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

To assess the hypothesis that beta blocker use and hypertension are associated with high lipoprotein(a) [Lp(a)] or with reduced basal fibrinolytic activity, the authors studied relationships of hypertension and beta blockers to Lp(a), lipids, lipoproteins, apolipoproteins, and basal fibrinolytic activity in 385 patients consecutively referred for diagnosis and therapy of hyperlipidemia. A second aim was to determine possible gender differences in fibrinolytic activity among patients with hypertension. Ninety-nine patients (58 women [88% post-menopausal] and 41 men) had drug-treated hypertension. In women, hypertension was a positive, independent predictor of the major inhibitors of fibrinolysis, plasminogen activator inhibitor antigen (p = 0.017), and plasminogen activator inhibitor activity (p = 0.004). In men and women, major risk factors for atherosclerosis were significant, independent predictors of reduced basal fibrinolysis. Median Lp(a) in the 99 patients with hypertension (16 mg/dL) did not differ from Lp(a) (18 mg/dL) in normotensive patients (p > 0.1). Of the 385 patients, the 39 beta blocker users had higher plasminogen activator inhibitor activity (p = 0.01), higher triglyceride (p = 0.02) levels, and higher Quetelet Indices (p = 0.01) than non-users (n = 346). After covariance adjusting for age, Quetelet Indices, sex, and triglycerides, plasminogen activator inhibitor activity was not higher in beta blocker users than in non-users (p > 0.1). Median Lp(a) did not differ in beta blocker users (16 mg/dL) and in non-users (17 mg/dL), p greater than 0.1. Hypertensive, predominantly post-menopausal women are likely to have high plasminogen activator inhibitor activity and plasminogen activator inhibitor antigen with concurrent reduced fibrinolytic activity, as well as high fibrinogen levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta blockers, Lp(a), hypertension, and reduced basal fibrinolytic activity. 790 48

Three infants suffering from hepatosplenomegaly, pancytopenia, hyperlipidemia, low fibrinogen levels and fever are reported. Two patients died during the first year of life, the third one received allogenic bone transplantation and survives. Clinical and haematological features are consistent with diagnosis of hemophagocytic lymphohistiocytosis.
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PMID:[Erythrohemophagocytic lymphohistiocytosis. A clinical report of 3 cases]. 802

To clarify age-related and lipid-related hemostatic abnormalities in the elderly, we measured the plasma levels of active PAI-1 antigen (aPAI-1), tPA-PAI-1 complex (TPC), plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI), plasmin-alpha 2-PI complex (PIC), and D-dimer, together with the plasma levels of fibrinogen, factor VII (F VII), and thrombin-antithrombin III complex (TAT) and the serum lipid levels in 68 hyperlipidemic and 82 normolipidemic elderly subjects. The aPAI-1 ratio was calculated as aPAI-1/(aPAI-1 + TPC). In the normolipidemic elderly subjects, plasma PIC and D-dimer levels were much higher when compared with healthy young controls, and there was also a decrease in plasma plasminogen and alpha 2-PI levels, an increase in plasma TPC levels, and high plasma F VII and fibrinogen levels. In elderly subjects with type IIb hyperlipidemia, both the plasma aPAI-1 level and the aPAI-1 ratio were significantly increased, while the plasma PIC and D-dimer levels were reduced despite higher plasma F VII, fibrinogen and TAT levels. Both serum total cholesterol and triglyceride levels were correlated positively with plasma F VII and TAT levels and with the TAT/PIC ratio, while only serum triglyceride levels showed a positive correlation with plasma TPC and aPAI-1 levels and with the aPAI-1 ratio. Thus, an increase of fibrinolytic activity appears to occur as part of normal aging to balance the increase of procoagulant activity. However, an imbalance between thrombin activity (increased procoagulant activity) and plasmin activity (hypofibrinolysis) appears to occur in elderly individuals with hyperlipidemia, perhaps resulting in a predisposition to thromboembolic disease.
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PMID:Lipid-related hemostatic abnormalities in the elderly: imbalance between coagulation and fibrinolysis. 829 90

Erythrocyte aggregation (EA) was determined in a Myrenne aggregometer at stasis (EAMo) and low shear (EAM1) in 102 patients suffering from primary hyperlipoproteinemia (PHLP)-46 with familial hypercholesterolemia (FH); 28 with familial combined hyperlipemia (FCHL); 28 with primary hypertriglyceridemia (PHTG)-and in a control group (CG) of healthy matched subjects. EA was also determined in FH after the autologous plasma had been replaced by a control plasma. The following parameters were also measured: fibrinogen (Fbg), plasmatic lipids, apolipoproteins, glucose, HbA1 c and membrane erythrocyte lipids: cholesterol (C) and phospholipids (PL). An increase in both EAMo and EAM1 was observed in all the studied groups of patients. When erythrocytes of FH were resuspended in control plasma, EA normalized, but only in 75% of them. Fbg was elevated only in FH and FCHL. Membrane C was increased mainly in FH and FCHL. EA correlates with both Fbg and apolipoproteins. In FH, EA also correlates with membrane C/PL. In addition, a high significant correlation exists between EA and HbA1 c in FCHL. The results obtained suggest that not only Fbg and apolipoproteins but also possible changes in erythrocyte membrane could encourage EA in PHLP.
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PMID:Red blood cell aggregation and primary hyperlipoproteinemia. 830 49

Atherosclerotic cardiovascular disease is a complex problem involving lipid deposition, pressure, rheologic forces, carbohydrate tolerance and thrombogenesis. The major contributors identified through epidemiologic research include atherogenic personal attributes, living habits which promote them, signs of a compromised coronary circulation and host susceptibility to these risk factors. Of the atherogenic risk attributes, such as blood lipids, blood pressure, glucose tolerance and fibrinogen, each independently contributes to risk, and the risk associated with any one is compounded by the presence of the others. The risk associated with hypertension, hyperlipidemia or diabetes varies widely depending on the level of associated risk factors. Also, at a given level of total cholesterol, risk is greatly affected by the total/HDL cholesterol ratio, which provides a practical means for assessing the two-way traffic of cholesterol. In addition, living habits, such as cigarette smoking or lack of exercise, can independently affect the risk associated with any of the atherogenic traits. These living habits, obesity and diet can also affect the level of atherogenic risk factors and must be taken into account in assessing risk and implementing preventive measures. Finally, preclinical indicators of silent myocardial ischemia greatly augment the risk associated with a poor cardiovascular risk profile. Hence, ECG left ventricular hypertrophy, blocked intraventricular conduction, repolarization abnormalities and abnormal response to exercise on monitoring must be taken into consideration. Optimal risk predictions require a quantitative synthesis of risk factors into a composite estimate. Handbooks, hand calculators and PC software have been devised for office use based on multiple logistic risk formulations. These have been shown to accurately predict disease risk in a variety of American population samples, in elderly as well as young coronary candidates. Preventive management as well as risk estimation should be multifactorial if optimal results are to be achieved. Preventive strategies should include public health measures to alter the ecology so as to shift the distribution of risk factors to a more favorable level, health education to enable people to protect their own health and preventive medicine for high-risk candidates. Greater skill must be developed to carry out such interventions. In selecting drugs to correct hypertension, diabetes and lipid disorders, it is important to choose agents which do not adversely affect the composite risk profile.
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PMID:Long-term epidemiologic prediction of coronary disease. The Framingham experience. 832 76

There is considerable evidence to suggest that the identification and treatment of dyslipidaemia will reduce the risk of premature CHD, i.e. before the age of 65. Diagnosis of the cause of raised plasma lipid levels will enable appropriate decisions to be taken with regard to management. The cornerstone of treatment is nutritional counselling and attention to other major risk factors for CHD, particularly smoking and hypertension. For a small percentage of patients with severe hyperlipidaemia drug therapy is indicated. Appropriate drug choices need to be made based on the particular lipid abnormality to be treated. In general those patients with clinical vascular disease are treated more aggressively than those where the aim is primary prevention. More research is needed to determine individual risk more precisely and to allow proper targeting of therapy. Genetic factors, qualitative changes in lipoproteins, lipoprotein (a), fibrinogen, and other coagulation and thrombotic factors are likely to be important in individual risk assessment. There is no doubt that more information is needed from prospective studies of lipid-lowering therapy in terms of risk benefit for affected individuals. Hopefully the major studies currently underway will fill some of the gaps in our knowledge. Until then aggressive therapy with drugs should be reserved for those at highest risk where the benefit is likely to be greatest.
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PMID:Management of hyperlipidaemia: guidelines of the British Hyperlipidaemia Association. 834 30

Diabetes mellitus and hyperlipidemia are associated with coronary heart disease and with hypercoagulability, another independent risk factor for coronary heart disease. In 65 non-insulin-dependent diabetes mellitus patients [41 females, 24 males, median age 66 years (range 43-81 years)] treated with antidiabetic agents glycometabolic control (HbA1c), lipids (Quetelet index and blood lipids), and several coagulation parameters were studied in comparison with a reference group. Serum triglycerides were elevated [median (interquartile range) 2.3 (1.3) mmol/l vs. 1.6 (0.7) mmol/l in the controls (P < 0.001)], whereas the median lipoprotein(a) concentration was 65 (157) mg/l in the diabetic patients versus 44 (114) mg/l in the control group (not significantly different). Median high-density lipoprotein-cholesterol concentrations were slightly decreased in the diabetic patients: 1.2 (0.3) mmol/l compared with 1.3 (0.4) mmol/l in the control group (P < 0.02). Elevated levels of fibrinogen, fibrin monomers, thrombin-antithrombin III complex, and factor VIIIc were found in the diabetic patients and factor VII in male diabetic patients. These elevated coagulation parameters are indicators of an activated coagulation system in this patient group. By Spearman's rank test, only HbA1c values correlated with anti-thrombin III (r = 0.27, P < 0.03) and showed a tendency towards a correlation with lipoprotein(a) (r = 0.23, P < 0.07). Triglycerides correlated with the Quetelet index (r = 0.27, P < 0.03), high-density lipoprotein-cholesterol (r = -0.41, P < 0.001), and factor VII (r = 0.35, P < 0.01), whereas serum cholesterol concentrations correlated with factor VII (r = 0.27, P < 0.04) and with fibrin monomers (r = 0.29, P < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycometabolic control, lipids, and coagulation parameters in patients with non-insulin-dependent diabetes mellitus. 840 Mar 36

The cardiovascular risk factors blood pressure, overweight, hyperlipidaemia and several coagulation parameters were studied in a group of 54 otherwise healthy patients with essential hypertension of moderate severity. Of the 54 hypertensive patients, 43 were treated with anti-hypertensive drugs and 11 were not. The patients included in this study who were treated with anti-hypertensive drugs were still hypertensive in spite of their treatment. Lipoprotein levels and coagulation parameters did not differ between the untreated and treated hypertensive patients. Substantial percentages of patients were found to have hypertriglyceridaemia (46%), elevated LDL-cholesterol (28%) and elevated lipoprotein(a) concentrations (43%). Coagulation factors F VIIIc, fibrin monomer and factor VII in males were significantly elevated in comparison with a healthy reference group. These data are compatible with a moderate activation of the coagulation system. Correlations were established between systolic blood pressure and serum cholesterol (r = 0.43, p = 0.003), LDL-cholesterol (r = 0.34, p = 0.02) and triglycerides (r = 0.35, p = 0.01); Quetelet-index with fibrinogen (r = 0.37, p = 0.02) and thrombin-antithrombin III (r = 0.30, p = 0.04); and triglycerides with F VIIc (r = 0.34, p = 0.03) and fibrin monomer (r = 0.29, p = 0.04) respectively. These data link hypertension and hyperlipidaemia with increased coagulation activity and may contribute to our understanding of why these two cardiovascular risk factors accelerate atherogenesis.
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PMID:Coagulation factors and lipid composition of the blood in treated and untreated hypertensive patients. 846 17

Hyperlipidemia and elevated lipoprotein (a) [Lp(a)] levels have been linked to the development and progression of premature atherosclerosis. Two male caucasian patients (36 and 42 years old) with heterozygous familial hypercholesterolemia and extremely elevated Lp(a) concentrations, resistant to diet regimen and lipid lowering drugs, were treated with LDL-apheresis for 55 months (liposorber system, Kaneka, Japan) and 15 months (immunoadsorption system, special Lp(a) columns, Lipopak, Pocard, Russia). Lp(a) dropped on average by 50%, total cholesterol by 27%, LDL-cholesterol by 42%, triglycerides by 43% and the fibrinogen concentration by 16%. Prior to treatment, both patients had suffered three myocardial infarctions. Four and six coronary angiographies with two and four percutaneous transluminal angioplasties (PTCA) were necessary. Since the treatment with LDL-apheresis neither myocardial infarctions nor cardiac complaints have been observed, and both patients have reported better performance. Available data suggest that LDL-apheresis may be effective in the treatment of patients with extremely high Lp(a) concentration.
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PMID:LDL-apheresis in two patients with extremely elevated lipoprotein (a) levels. 856 5

Novel antihyperlipidemic micronized phenofibrate lipantil 200 M was tested for safety and efficacy (one 200 mg capsule a day for 3 months) in 27 patients having cholesterol level above 6.5 mmol/l. The effect emerged upon 1 month of administration and persisted till the end of the treatment. In combined hyperlipidemia triglycerides decreased by 45-60%, total cholesterol and LDL cholesterol by 10-12%. In isolated hyperlipidemia the latter two values appeared lower by 20-23 and 22-27%, respectively. After lipantil 200 M treatment HDL cholesterol went up by 9% in low baseline level (< 1 mmol/l) by 27%. No negative clinico-biochemical shifts were seen, while fibrinogen and uric acid reduced by 16%, apoB by 23-30%. Lipantil 200 M proved active against hyperlipidemia and is recommended for clinical practice.
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PMID:[The effect of micronized phenofibrate on the lipoproteins of the blood plasma at different initial lipid levels]. 864 40


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