was not increased; indeed, in many patients synthesis appeared to be decreased. While the data obtained in 29 patients were not always consistent, the bulk of the evidence suggests that, in all forms of hyperlipidemia except fat-induced hyperglyceridemia, the drug causes an increased output of cholesterol while simultaneously inhibiting any compensatory increase in cholesterol synthesis. Therefore, it appeared that the increased excretion of steroids was most likely derived from cholesterol stored in tissues. This conclusion was strengthened by finding that long-term administration of the drug can cause marked reduction in body pools of cholesterol. These findings are reflected clinically by resolution of skin and tendon xanthomatosis. However, it is not yet known whether the accumulation of cholesterol in arterial walls that is part of the process of atherogenesis can be inhibited or reversed by the drug.

Adult↗
PubMed1984

Apolipoprotein E polymorphism and hyperlipidemia.

We tested apolipoprotein E phenotypes in 1557 normolipidemic factory workers and 822 hyperlipidemic hospital patients. We distinguished six different apolipoprotein E phenotypes and determined their frequencies in normolipidemia (factory workers), hypertriglyceridemia, hypercholesterolemia, and mixed hyperlipidemia. For the three homozygous phenotypes E3/3, E4/4, and E2/2, the percentage distribution in the normolipidemic group was 62.2%, 2.2%, and 0.9%, respectively; for the three heterozygous phenotypes E4/3, E3/2, and E4/2, we determined frequencies of 19.9%, 11.7%, and 2.9%, respectively. A higher prevalence of E2/2 homozygosity was observed in hypertriglyceridemic persons (2.5%) and persons affected by mixed hyperlipidemia (5.0%). E4/4 homozygosity occurred more often among hypercholesterolemic patients (5.0%) than normolipidemic persons (2.2%). These data suggest that E2/2 homozygosity and E4/4 homozygosity both predispose to hyperlipidemia. Patients affected by mixed hyperlipidemia should be investigated for their apolipoprotein E polymorphism because of the possible linkage of apolipoprotein E2/2 homozygosity, hyperlipidemia, and atherosclerosis.

Adult↗
PubMed1993

[Diffusion of lipid fractions through the barrier of cantharidin blisters in hyperlipidemias under conditions of clofibrate and rutinosid interaction].

Diffusion of lipid fractions from blood to fluid in blister induced by cantharidal ointment, applied on the forearm skin, was studied in 54 patients, thereof 18 with normlipidemia, 13 having type II hyperlipidemia, 23 with type IV hyperlipidemia. Concentrations of triglycerides, phospholipids, free fatty acids, total cholesterol, HDL-cholesterol and LDL--cholesterol were studied in blood and fluid before treatment, 10 days after applying clofibrate, 20 days after clofibrate application, and 10 days following the application of rutinosid, i.e. upon completion of therapy. After the treatment it was observed that in all the patients the concentration of lipid fractions in blood was lowered, except for HDL-cholesterol, the level of which was elevated, as was the concentration of all the fractions in the blister fluid. Lipid concentration in serum, with the exception of free fatty acids, was invariably higher than in blister fluid. Free fatty acids, LDL-cholesterol and HDL-cholesterol diffused from blood to fluid in a greater percentage. Lipid fraction concentration in fluid depended mainly on the concentration of HDL-cholesterol and triglycerides in the blood. In normlipidemia, the highest percentage of lipid fractions was diffused to blister fluid; the percentage was lower in type IV hyperlipidemia, the lowest being in type II hyperlipidemia. Clofibrate hypolipemia action correlated best with with HDL-cholesterol and triglyceride activity. After the treatment, the elevated diffusion of all the fractions from blood to blister fluid was, in my opinion, consistent with lipid metabolism, venoruton, as vessel tightening drug, may play a protective role in relation to endothelia in hyperlipidemia.

Administration, Cutaneous↗
PubMed1994

[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia].

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.

Adult↗
PubMed1997

Efficacy and safety of fenofibrate or gemfibrozil on serum lipid profiles in Chinese patients with type IIb hyperlipidemia: a single-blind, randomized, and cross-over study.

BACKGROUND: The purpose of the study was to evaluate the effects and safety of fenofibrate or gemfibrozil on plasma lipid profiles in Chinese patients with type IIb hyperlipidemia. METHODS: Patients with previously diagnosed type IIb hyperlipidemia were initially evaluated in this single-blind, randomized, cross-over study. Only those who had persistent hyperlipidemia after a two-month diet control period were included. The patients were randomized to either fenofibrate 100 mg tid or gemfibrozil 600 mg bid for three months, then shifted to alternate drug for another three months after a two-month washout period. During the whole 10-month period, a prudent diet was maintained. Each patient was followed up at Out-patient Clinic regularly for diet interview, compliance and possible adverse events. RESULTS: A total of 12 patients, 11 males and 1 female, completed the whole study. After a three-month treatment of fenofibrate, there was significant reduction in plasma total cholesterol (22.7%, p < 0.001), total triglycerides (43.2%, p < 0.001), and low-density lipoprotein (LDL)-cholesterol (25.7%, p = 0.001). Serum high density lipoprotein (HDL) cholesterol was also increased by 30.2% (p = 0.055). On the other hand, only total triglyceride was significantly reduced by 36.5% (p = 0.005) with gemfibrozil treatment. There was no significant change of serum total, HDL- and LDL-cholesterol after the three-month treatment of gemfibrozil. Besides, serum uric acid and alkaline phosphatase were significantly reduced with fenofibrate but not with gemfibrozil treatment. There was no obvious adverse event noted during each treatment period with either drug. CONCLUSIONS: The findings suggest that in Chinese patients with type IIb hyperlipidemia, both fenofibrate and gemfibrozil can safely and significantly reduce serum triglyceride. Fenofibrate, but not gemfibrozil, could also reduce serum total cholesterol, LDL and uric acid. The results were compatible with the findings of previous studies in western patients with hyperlipidemia.

Adult↗
PubMed2001

[Study on apoE gene polymorphism in Chinese type II b hyperlipidemia].

OBJECTIVE: To study apolipoprotein(apo) E polymorphism and its relationship with plasma lipids and apolipoproteins levels in Chinese patients with type II b hyperlip oproteinemia. METHODS: apoE genotypes were assayed by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) method, serum lipids were determined by enzyme method, and apolipoproteins were measured by radial immunodiffusion assay in 74 type II b hyperlipidemia patients whose fasting serum lipids levels were TG > or = 2.26 mmol/L, TC > or = 6.21 mmol/L and in 230 healthy subjects whose fasting serum lipids levels were TG < 1.82 mmol/L, TC < 6.21 mmol/L from a population of Chinese Han nationality in Chengdu area. RESULTS: Compared with the control group, the serum TG, TC, LDLC, nHDLC, apoA II, apoB100, apoC II, apoC III, apoE levels and TG/HDLC ratio in patients with type II b hyperlipidemia were significantly increased(P < 0.001), and the serum HDLC levels and apoE/apoC III ratio were significantly decreased (P < 0.05). ApoE3/3 genotype and allele epsilon 3 frequency in type II b hyperlipidemia group and control group were both the highest. In type II b hyperlipidemia group, allele epsilon 2 frequency tended to increase and allele epsilon 4 frequency tended to decrease as compared with those in the control group (P > 0.05). In type II b hyperlipidemia group the genotype of apoE2 was associated with higher serum TG, apoC II, apoE levels and apoE/apoC III ratio when compared with the genotype of apoE3; the genotype of apoE4 was associated with higher serum TC, nHDLC and apoE levels when compared with the genotypes E3 and E2 (P < 0.001). CONCLUSION: The alleles epsilon 2 and epsilon 4 are associated with serum TG, TC, nHDLC, apoC II and apoE levels to some extent in type II b hyperlipide in Chinese population.

Adult↗