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Biomedical subjects

A Vayá

Publications and source records attributed to A Vayá.

At least 19 recordsLinked to original sources
PubMed2003

Erythrocyte aggregability and disaggregability in thalassemia trait carriers analyzed by a laser backscattering technique.

Erythrocyte aggregability was determined by a laser backscattering light technique in 23 beta minor thalassemia carriers and in 36 age and sex matched controls. The aggregation time (Ta) was statistically higher in cases than in controls (2.8 +/- 1.0 vs 2.3 +/- 0.4, p < 0.05) and the aggregation index at 10 sec (AI10) was statistically lower (25.1 +/- 5.7 vs 28.2 +/- 3.8, p < 0.05), suggesting both parameters a statistically lower erythrocyte aggregability tendency. However, the total disaggregation threshold (gammaD) was statistically higher in cases than in controls (134.4 +/- 34.1 vs 105.1 +/- 33.1, p < 0.05), indicating that once aggregates are formed a higher shear rate is needed to break them up. No differences were observed in plasmatic factors, i.e., fibrinogen, total cholesterol and triglycerides, that could have influenced erythrocyte aggregation. A negative statistically significant correlation was found between erythrocyte indexes and the total disaggregation threshold. The lower erythrocyte aggregation found in minor thalassemia carriers could be attributed in part to the morphological alterations, although others mechanisms such as modifications in the membrane structure of the RBC can not be ruled out.

Adolescent↗
PubMed2002

Plasma lipids and blood fluidity in patients with polygenic hypercholesterolaemia treated with fluvastatin.

The clinical benefit brought about by HMG-CoA reductase inhibitors (statins) may not entirely be due to their lipid-lowering effect. Further investigation is necessary in order to determine the significance of ancillary effects to the clinical benefit of statin treatment. We studied 27 polygenic hypercholesterolaemia (PHC) patients before and 3 and 6 months after fluvastatin treatment. A control group of 38 normal, sex and age matched, subjects were also studied. The following parameters were measured: haematimetry, serum lipids and general biochemistry, apo-A/B and lipoproteins, fibrinogen, blood filterability, red blood cell aggregation, blood and plasma viscosity. PHC patients showed lower blood filterability (16.00+/-0.99 vs 19.90+/-2.90 microl/s), higher plasma fibrinogen (274.8+/-41.5 vs 241.6+/-43.2 mg/dl), increased erythrocyte aggregation at low shear stress (8.10+/-1.15 vs 7.19+/-1.29) and increased plasma viscosity (1.26+/-0.06 vs 1.23+/-0.05 mPa.s). Notable lipid changes after 6 months fluvastatin treatment were not accompanied by measurable changes in the haemorheological alterations of the PHC patients.

Adult↗
PubMed2001

Relationship between fibrinogen protein and fibrinogen function in postmyocardial infarction patients.

The present study investigates the association between increases in the concentration and function of plasma fibrinogen in two groups of patients with chronic ischemic heart disease (11 with recurrent ischemic events and 19 free of these episodes) and in 34 healthy controls. The fibrinogen function index (fibrinogen function per unit of fibrinogen protein) (FgFI) was used as a measure of the fibrinogen clotting potential. The prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin (TAT) were used as procoagulant markers. Plasma sialic acid (SA) was also evaluated as an inflammatory marker. No differences were found between FgFI (1.06+/-0.13 vs. 1.02+/-0.13), F1+2 (1.2+/-0.5 vs. 1.1+/-0.4 nmol/l) and TAT (2.5+/-1.3 vs. 2.5+/-0.7 microg/ml) in postinfarction patients without recurrent coronary ischemic events and the control group. However, postinfarction patients who suffered recurrent coronary ischemic events had significantly higher FgFI than patients without these symptoms (1.19+/-0.09 vs. 1.06+/-0.13), P<.01) and than the control group (1.19+/-0.09 vs. 1.02+/-0.13, P<.001). Moreover, the F1+2 (1.4+/-0.5 vs. 1.1+/-0.4 nmol/l, P<.05) and TAT (3.6+/-3.3 vs. 2.5+/-0.7 microg/ml, P<.05) were significantly higher in patients who suffered recurrent coronary ischemic events than in the control group. However, F1+2 and TAT were not different between patients with and without these symptoms. The fibrinogen protein (Fg-protein) concentration and high molecular weight fibrinogen (HMW-Fg) levels were significantly higher in both postinfarction patient groups than in the control group and in postinfarction patients with recurrent coronary ischemic events than in postinfarction patients without these symptoms. The plasma SA levels were significantly increased in postinfarction patients with and without recurrent coronary ischemia as compared with the control group. A positive correlation was found between fibrinogen and SA levels (r=.5, P<.01). In conclusion, our study indicates that the procoagulant factors, among which we include fibrinogen, F1+2 and TAT play a very active role in recurrent ischemic events in postmyocardial infarction patients. High plasma concentrations of both fibrinogen and SA suggests that fibrinogen becomes elevated as a consequence of inflammatory processes. The FgFI as an indicator of clotting potential of fibrinogen appears to be associated with ischemic events in chronic coronary artery disease.

Adult↗
PubMed2001

Upper extremity deep vein thrombosis in a young patient double heterozygous for factor V Leiden and prothrombin G20210A mutation.

We report on a 19-year-old girl with upper extremity deep vein thrombosis after catheter indwelling whose thrombophilic study disclosed the coexistence of factor V Leiden and the prothrombin G20210A mutation. The family study identified five other members who were also heterozygous for both mutations. This is the first case of upper extremity deep vein thrombosis with the co-inheritance of both genetic defects. It provides further evidence that thrombophilic defects mostly require additional triggering factors to induce a thrombotic event and suggests that in young patients with this venous thrombotic location, a thrombophilic search should be performed even when there are other acquired thrombotic risk factors.

Adult↗
PubMed2001

Spontaneous cervical epidural hematoma associated with oral anticoagulant therapy.

A 54-year-old woman who was on anticoagulant treatment with acenocoumarol for a mitral prothesis developed a cervical spinal epidural hematoma, probably triggered by coughing fits together with supratherapeutic anticoagulation. Because of the subacute evolution of the hematoma, it was not diagnosed until the patient was admitted to the hospital with profuse hemorrhages. Given the subacute nature of the hematoma, along with the favorable evolution, conservative treatment with dexamethasone was decided upon, and it was resolved with almost no sequelae. This unusual clinical entity definitely should be suspected in patients on anticoagulants who complain of severe localized neck pain, most often with radicular irradiation.

Acenocoumarol↗
PubMed2001

Factor V Leiden and prothrombin G20210A in relation to arterial and/or vein rethrombosis: two cases.

The factor V Leiden (FV Leiden) and prothrombin G20210A mutations, are the most common established genetic risk factors for deep vein thrombosis (DVT). However, the relationship between these mutations and arterial thrombotic syndromes (coronary heart disease, myocardial infarction, stroke) has not been established. Some studies have suggested a relationship between them, but other authors have considered it unlikely that these anomalies are a major risk factor for arterial thrombosis. From the clinical point of view, a question arises concerning the risk of repeated thrombosis in patients carrying one of these two mutations. The question is whether the recurrence is attributable to the mutations or to the presence of additional circumstantial risk factors. As the risk of repeated thrombosis varies considerably from one patient to another, decisions about long-term treatment require weighing the persistence of risk factors for vascular disease (venous and arterial), especially in selected cases such as young patients or patients with thrombosis of unusual localization.

3' Untranslated Regions↗
PubMed2001

The effect of acenocoumarol on hemorheological parameters.

The effect of acenocoumarol on hemorheological variables was measured in 35 non-valvular chronic atrial fibrillation patients before starting oral anticoagulant therapy (basal) and one and two months after beginning treatment (INR-2,3). Fibrinogen increased significantly from the basal situation: 332+/-99 mg/dl to 386+/-96 mg/dl in the second month (p<0.05). However, this small increase in fibrinogen is not large enough to mediate other rheological changes, and whole blood filterability, blood viscosity, plasma viscosity and erythrocyte deformability and aggregability remained unchanged after treatment. These results suggest that acenocoumarol does not affect rheological parameters and can therefore be used as a "neutral drug" for rheological studies in cardiovascular patients under oral anticoagulant therapy.

Acenocoumarol↗
PubMed2001

Low level of circulating activated protein C is a risk factor for venous thromboembolism.

The levels of circulating activated protein C (APC) reflect in vivo protein C activation. The aim of this study was to determine whether a low APC level is an independent risk factor for venous thromboembolism (VTE). We measured APC in 160 patients with a history of VTE and without recognized thrombophilic defects, and in 199 healthy individuals. The mean (+/- SD) APC level was lower in patients (0.99 +/- 0.44 ng/ml) than in controls (1.19 +/- 0.41 ng/ml) (p < 0.0001), and showed a different distribution in the two groups. Thirty-eight patients (23.7%) had APC levels below the 5th percentile of the control group (<0.69 ng/ml) and 57 patients (35.6%) had APC levels below the 10th percentile (<0.77 ng/ml). APC levels <0.69 ng/ml increased the risk of a single or recurrent episode of VTE 4.2-fold (95% confidence interval, 2.0-9.0) or 6.9-fold (2.6-17.9). respectively, and APC levels <0.77 ng/ml increased these risks 3.4-fold (1.9-6.2) or 5.1-fold (2.3-11.2), respectively, compared with controls. Familial studies revealed that in some cases the low APC phenotype seems to be hereditary. We conclude that a low level of circulating APC in individuals without any of the most recognized thrombophilic defects is a prevalent, independent risk factor for VTE, and that it predisposes to recurrent VTE.

Adult↗
PubMed2000

PAI-1 promoter 4G/5G genotype as an additional risk factor for venous thrombosis in subjects with genetic thrombophilic defects.

Impaired fibrinolysis as a result of increased plasminogen activator inhibitor-1 (PAI-1) levels in plasma is a common finding in patients with deep vein thrombosis (DVT). A 4G/5G polymorphism in the promoter region of the PAI-1 gene has been reported to influence the levels of PAI-1. The 4G allele was found to be associated with higher plasma PAI-1 activity (act), but contradictory results on the incidence of the 4G allele in DVT patients have been reported. The aim of this study was to analyse whether the PAI-1 promoter 4G/5G genotype increases the risk of venous thrombosis in subjects with thrombophilic defects, and to determine the distribution of the PAI-1 4G/5G genotype and its relation to plasma PAI-1 levels in 190 unrelated patients with DVT in comparison with a control group of 152 healthy subjects. No differences between the 4G/5G allele distribution in the DVT group (0.43/0.57) and in the control group (0.42/0.58) were observed. However, the presence of the 4G allele significantly increased the risk of thrombosis in patients with other thrombophilic defects. Significantly higher PAI-1 levels were observed in DVT patients than in the controls. Our results also showed significant differences in the plasma levels of PAI-1 antigen (ag) and PAI-1 act among the 4G/5G genotypes in DVT patients. A multivariate analysis revealed that, in the DVT group, PAI-1 ag levels were influenced by the 4G allele dosage, triglyceride levels and body mass index (BMI). The influence of the 4G allele dosage on PAI-1 levels was independent of the triglyceride levels and BMI. In the control group, no significant correlation between PAI-1 levels and 4G allele dosage was observed. In conclusion, the PAI-1 promoter polymorphism was found to have an influence on PAI-1 levels in DVT patients and on the risk of venous thrombosis in subjects with other genetic thrombophilic defects.

Adult↗
PubMed2000

Congenital and acquired thrombotic risk factors in women using oral contraceptives: clinical aspects.

We describe the thrombophilic and clinical characteristics of a group of patients who suffered venous thrombosis (VT) (n = 36) and ischemic stroke (n = 8) while taking oral contraceptives (OC). Our purpose is to ascertain whether there are differences between users of second and third generation progestogen and to investigate the influence of concurrent congenital and acquired risk factors (other than OC) on the onset of the thrombosis. The group of patients included 36 women with VT and eight with ischemic stroke. The patients' recognized predisposing factors were recorded. We also considered age, length of time on OC, types of OC, rethrombosis, family history of VT, and the presence of thrombophilic genetic defects. In the group of patients with VT, 54% were treated with second generation OC (n = 23), and 30% (n = 11) were treated with third generation OC. We found no significant statistical differences with respect to age and length of time on OC between the two types of OC. The prevalence of genetic defects in these patients--factor V (FV) Leiden, prothrombin G20210A mutation and protein S deficiency--was 19% (n = 7), 17% (n = 6), and 8% (n = 3) respectively. We observed the shortest time lapse between initiating OC and the first thrombotic event in carriers of FV Leiden and in patients with combined defects, but the differences were not significant. In patients with ischemic stroke, 50% were treated with second generation OC and 50% were treated with third generation OC. Prothrombin G20210A mutation was detected in two patients. In both patients,the stroke occurred earlier than in the rest of the patients, but these differences were not statistically significant. With respect to preventing thrombotic events in these patients, our data suggest that OC therapy should be avoided in patients with a previous history of thrombosis and in patients with an evident thrombotic tendency in the family. In patients in whom the family history of thrombosis is not very evident, it would be recommended to screen for FV Leiden, prothrombin G20210A mutation, and protein S, and to rule out OC if the patient does in fact have one of these risk factors. Moreover, if a patient develops a thrombotic complication while taking OC, an evaluation to search for a thrombophilic defect is warranted, and at the same time, alternative methods of contraception should be considered.

Adolescent↗
PubMed2000

Portal vein thrombosis associated to prothrombin G20210A mutation and protein C deficiency.

We describe a patient with left branch portal vein thrombosis involving two thrombophilic alterations, the prothrombin G20210A mutation and protein C deficiency. In spite of not being under anticoagulant treatment, the thrombus in the portal vein underwent complete and spontaneous lysis. No other risk factors were detected and no family history related to thrombosis was found.

Adenine↗
PubMed2000

Intracardiac thrombosis in a case of Behcet's disease associated with the prothrombin 20210G-A mutation.

Thrombosis occurs in 20 to 30% of patients with Behçet's disease (BD), but the precise pathogenic mechanism underlying the thrombotic tendency in these patients is not well known. Venous thromboses are commonly located in the lower extremities, but right intracardiac thrombi are extremely rare. We report for the first time on a young patient with BD associated the 20210G-A prothrombin gene mutation and right intracardiac thrombosis. We suggest that the association of BD with this newly recognized prothrombotic genetic mutation may have contributed to the development of the thrombotic event in this patient.

Adolescent↗
PubMed2000

Quantification of D-dimer using a new fully automated assay: its application for the diagnosis of deep vein thrombosis.

BACKGROUND AND OBJECTIVE: A D-dimer assay can be helpful to rule out thromboembolism provided it is sensitive, reliable, fast and easy to perform. Tests based on the ELISA methodology have a high diagnostic sensitivity, and are therefore adequate for excluding deep venous thrombosis (DVT). The drawbacks are their long assay times, unsuitability to be run on single samples and cost. New methods have been developed, based either on the same principle, by immunofiltration or by microlatex immunoturbidimetric assays which seem to reach the high sensitivity and negative predictive value (NPV) required, but allowing fast and quantitative single sample analysis. The aim of this work was to evaluate one rapid test, a fully automated quantitative assay (IL Test D-dimer, run on an ACL 7000 coagulation analyzer, Instrumentation Laboratory). DESIGN AND METHODS: We compared the diagnostic value of IL Test for DVT with that of an ELISA (Dimertest Gold EIA Agen Biomedical Limited, Acacia Ridge, Australia). Eighty-six patients (43 men, 43 women, mean age: 61 years) showing DVT symptoms formed the population for this non-randomized controlled trial in a referral center. The diagnosis of DVT based on the clinical history, was confirmed by serial compression ultrasonography (CUS) with Doppler flow in 62 patients. RESULTS: The IL Test D-dimer proved to be rapid, automated and well suited for individual tests with a good reproducibility in three control plasmas with different concentrations of D-dimer (coefficient of variation range 0.54-3. 87%). Its performance was comparable to that of the Dimertest Gold EIA, as indicated by the areas under the receiver operating characteristic curves (Dimertest Gold EIA 0.748; IL Test D-dimer 0.70). On the basis of kappa coefficients, there was a good concordance between the Dimertest Gold EIA and IL Test D-dimer when the receiver operating characteristic (ROC) curves suggested cut-offs were used. The sensitivity (98.3%) and NPV (88.9%) shown by IL Test D-dimer are comparable or even better than those obtained for EIA (95%, 80%, respectively). INTERPRETATION AND CONCLUSIONS: This study shows that the new method can be included in prospective clinical trials to test the utility of D-dimer measurement in combination with other non-invasive diagnostic procedures in the management of DVT diagnosis.

Adolescent↗
PubMed2000

Risk of venous thrombosis in carriers of the prothrombin G20210A variant and factor V Leiden and their interaction with oral contraceptives.

BACKGROUND AND OBJECTIVES: The prothrombin G20210A mutation and factor V Leiden have been found to be associated with an increased risk of venous thrombosis, but the reported prevalences of the prothrombin gene variant both in the normal population and in patients with deep venous thrombosis (DVT) vary greatly in the literature. Moreover, the influence of oral contraceptives (OC) on thrombotic events in patients with the prothrombin G20210A variant has not been well established. In this study we evaluate both circumstances. DESIGN AND METHODS: A case-control study was run on 229 patients with DVT and 246 healthy controls. The patients' history of thrombosis and acquired thrombotic risk factors, especially OC, were recorded. Prothrombin G20210A mutation, factor V Leiden, antithrombin, heparin II cofactor, plasminogen and proteins C and S were evaluated. RESULTS: Seven and a half percent of the patients and 2.9% of the controls were carriers of the prothrombin mutation, while 12.2% of the patients and 1.6% of the controls had factor V Leiden. Among the 229 DVT patients there were 130 patients with clinically suspected thrombophilia (first thrombotic event occurring before the age of 45 years or positive family history of thrombosis or recurrent venous thrombosis). Ten percent of these 130 patients were carriers of the prothrombin G20210A mutation and 18.5% had the factor V Leiden mutation. The odds ratios (OR) for DVT risk were: 2.4 (95% CI, 1.0-6.3) for the total DVT patients and 5.2 (95% CI, 1.4-19.5) for the patients with clinically suspected thrombophilia with the prothrombin mutation. The risk of thrombosis was 6.9 (95% CI, 2.3-20.6) for the DVT patients and 14.3 (95% CI, 3.3-64.6) for the patients with clinically suspected thrombophilia with factor V Leiden. Fifty-five percent of the patients with combined congenital defects (prothrombin mutation G20210A plus another congenital defect) had recurrent thrombosis. In women receiving OC the risk of DVT was 3.5 (95% CI, 1.5-8.2) that of the patients not receiving OC. When women with combined defects were also taking OC, the risk of thrombosis increased significantly. INTERPRETATION AND CONCLUSIONS: The prevalence of the prothrombin G20210A mutation in the healthy population in our study is similar to that observed in other southern European countries. The prothrombin G20210A mutation does not by itself seem to be a high thrombotic risk factor. However, when it is present together with other thrombotic risk factors, the predicted risk of thrombotic events increases. The use of OC by women with the prothrombin G20210A variant or FV Leiden, either alone or combined with other thrombotic risk factors, was associated with a significant increase in the risk of venous thrombosis.

Adult↗