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)

The kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195 +/- 57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298 +/- 824 platelets/microliter/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8 +/- 0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.
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PMID:Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia. 343 47

Plasma level of beta-thromboglobulin (beta TG), a useful marker of in vivo platelet "release reaction,"was determined by radioimmunoassay in 69 patients, with three types of primary hyperlipidemia (IIa, IIb, IV) and compared with the findings in age- and sex-matched healthy controls and 57 patients with established atherosclerosis and peripheral vascular disease. Malondialdehyde (MDA) formation, used for assessment of prostaglandin synthesis, was determined in 51 and plasma platelet factor 4 (PF4), measured by radioimmunoassay, in 48 of the patients with hyperlipidemia. Results were correlated to five serum lipids and lipoprotein levels in the patients with hyperlipidemia. beta TG was significantly increased in the patients with hyperlipidemia and peripheral vascular disease, compared to those in the controls (p < 0.001); it was significantly higher in the patients with hyperlipidemia than in those with peripheral vascular disease. PF4 and MDA formation were also increased in the patients with hyperlipidemia, and significantly higher levels of MDA were obtained in patients with type IIb and type IV hyperlipidemia than in those with type IIa hyperlipidemia (p < 0.02). beta TG and MDA correlated weakly with total serum cholesterol triglycerides and very low density lipoprotein-triglyceride. There was also a significant correlation between beta TG and PF4, and MDA production. These results indicate that in vivo platelet "release reaction" and MDA formation are increased in hyperlipidemic patients. The release reaction is more enhanced in those with hyperlipidemia than in the patients with peripheral vascular disease. They suggest that the abnormal platelet function is related to the elevated levels of serum lipids and lipoproteins in the hyperlipidemic patients and not only to the atherosclerotic changes associated with hyperlipidemia.
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PMID:Enhanced in vivo platelet release reaction and malondialdehyde formation in patients with hyperlipidemia. 645 May 32

The present study was conducted to determine whether alimentary lipemia alters platelet activity in vivo. Normolipidemic volunteers were given a fatty meal and platelet function was assessed before, and 3 and 6 h after the meal. Platelet aggregability and secretion was determined using whole blood flow cytometry (expression of platelet P-selectin and fibrinogen binding), filtragometry ex vivo (reflecting platelet aggregability in vivo) and by measurements of platelet specific products in plasma (beta-thromboglobulin and platelet factor 4). Plasma triglycerides increased from 0.8 (0.6:1.1; median, 25th and 75th percentiles) to 1.7 (1.0:2.3) mmol/l at 3 h and returned to baseline after 6 h (P < 0.001, one-way ANOVA). Apo B-100 and apo B-48 were both markedly increased 3 h postprandially in the Sf 60-400 fraction (large VLDLs, P < 0.001 for both), whereas the Sf 20-60 (small VLDLs) and Sf 12-20 fractions (IDL) did not change. The platelet function assessments revealed that the percentage of platelets expressing P-selectin increased by 40% (5%; 64%) after 3 h and by 51% (- 7%; 85%) 6 h postprandially in unstimulated samples (P < 0.05 for both). In samples stimulated by ADP in vitro P-selectin expression increased by 45% (6%; 58%) after 3 h and by 30% (12%; 58%) (P<0.01 for both) after 6 h at 0.1 microM. Platelet P-selectin expression was less influenced at higher ADP concentrations. The plasma levels of beta-thromboglobulin (approximately 20 ng/ml) and platelet factor 4 (approximately 0.3 ng/ml) were not affected by the fat load. Flow cytometric analyses of fibrinogen binding and filtragometry measurements also failed to reveal any postprandial alterations. The present finding of enhanced platelet P-selectin expression suggests that platelets are mildly sensitized postprandially. Whether this is of importance for thrombus formation and atherosclerosis needs to be studied further.
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PMID:Alimentary lipemia enhances the membrane expression of platelet P-selectin without affecting other markers of platelet activation. 956 42