Search PubMed⌕ Search

Biomedical subjects

R Marin

Publications and source records attributed to R Marin.

65 records · Page 4Linked to original sources
PubMed1986

Lipoprotein modifications during dietary treatment in patients with primary type V hyperlipoproteinaemia.

Type V hyperlipoproteinaemia is a disorder of lipid transport characterized by the accumulation in serum of chylomicrons and very low density lipoproteins. The purpose of the study was the analysis of serum lipids and lipoproteins by ultracentrifugation in nine patients with primary type V hyperlipoproteinaemia before and during dietary treatment. After 30 days of balanced isocaloric diet mean serum triglycerides fell from 25.4 +/- 15.0 (mean +/- SD) to 2.8 +/- 1.7 mmol l-1. At the same time the chylomicrons and the very low density lipoproteins of flotation rate higher than 100 disappeared from the serum while the remaining very low density lipoproteins maintained unaltered their normal protein-lipid composition. After 30 days the low density lipoproteins increased significantly in concentration (from 1.6 +/- 0.8 to 4.1 +/- 1.1 mmol l-1 cholesterol) and their percentage content of cholesterol and triglyceride was increased and reduced, respectively. The highest concentration of intermediate density lipoprotein cholesterol was observed after 15 days of treatment (1.2 +/- 0.6 mmol l-1. The abnormally low concentrations and the physicochemical properties of the high density lipoproteins remained unchanged throughout the study (from 0.6 +/- 0.2 to 0.8 +/- 0.2 mmol l-1 cholesterol concentration) and no high density lipoproteins two (HDL2) were observed at any time. The effects of this treatment were an increase in low density and marginal change in high density lipoproteins which are considered, respectively, a positive and a negative risk factor for atherosclerosis.

Adult↗
PubMed1986

Modifications of plasma lipoproteins after lipase activation in patients with chylomicronemia.

Lipoprotein lipase (LPL) and hepatic lipase (HL) are enzymatic activities involved in lipoprotein metabolism. The purpose of this study was to analyze the physicochemical modifications of plasma lipoproteins produced by LPL activation in two patients with apoC-II deficiency syndrome and by HL activation in two patients with LPL deficiency. LPL activation was achieved by the infusion of normal plasma containing apoC-II and HL was released by the injection of heparin. Lipoproteins were analyzed by ultracentrifugation in a zonal rotor under rate flotation conditions before and after lipase activation. The LPL activation resulted in: a reduction of plasma triglycerides; a reduction of fast-floating very low density lipoprotein (VLDL) concentration; an increase of intermediate density lipoprotein (IDL), which maintained unaltered flotation properties; an increase of low density lipoproteins (LDL) accompanied by modifications of their flotation rates and composition; no significant variations of high density lipoprotein (HDL) levels; and an increase of the HDL flotation rate. The HL activation resulted in: a slight reduction of plasma triglycerides; a reduction of the relative triglyceride content of slow-floating VLDL, IDL, LDL2, and HDL3 accompanied by an increase of phospholipid in VLDL and by an increase of cholesteryl ester in IDL; and a reduction of the HDL flotation rate. These experiments in chylomicronemic patients provide in vivo evidence that LPL and HL are responsible for plasma triglyceride hydrolysis of different lipoproteins, and that LPL is particularly involved in determining the levels and physicochemical properties of LDL. Moreover, in these patients, the LPL activation does not directly change the HDL levels, and LPL or HL does not produce a step-wise conversion of HDL3 to HDL2 (or vice versa) but rather modifies the flotation rates of all the HDL molecules present in plasma.

Adult↗
PubMed1984

Characterization with zonal ultracentrifugation of low-density lipoproteins in type V hyperlipoproteinemia.

Low-density lipoproteins (density = 1.019-1.063 g/ml) were isolated in 10 subjects with type V hyperlipoproteinemia by ultracentrifugation in a zonal rotor under rate flotation conditions. Plasma LDL concentrations in these patients were extremely reduced, as well as being heterogeneous, and two different subclasses consisting of LDL2 (density = 1.019-1.045 g/ml) and LDL3 (density = 1.045-1.063 g/ml) were observed. LDL2 and LDL3 have similar electrophoretic mobilities in beta position in agarose gel, and their diameters, calculated from gel filtration studies, were inversely proportional to their densities. LDL2 and LDL3 have a mean hydrated density of 1.034 and 1.054 g/ml, respectively. In comparison with normal LDL2, the LDL2 and LDL3 of hypertriglyceridemic subjects are particularly rich in triacylglycerols and poor in cholesteryl esters and free cholesterol, while they have an increasing amount of proteins. The protein moiety is composed almost exclusively of apolipoprotein B-100 in IDL, LDL2 and LDL3 ; in addition, IDL also contain apolipoprotein C peptides. This characterization of LDL heterogeneity in type V hyperlipoproteinemia should be considered in interpreting kinetic data in human normal and pathological lipid metabolism and in evaluating the atherogenic risk of hypertriglyceridemia.

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↗
PubMed1984

Mediastino-abdominal lipomatosis: deep accumulation of fat mimicking a respiratory disease and ascites. Clinical aspects and metabolic studies in vitro.

We report on clinical and metabolic studies of a newly delineated lipomatosis, characterised by an abnormal mediastinal and abdominal accumulation of fat, without obesity. The clinical features, which occurred in all the patients studied, are: Exertional dyspnoea due to a space-occupying mediastinal accumulation of fat, without evidence of cardiac or pulmonary disease. A pseudo-ascitic abdominal enlargement, due to intra- and retroperitoneal accumulation of fatty tissue. Insulin-independent diabetes mellitus. Type IV hyperlipidaemia and elevated levels of plasma uric acid were observed in four patients. Intra-abdominal lipomatous tissue, obtained during laparoscopy from four patients, demonstrated a reduced lipolytic response to beta-adrenergic stimulation. Thus, fat deposition in the abdominal and mediastinal areas could be causally related to defective lipid mobilization in lipomatocytes. Lipoprotein lipase activity in abdominal adipose tissue were normal in two patients (10.0 and 10.6 nmol/g/min) and markedly elevated in another two patients (37.3 and 49.9 nmol/g/min), as compared with controls (12.7 +/- 2.1 nmol/g/min). When expressed on per cell basis, LPL activity in lipomatous tissue was significantly higher than in control tissue (3.21 +/- 1.1 nmol/10(5) cell/min vs 0.92 +/- 0.16 nmol/10(5) cell/min). Lipoprotein fractionation did not demonstrate consistent modification of the serum lipoprotein pattern. HDL and HDL2 cholesterol values were reduced, even in patients with elevated LPL activity in adipose tissue.

Abdominal Neoplasms↗
PubMedDate not supplied

Randomised trial of nadolol alone or with isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis. Gruppo-Triveneto per L'ipertensione portale (GTIP)

BACKGROUND: The risk of having a first cirrhosis-associated variceal bleed is lowered by about 50% by beta-blockers. Use of beta-blockers is currently recommended for patients with cirrhosis and oesophageal varices that are at risk of bleeding. We aimed to test the effectiveness of isosorbide mononitrate as an adjunct to the beta-blocker nadolol in the prophylaxis of first variceal bleeding in these patients. METHODS: We did a randomised multicentre study to compare the non-selective beta-blocker, nadolol, with nadolol plus isosorbide mononitrate in 146 relatively well (Child-Pugh score < or = 11) patients who had oesophageal varices at risk of bleeding. Patients on nadolol alone received a single oral 40 mg daily dose. Every second day the dose was titrated to achieve 20-25% decrease in resting heart rate (maximum dose 160 mg daily). Patients receiving both drugs received nadolol as above then isosorbide mononitrate was added starting with 10 mg orally twice daily, which was increased to 20 mg unless hypotension or severe headache occurred. The main endpoint was the occurrence of variceal bleeding of any severity. Patients were followed up for up to 40 months. FINDINGS: During the study period 11 of 74 patients from the nadolol alone group and four of 72 from the nadolol plus isosorbide mononitrate group had variceal bleeding (log-rank test p = 0.03). Cumulative risk of variceal bleeding was 18% in the nadolol group and 7.5% in the combined treatment group (95% CI for difference 1-25%). Two patients in each group had a non-variceal bleed related to portal hypertension. 14 patients from the nadolol only group and eight from the combined treatment group died during the study period (log-rank test p = 0.09). Four and eight patients, respectively, had to discontinue one of the drugs because of side-effects. INTERPRETATION: Nadolol plus isosorbide mononitrate is significantly more effective than nadolol alone in the primary prophylaxis of variceal bleeding in relatively well patients with cirrhosis, and has few side-effects.

Administration, Oral↗
PubMedDate not supplied

A case of idiopathic fecal incontinence. Evaluation and management.

Idiopathic fecal incontinence is a clinical entity described mostly in the colorectal surgical literature and seldom encountered by the physiatrist. Evidence exists suggesting neuropathic injury to the external anal sphincter. Several reports have linked this syndrome to the descending perineum syndrome. A final answer to this diagnostic puzzle is yet to be found. This article presents a case of probable "idiopathic" fecal incontinence presenting during an evaluation for low back pain. Full evaluation yielded a denervating lesion of unknown etiology to the pudendal nerve. The patient was managed with a bowel program without success. Because physiatrists often find themselves managing cases of neurogenic bowel or bladder, it is important for the physiatrist to have a thorough understanding of idiopathic fecal incontinence. A discussion of the differential diagnosis and management of fecal incontinence is included.

Adult↗