[Importance of the determination of Lp(a) in the prevention of coronary risk].
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Biomedical subjects
Publications and source records attributed to S Masdeu.
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Serum concentration of apoprotein A-I (apo A-I) and cholesterol content in high density lipoprotein (HDL) subfractions have been studied in 19 men and 11 women at the end stage of chronic renal failure undergoing hemodialysis. HDL2 cholesterol concentration was decreased in males [0.33 +/- 0.12 (mean +/- SD) mmol/l, controls 0.45 +/- 0.09 mmol/l; p less than 0.001]; in females HDL2 cholesterol was also decreased although without statistical significance (0.45 +/- 0.15 vs. 0.55 +/- 0.10 mmol/l). HDL3 cholesterol was significantly decreased in men (0.65 +/- 0.11 vs. 0.77 +/- 0.04 mmol/l; p less than 0.001) and also in women (0.61 +/- 0.12 vs. 0.82 +/- 0.07 mmol/l; p less than 0.005). However, serum concentration of apo A-I was within the normal range (1.13 +/- 0.16 milligram in males and 1.25 +/- 0.17 milligram in females; controls 1.24 +/- 0.17 and 1.35 +/- 0.19 milligram, respectively). The raised apo A-I/HDL2 cholesterol ratio in both men and women suggests the existence of qualitative changes in HDL subfractions as has been proposed in previous studies measuring total apo A and total HDL cholesterol in patients with chronic renal failure receiving hemodialysis. These abnormalities in the relative composition of HDL subfractions could play an important role as a vascular risk factor in patients with chronic renal failure undergoing hemodialysis.
Serum concentration of apoprotein A, high density lipoprotein (HDL)-cholesterol and HDL-phospholipids has been studied in thirteen consecutive episodes of diabetic ketoacidosis. In three patients with type I diabetes mellitus HDL2 and HDL3 subfractions were also measured. Patients with type I diabetes showed greatly decreased HDL-cholesterol concentration on admission which increased into the normal range after insulin treatment, while HDL-phospholipids decreased during treatment and apoprotein A remained almost unmodified. In three patients with type I diabetes a virtual absence of HDL2-cholesterol subfraction was observed, which rose to normal values during recovery. Conversely, in type II diabetes mellitus HDL-cholesterol was slightly reduced on admission, and tended to decrease during recovery. These findings imply the existence of abnormalities in the qualitative composition of HDL, and indicate that HDL-cholesterol can fluctuate much more rapidly than previously thought.
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Serum concentrations of high density lipoproteins (HDL)-cholesterol, apoprotein A and apoprotein B has been studied in 13 patients with chronic renal failure treated with hemodialysis and in 12 patients with functioning renal graft. 5 patients on hemodialysis and 6 with a renal graft had hypertriglyceridemia. In the hemodialyzed patients, the increase in triglycerides was associated to a decreased concentration of serum apoprotein B. HDL-cholesterol was substantially reduced in the hemodialyzed patients without this being associated with a drop in serum apoprotein A concentration, thus suggesting that there are changes in the qualitative composition of the HDL. In renal graft recipients, the HDL-cholesterol and the apoprotein A concentration were increased. It is suggested that the risk of developing accelerated atheromatosis in patients carrying a renal graft cannot be related to changes in HDL. In patients undergoing hemodialysis, the development of atheromatosis would be related to decreased concentration and also qualitative changes in the HDL together with the increase in the VLDL and LDL.
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Concentrations of apoprotein A in whole serum, and cholesterol and phospholipids concentrations in the high-density lipoprotein fraction of serum were measured after the precipitation of low-density and very-low-density lipoproteins with sodium phosphotungstate-Mg2+ in 23 patients with liver cirrhosis, 19 patients with extrahepatic biliary obstruction, and 20 healthy control subjects. Patients with cirrhosis and cholestasis showed approximately one-half as much cholesterol and apoprotein A in the nonprecipitable high-density lipoprotein fraction as normal subjects did. High-density lipoprotein phospholipids concentrations in those patients were normal or slightly increased, however, which is about double what one would expect from the apoprotein A and cholesterol content.
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The serum levels of cholesterol bound to high density lipoproteins (HDL-C) were determined by the heparin-manganese chloride precipitation method in 306 subjects, 182 male with ages ranging from 11 to 81 years, and 124 female with ages ranging from 7 to 78 years. Twenty six subjects belonged to a lacto-vegetarian community, while the remaining 280 were healthy volunteers, factory workmen sampled during a regular check-up, and either outpatients or inpatients being evaluated for minor illnesses or minor surgery. None of the subjects had arteriosclerosis or a metabolic disease and, with the exception of the lacto-vegetarians, they were all consuming a normal diet. HDL-C concentrations varied very little among the different age groups. Females had HDL-C values slightly superior to those of males. No significant differences were found between smokers and non-smokers, alcohol drinkers and non-drinkers, and regularly exercising and sedentary people. HDL-C concentrations were independent of total cholesterol and triglyceride levels. Females under oral contraceptive treatment had lower HDL-C levels than control females, but the differences were not statistically significant. Compared with age and sex-matched controls, the lactovegetarians showed similar HDL-C concentrations.
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Serum high-density lipoprotein cholesterol (HDL-C) has been determined in 85 patients with peripheral vascular disease (PVD) and in 72 healthy control subjects. HDL-C levels were significantly decreased in patients with PVD. Considering other vascular risk factors as diabetes mellitus, smoking and hypertension, there were no differences in HDL-C levels. Twenty-three patients received heparin as treatment, this subgroup showed a HDL-C levels higher than patients who were not under heparin therapy. The possible clinical implications of these facts are discussed.
It is generally accepted that the bile acids are responsible for pathologies as a result of deficiency or by toxic action. Quantitative deficiency is difficult to evaluate but the normal pool of bile acids is generally considered to be between 2 and4 grams. Daily loss and replacement by synthesis is thought to be between 500 and 700 mg. There is experimental evidence to demonstrate the toxic action of certain bile acids on metabolic structures and processes. There is no doubt that alterations in the metabolism of bile acids give rise to certain pathologic aspects in some diseases of the gastrointestinal tract or the hepatobiliary system. There are other conditions, on the other hand, in which the study of these acids may reveal significant physiopathologic implications. The first group includes terminal ileopathy, blind loop syndrome, gastric ulcer, gastritis, cholestasis, cirrhosis of the liver, and cholelithiasis. In the second group are such diverse conditions as acute pancreatitis, cancer of the colon, endocrine disturbances, some hyperlipidemias, and others. Much of the present day understanding of the physiopathology of the bile acids will probably have to be revised in the nex few years, in view of the rapid advances being made in this field.