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Biomedical subjects

M R Baiocchi

Publications and source records attributed to M R Baiocchi.

At least 19 recordsLinked to original sources
PubMed2001

Relationship of early carotid artery disease with lipoprotein (a), apolipoprotein B, and fibrinogen in asymptomatic essential hypertensive patients and normotensive subjects.

BACKGROUND: We investigated the relationships between plasma lipids and lipoprotein fractions and carotid artery lesions (CAL) in 177 cerebro-vascularly asymptomatic subjects, of whom 107 were primary hypertensive patients and 70 normotensive controls. METHODS: The prevalence and severity of CAL, as assessed by calculating a score of severity (score of CAL) and the maximal stenosis of both sides, as well as the intimal-medial thickness (IMT) were evaluated with a high-resolution echo-Doppler technique. We measured total serum cholesterol, triglycerides, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, lipoprotein (a) [Lp(a)], Apo (apolipoprotein)AI, ApoAII, ApoB, and fibrinogen. RESULTS: Both the prevalence (59.4% vs 26.2%) and severity of sex- and age-adjusted and unadjusted CAL and IMT were significantly higher in hypertensive patients than in controls. Regression analysis showed different predictors of IMT and maximal stenosis. The variables that remained in the model were age, mean blood pressure (BP), and smoking for IMT; pulse pressure, known duration of hypertension (HT), fibrinogen, and ApoB for the score of CAL; and the last four variables along with age and mean BP for maximal stenosis. Furthermore, we identified a link between the atherogenic lipoprotein fractions Lp(a) and ApoB, fibrinogen and early carotid artery atherosclerotic changes. CONCLUSIONS: The different correlates of IMT, CAL, and maximal degree of stenosis suggest that they reflect different events occurring in the arterial wall in response to aging, HT, and other risk factors, rather than simply different stages of the same atherosclerotic process.

Adult↗
PubMed1996

Carotid artery lesions in patients with nondiabetic chronic renal failure.

Atherosclerotic complications are the leading cause of death in chronic renal failure (CRF) patients. Therefore, we wished to investigate the prevalence of carotid artery lesions (CALs) in these subjects. Two groups were evaluated by high-resolution echo Doppler: group 1 included 103 patients (68 males and 35 females) affected by nonnephrotic CRF and group 2 included 100 control subjects (60 males and 40 females). The prevalence of hypertension was 84% in both groups. The exclusion criteria included diabetes mellitus and symptoms of cerebrovascular disease. In the two groups we evaluated clinical history, physical examination, total cholesterol, triglycerides, fibrinogen, blood cell counts, blood urea nitrogen, creatinine, 24-hour proteinuria, and urine analysis. In group 1 patients the following lipid profile parameters were also evaluated: low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, lipoprotein(a), ApoAI, ApoAII, and ApoB. Group 1 had higher triglycerides and fibrinogen than group 2. A lower body mass index was found in group 1 than in group 2. The prevalence of CALs was significantly higher in the CRF patients than in the control subjects (62% v 47%; P = 0.04). The difference between the two groups was more striking among normotensive patients (62% v 19%; P = 0.03). All CRF patients affected by peripheral arterial disease and 86% of those having coronary artery disease had associated CALs. In CRF patients the severity of CALs was positively correlated to age, white blood cell count, triglycerides, and fibrinogen. Nondiabetic CRF patients have a higher prevalence of carotid artery lesions than control subjects. Several factors besides hypertension, including lipids, blood coagulation, and leukocytes, could contribute to the accelerated atherosclerosis of CRF patients.

Adult↗
PubMed1991

Specialized physical training programs: effects on serum lipoprotein cholesterol, apoproteins A-I and B and lipolytic enzyme activities.

To determine the effects of different types of physical training on lipid metabolism, serum lipids, lipoprotein cholesterol, apoproteins A-I and B, hepatic (HTGL), extrahepatic (LPL) and total (PHLA) post-heparin lipoprotein lipase activities were studied in elite athletes engaged in aerobic ("B", no. 13), anaerobic ("C", no. 17) and mixed ("D", no. 9) training programs and in a group of sedentary controls ("A", no. 15). In the aerobic and mixed groups serum triglycerides were significantly lower compared to sedentary controls while total serum cholesterol and LDL cholesterol, as well as serum apoprotein B levels were only slightly lower. HDL cholesterol and HDL2 cholesterol were slightly higher while serum cholesterol/HDL cholesterol (2.89 +/- 0.37 vs 3.6 +/- 0.47, p less than 0.01) and LDL cholesterol/HDL cholesterol (1.69 +/- 0.38 vs 2.23 +/- 0.43, p less than 0.05) ratios were significantly lower only in aerobic athletes compared to the control group. PHLA and LPL activities were slightly higher in the aerobic group than in controls, while PHLA and HTGL were significantly lower in aerobic and mixed athletes. No significant correlations were found between HDL cholesterol and energy expenditure during training, indexes of adipose mass or lipolytic enzyme activities. The results of this cross-sectional study seem to indicate that specialized training programs have a different effect on lipoprotein pattern and lipolytic enzyme activities, and only aerobic exercise has a potentially antiatherogenic effect.

Adult↗
PubMed1990

Serum lipids, lipoprotein analysis and apoprotein A-I, A-II and B levels in Friedreich's ataxia.

Serum lipid, lipoprotein and apoprotein parameters were evaluated in 15 patients (7 males and 8 females) with Friedreich's ataxia. Serum lipid levels in patients showed no significant differences compared to controls. Small reduction in serum phospholipid and in total HDL and HDL3 cholesterol levels were observed, and the female patients presented a slight reduced total cholesterol level; among the serum apoproteins, apo B was reduced only in the males. The most interesting findings concerned the lipoproteins, since both lipid and protein masses of the VLDL, LDL and HDL2 fractions were reduced. In reference to lipoprotein composition, however, HDL2 was the most modified fraction, showing an important protein reduction. From this point of view, this lipoprotein seems the most responsible for the changes observed in our patients. The meaning of this modified lipoprotein pattern in the pathophysiology of Friedreich's ataxia is not clear.

Adolescent↗
PubMed1988

Lipoprotein pattern and plasma lipoprotein lipase activities in patients with primary biliary cirrhosis. Relationship with increase of HDL2 fraction in Lp-X-positive and Lp-X-negative subjects.

Plasma lipids, apoprotein A-I and B in serum and in lipoprotein fractions (VLDL + LDL, HDL2, and HDL3) obtained by preparative ultracentrifugation, as well as postheparin lipoprotein lipase activity (H-TGL and LPL) were evaluated in 17 subjects with primary biliary cirrhosis (stage II and III) subdivided into two groups according to the presence or absence of lipoprotein X (Lp-X). A reduction in total lipoprotein lipase activity was observed in both patient groups, compared to controls (P less than 0.01); the hepatic lipoprotein lipase was significantly reduced (P less than 0.01) only in the Lp-X-positive group. The lipid (477.8 +/- 154.3 vs 239.6 +/- 51.1; P less than 0.01) and protein (147.4 +/- 37.1 vs 83.3 +/- 19.7; P less than 0.01) masses in the VLDL + LDL fraction of the Lp-X-positive group were increased compared to controls. In the same group, the HDL2 fraction also showed an increase in lipid (186.6 +/- 80.0 vs 77.9 +/- 21.6; P less than 0.01) and protein (133.9 +/- 60.0 vs 67.9 +/- 16.5; P less than 0.01) masses; in addition, the HDL2 percent lipid composition was different in the two patient groups, showing a decrease in esterified cholesterol (20.4 +/- 3.6 vs 25.7 +/- 2.2; P less than 0.01) and an increase in phospholipids (59.2 +/- 2.9 vs 54.8 +/- 2.6; p less than 0.01) in the Lp-X-positive group.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins B↗
PubMed1987

Analbuminaemia: a natural model of metabolic compensatory systems.

Important clinical signs are usually not present in analbuminaemia, a congenital condition inherited as an autosomal recessive trait, but several biochemical alterations in proteins, cholesterol, phospholipids and plasma beta lipoproteins have been observed. We studied two sibs, R.U. and R.R., with this disease and observed a striking increase in the variables mentioned above as well as a high LDL fraction with concomitant increase in apo B; increases in HDL3 and apo A-I and A-II levels were also observed. The lipoproteins, however, were not altered in morphology but showed a slight increase in lipid/protein ratio. Post-heparin lipolytic activity was normal in the male patient and reduced in the female while LCAT enzyme activity instead was increased in both. Fatty acids bound to phospholipids and serum cholesterol were mostly monounsaturated. Free fatty acid concentration was normal and they appeared mostly bound to the LDL and HDL3 fractions, which are increased in this disease and appear to replace albumin in one of its main carrier functions.

Apoproteins↗
PubMed1986

Effect of probucol treatment on lipoprotein cholesterol and drug levels in blood and lipoproteins in familial hypercholesterolemia.

Twelve patients with mild and 3 with severe hypercholesterolemia were stabilized with an isocaloric diet containing less than 300 mg cholesterol daily with a P/S ratio of 1.8, and placebo period of 4 weeks. They were administered 1000 mg probucol daily for 12 weeks, followed by placebo for 6 weeks. In patients with mild disease, a significant cholesterol reduction was achieved in serum, LDL, and HDL (maximum decrease, 17%, 13%, and 31%, respectively). While HDL3 cholesterol was reduced significantly throughout the period (P less than 0.001), HDL2 cholesterol showed a significant decrease only at the 4th week of treatment (P less than 0.001), and returned to basal levels at the 8th and 12th treatment weeks. Serum apo B levels decreased only slightly, but the HDL-apo A-I fall was significant with a reduction in the HDL-CH/HDL-apo A-I ratio throughout the treatment period. In 3 patients with severe disease, cholesterol decrease in serum and in VLDL, LDL and HDL fractions varied, but on the whole was lower than in patients with mild disease. A decrease in VLDL-CH and HDL-CH was present in all 3, but LDL-CH levels were only slightly lowered in 2 patients, and unchanged in the third. Serum probucol levels fell 66% from the 4th to the 12th treatment week, and in parallel, the percentage of lipoprotein-bound drug increased about 2-fold. It is suggested that these changes in pharmacokinetics as well as the cholesterol-lowering effect of the drug may be due to a change in lipoprotein composition or structure.

Adult↗
PubMed1986

Apolipoprotein C-II deficiency syndrome. Clinical features, lipoprotein characterization, lipase activity, and correction of hypertriglyceridemia after apolipoprotein C-II administration in two affected patients.

Two patients (brother and sister, 41 and 39 yr of age, respectively) have been shown to have marked elevation of plasma triglycerides and chylomicrons, decreased low density lipoproteins (LDL) and high density lipoproteins (HDL), a type I lipoprotein phenotype, and a deficiency of plasma apolipoprotein C-II (apo C-II). The male patient had a history of recurrent bouts of abdominal pain often accompanied by eruptive xanthomas. The female subject, identified by family screening, was asymptomatic. Hepatosplenomegaly was present in both subjects. Analytical and zonal ultracentrifugation revealed a marked increase in triglyceride-rich lipoproteins including chylomicrons and very low density lipoproteins, a reduction in LDL, and the presence of virtually only the HDL3 subfraction. LDL were heterogeneous with the major subfraction of a higher hydrated density than that observed in plasma lipoproteins of normal subjects. Apo C-II levels, quantitated by radioimmunoassay, were 0.13 mg/dl and 0.12 mg/dl, in the male and female proband, respectively. A variant of apo C-II (apo C-IIPadova) with lower apparent molecular weight and more acidic isoelectric point was identified in both probands by two-dimensional gel electrophoresis. The marked hypertriglyceridemia and elevation of triglyceride-rich lipoproteins were corrected by the infusion of normal plasma or the injection of a biologically active synthesized 44-79 amino acid residue peptide fragment of apo C-II. The reduction in plasma triglycerides after the injection of the synthetic apo C-II peptide persisted for 13-20 d. These results definitively established that the dyslipoproteinemia in this syndrome is due to a deficiency of normal apo C-II. A possible therapeutic role for replacement therapy of apo C-II by synthetic or recombinant apo C-II in those patients with severe hypertriglyceridemia and recurrent pancreatitis may be possible in the future.

Adult↗
PubMed1985

Selective determination of cholesterol in high density lipoprotein subfractions (HDL2 and HDL3) in patients with cerebral and peripheral arteriosclerosis.

Cholesterol levels in high density lipoprotein subfractions (HDL2 and HDL3) were evaluated in 69 patients (55 males, average age +/- SD 58.3 +/- 8.8, and 14 females, average age +/- SD 63.1 +/- 10.3) with extra-coronary arteriosclerosis (lower limbs, supraaortic trunks and both sites), and in 79 healthy age-matched control subjects. HDL cholesterol was significantly reduced in male and female patients. The HDL cholesterol decrease was due to a fall in both HDL2 and HDL3 cholesterols; nonetheless, an analysis of the HDL2-cholesterol/HDL3-cholesterol ratio disclosed that HDL2 cholesterol was the most reduced. Slightly higher plasma cholesterol and triglyceride levels were found in the patients as well as a higher plasma cholesterol/HDL-cholesterol ratio. On the contrary, the HDL2-cholesterol/HDL3-cholesterol ratio was significantly reduced in the patients. These preliminary findings suggest that, as in ischemic heart disease, the HDL cholesterol reduction in cerebral and peripheral arteriosclerosis is also mainly due to a reduction in the HDL2 subfraction. These results also lend further support to the proposal that determination of the HDL subfractions is useful for a better assessment of the risk profile for arteriosclerosis.

Aged↗
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

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↗
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↗