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Biomedical subjects

I Alberca

Publications and source records attributed to I Alberca.

At least 19 recordsLinked to original sources
PubMed2006

Hyperhomocysteinemia is a risk factor of recurrent coronary event in young patients irrespective to the MTHFR C677T polymorphism.

Despite the well-known pro-coagulant effect of hyperhomocysteinemia, data is limited regarding the result on recurrent coronary event (RCE) in young people. One hundred and forty patients <55 years old with a first acute coronary syndrome (ACS) were prospectively followed for a mean (+/-S.D.) follow-up of 49+/-14 months in order to investigate the relationship between homocysteine levels (tHcy) at admission and the incidence of RCE. The tHcy values were divided into quartiles to examine their relationship with end points. Furthermore, we determined the effect of C677T methylene tetrahydrofolate reductase (MTHFR) polymorphism, as well as other risk factors for developing a RCE. The median plasma homocysteine concentration was 9.6 mumol/L (interquartile range, 3.7). In the screening of MTHFR C677T polymorphism in patients with ACS, the T allele frequency was 0.4 and the genotype frequency distributions were in Hardy-Weinberg equilibrium. At time of final evaluation, 49 (35%) of the 140 valuable patients had developed a RCE. Increasing numbers of RCE were observed for increasing quartiles of tHcy according to Kaplan-Meier survival (Log-rank test=0.0092). The MTHFR C677T polymorphism was not associated with an increased incidence of RCE. In multivariate analysis, the variables independently associated with a higher risk of RCE were age older than 45 years [HR=2.7; (95% CI, 1.3-6.1); p=0.030], body mass index more than 25 [HR=2.6; (95% CI, 1.1-5.9); p=0.034] and tHcy levels into quartile 4 (tHcy>12.37 mumol/L) [HR=2.5; (95% CI, 1.1-4.7); p=0.04]. Elevated plasma homocysteine level at admission is an independent risk factor for RCE after the first episode of ACS in young patients irrespective of the status of MTHFR C677T.

Acute Disease↗
PubMed2004

Partial androgen deficiency in aging type 2 diabetic men and its relationship to glycemic control.

Aging in the male is associated with both a higher incidence of type 2 diabetes and hypogonadism. However, little information is available about the complex of symptoms and hormonal changes related to partial androgen deficiency in aging (called andropause) in type 2 diabetic men. Here, for the first time, we used a combination of clinical and hormonal criteria to define andropause and to analyze the relationships between the androgen environment and glucose metabolism in 55 type 2 diabetic men (63.6 +/- 7.9 years, mean +/- SD). Low plasma levels of total testosterone (< or =3.4 ng/mL) and free testosterone (< or =11 pg/mL) were found in 20% and 54.5%, respectively, of the diabetic men. The fraction of diabetic men with subnormal levels of total testosterone increased with aging: 14.2% (50 to 59 years), 17.4% (60 to 69 years) and 36% (> 70 years). The corresponding figures for subnormal values of free testosterone were 38%, 69.6%, and 54.5%, respectively. In the whole group of type 2 diabetic men, no significant linear correlations between total or free testosterone with fasting plasma glucose, insulin, C-peptide, or fructosamine values could be established. Total testosterone was positively correlated with glycosylated haemoglobin (HbA(1c)) levels (r =.322, P =.01). Although fasting plasma glucose was marginally higher in aging type 2 diabetic patients with andropause than in those without andropause (162 +/- 6.9 v 139 +/- 8.9, mean +/- SEM, P =.05), there were no differences between both subgroups for plasma fasting insulin, C-peptide, fructosamine, or HbA(1c) levels. Replacement therapy (150 mg intramuscular [IM] of enanthate of testosterone every 14 days for 6 months) was applied in 10 type 2 diabetic men with clinical features of andropause associated with subnormal concentrations of serum testosterone. The treatment induced significant increases in total plasma testosterone (baseline: 3.9 +/- 0.3; at 6 months: 7.1 +/- 0.9 ng/mL, mean +/- SEM, P =.003) and free testosterone (baseline: 9.3 +/- 0.6; at 6 months 17.6 +/- 2.4 pg/mL, P =.003), but had a neutral effect on overall glycemic control. These data show a high prevalence of andropause in aging type 2 diabetic men and suggest that the endogenous androgen environment, as well as correction of the partial androgen deficiency, do not have a meaningful effect on glycemic control.

Adult↗
PubMed1999

Antiphosphatidylserine antibodies in patients with autoimmune diseases and HIV-infected patients: effects of Tween 20 and relationship with antibodies to beta2-glycoprotein I.

Antiphospholipid antibodies (aPL) react with negatively charged phospholipids, which may often be complexed with a protein cofactor such as beta2 glycoprotein (beta2GPI) and prothrombin. Cofactor requirements may be assessed by measuring antibodies to beta2GPI or by adding Tween 20 to some reagents in the assays for aPL (anticardiolipin and antiphosphatidyIserine). We have measured anticardiolipin antibodies (aCL), antiphosphatidylserine antibodies (aPS), and anti beta2 glycoprotein antibodies (abeta2GPI) in the serum of 10 normal subjects, 20 patients with systemic autoimmune diseases (SAD) diagnosed as having systemic lupus erythematosus (SLE) or antiphospholipid syndrome (APS), and 12 patients with HIV infection. Adding Tween 20 to aPS, the assay couldn't differentiate protein cofactor dependent from independent antibodies, but this can be done by measuring abeta2GPI (P= 0.0008). There was a significant correlation between aCL and a(beta)2GPI in the control group and in the patients with SAD, but not in the HIV-positive (HIV+) patients. After excluding the HIV+ patients, the best Spearman correlation was obtained between a(beta)2GPI and aCL (0.64, P< 0.0005). In 3 out of 7 patients with positive a(beta)2GPI and in 5 out of 6 patients with moderate or high positive aCL of the group of SAD, there was a history of venous thrombosis. The presence of moderate or high values of aCL either alone or together with a(beta)2GPI was significantly associated with a history of venous thrombosis (P < 0.05). Moderate or high aCL concentrations and their association with a(beta)2GPI seems to be useful for the assessment of the risk of venous thrombosis in unselected patients with SLE or APS.

Adult↗
PubMed1998

Changes in coagulation and fibrinolysis in the postoperative period immediately after kidney transplantation in patients receiving OKT3 or cyclosporine A as induction therapy.

Different immunosuppressive agents, in particular OKT3, have been implicated as causative factors in the risk for renal thrombosis in the period immediately after kidney transplantation. Also, in different types of vascular surgery, a state similar to hypercoagulation has been reported. To assess the extent to which OKT3, cyclosporine A (CsA), and surgery itself affect coagulation and fibrinolysis, a study was conducted of 20 patients divided into two groups: group A, 10 patients received OKT3 (first dose during the induction of anesthesia); and group B, 10 patients received CsA (first dose at least 2 hours before transplantation). Basal determinations and determinations at 2, 4, and 24 hours after the induction of anesthesia were made. No differences were found between the groups with respect to the clinical and usual coagulation parameters. The following were studied in both groups: (1) markers of coagulation activity (prekallikrein [PKK] levels and formation of thrombin-antithrombin complexes [TATc]), (2) inhibitors and suppressors of hemostasis (antithrombin III [AT-III] and protein C [PC] activity), (3) markers of fibrinolysis activation (levels of plasminogen [PLG] and of alpha2-antiplasmin [alpha2-APL]), and (4) markers of endothelial damage (tissue plasminogen activator [TPA] and thrombomodulin [TMD]). In both groups, an important formation of TATc was observed early, together with a decrease in PKK levels and consumption of both AT-III and PC, which reached their lowest levels at 24 hours. This points to an activation of coagulation through the intrinsic route and a secondary consumption of hemostasis inhibitors, both possibly caused by surgery. A consumption of PLG and alpha2-APL was also observed, reflecting stimulation of the fibrinolytic system and a physiological response to the activation of coagulation. A greater release of endothelial TPA was only observed in the patients receiving OKT3 (P < 0.0001), possibly signaling endothelial activation. It is concluded that surgical stress could be the major factor triggering the alterations seen in hemostasis and their possible consequences.

Adult↗
PubMed1998

Natural anticoagulant proteins and antiphospholipid antibodies in systemic lupus erythematosus.

OBJECTIVE: Thrombosis is a relatively common complication in patients with systemic lupus erythematosus (SLE) and is strongly associated with the presence of antiphospholipid antibodies (aPL). The mechanism involved in the pathogenesis of this prothrombotic state remains obscure. We studied 4 natural anticoagulant proteins: protein C, protein S, antithrombin III, and plasminogen in 50 patients diagnosed with SLE. METHODS: Protein C, antithrombin III, and plasminogen were measured by chromogenic substrates and total and free protein S by electrophoresis. We also determined the prevalence of different aPL (lupus anticoagulant and antibodies against cardiolipin, phosphatidylserine, and phosphatidylinositol). RESULTS: Ten patients (20%) had a history of thrombosis. Some type of aPL was present in 26 patients (52%). Nine of the 10 patients with history of thrombosis had aPL (p = 0.007). Functional assays for protein C, antithrombin III, and plasminogen were in the normal range in all patients. Low free protein S levels were documented in 19 patients and were associated with the presence of aPL (13/19 were aPL positive) (p < 0.05). Only 4 patients with acquired free protein S deficiency had a history of thrombosis. CONCLUSION: This study shows an association between aPL and reduced free protein S levels in patients with SLE. Further studies are needed to determine the mechanism and role of this acquired deficiency in the pathogenesis of thrombotic episodes in patients with SLE.

Adolescent↗
PubMed1994

[Control of oral anticoagulant treatment using an automated method].

PURPOSES: To evaluate the reproducibility of an automated method (IL test Pro-IL-Complex) in the control of oral anticoagulant therapy. PATIENTS AND METHODS: Samples from patients subjected to oral anticoagulants were analysed with two different methods in order to compare the International Normalized Ratio (INR). The results were studied with the regression analysis and the statistical SPSS programme. RESULTS: Two INR values were attained in 422 samples studied with Thrombotest and Pro-IL Complex. The correlation coefficient (r) between both values was 0.94. When establishing anticoagulation limits of 2.0 and 4.8 for Thrombotest and 1.66 and 4.2 for Pro-IL Complex, the percentage of coincidence between the two methods was above 90%. These findings were more evident when analysing separately those patients with coronary or vascular disease subjected to chronic anticoagulant treatment. CONCLUSIONS: These findings show that Pro-IL Complex test renders results similar to those attained with Thrombotest. Since the former is an automated method available for most of the coagulometers used in clinical laboratories, its easy management, rapidity and possibility for using computerized data are most valuable.

Anticoagulants↗
PubMed1993

[Primary antiphospholipid syndrome in juvenile ischemic stroke].

Results obtained in three patients with juvenile ischemic stroke and criteria of primary antiphospholipid syndrome is reported. These patients are selected out from a series of 12 patients with 18-mounts follow-up. Lupic anticoagulant and anticardiolipin antibodies were found in two of three patients and one patient show anticardiolipin antibodies with negative lupic anticoagulant. All others coagulation proteins examined (antithrombin III, plasminogen, protein C and protein S) were normal. We conclude that antiphospholipid antibodies are associated with increase risk of thrombosis. Therefore should be systematically investigated in juvenile ischemic stroke of unknown aetiology.

Adult↗
PubMed1991

[Antibodies against hepatitis C virus in hemophiliacs: correlation with peripheral blood lymphocyte populations].

The presence of antibodies (Abs) against hepatitis C virus (HCV) was analyzed in 26 haemophiliac patients; a prevalence of 38% was found in the total series and 56% in the treated patients. There were no cases with a positive serology among the three patients who had only received pasteurized factor. The frequency of detection of anti-HCV was higher in the patients who had a positive serology for HIV (67%) and hepatitis B virus (56%) than in the seronegative patients (24 and 29%, respectively). The patients with HCV Abs showed a decrease in the helper (CD4+) lymphocytic population, mainly due to the decrease in the helper inducer (CD4+/Leu8-) cells, such alterations being more evident in the patients who also were HIV+ who showed as well an increase in the T-cell activated lymphocytes (CD3+/la+) and a decrease in CD16+ natural killer cells. These results suggest that the lymphocytic alterations found in the patients with anti-HCV Abs are not specific and would rather be related to the presence or not of HIV infection.

Hemophilia A↗
PubMed1991

Incidence and clinical characteristics of hereditary disorders associated with venous thrombosis.

At present, different congenital defects in several proteins--antithrombin III (AT III), protein C (PC), protein S (PS), and plasminogen (PLG)--are known to be causes of hereditary predisposition to thrombosis (thrombophilia). The incidence of these hereditary disorders in our 204 patients (106 males and 98 females) with venous thromboembolism were 4% (three cases deficient in PC, three in PS, two in PLG, and one patient in AT III). Their families were studied. In all cases the disorders were inherited as an autosomal dominant trait. The first thrombotic episodes occurred at a age of below 40 years. There was no relationship between protein levels and the occurrence of thrombosis, although a significant relationship was observed between a positive history of thromboembolic disease and a diagnosis of protein deficiencies. We evaluated the differences between primary thrombosis and secondary thrombosis. The most common thrombotic sites were the deep veins. There were no differences between males and females. Evaluation of PC, PS, AT III, and PLG in patients with thromboembolic disease should be considered.

Adolescent↗
PubMed1990

Subcutaneous desmopressin (DDAVP) shortens the prolonged bleeding time in patients with liver cirrhosis.

The intravenous infusion of 1-deamino-8-D-arginine vasopressin (DDAVP) shortens the prolonged bleeding time in patients with congenital or acquired bleeding disorders, including patients with uremia or liver cirrhosis. We carried out a double-blind, placebo-controlled crossover study in ten patients with liver cirrhosis to evaluate whether or not their prolonged bleeding times could be shortened by subcutaneous injections of DDAVP (0.3 microgram/kg), a more practical route of administration than intravenous infusions. One hour after DDAVP injection the bleeding time was significantly shortened (p less than 0.05). After 4 h, however, the bleeding time shortening was no longer statistically significant. There was no bleeding time change after placebo. Plasma levels of von Willebrand factor antigen (vWF:Ag) did not significantly increase after DDAVP or placebo. The study shows that subcutaneous DDAVP is an alternative method for short-term shortening of the bleeding time in liver cirrhosis.

Adolescent↗
PubMed1990

[Plasminogen deficiencies in 2 Spanish families. Response to the administration of DDAVP].

We describe two families with heterozygous plasminogen deficiency. In the first the patient was a 27 year-old female who suffered an acute episode of ischemic cerebrovascular disease affecting the left temporal lobe documented by arteriographic, gammagraphic and CAT studies. She had no family history of thrombotic conditions. In the other family the propositus was a 31 year-old man with spontaneous deep venous thrombosis in the left leg. His father was also symptomatic, with a history of recurrent thrombotic complications after predisposing factors, that included multiple venous thrombosis and a pulmonary embolism. Laboratory data showed normal hemostasis test results. Antigenic and functional levels of protein C, protein S and antithrombin III were within normal limits. The only abnormality found was decreased plasminogen activity in plasma; antigenic and functional levels were reduced to about half-normal levels. In both cases crossed immunoelectrophoresis revealed a normal migration pattern of plasminogen. Thus, we conclude that our patients were carriers of congenital hypoplasminogenemia or familial type I plasminogen deficiency, due to decreased synthesis. We also reported on fibrinolytic response to infusion of DDAVP, a synthetic analogue of the antidiuretic hormone. Fibrinolytic activity was normal in basal conditions as well as in response to DDAVP infusion.

Adult↗
PubMed1988

Changes of contact phase proteins during haemodialysis.

Functional and immunological activities of factors XII and XI, Prekallikrein, high molecular weight kininogen and C-1-esterase inhibitor were studied in eight patients before, during and after haemodialysis. During and after dialysis sessions a significant decrease in the functional activities of Prekallikrein and high molecular weight kininogen (p less than 0.05) could be detected, whereas their immunological levels did not change. Furthermore C-1-esterase inhibitor increased after dialysis (p less than 0.05). These results indicate activation of the kinin system during haemodialysis.

Adult↗
PubMed1987

Intravenous and subcutaneous administration of desmopressin (DDAVP) to hemophiliacs: pharmacokinetics and factor VIII responses.

When desmopressin (DDAVP) is given to mild and moderate hemophiliacs intravenously (i.v.) or subcutaneously (s.c.), there is a very large between-patient variability for peak levels of factor VIII coagulant activity (VIII:C). To evaluate whether or not between-patient variability is related to DDAVP levels achieved in plasma, we measured drug levels in 14 hemophilic volunteers (VIII:C 2 to 31 U/dL) who were randomly given 0.3 micrograms/Kg of i.v. or s.c. DDAVP and crossed-over to the other treatment after an interval of 15-30 days. Peak DDAVP levels (Cmax) were higher for i.v. DDAVP (p less than 0.02), times to peak levels (tmax) were shorter for i.v. DDAVP (p less than 0.001). There was no difference between the i.v. and s.c. routes for plasma DDAVP time curve (AUC) and half-life (t 1/2), but there was much larger variability for pharmacokinetic parameters with i.v. than with s.c. DDAVP. Post-DDAVP VIII:C increased 3.4 +/- 1.6 fold (i.v.) and 3.3 +/- 1.3 fold (s.c.) over baseline levels, with no significant correlation between peak VIII:C and DDAVP levels for either route of administration. These findings establish the s.c. route of DDAVP administration to be bioequivalent in effect to the i.v. route, albeit with less variability. At the DDAVP dosage used in this study and currently recommended for therapy, the VIII:C response is neither a function of the rate of absorption of the compound nor of the magnitude of its plasma concentration.

Deamino Arginine Vasopressin↗