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Josep M Simó

Publications and source records attributed to Josep M Simó.

5 recordsLinked to original sources
PubMed2003

Evaluation of a fully-automated particle-enhanced turbidimetric immunoassay for the measurement of plasma lipoprotein(a). population-based reference values in an area with low incidence of cardiovascular disease.

OBJECTIVES: Lipoprotein(a) has been proposed as an independent risk factor for cardiovascular disease. This lipoprotein possesses a marked size polymorphism that makes difficult to measure accurately its concentration in plasma. The International Federation of Clinical Chemistry recently recommended to carefully evaluate new commercial methods for lipoprotein(a) measurement to discard the possible influence of lipoprotein(a) isoforms on immunoreactivity. They also recommended to perform population-based studies for different ethnic and geographic groups. Therefore, in the evaluation of a fully automated, particle-enhanced turbidimetric immunoassay for the measurement of lipoprotein(a) we have determined its reference interval in the Spanish population, an area with the lowest incidence of cardiovascular disease in Europe. DESIGN AND METHOD: We evaluated a commercial kit of reagents calibrated against the Proposed Reference Material and determined the effect of lipoprotein(a) size polymorphism on the measurements. A population-based study was carried out in two different villages on the Mediterranean coast of Spain. RESULTS: Imprecision at different lipoprotein(a) concentrations ranged between 3.0 and 15.4%. Recovery was 98.5 +/- 2.1. Detection limit was 4.8 nmol/L. There were no significant interferences from lipemia, jaundice, hemolysis, paraproteinemia, apolipoprotein B or plasminogen. We did not observe any effect of the lipoprotein(a) size polymorphism on the measurements. Mean (and SD) values for plasma lipoprotein(a) (n = 369) were 53.6 (65.3) nmol/L, the median was = 25.3 nmol/L and range varied between <4.8 and 356.0 nmol/L. CONCLUSION: The present article presents an accurate and practical assay for measuring plasma lipoprotein(a) concentrations and describes its reference values in a population of Spanish Caucasians. Our results are similar to those obtained in other Caucasian populations (between 10 and 25% higher than in participants of the CARDIA study).

Adolescent↗
PubMed2003

Differences between genotyping and phenotyping methods for assessing apolipoprotein(a) size polymorphisms.

The aim of the present study was to analyze, on a double-blind basis, the relationships between the apolipoprotein(a) (apo(a)) gene and protein size polymorphisms in healthy volunteers (n = 99) and patients with premature myocardial infarction (n = 91). Apo(a) genotypes were determined by pulse-field electrophoresis and phenotypes were separated by sodium dodecyl sulfate-agarose gel electrophoresis. Results showed that phenotyping overestimated apo(a) size with respect to genotyping (mean (SD) = 3.7 (3.4) kringle units; p < 0.001) in subjects with a double-band genotype, although both measurements were highly correlated (r = 0.83; p < 0.001). We also observed that the protein band in subjects with a single-band phenotype was related more closely to the smallest allele than to the largest allele band. The correlation of plasma lipoprotein(a) (Lp(a)) concentration was stronger with the phenotype than with the genotype. We hypothesize that post-translational modifications in the apo(a) molecule may be the most plausible explanation for the discrepancies observed. In conclusion, the present study highlights the dissimilarities between phenotyping and genotyping methods for the measurement of apo(a) size and suggests that laboratories should carefully consider these relationships and the transfer of results between such methodologies.

Age of Onset↗
PubMed2002

Impaired vitamin E status in patients with parenchymal liver cirrhosis: relationships with lipoprotein compositional alterations, nutritional factors, and oxidative susceptibility of plasma.

Vitamin E is a lipid-soluble vitamin and an important antioxidant that protects lipoproteins and cell membranes from lipid peroxidation. The aims of the present study were to investigate, in patients with parenchymal liver cirrhosis, the following: (1) nutritional and vitamin E status in relation to compositional changes in lipoproteins; and (2) the effects of these alterations on the patients' plasma susceptibility to copper-mediated oxidation. Patients (n = 55) with liver cirrhosis and 25 healthy volunteers had vitamin E in serum and in isolated lipoprotein fractions analyzed by high-performance liquid chromatography (HPLC). Plasma susceptibility to peroxidation was measured by incubation with Cu(2+). Nutritional status was assessed by anthropometry. Vitamin E concentration was significantly decreased (P <.001) in the serum and in very-low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) in cirrhotic patients. The decrease was related to the degree of liver impairment. There were significant correlations between cholesterol and vitamin E concentrations in serum and in all the lipoprotein fractions (r between 0.72 and 0.89; P <.001) in cirrhotic patients, but there were no significant relationships between vitamin E and any of the anthropometric indices of nutritional status. The plasma maximal oxidation rate was significantly increased in cirrhotic patients (P <.01) and was inversely related to the serum concentration of vitamin E (P <.05). We conclude that lipoprotein alterations and not nutritional factors should be regarded as major factors explaining serum vitamin E reduction in patients with parenchymal liver cirrhosis, and that vitamin E depletion is associated with an increased plasma susceptibility to oxidation.

Adult↗
PubMed2002

Heterozygous apolipoprotein (a) status and protein expression as a risk factor for premature coronary heart disease.

Exactly how apolipoprotein a [APO(a)] isoform size affects the degree of cardiovascular risk associated with high lipoprotein a [LP(a)] levels is not fully understood. Using a sodium dodecyl sulfate-agarose APO(a) & LP(a) phenotyping method, we assessed the role of APO(a) size heterogeneity according to the number of kringle 4 repeats and the differential APO(a) protein expression in 91 male Spanish patients with premature coronary heart disease (CHD) compared with 99 healthy Spanish men. CHD patients had significantly increased median plasma LP(a) levels (0.31 g/L) and a higher percentage of subjects with LP(a) levels of 0.30 g/L or greater (51%) than controls (0.15 g/L and 23%, respectively). Patients with the double-band phenotype had significantly higher plasma LP(a) levels (median 0.37 g/L) compared with those expressing a single-band phenotype (median 0.20 g/L; P =.018) and with their corresponding controls (median 0.15 g/L; P <.001). The double-band phenotype and LP(a) values of 0.30 g/L or greater had a significant association with CHD (odds ratio [OR] 6.47, 95% confidence interval [CI] 2.51-16.7), stronger than that observed for the entire group (OR 4.19, 95% CI 1.97-8.90). The adjusted OR for the APO(a) protein pattern that equally expressed both isoforms indicates an independent association with premature CHD (OR 3.33; 95% CI 1.08-10.3). These results suggest that APO(a) phenotyping might be used in subjects with hyperlipoproteinemia a as a powerful marker to assess the risk of premature CHD because heterozygous status, mainly when both isoforms are equally expressed, is associated with higher cardiovascular risk.

Apolipoproteins A↗