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Showing papers by "Michael Aviram published in 1984"


Journal ArticleDOI
01 Jan 1984-Nephron
TL;DR: A harmful effect of L-carnitine replacement therapy when given in high doses is suggested, causing aggravation of uremic hypertriglyceridemia and increased platelet aggregation in patients predisposed to thromboembolic phenomena.
Abstract: Uremic patients undergoing chronic hemodialysis demonstrate a secondary systemic carnitine deficiency. We studied the effect of carnitine replacement with high doses ( L -carnitine, 3

57 citations


Journal ArticleDOI
TL;DR: The abnormal lipid and protein composition of the lipoproteins derived from hypercholesterolaemic patients appears to be the cause of platelet hyperactivity observed in these patients.
Abstract: Increased platelet activation has been shown to be a feature of patients with familial hypercholesterolaemia. Plasma lipoprotein concentration and composition were studied in eleven male patients with familial hypercholesterolaemia and in ten age-matched healthy controls. Increased levels of cholesterol were found in very-low- and low-density lipoproteins (53 and 275%, respectively), whereas in high-density lipoprotein, both cholesterol and apolipoprotein A-I were decreased by 21 and 26%, respectively. On incubation of gel-filtered platelets derived from normolipidaemic controls with identical concentrations of lipoproteins derived from either nomolipidaemic controls or hypercholesterolaemic patients very-low- and low-density lipoproteins from the patients caused significantly greater thrombin-induced platelet aggregation (P less than 0.01). High-density lipoprotein from normal subjects reduced platelet release by 22%, whereas the patients' high-density lipoprotein had no significant effect on platelet release. Lipoprotein-deficient plasma from both groups augmented platelet function to a similar extent. Lipoprotein composition has an important effect on platelet function in vitro. The abnormal lipid and protein composition of the lipoproteins derived from hypercholesterolaemic patients appears to be the cause of platelet hyperactivity observed in these patients.

40 citations


Journal ArticleDOI
TL;DR: Results support the following conclusions: platelet activation by LDL in normal subjects is through the arginine-rich apoprotein-binding site; more than one binding site for LDL exists on platelets; under certain circumstances, LDL binding can cause a reduction in platelet activity.
Abstract: The binding of low-density lipoproteins (LDL) as well as LDL modified by cyclohexanedione (CHD-LDL) to gel-filtered platelets (GFP) and its effect on platelet function were studied in normal and in homozygous familial hypercholesterolaemic (HFH) subjects. Only normal-derived LDL could significantly compete with normal 125I-labelled LDL for binding to normal platelets. When GFP from normal subjects were incubated with normal LDL at concentrations of 25-200 micrograms of protein/ml, platelet aggregation in the presence of thrombin (0.5 i.u./ml) was increased by 65-186%. CHD-LDL, at similar concentrations, caused the opposite effect and decreased platelet aggregation by 26-47%. Both LDL and CHD-LDL (100 micrograms/ml) from HFH patients, when incubated with normal GFP, caused a significant reduction in platelet aggregation (33 and 50% respectively). When HFH-derived platelets were used, both patient LDL and CHD-LDL (but not the normal lipoprotein) could markedly compete with the patient 125I-labelled LDL for binding to the platelets. LDL and CHD-LDL (100 micrograms/ml) from normal subjects decreased aggregation of HFH-platelets by 52 and 85% respectively, while corresponding concentrations of LDL derived from HFH subjects (HFH-LDL) and CHD-LDL derived from HFH subjects (CHD-HFH-LDL) increased platelet aggregation by 165 and 65% respectively. The present results support the following conclusions: platelet activation by LDL in normal subjects is through the arginine-rich apoprotein-binding site; more than one binding site for LDL exists on platelets; under certain circumstances, LDL binding can cause a reduction in platelet activity; specificity for LDL binding to the platelets resides in different regions of the lipoprotein in HFH and in normal subjects. We have thus suggested a model for LDL-platelet interaction in normal and in HFH subjects.

30 citations


Journal ArticleDOI
TL;DR: The release of serotonin and β-thromboglobulin are used in the dense and α granules in order to evaluate the effect of plasma lipoproteins on platelet release from these granules.

21 citations


Journal ArticleDOI
TL;DR: The abnormal lipoproteins in these patients may contribute to their abnormal in vitro platelet aggregation, and little correlation between lipoprotein disorders and clinical condition was found.

14 citations


Journal ArticleDOI
TL;DR: Plasma lipids and lipoproteins were studied in patients with benign monoclonal gammopathy, patients with multiple myeloma and seven patients with Waldenström's macroglobulinaemia and no correlation was found between the severity of the disease and plasma lipid pattern.
Abstract: Plasma lipids and lipoproteins were studied in 21 patients with benign monoclonal gammopathy, 21 patients with multiple myeloma and seven patients with Waldenstrom's macroglobulinaemia. Results were compared with those of a control group, age and sex matched. Low plasma cholesterol levels in all three patient groups were associated with low HDL-cholesterol concentrations. Apo A-I, but not apo B, was significantly reduced. Sixty per cent of the patients exhibited an extra lipid band on plasma lipoprotein electrophoresis, which could be an immunoglobulin-lipid complex. In these patients plasma and LDL-cholesterol levels were significantly lower than in those patients in whom this band was absent. No correlation was found between the severity of the disease and plasma lipid pattern.

12 citations


Journal ArticleDOI
TL;DR: Study of platelet adhesion function in 13 patients with established Behçet's disease, 5 with venous thrombosis and 8 with no involvement of veins, as well as in 30 age and sex matched healthy controls found no pathology in concentration or function of coagulation parameters.
Abstract: The coagulopathy observed in Behcet's disease has defied explanation. No pathology in concentration or function of coagulation parameters has been demonstrated. We have studied platelet adhesion function in 13 patients with established Behcet's disease, 5 with venous thrombosis and 8 with no involvement of veins, as well as in 30 age and sex matched healthy controls. Platelets derived from 10 of the 13 Behcet's patients exhibited significantly increased adhesion as compared to the controls (p<0.01). The platelets of 11 of the 13 tested patients showed significantly increased aggregation in response to adenosine diphosphate (ADP) and epinephrine incomparison to those from controls (p<0.01). However, no correlation between disturbed platelet function and the clinical occurrence of the thrombotic phenomenon was noted. It is suggested that the thrombotic tendency may be related to platelet abnormality while the generation of the actual process is dependent on other factors which await elucidation.

8 citations



Journal ArticleDOI
TL;DR: The method was shown to be dependent on the surface properties of the test slide, on which platelets are deposited, thus proving its suitability to elucidate variations in the surface interaction of the platelets.
Abstract: A simple stagnation flow method for the determination of platelet adhesivity has been developed. The sensitivity of the method to its main operational parameters was tested, resulting in recommended standard flow conditions. The method was shown to be dependent on the surface properties of the test slide, on which platelets are deposited, thus proving its suitability to elucidate variations in the surface interaction of the platelets. Normal values were established for males and females.

1 citations


Journal ArticleDOI
TL;DR: The plant protein diet had a marked hypocholesterolemic effect, and induced a reduction in the cholesterol and in the protein VLDL + LDL to HDL ratios that were used as atherogenic parameters.

1 citations