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

The effect of Etofibrate, a chemical compound of the two antihyperlipidemic agents Clofibrate and nicotinic acid, on elevated plasma fibrinogen and plasminogen concentrations was investigated in a 6 months' survey in 25 patients with different types of primary hyperlipidemia. A consistent reduction of fibrinogen levels to normal occurred after 6 months' therapy, whereas the effect on plasminogen concentrations was weaker and not significant. The fibrinogen-lowering effect of Etofibrate was not related to the pretreatment levels but nearly equal in all cases. The possible consequences on the hemostatic system are discussed. On account of the low daily dosage, apart from a slight flush, no side-effects were noted.
 ...
PMID:Influence of Etofibrate on plasma fibrinogen and plasminogen concentrations in patients with different forms of primary hyperlipoproteinemia. 100 13

It is well known that in thrombotic disease the alteration of biological factors such as antithrombin III, protein C, and protein S deficiency, and congenital disfibrinogenimias and displasminogenemias are determining factors being the acquired alterations not so well known. With this in mind was studied 85 patients with arterial thrombosis and 196 with venous thrombosis, who were again divided into three groups: unique or of repetition, less or more than 35 years and with or without immediate apparent cause. The general clinical-biological profile in patients with thrombosis in whom a congenital deficit is not detected, can help establish prognosis and treatment in these patients. In our patients, together with the importance of factors such as obesity, hyperlipemia, and tabaquism, an increase in fibrinogen (Fg), antigenic Factor VII (vWF:Ag), total protein S is observed as well as a decrease in total fibrinolytic activity related to an increase in the inhibitor of the plasminogen tissue activator (PTA).
 ...
PMID:[Hemostasis profiles in thrombotic disease]. 178 55

Increased cholesterol levels above 200 mg/dl, LDL levels above 130 mg/dl and total cholesterol/HDL ratio above 4.5 in males and above 5.0 in females are recognized as indicators of increased risk of atherosclerosis. Risk associated to increased triglyceride levels (above 200 mg/dl) must be judged in relation to associated factors such as family history of coronary heart disease, presence of remnants (type III hyperlipidemia), presence of Lp(a), increased levels of Apo B, reduced levels of HDL2 or Apo A1. VLDL and chylomicron remnants and Lp(a) have an atherogenic power in vitro 2 to 4 times that of LDL. There is a correlation between hypertriglyceridemia and reduced HDL2 and Apo A1 levels. Hypertriglyceridemia is frequently associated to other risk factors like diabetes, obesity, hyperinsulinism, and high blood pressure. Finally, VLDL may elevate levels of plasma plasminogen inhibitor. Thus, hypertriglyceridemia should be investigated when, evaluating risk of atherosclerosis.
 ...
PMID:[Cholesterol and triglycerides in atherosclerosis: epidemiologic and physiopathologic considerations]. 184

Effect of corticosteroids (steroids) on some hemostatic parameters was serially studied in 23 children with minimal change nephrotic syndrome (MCNS). Increased platelet count, erythrocyte sedimentation rate (ESR), cholesterol, fibrinogen, fibrin(ogen) degradation products (FDP), alpha 2-macroglobulin (alpha 2M), alpha 2-antiplasmin (alpha 2AP) and protein C, and reduced antithrombin III (ATIII) and plasminogen (Plg) were noted in relapse before steroid therapy began. With institution of oral prednisolone, FDP started to fall, and platelet count, cholesterol, alpha 2M, ATIII, Plg, alpha 2AP and protein C started to increase despite unchanged nephrotic state from that before the therapy. In remission induced by prednisolone, platelet count, cholesterol, alpha 2M, ATIII, Plg, alpha 2AP and protein C were still increased, but normalized off therapy. ESR, fibrinogen, FDP, alpha 2M and protein C correlated inversely with serum albumin and directly with cholesterol and urine protein excretion. In contrast, ATIII and Plg correlated directly with serum albumin and inversely with cholesterol and urine protein excretion. A direct correlation was only noted between alpha 2AP and the dose of prednisolone. The data indicate that steroids appear to be a thrombogenic factor by accerelating thrombocytosis and hyperlipidemia, and by reducing plasma fibrinolysis in children with MCNS.
 ...
PMID:Effect of corticosteroids on some hemostatic parameters in children with minimal change nephrotic syndrome. 207 95

Seventy-one healthy subjects, aged 20 to 60, 19 males and 52 females, body mass index (BMI) 19 to 40, were enrolled in the study. None of them were smokers, or affected by hyperlipidemia, arterial hypertension or impaired glucose tolerance. We measured plasminogen activators inhibitor (PAI) activity, C-peptide levels, plasma fibrinolytic activity. We found a correlation between BMI and plasma fibrinolytic activity (r = -0.382, p less than 0.005), between BMI and PAI (r = 0.353, p less than 0.005), between BMI and C-peptide (r = 0.694, p less than 0.001) and between PAI and C-peptide (r = 0.404, p less than 0.02). Our data show a correlation between obesity and low fibrinolytic activity, probably due to high PAI levels. In obesity impaired fibrinolytic activity, maybe linked to hyperinsulinemia, could induce thrombophilic state.
 ...
PMID:[Relations between overweight, thrombophilia and cardiovascular risk]. 211 69

To elucidate the mechanism for thrombus formation in hypoalbuminemic and hyperlipidemic subjects, the experimental thrombus formation was analyzed in Nagase analbuminemic rats (NAR). The mutant rat reveals similar biochemical findings to those of NS, such as hyperlipidemia. When thrombus was induced in a small branch of the mesenteric artery by inserting a glass micropipette, thrombus formation was observed within 4 min in NAR and Sprague-Dawley rat (SDR). In SDR, the thrombus gradually grew up in size and detached from the inserted glass micropipette within 4 min after its formation. In contrast, the thrombus formed in NAR did not dissociate from the micropipette until 10-13 min after its formation. The maximum size of the thrombus formed in NAR was about 4 times larger than that in SDR. In the presence of fibrin, the plasma samples from NAR inhibited the activity of tissue-plasminogen activator (t-PA) 1.7 times more potently than did SDR plasma. Plasma gamma 2-plasmin inhibitor activity was significantly higher than that in SDR. Albumin significantly enhanced the t-PA-catalyzed activation of plasminogen, suggesting that the serum albumin might contribute, at least in part, to the plasma fibrinolytic activity. Thus, the higher thrombogenic potential in NAR than in SDR might be due to the reduced thrombolytic activity in NAR.
 ...
PMID:Dynamic aspects of thrombus formation in mutant analbuminemic rats. 238 31

In this work we investigated the influence of hyperlipemia on the fibrinolytic system and also attempted to determine whether vascular lesions may modify the response of plasminogen activators to hyperlipemia. The study was made on rats. Three different diets were administered to the animals, two of the diets only increased the levels of plasmatic lipids in the animals (hyperlipemic groups), but the third induced hyperlipemia and lipid infiltration in aorta (arteriosclerotic group). Fibrinolytic activity was evaluated in the plasma, on the aorta endothelial surface and in aorta wall. In the plasma, plasminogen activator (PA) activity was increased in the hyperlipemic and arteriosclerotic groups compared to control group, however, the activity of fibrinolysis inhibitors was also increased. On the endothelial surface and in the aorta wall, fibrinolytic activity was increased in the groups which received hyperlipidic diets but in the arteriosclerotic group only the endothelial surface showed a clear increase of fibrinolytic activity. A positive correlation was observed between PA activity and levels of hyperlipemia. However, no correlation has been shown between fibrinolytic activity in the aorta with cholesterol and triglyceride levels in this vascular wall.
 ...
PMID:Hyperlipemia, fibrinolysis and arteriosclerosis. 338 9

Blood coagulation and fibrinolysis in pregnancy with or without hyperlipidemia were studied. Blood samples were taken from 36 cases with early pregnancy, 59 cases with late pregnancy, and the relationship between the hemostatic changes and the concentrations of lipids was examined. The following results were obtained: 1. In early pregnancy, all cases were non-hyperlipidemic, but in 41% of late pregnancy cases, hyperlipidemia was found. 2. In late pregnancy without hyperlipidemia, shortening of prothrombin time and activated partial thromboplastin time, increases in platelet epinephrine, collagen aggregation, fibrinogen, and plasminogen, and a decrease in alpha 2-plasmin inhibitor were marked compared with those in early pregnancy without hyperlipidemia. 3. In late pregnancy with hyperlipidemia, the platelet count and fibrinogen were increased, and prothrombin and activated partial thromboplastin time were shortened compared with late pregnancy without hyperlipidemia. The platelet epinephrine aggregation was slightly decreased. Antithrombin III was increased and alpha 2-plasmin inhibitor was slightly decreased. 4. In the same subjects, the relationship between changes in blood coagulation and fibrinolysis in early and late pregnancies and total cholesterol was studied by the independent matched pair test. There were significant correlations (p less than 0.02, p less than 0.05) between activated partial thromboplastin time (r = -0.5998) and fibrinogen (r = 0.6230). From these results the author concluded that late pregnancy was a hypercoagulable state and this tendency was more obvious in late pregnancy with hyperlipidemia.
 ...
PMID:[Hemostatic changes during pregnancy in reference to hyperlipidemia]. 339 35

Fat overload syndrome is a rare complication of intravenous fat emulsion therapy. It is characterized by sudden elevation of the serum triglyceride level, fever, hepatosplenomegaly, coagulopathy, and variable end-organ dysfunction. The illness is generally discrete, and symptoms regress as the lipemia clears. The transient nature of the syndrome has allowed only speculation as to its pathogenesis. The authors report an autopsy study of a child who died during an acute episode of fat overload and document the causative role of fat sludging in the associated end-organ failure. In addition, they offer evidence that the coagulopathy, previously an enigma, results from primary fibrinolysis, possibly caused by release of tissue plasminogen activators from the damaged endothelial cells.
 ...
PMID:Fat overload syndrome. An autopsy study with evaluation of the coagulopathy. 339 63

Many human atherosclerotic lesions, showing no evidence of fissure or ulceration, contain a large amount of fibrin which may be in the form of mural thrombus on the intact surface of the plaque, in layers within the fibrous cap, in the lipid-rich centre, or diffusely distributed throughout the plaque. Small mural thrombi are invaded by SMCs and collagen is deposited in patterns closely resembling the early proliferative gelatinous lesions. In experimental animals, thrombi are converted into lesions with all the characteristics of fibrous plaques, and in saphenous-vein bypass grafts, fibrin deposition is the main cause of wall thickening and occlusion. There seems little doubt that fibrin deposition can both initiate atherogenesis and contribute to the growth of plaques. Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease. Fibrin may stimulate cell proliferation by providing a scaffold along which cells migrate, and by binding fibronectin, which stimulates cell migration and adhesion. Fibrin degradation products, which are present in the intima, may stimulate mitogenesis and collagen synthesis, attract leukocytes, and alter endothelial permeability and vascular tone. In the advanced plaque fibrin may be involved in the tight binding of LDL and accumulation of lipid. Thus there is extensive evidence that enhanced blood coagulation is a risk factor not only for thrombotic occlusion, but also for atherogenesis. Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.
 ...
PMID:Fibrinogen, fibrin and fibrin degradation products in relation to atherosclerosis. 352 31


1 2 3 Next >>