PubMed Health⌕ Search

Biomedical subjects

J Pedro-Botet

Publications and source records attributed to J Pedro-Botet.

At least 73 records · Page 4Linked to original sources
PubMed1993

Serum lipoprotein(a) concentration in patients with chronic renal failure receiving haemodialysis: influence of apolipoprotein (a) genetic polymorphism.

Serum lipoprotein(a) (Lp(a)) was measured in 101 men with end-stage chronic renal failure (CRF) receiving haemodialysis and in 101 age-matched male controls. Apolipoprotein(a) genetic polymorphism was determined by immunoblotting in 100 patients and in 92 controls. Patients with CRF on haemodialysis had significantly greater serum Lp(a) than controls. Apolipoprotein(a) phenotype frequencies in patients with CRF did not differ from those of the control group. Both patients and controls with phenotype S2 had greater serum Lp(a) than those with phenotype S4. It should be emphasized that serum Lp(a) was significantly greater in patients on haemodialysis than controls, both for those with phenotype S2 and those with S4. Increased serum Lp(a) together with other lipoprotein abnormalities in patients with CRF on haemodialysis imply an increased cardiovascular risk. Genetic polymorphism clearly influences serum Lp(a) both in controls and patients. In the latter group CRF itself, dialysis, or both, also play a role in increasing Lp(a).

Adult↗
PubMed1992

[Coronary heart disease and lipoprotein (a): relationship with other lipid cardiovascular risk factors].

BACKGROUND: Lipoprotein (Lp) (a) is considered a risk factor for early coronary heart disease (CHD), and a discriminant cutoff of Lp(a) concentration has been suggested. METHODS: Serum Lp(a) concentrations have been determined by enzymoimmunoassay in 66 men with CHD and in 100 healthy control men. Serum cholesterol, serum triglycerides, high density lipoprotein (HDL)-cholesterol, and apoprotein (apo) A-I were also determined. RESULTS: Serum Lp(a) concentration was 21.7 +/- 16.9 mg/dl (mean +/- SD) in patients and 12.5 +/- 12.5 mg/dl in controls (p less than 0.001). Serum cholesterol was 5.63 +/- 1.22 mmol/l and 5.29 +/- 1.00 mmol/l (p less than 0.05) respectively; serum triglycerides were 1.99 +/- 1.23 mmol/l and 1.29 +/- 0.61 mmol/l (p less than 0.001) respectively; HDL-cholesterol was 0.97 +/- 0.27 mmol/l and 1.07 +/- 0.30 mmol/l (p less than 0.05) respectively; and apo A-I was 94 +/- 15 mg/dl and 144 +/- 41 mg/dl (p less than 0.001) respectively. Lp(a) concentrations were not correlated with other well-recognized cardiovascular risk lipidic factors, nor influenced by age either body mass index. Using 20 mg/dl as discriminant Lp(a) concentration between patients and controls, a ratio 2:1 in patients with respect to controls has been observed and exceeded some more when the threshold level was put on 30 mg/dl. A subset of normocholesterolemic and normotriglyceridemic patients (n = 17) and controls (n = 49) had serum Lp(a) concentration of 22.7 +/- 16.3 mg/dl and 9.1 +/- 8.2 mg/dl (p less than 0.001) respectively. CONCLUSIONS: Increased concentration of Lp(a) constitutes an independent risk factor for CHD. On the other hand, Lp(a) concentrations of 20 mg/dl or 30 mg/dl as risk threshold levels are well-defined.

Adult↗
PubMed1992

Lipoprotein abnormalities in hyperlipidemic and normolipidemic men on hemodialysis with chronic renal failure.

Lipids, lipoproteins, apolipoproteins (apo) and apo E polymorphism were determined in 101 men with chronic renal failure (CRF) were were on hemodialysis and 101 healthy controls matched for age and sex. Patients with CRF on hemodialysis had significantly higher levels of serum triglycerides, very-low-density lipoprotein (VLDL) cholesterol, intermediate-density lipoproteins (IDL), and lower levels of low- and high-density lipoproteins (LDL and HDL, respectively) than controls. Regarding apolipoproteins, serum apo B concentrations were decreased. Apo C-III concentrations in sera and in VLDL and HDL fractions were significantly increased in 35 hemodialysis patients compared with 32 controls. Seventy-eight of the 101 CRF patients had normal serum cholesterol and triglycerides (less than 5.2 mmol/liter and less than 2.3 mmol/liter, respectively). However, this subgroup also showed a significant increase in VLDL-triglycerides and serum apo E concentration in addition to changes observed in the group as a whole. Apo E polymorphism in our study population did not differ from that reported for other European populations. According to the different apo E phenotypes, lipids and lipoprotein composition showed no significant differences in controls or patients. We conclude that accumulation of triglyceride-rich lipoproteins in patients with CRF on hemodialysis may thus be at least in part related to the enrichment of apo C-III in VLDL and HDL fractions. Lipoprotein profile in hemodialysis patients, including those with normal serum cholesterol and triglyceride levels, is consistent with high cardiovascular risk.

Adult↗
PubMed1992

Effect of bezafibrate on lipoprotein (a) and triglyceride-rich lipoproteins, including intermediate-density lipoproteins, in patients with chronic renal failure receiving haemodialysis.

The effect of bezafibrate, at doses of 200 mg three times weekly throughout a period of 10 weeks, on lipoprotein (a) and triglyceride-rich lipoproteins including intermediate-density lipoproteins (IDL) has been studied in 12 patients with chronic renal failure receiving haemodialysis. No side-effects were observed, and serum creatine phosphate kinase values remained within normal limits throughout the duration of the study. Serum cholesterol, triglycerides and apoprotein (apo) B significantly decreased after bezafibrate, whereas apo A-I increased significantly. Serum lipoprotein (a) decreased after bezafibrate, although differences reached no statistical significance. The very-low-density lipoproteins (VLDL) cholesterol and the VLDL triglycerides decreased from 0.93 +/- 0.45 mmol/l (Mean +/- SD) to 0.54 +/- 0.27 mmol/l (P less than 0.05) and from 1.50 +/- 0.58 mmol/l to 0.91 +/- 0.35 mmol/l (P less than 0.01) respectively. The IDL cholesterol and IDL triglycerides decreased from 0.44 +/- 0.35 mmol/l to 0.20 +/- 0.18 mmol/l (P = NS) and from 0.46 +/- 0.35 mmol/l to 0.17 +/- 0.12 mmol/l (P less than 0.05) respectively. These data, with a substantial improvement of the lipoprotein profile in patients with chronic renal failure on haemodialysis after treatment with bezafibrate, suggest a decrease in the coronary heart disease risk.

Adult↗
PubMed1992

Pulmonary tuberculosis in HIV-infected patients with normal chest radiographs.

SUBJECTS: Three HIV-infected patients with active pulmonary non-disseminated tuberculosis and normal chest radiograph at clinical presentation and during follow-up are reported. Patients had cough and fever but no other specific symptoms. Löwenstein cultures of specimens from bronchoalveolar lavage in two cases and induced sputum in one yielded Mycobacterium tuberculosis. CONCLUSIONS: The diagnosis of tuberculosis in HIV-infected patients depends greatly on clinical suspicion by the physician, because of its atypical presentation. Failure to perform appropriate diagnostic tests in HIV-infected patients who present with suspected pulmonary disease will result in underdiagnosis and undertreatment of tuberculosis.

Adult↗
PubMed1992

Lipoprotein profile in men with peripheral vascular disease. Role of intermediate density lipoproteins and apoprotein E phenotypes.

BACKGROUND: The role of lipoprotein disturbances in the development of peripheral vascular disease (PVD) has not been sufficiently clarified. METHODS AND RESULTS: The relations among concentrations of intermediate density lipoproteins (IDL), apoprotein (apo) B, apo E, and other lipoproteins were studied in 102 men with PVD and 100 healthy men who formed the control group. Patients with PVD had significantly higher levels of serum triglycerides, very low density lipoprotein (VLDL) cholesterol, VLDL triglycerides, VLDL proteins, IDL cholesterol, and IDL triglycerides and lower levels of high density lipoproteins (HDL) than controls. Serum cholesterol and triglycerides were normal in 30 patients (cholesterol, less than 5.2 mmol/l; triglycerides, less than 2.3 mmol/l), who had significant increases in IDL triglycerides and significant decreases in HDL cholesterol compared with the 47 controls, who had normal cholesterol and triglyceride levels. Patients with more severe distal involvement showed higher cholesterol and triglycerides carried by IDL and a greater reduction in HDL cholesterol. Smoking patients with PVD showed increased VLDL cholesterol and VLDL triglycerides and lower HDL concentrations. Apo E polymorphism in our study population does not differ from that reported for other European populations. Alleles epsilon 2 and epsilon 4 had a major impact on serum triglycerides and VLDL lipids in our patients with PVD. CONCLUSIONS: Lipoprotein disturbances are a major risk factor for PVD. IDL abnormalities play an important role in the development and severity of PVD and should also be considered a vascular risk factor in normocholesterolemic and normotriglyceridemic patients.

Adult↗
PubMed1992

Lipoprotein and apolipoprotein profile in men with ischemic stroke. Role of lipoprotein(a), triglyceride-rich lipoproteins, and apolipoprotein E polymorphism.

BACKGROUND AND PURPOSE: The role of lipoprotein abnormalities in the development of ischemic cerebrovascular disease has not been sufficiently clarified. The aim of this study was to identify the lipoprotein profile in ischemic cerebrovascular disease and the possible role of apolipoprotein E polymorphism. METHODS: The relation between the concentrations of lipoprotein(a), intermediate density lipoproteins, apolipoprotein A-I, apolipoprotein B, apolipoprotein E, and other lipoproteins was studied in 100 men with ischemic cerebrovascular disease (48 atherothrombotic, 28 lacunar, and 24 of unknown type) and in 100 healthy age-matched men as a control group. RESULTS: Patients with ischemic cerebrovascular disease had significantly higher levels of lipoprotein(a), lipids carried by intermediate density lipoproteins, and low density lipoprotein cholesterol and lower levels of high density lipoproteins than control subjects. Patients with atherothrombotic infarction had higher total serum cholesterol and low density lipoprotein cholesterol concentrations than patients with lacunar infarction. To assess lipoprotein abnormalities in normolipidemic subjects, a subgroup of 38 patients with ischemic cerebrovascular disease and 53 control subjects, both with serum cholesterol levels < 5.2 mmol/l (200 mg/dl) and triglycerides < 2.3 mmol/l (200 mg/dl), was analyzed. Serum lipoprotein(a), lipids carried by very low density lipoproteins and intermediate density lipoproteins, and low density lipoprotein triglycerides were significantly higher in normolipidemic patients compared with normolipidemic control subjects, whereas high density lipoprotein cholesterol levels were lower. Apolipoprotein E polymorphism in our ischemic cerebrovascular patients differed from that of the control group, with the epsilon 4 allele being more prevalent. CONCLUSIONS: Increased serum lipoprotein(a) levels and intermediate density lipoprotein abnormalities together with decreased high density lipoprotein levels are major risk factors for ischemic cerebrovascular disease, even in normocholesterolemic and normotriglyceridemic subjects. Finally, the epsilon 4 allele could probably be a predisposing genetic marker for ischemic cerebrovascular disease.

Adult↗
PubMed1991

[Changes in high density lipoproteins in peripheral vascular disease].

BACKGROUND: It is well known that lipid and lipoprotein disturbances play an important role in the development of atherosclerosis. However, the changes in the high density lipoprotein (HDL) composition in patients with peripheral vascular disease (PVD) and its relation to the severity of ischemia of the lower limbs need to be clarified. METHODS: HDL abnormalities have been studied in 102 men with PVD and in 100 age-sex-matched controls. History of smoking was recorded in 88 patients, but only 58 were smokers at the time of the study; 35 of controls were smokers. RESULTS: Serum triglycerides were 1.66 +/- 0.85 mmol/L (mean +/- SD) in patients and 1.29 +/- 0.61 mmol/L in controls (p less than 0.001). HDL-cholesterol was 0.97 +/- 0.27 mmol/L and 1.08 +/- 0.28 mmol/L (p less than 0.01) respectively; HDL-proteins were 1.16 +/- 0.21 g/L and 1.25 +/- 0.17 g/L (p less than 0.005) respectively. No significant differences were observed when serum apoprotein (apo) A-I and HDL-triglycerides levels were compared between patients and controls. Smoker patients showed a significant increase in serum triglycerides (p less than 0.005) and a lower HDL-cholesterol concentrations (p less than 0.005) compared with non smoker patients. Patients with more severe distal involvement according to the arm-ankle pressure index showed a significantly greater reduction in HDL-cholesterol (p less than 0.05). CONCLUSIONS: HDL-cholesterol is the best marker of PVD, and the degree of severity of ischemia was associated with greater decrease in HDL-cholesterol. Apo A-I has not been revealed as a risk marker for PVD.

Adult↗
PubMed1991

Serum lipoprotein (a) levels in men with peripheral vascular disease.

The authors quantified serum lipoprotein (a) (Lp) (a) by enzymo-immuno-analysis in 86 outpatient men suffering peripheral vascular disease (PVD) and in 53 age-matched healthy men. They further measured serum cholesterol, serum triglycerides, low density lipoproteins-cholesterol, high density lipoproteins (HDL)-cholesterol and serum apolipoprotein B. Serum triglycerides were significantly increased in patients with PVD versus controls (148 +/- 8 and 114 +/- 7 mg/dL, mean +/- SEM). HDL-cholesterol levels were significantly lower in patients versus controls (36 +/- 1 and 43 +/- 2 mg/dL, respectively). Serum Lp(a) levels in patients with PVD were 20 +/- 2 mg/dL, whereas in controls they were 16 +/- 3 (p: NS). Serum Lp(a) concentrations were identical in smoker and nonsmoker patients. There was no correlation between Lp(a) concentration and the other lipid parameters. Conversely, as occurs in coronary heart disease and in cerebrovascular disease, Lp(a) does not seem to be a marker for PVD, although a trend toward a higher mean levels was found.

Adult↗
PubMed1991

High density lipoprotein subfractions and physical activity: changes after moderate and heavy exercise training.

The changes in high density lipoprotein (HDL) subfractions have been studied in 106 young healthy men after two months of physical training at a military base. Forty subjects were placed on a heavy intensity training program (HITP) with a daily average energy expenditure estimated as 3,504 Kcal, and 66 subjects followed a moderate intensity training program (MITP) with an average energy expenditure estimated as 2,942 Kcal/day. The HITP group reduced their body fat while HDL-cholesterol, HDL2-cholesterol and apoprotein (apo) A-I increased by 8.4%, 30% and 16.9% respectively (p less than 0.001). Body fat of MITP subjects did not change and HDL-cholesterol, HDL2-cholesterol and apo A-I increased by 5.6% (p less than 0.05), 17.1% (p less than 0.001) and 5.6% (p less than 0.05), respectively. The increase in serum apo A-I level was significantly higher (p less than 0.005) in the heavy intensity training group. The apo A-I/A-II ratio increased significantly in both groups (p less than 0.001), reflecting an increase in the HDL2/HDL3 ratio. This is in agreement with the significant increase in HDL2-cholesterol in both groups (p less than 0.001) with no change or decrease in HDL3-cholesterol.

Adolescent↗
PubMed1991

Influence of intermediate-density lipoproteins on the accuracy of the Friedewald formula.

Values of low-density lipoprotein (LDL) cholesterol (C) according to the Friedewald formula (Clin Chem 1972;18:499-502) were compared with those obtained by lipoprotein fractionation in 98 healthy subjects (control group), 135 specimens from patients with peripheral vascular and cerebrovascular disease (atherosclerotic group), and 45 with chronic renal failure on hemodialysis (CRF group). All had concentrations of total cholesterol between 3.23 and 7.76 mmol/L (1.25-3.00 g/L) and triglycerides less than 3.39 mmol/L (less than 3.00 g/L). The percentage error of calculated LDL-C was 4% in controls with a cholesterol/triglycerides (C/TG) ratio for very-low-density lipoprotein (VLDL) of 0.20, but greater than 60% in those with a (C/TG)VLDL ratio of 0.40. The percentage of error in sera of patients with atherosclerosis and chronic renal failure was higher than in controls with a similar mean (C/TG)VLDL ratio. The percentage of error of calculated LDL-C increases progressively with the increase in the C/TG intermediate-density lipoprotein (IDL) ratio, both in controls and in the atherosclerotic and CRF groups. Similar findings are observed when the mean percentage of error of measured LDL-C is evaluated. The percentage of error from calculated LDL-C in the atherosclerotic and CRF groups is significantly lower than that obtained by comparison of LDL-C separated by ultracentrifugation when the "broad cut" LDL (IDL plus LDL, both by ultracentrifugation) was used. The high percentage of errors found in the groups of patients studied underlines the need for caution when assessing the reliability of the Friedewald formula, particularly in cases in which disturbances in IDL composition are suspected.

Arteriosclerosis↗