Search PubMed⌕ Search

Biomedical subjects

R Fellin

Publications and source records attributed to R Fellin.

At least 91 records · Page 5Linked to original sources
PubMed1985

Decreased number of PGD2 binding sites on platelets from patients with type IIa hyperlipoproteinemia.

Platelets from patients with familial hypercholesterolemia (type IIa hyperlipoproteinemia), a condition associated with a high prevalence of atherosclerosis and its ischemic complications, are claimed to be hyperresponsive to aggregating stimuli. We investigated the platelet responsiveness to and the binding of PGD2, a potent endogenous inhibitor of platelet aggregation via stimulation of adenylate cyclase, in a group of 7 patients affected by IIa hyperlipoproteinemia (IIa HLP) and in a control group of 10 healthy subjects. Inhibition by PGD2 of ADP-induced platelet aggregation was significantly lower in IIa HLP patients than in controls. The number of binding sites for PGD2 of platelets from IIa HLP patients was significantly reduced in comparison with that from controls (93 +/- 19 and 232 +/- 23 receptors/platelet, respectively), whereas the affinity for PGD2 was comparable to that of controls (Kd = 68.8 +/- 19.8 nM in patients and 66.1 +/- 15.9 nM in controls). The reduced number of platelet PGD2 binding sites in IIa HLP patients may account for the impaired sensitivity to PGD2 shown in vitro by platelets and may contribute to the increased tendency to thrombotic manifestations observed in IIa HLP.

Adolescent↗
PubMed1985

[Effect of sulodexide on hemorheological parameters in a group of patients with peripheral arteriosclerotic vascular disease].

The aim of this study was the evaluation of some hemorheological and metabolic parameters in a group of patients affected by peripheral artery disease treated with sulodexide. A double-blind with cross-over treatment was used. The results demonstrate that sulodexide reduces blood viscosity and triglyceride levels. This action may have a role in order to modify clinical symptoms and evolution of atherosclerosis.

Arteriosclerosis↗
PubMed1984

Apolipoprotein C-II deficiency. The role of apolipoprotein C-II in the hydrolysis of triacylglycerol-rich lipoproteins.

Kinetic studies were performed incubating lipoprotein lipase and hepatic triacylglycerol lipase from human postheparin plasma with triacylglycerol-rich lipoproteins from two patients with apolipoprotein C-II deficiency. These lipoproteins differed in their lipid and apolipoprotein composition from normal very-low-density lipoproteins and chylomicrons. The addition of isolated apolipoprotein C-II and normal or apolipoprotein C-II-deficient high-density lipoproteins caused an increase of Vmax and a decrease of the Km for lipoprotein lipase-induced hydrolysis. Hepatic triacylglycerol lipase activity was not influenced by the presence of apolipoprotein C-II in the incubation medium, but was inhibited by increasing amounts of high-density lipoproteins. Binding studies were performed in order to analyze the interactions between lipolytic enzymes, apolipoprotein C-II, and triacylglycerol-rich lipoproteins. Apolipoprotein C-II was, as expected, rapidly taken up by apolipoprotein C-II-deficient very-low-density lipoproteins and chylomicrons when they were incubated with normal high-density lipoproteins or with the purified apolipoprotein. This uptake was inhibited by the addition of increasing amounts of lipoprotein lipase in conditions in which no lipolysis could occur. Binding of lipoprotein lipase to apolipoprotein C-II-deficient very-low-density lipoproteins or chylomicrons was not affected by the addition of apolipoprotein C-II when an excess of triacylglycerol-rich lipoprotein was present. The stability of lipoprotein lipase was also studied. Apolipoprotein C-II and high-density lipoproteins were unable to prolong the half-life of the enzyme activity, while triacylglycerol-rich particles effectively stabilized lipoprotein lipase. We conclude that binding of lipoprotein lipase to the substrate surface is not affected by apolipoprotein C-II. It is more likely that the peptide catalyzes the conversion of lipoprotein lipase from a less to a more active form.

Adult↗
PubMed1984

Evaluation of HDL2 and HDL3 cholesterol by a precipitation procedure in a normal population and in different hyperlipidemic phenotypes.

Gidez et al described a double precipitation method with polyanions to separate high density lipoprotein (HDL) subfractions, using sodium heparin to precipitate very low density lipoprotein (VLDL) and low density lipoprotein (LDL) first, and dextran sulphate 15000 to precipitate HDL2 from total HDL afterwards. This method has shown a very good correlation with the data from the analytical and preparative ultracentrifuge. The aim of this work is to use this method to analyse HDL2 and HLD3 levels in a population living in our district. We studied 163 subjects considered as 'normal' on the basis of anamnestic and clinical evaluation and routine analysis and 47 subjects with familial hyperlipoproteinemia (types IIa, IIb, and IV). The results obtained confirmed both the difference in HDL and particularly HDL2 levels between the sexes which other authors had observed with reference methods, and the significant negative correlation between plasma triglycerides and HDL2 levels. This method may be applied easily, is rather cheap and, therefore, may be used more often in future.

Adult↗
PubMed1984

The plasma lipoproteins in familial chylomicronemia. Analysis by zonal ultracentrifugation.

Familial chylomicronemia is a rare genetic disorder attributable to the absence of lipoprotein lipase activity or the absence of apo-CII, i.e., the cofactor for the same enzyme. Plasma lipoproteins were analyzed by zonal ultracentrifugation under rate flotation conditions in four patients with lipoprotein lipase deficiency and two patients with apo-CII deficiency. Lipoproteins of density less than 1.006 gm/ml, and particularly lipoproteins with Sf greater than 100, were present in very high concentrations. Low levels of density greater than 1.006 gm/ml lipoproteins were observed. This fraction was composed of some different and discrete lipoprotein populations: intermediate-density lipoproteins (in three of six patients, density = 1.006 to 1.019 gm/ml); low-density lipoprotein LDL2 (in all patients, density = 1.019 to 1.045 gm/ml); low-density lipoprotein LDL3 (in all patients, density = 1.045 to 1.063 gm/ml); high-density lipoprotein HDL2 (in four of six patients); and high-density lipoproteins HDL3 (in all patients). LDL3 was never observed in normal participants by means of zonal ultracentrifugation; this subclass of low-density lipoproteins seems to correspond to LDL particles of very low Sf (2 to 5) previously identified by analytical ultracentrifugation in patients with severe hypertriglyceridemia. LDL3 was isolated by means of zonal ultracentrifugation as a single and discrete peak in all patients. Lipoproteins of density greater than 1.006 gm/ml were rich in triglycerides and poor in cholesterol in comparison with normal lipoproteins. The heterogeneity of low-density lipoproteins (particularly the appearance of LDL3), low levels of total high-density lipoproteins, and lower HDL3 flotation rate than normal are typical aspects of serum lipoproteins in these patients. No significant differences in the lipoprotein profiles of the patients with lipoprotein lipase deficiency in comparison with patients with apo-CII deficiency were found. In both groups of patients, the plasma lipoproteins profile and the altered lipoprotein composition could be related to the impaired catabolism of triglyceride-rich lipoproteins caused by the absence of lipoprotein lipase activity.

Apolipoprotein C-II↗
PubMed1983

Characterization of hyperlipidemia in two patients with analbuminemia.

The results of plasma lipid and lipoprotein analysis in two related patients, brother (R.U.) and sister (R.R.) with analbuminemia, and three first-degree relatives (parents and sister) are reported. Both patients showed a remarkable increase in cholesterol and phospholipid levels, and there was a corresponding increase in serum apo B and apo A-I. This hyperlipidemia is due to a selective increase in LDL and HDL concentrations. R.U. showed an increase in both HDL2- and HDL3-cholesterol, R.R. only in HDL3-cholesterol. VLDL concentration was reduced in R.U. and normal in R.R. The plasma lipoprotein electrophoretic pattern did not correspond to any of the phenotypes in Fredrickson's classification. Composition of the different lipoprotein fractions was normal in the patients and family members. Serum FFA level in R.R. was very low. An increase in the plasma protein fractions, particularly the transport fractions, was confirmed in both patients. The possible pathophysiology of the hypercholesterolemia in these patients is discussed. Unlike other reported cases, clinical signs of atherosclerotic complications were absent.

Adult↗
PubMed1983

Familial lipoprotein lipase and apolipoprotein C-II deficiency. Lipoprotein and apoprotein analysis, adipose tissue and hepatic lipoprotein lipase levels in seven patients and their first degree relatives.

Plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic lipase (H-TGL) were studied in 7 patients with familial hyperchylomicronemia from four different families. Their first-degree relative were also studied. The patients were heterogeneous for the genetic defect; LPL activity was absent in five patients (LPL deficiency) but normal in two. However, these two did not have apo C-II, the physiological activator of LPL (C-II deficiency). There were no significant differences in the clinical picture between patients with LPL deficiency and C-II deficiency. In both mutants, marked hypertriglyceridemia was due to an accumulation of lipoproteins of density less than 1.006 g/ml. The LDL fraction was very reduced and abnormal in composition, presenting a CH/TG ratio of 0.5. The plasma apolipoprotein B (apo B) level was low (67 +/- 5.5 mg/dl) and was transported mainly in the VLDL fraction (26 +/- 3.2 mg/dl) rather than in the LDL fraction (15 +/- 1.4 mg/dl). Very low levels of cholesterol and apolipoprotein A-I in HDL subfractions HDL2 and HDL3 were also recorded. Only 3 out of the 24 first-degree relatives of patients with LPL deficiency showed even a small increase in plasma triglycerides, but 15 had low or low to normal LPL values. H-TGL levels were normal in all subjects. The 4 first-degree relatives of C-II deficiency patients showed normal levels of plasma lipids. LPL and H-TGL, and 2 children of 1 patient showed normal distribution of apo C peptides in their VLDL. A block in chylomicron catabolism, due to the absence of LPL or apo C-II, may lead to a massive accumulation of lipoproteins with a density less than 1.006 g/ml, and a drastic reduction in the LDL and HDL fractions. Low LPL values in the first-degree relatives of LPL deficiency patients might represent a biochemical marker for healthy carriers of LPL deficiency.

Adipose Tissue↗
PubMed1983

Metabolic abnormalities in multiple symmetric lipomatosis: elevated lipoprotein lipase activity in adipose tissue with hyperalphalipoproteinemia.

Lipoprotein lipase activity in lipomatous tissue, post-heparin lipoprotein lipase activity in plasma, and the composition and concentration of serum lipoproteins were studied in 15 patients with Multiple Symmetric Lipomatosis (MSL). Extremely elevated lipoprotein lipase activity in adipose tissue was found in MSL patients. Total and hepatic post-heparin plasma lipolytic activity was normal, while a moderate but statistically significant increase of extrahepatic lipolytic activity was present. An abnormal composition of serum lipoproteins, characterized by a significant increase in high density lipoproteins, namely HDL2 subfraction, and apoprotein A-I, was demonstrated. A concomitant decrease in and abnormal composition of low density lipoproteins were found. This lipoprotein pattern is consistent with a newly recognized type of hyperalphalipoproteinemia. Significant correlations were found between serum HDL2 cholesterol values and lipoprotein lipase activity in adipose tissue (as well as between serum VLDL-triglyceride and HDL2 cholesterol values). These observations confirm the role of adipose tissue lipoprotein lipase in triglyceride-rich lipoprotein catabolism. The elevated levels of lipoprotein lipase activity in adipose tissue, in addition to a previously demonstrated decrease in adrenergic-stimulated lipid mobilization, could account for both the abnormal fat accumulation in lipomatous fat cell and for hyperalphalipoproteinemia in MSL patients. The occurrence of MSL in two brothers suggests an inherited enzymatic defect, indicating MSL as a "triglyceride storage disease in adipose tissue".

Adipose Tissue↗
PubMed1980

Relationship between triglyceride-rich lipoprotein (chylomicrons and VLDL) and HDL2 and HDL3 in the post-prandial phase in humans.

In order to evaluate the relationship between triglyceride-rich lipoproteins (chylomicrons and VLDL) and HDL during alimentary lipaemia, 12 healthy volunteers, 6 male and 6 female (aged 20--40 yrs), were studied. Cholesterol, phospholipid, triglyceride and protein were evaluated in whole serum, VLDL, LDL and HDL (successively subfractionated in HDL2 and HDL3). Blood samples were collected in a fasting state, 4.5 and 9 h after a 1500 calorie meal (20% protein, 40% carbohydrate, 40% fat). A striking increase in triglyceride-rich lipoproteins after 4.5 h was observed in both sexes, but was more pronounced in males. An increase in phospholipid and triglyceride as well as a slight reduction in cholesterol was evident in HDL after 4.5 h. At the same time both lipids and proteins were decreased in HDL3 and increased in HDL2. This phenomenon is more evident in females, who showed a significantly higher basal HDL2 level. These results suggest a possible metabolic relationship in the post-prandial phase between triglyceride-rich lipoproteins and HDL, and an inverse correlation between HDL2 and HDL3.

Adult↗
PubMed1978

Lipoprotein-X and diagnosis of cholestasis: comparison with other biochemical parameters and liver biopsy.

The presence or absence of histological signs of cholestasis (on the basis of liver specimens obtained by means of liver biopsy) was compared with total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, ornithine carbamoyltransferase, serum glutamic oxaloacetic transaminase levels and LP-X test in 157 patients suffering from different liver diseases. The LP-X test was positive in 93% of the 59 cases in whom histological evidence of cholestasis was observed and negative 95% of the 98 cases in whom histological examination was negative. LP-X concurs more frequently with the histological picture than do total bilirubin and alkaline phosphatase. These data confirm that LP-X test is more specific than the tests traditionally used to demonstrate or exclude cholestasis. An increment in gamma-GT levels was observed in 97% of the patients with a positive LP-X test. These clinical results have been discussed in the light of recent data regarding the mechanism of lipoprotein-X formation and the possible relationships between LP-X and gamma-glutamyl transpeptidase.

Adolescent↗
PubMed1978

Long-term trial with colestipol plus clofibrate in familial hypercholesterolemia.

Twenty subjects with familial hypercholesterolemia (12 Type IIa and 8 Type IIb), previously treated with Colestipol for 16 months, were subjected to therapy with Colestipol (15 g/day) + clofibrate (2 g/day) for 15 months. During the second treatment period these patients continued to follow the isocaloric hypocholesterolemic diet initiated during the original trial. In Type IIa patients, the association of these drugs enhanced the decrease in plasma cholesterol levels. The total mean decrease was -40 +/- 17 mg/dl (P less than 0.05). In Type IIb patients, on the other hand, the association of clofibrate with Colestipol induced an increase in plasma cholesterol levels. The total mean increase was +24 +/- 7 mg/dl (P less than 0.05). A markedly significant decrease in plasma triglyceride levels was observed in this group (- 107 +/- 30; P less than 0.01). These results seem to indicate that, in Type IIa, clofibrate increased the resin's hypocholesterolemic effect. In Type IIb, on the other hand, the association of these drugs did not seem to be indicated since a marked hypotriglyceridemic effect was accompanied by an increase in plasma cholesterol levels. These results are briefly discussed in the light of recent data obtained on the effects of Colestipol and clofibrate on lipoprotein metabolism.

Adult↗
PubMed1976

Formation of lipoprotein-X. Its relationship to bile compounds.

In this study we have demonstrated that in native bile, lipids are organized in the form of a lipoprotein (bile LP) carrying albumin as apoprotein. The lipid composition of bile LP is almost identical to lipoprotein-X (LP-X, the characteristic lipoprotein of cholestasis). However, it differs from LP-X inits protein/lipid ratio and immunological and electrophoretic characteristics. Bile lipoprotein can be converted into "LP-X-like" material in vitro by adding albumin or serum to native bile. The LP-X-like material formed in vitro has physicochemical and chemical characteristics similar or identical to LP-X isolated from serum. As bile lipoprotein can be converted into LP-X-like material by the addition of albumin to bile, LP-X can be converted into bile-LP-like particles by adding bile salts to a LP-X-positive serum. Furthermore, experimental connection of the common bile duct to the vena cava is followed after a few hours by the appearance of LP-X-like material in the plasma. These facts taken together strongly suggest that bile LP is a precursor lipoprotein for LP-X and that it refluxes into the plasma pool under cholestatic conditions.

Animals↗