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)

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.
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PMID:Nephrotic syndrome: a platelet hyperaggregability state. 293 Sep 39

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.
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PMID:[Hemostatic changes during pregnancy in reference to hyperlipidemia]. 339 35