Search PubMed⌕ Search

Biomedical subjects

J Aznar

Publications and source records attributed to J Aznar.

At least 37 records · Page 2Linked to original sources
PubMed1998

Influence of lipoprotein (a) levels and isoforms on fibrinolytic activity--study in families with high lipoprotein (a) levels.

Increased levels of lipoprotein (a) [Lp(a)] have been considered an independent risk factor for cardiovascular disease, but the mechanism behind this relationship is not completely understood. A high concentration of Lp(a) may interfere with fibrinolysis because of the structural similarity between apo(a) and plasminogen. The aim of the present study was to examine the influence of apo(a) levels and isoforms on fibrinolytic activity in 82 subjects from 24 families in which the Lp(a) levels were > or =30 mg/dl in at least one child and one parent. Several fibrinolytic parameters, including plasmin generation by fibrin-bound tissue plasminogen activator, the lipid profile and apo(a) isoforms were studied. Subjects with high circulating Lp(a) levels (n = 44) had significantly reduced plasmin generation compared with their relatives with normal Lp(a) levels (n = 38). A significant inverse correlation between Lp(a) levels and plasmin generation was observed. The individuals with a combination of high levels of plasma Lp(a) and a major apo(a) isoform < or =580 kD molecular weight show the lowest fibrinolytic activity. A high correlation was found between the levels of apo(a) isoforms in children and the levels of the corresponding parental apo(a) isoforms. We conclude that the antifibrinolytic effect of Lp(a) in subjects with two apo(a) isoforms may depend not only on the total plasma level of Lp(a) but also on the relative concentration of the small apo(a) isoform.

Adolescent↗
PubMed1998

Anaerobic bacteria in men with urethritis.

AIM: Investigation of the urethral flora in men with urethritis, with particular reference to anaerobic bacteria. METHODS: Multiple cultures were performed on three urethral samples from 110 men attending the STD Clinic of the School of Medicine in Seville: 35 with no evidence of urethritis (control group), and 75 with urethritis (17 gonococcal urethritis (GU) and 58 non-gonococcal urethritis (NGU)). In the 58 men with NGU, Chlamydia trachomatis was isolated in 16 (27.5%), Ureaplasma urealyticum in 18 (31%), Trichomonas vaginalis in two (3.4%) and no pathogens were isolated in the remaining 22 (38%) patients. RESULTS: Aerobic flora, mainly Staphylococcus spp., were isolated less frequently (41%) in patients with GU than in the control group (80%), and those with NGU (72%). Anaerobic flora were isolated in 62% of patients, with similar isolation rates in each group. Gram-negative anaerobes were more frequently isolated in men with urethritis, especially NGU, compared to controls (P < 0.05). Prevotella spp. and Bacteroides spp. were significantly more frequently isolated in patients with NGU, including Chlamydia-negative NGU. Fusobacterium spp. were more frequent in the Chlamydia-positive NGU than in the controls (P < 0.05). P. magnus was the most frequent anaerobic species found in the control group, while P. prevotii was most frequently seen in the urethritis group. B. ureolyticus, P. prevotii and P. tetradius were more frequent on the NGU group (P < 0.05). B. ureolyticus was commoner in patients with Chlamydia-negative NGU, while P. tetradius and P. asaccharolytica was commoner in those where C. trachomatis was isolated than in the control group. CONCLUSION: Urethral microflora isolated showed ten bacterial genus and 25 different species of anaerobes. The spectrum of these microflora changed with the presence of urethritis and varied with its aetiology.

Adult↗
PubMed1998

Alterations in erythrocyte aggregability in diabetics: the influence of plasmatic fibrinogen and phospholipids of the red blood cell membrane.

In order to ascertain whether the increased aggregability observed in the red blood cells of diabetic patients is induced exclusively by plasma factors or is also influenced by membrane lipids, we examined the phospholipids of the erythrocyte membrane, the plasma fibrinogen concentration and erythrocyte aggregation in 86 insulin and non insulin-dependent diabetic patients. The data obtained show that the erythrocyte aggregability of the diabetic patients is higher than that of the control group (10.0+/-2.4 vs. 7.8+/-1.6%). This increased aggregability correlates not only with a higher fibrinogen concentration but also with changes observed in the membrane phospholipids. The percentage of sphingomyelin (SP) in the patients is higher than in the controls (22.6+/-6.8 vs. 18.4+/-5.4%) and that of phosphatidylserine (PS) is lower (9.5+/-6.1 vs. 12.1+/-5.1%). No differences in the percentages of the other two phospholipids identified (phosphatidylcholine, PC, and phosphatidylethanolamine, PE) were observed. The increase in the saturated nature of the phospholipids of the erythrocyte membrane, which can be measured by the (SP + PC)/(PE + PS) ratio, is statistically related (r = 0.39; p < 0.05) to the increased red blood cell aggregability observed in these patients.

Adult↗
PubMed1998

The cholesterol/phospholipid ratio of the erythrocyte membrane in children with familial hypercholesterolemia. Its relationship with plasma lipids and red blood cell aggregability.

The cholesterol/phospholipid ratio (C/PL) of the red blood cell membrane, plasma lipids and erythrocyte aggregability were evaluated in 20 children with familial hypercholesterolemia (age: 10.4+/-4.6 years) but without detectable vascular injury. The results indicate that hypercholesterolemic children have a higher erythrocyte membrane C/PL ratio than the control group (0.81+/-0.23 vs. 0.65+/-0.08, p < 0.01). This membrane lipid alteration correlates inversely with the plasma concentration of HDL-cholesterol (r = -0.558, p < 0.010). The patients also showed greater erythrocyte aggregability than the control group (8.21+/-1.11 vs. 6.25+/-1.24, p < 0.001), but this does not seem to correlate with the changes observed in the lipid composition of the cell membrane. These results suggest that from childhood, people with familial hyper-cholesterolemia show alterations in the lipid composition of the red blood cell membrane that are related to the changes observed in plasma lipids and appear prior to atherosclerotic vascular symptoms.

Child↗
PubMed1998

Erythrocyte deformability in young familial hypercholesterolemics.

In order to ascertain whether young familial hypercholesterolemic subjects without atherosclerotic lesions demonstrable on a carotid echo-Doppler show decreased erythrocyte deformability, we determined the erythrocyte elongation index (EEI) by means of a shear stress diffractometer (Rheodyn SSD) in twenty-four children with heterozygous familial hypercholesterolemia (FH), aged 12 +/- 3 years, and their corresponding affected parent. The parents were twenty-three adults with heterozygous FH aged, 32 +/- 6 years. The control group was made up of a similar number of well matched healthy volunteers. The EEI at 6, 12, 30 and 60 Pa showed no statistical differences between FH children and their control group, or between FH parents and their control group. No correlations were found between EEI and plasma lipids or lipoproteins at any of the shear stresses used. These results suggest that the red blood cells of young familial hypercholesterolemic subjects who show no deterioration of the vascular tree are not less deformable than those of healthy normolipemic subjects, and that dyslipemia itself does not produce alterations that damage the rheological properties of the red blood cell.

Adolescent↗
PubMed1998

Plasma thrombomodulin is not increased in familial hypercholesterolemic children with rheological alterations.

In order to ascertain whether hemorheological alterations precede the atherosclerotic lesion in familial hypercholesterolemia (FH), we studied the lipid and hemorheological profile of 29 heterozygous FH children (12 males and 17 females), aged 12+/-3 years, and a well-matched control group (CG), and assessed their plasma thrombomodulin level as an early marker of endothelial injury. No differences were found between FH children's plasma thrombomodulin values (31.7+/-11.2 ng/ml) and those of the CG (27.8+/-15 ng/ml). However, the rheological variables of FH children and the CG were statistically different (p < 0.001) for fibrinogen (Fbg): 266+/-48 mg/dl vs. 205+/-32 mg/dl; erythrocyte aggregation at stasis (EAM0): 4.6+/-1.2 vs. 3.3+/-0.9; erythrocyte aggregation at low shear (EAM1): 7.9+/-1.7 vs. 6.1+/-0.8; and plasma viscosity (PV): 1.18+/-0.03 cP vs. 1.12+/-0.04 cP. Correlations between rheological parameters and lipids were found. The normal values obtained in FH children for plasma thrombomodulin suggest that the hemorheological alterations appear prior to the vascular injury, are in part related to dyslipemia and could contribute to the development of the atherosclerotic process by modifying blood flow conditions.

Adolescent↗
PubMed1998

Hemorheological changes in children with polygenic hypercholesterolemia.

In order to ascertain whether polygenic hypercholesterolemia (PH), the most common cause of small increases in plasma lipids during childhood, is associated with rheological alterations, we determined the hemorheological and lipid profile of 21 PH children (12 males, 9 females) and a well-matched control group (CG). In addition, a carotid ultrasound was done on all the PH children, but showed no alterations. When compared with the CG, PH children showed increased erythrocyte aggregation both at stasis (EAM0) (4.39+/-1.15 vs. 3.75+/-1.02), p < 0.05, and at low shear rate (EAM1) (8.22+/-1.42 vs. 7+/-1.39), p < 0.01, and increased plasma viscosity (PV) (1.19+/-0.04 cP vs. 1.15+/-0.04 cP), p < 0.01. These results reinforce the hypothesis that lipid metabolic alterations are associated with specific rheological modifications in absence of a demonstrable atherosclerotic lesion.

Apolipoproteins↗
PubMed1998

[Characterization of the rpoB gene mutations in clinical isolates of rifampicin-resistant Mycobacterium tuberculosis].

OBJECTIVES: Characterization and frequency of the rpoB gene mutations associated with rifampin resistance in Mycobacterium tuberculosis clinical isolates in Sevilla. METHODS: Characterization of rpoB mutations in 21 rifampicin-resistant strains of M. tuberculosis isolated during a three-year period (1994-1996) by three different molecular methods: a nonradioactive Single-strand conformation polymorphism (SSCP) analysis, DNA sequence analysis and a commercial method the line probe assay InnoLiPA. RESULTS: Five distinct rpoB mutations were identified. Ser531-->Leu mutation was detected in 14 strains (66.7%), H526-->Asp in 3 strains (14.3%), Ans512-->Ser in 1 strain (4.8%), Glu513-->Leu in 1 strain (4.8%). A nine nucleotide deletion (codon 510-513) was found in one strain (4.8%) while in the remaining resistant strain (4.8%) no mutation was detected. CONCLUSIONS: The frequency of the different mutations found in the rpoB gene, associated with rifampicin resistance in Mycobacterium tuberculosis clinical isolates in Seville, are similar to those previously reported. However, two new mutations has been detected: a nine nucleotide deletion (codon 510-513), and the Asn512-->Ser point mutation. The characterization of the mutations in the rpoB gene could serve as epidemiological marker for the rifampicin resistant clinical isolates of M. tuberculosis.

Amino Acid Substitution↗
PubMed1998

Hemorheological alterations and hypercoagulable state in deep vein thrombosis.

Deep vein thrombosis (DVT) seems to be related to a hypercoagulation and definite hemorheological alterations, but the importance of these alterations in the development of thrombotic events in the deep vein system has not been established. The present study examines both aspects in a group of 55 patients with DVT; the presence of a hypercoagulable state was assessed by quantifying the prothrombin fragment 1+2 (F1+2) and the thrombin-antithrombin III complex (T-AT), and the main hemorheological parameters were evaluated in the acute state and 6 and 12 months later. The results show marked hemorheological, F1+2, and TAT alterations in the acute phase. After 12 months the pattern shows a modest improvement, but erythrocyte aggregation, fibrinogen, F1+2 and T-AT remain increased with respect to the control group (8.51 +/- 1.43; 331 +/- 81 mg/dl; 1.33 +/- 0.60 nmol/l; 3.54 +/- 1.71 ng/ml vs. 8.10 +/- 1.40; 230 +/- 38; 0.94 +/- 0.40; 1.56 +/- 0.59, respectively). These data suggest that the thrombotic event could be influenced by the previous rheological situation and hypercoagulable state.

Acenocoumarol↗
PubMed1997

Prothrombotic effects of erythrocytes on platelet reactivity. Reduction by aspirin.

BACKGROUND: Aspirin effectively reduces the incidence of secondary vascular occlusive events in only 25% of patients. Low-dose aspirin as currently used blocks platelet production of prothrombotic thromboxane A2 and allows endothelial synthesis of antithrombotic prostacyclin. This regimen minimizes gastrointestinal toxicity. We previously showed that intact erythrocytes markedly enhance platelet reactivity. Therefore we investigated whether supplementation of low-dose aspirin with a single high dose at 2-week intervals could more effectively block erythrocyte promotion of platelet reactivity. METHODS AND RESULTS: Effects of different aspirin regimens on erythrocyte enhancement of platelet reactivity in normal volunteers were measured with the use of an assay that evaluates both platelet activation and recruitment. After 15 days of daily ingestion of 50 mg aspirin, reactivity of platelets alone was inhibited. However, erythrocyte promotion of platelet activation and recruitment was only inhibited by approximately 50% and persisted in the total absence of thromboxane synthesis. In contrast, if 50 mg/d aspirin was preceded by a single loading dose of 500 mg aspirin, the erythrocyte prothrombotic effect was strongly inhibited (approximately 90%) for 2 to 3 weeks. However, over time, erythrocytes "escaped" from this inhibition, and once again became prothrombotic, even on a daily regimen of 50 mg aspirin. CONCLUSIONS: For clinical purposes, we recommend a loading dose of aspirin (500 mg), followed by daily administration of 50 mg. The loading dose should be repeated at 2-week intervals. This regimen blocks recovery of the erythrocyte capacity to promote platelet reactivity and may amplify the therapeutic potential of aspirin in cardiovascular disease.

Adult↗
PubMed1997

Activated protein C resistance phenotype in patients with antiphospholipid antibodies.

The effect of antiphospholipid antibodies (aPL) on the action of activated protein C (APC) was examined in 32 patients: 19 with lupus anticoagulant (LA), 6 with anticardiolipin antibodies (aCL), and 7 with LA and aCL. Eighteen patients had a ratio of activated partial thromboplastin time (APTT) with APC to APTT without APC (APTT ratio) <2.06 (cut-off level) and no factor V Leiden mutation; these patients showed APC-resistance (APC-R) phenotype. The mean prolongation of APTT after addition of APC in a control group was 45.3 seconds, with a lower limit of 31.4 seconds. Only 3 of the 18 patients with low APTT ratio had a prolongation of <31.4 seconds; they were classified as true APC-R phenotype, whereas the other 15 patients were classified as spurious APC-R. Of the 3 patients with true APC-R, 2 had deep venous thrombosis, 1 with pulmonary embolism, and the third had recurrent abortion. Of the other 15 patients, 2 had had ischemic stroke, 1 had recurrent abortion, and 12 were asymptomatic. Circulating APC level was measured in 14 of the 18 aPL patients with a low APTT ratio; it was lower than the normal lower limit in 4 patients and within the lower limit in 2. Three of the 4 patients with reduced APC levels had a history of thrombosis. We conclude that patients with aPL who show APC-R phenotype due to a low APTT ratio without the factor V Leiden mutation can be classified into two groups: true and spurious APC-R phenotype. Since those with true APC-R phenotype could have greater thrombotic risk, adequate classification of these patients is important. Moreover, aPL can sometimes interfere with the activation of protein C, thus reducing the circulating levels of APC, and this could constitute another thrombotic risk factor.

Abortion, Habitual↗
PubMed1997

The effect of thrombin on the dynamic exchange between intraplatelet and extraplatelet fibrinogen.

We examined the distribution of platelet fibrinogen and the exchange between intra- and extra-platelet fibrinogen in unstimulated and thrombin-stimulated platelets. In unstimulated platelets 60% of platelet fibrinogen was found in the soluble platelet fraction and 40% in the insoluble one. In platelets activated with thrombin, changes took place in the distribution of intraplatelet fibrinogen but not in the total fibrinogen content. At > or = 0.5 U/ml of thrombin the fibrin(ogen) content of the insoluble and soluble fractions was approximately 80% and 20%, respectively. When we evaluated how extraplatelet fibrinogen affects the content and distribution of intraplatelet fibrinogen, we found that when unlabelled fibrinogen was added to unstimulated and thrombin-stimulated platelets the content and distribution of intraplatelet fibrinogen remained unaltered. However, when 125I-fibrinogen was added, it was incorporated into unstimulated and thrombin-stimulated platelets. In unstimulated platelets, 70% of the incorporated 125I-fibrinogen was in the soluble fraction and 30% in the insoluble. In thrombin-stimulated platelets the distribution of the incorporated 125I-fibrinogen was 62% and 38% in soluble and insoluble fractions respectively. MoAb to GPIIb-IIIa produced 80% and 60% inhibition of 125I-fibrinogen incorporation by unstimulated and thrombin-stimulated platelets. Our data showed dynamic exchange between intraplatelet and extraplatelet fibrinogen both in unstimulated and thrombin-stimulated platelets mediated mainly by GPIIb-IIIa.

Blood Platelets↗
PubMed1997

Molecular epidemiology of Mycobacterium tuberculosis strains isolated during a 3-year period (1993 to 1995) in Seville, Spain.

The genetic polymorphism of Mycobacterium tuberculosis strains isolated in Seville, Spain, was studied by using computer-assisted analysis of the IS6110 fingerprint in order to determine the current situation and to evaluate the human-to-human transmission of this pathogen. One hundred seventy-six isolates from 175 patients among the 205 patients diagnosed with tuberculosis (TB) during a 3-year period (1993 to 1995) were cultured and analyzed. One hundred nine patients (62%) were infected with genetically different isolates, and 67 isolates (38%) were grouped into 19 clusters. These results demonstrate that the level of clustering of strains in Seville is intermediate between those in developed and developing countries. Epidemiological relatedness was shown for isolates from only 10 of these clusters. Active and high transmission rates exist in children and in human immunodeficiency virus (HIV)-infected adults, while in non-HIV-infected adults this transmission rate is moderate. Although transmission from children to adults is uncommon, the probability of transmission from HIV-infected patients to young adults not infected with HIV may be higher. On the basis of these observations, we predict a constant rise in the rate of TB transmission among HIV-infected patients and probably in young adult patients not infected with HIV if measures for the effective prevention of TB among the HIV-infected population are not implemented.

Adolescent↗
PubMed1997

Modulatory effect of erythrocytes on the platelet reactivity to collagen in IDDM patients.

Platelets participate in the atherothrombotic complications of diabetes. Recent data demonstrate that platelet reactivity can be modulated via cell-cell interactions with erythrocytes and neutrophils. In this study, platelet reactivity was evaluated in 30 IDDM patients. We used an analytical procedure that permits an independent evaluation of platelet activation (granule release, eicosanoid formation) and platelet recruitment (pro-aggregatory activity of cell-free releasates) after platelet stimulation with collagen in the presence or absence of other blood cells. The interaction between platelets and erythrocytes (hematocrit 40%) resulted in a marked enhancement of platelet activation (5HT, betaTG, TXA2 release) and recruitment in both patients and control subjects. The erythrocyte enhancement of platelet TXA2 synthesis and recruitment was significantly higher in the patients, while no differences were detected in platelet granule release. The elevated platelet recruitment in the IDDM patients was found to be due to 1) increased susceptibility of diabetic platelets to the prothrombotic effect of erythrocytes and 2) the greater response of diabetic platelets to their own cell-free releasate. Patients with poor metabolic control (elevated HbA1c) or longer evolution time had an even greater platelet recruitment. The presence of microalbuminuria is not related to the platelet recruitment. Since platelet recruitment is an essential step in thrombus growth, its enhancement may favor thrombotic complications in IDDM.

Adolescent↗