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J Fontcuberta

Publications and source records attributed to J Fontcuberta.

At least 109 records · Page 6Linked to original sources
PubMed1994

[Comparative multicenter study of a rabbit high-sensitivity thromboplastin and a recombinant thromboplastin with synthetic phospholipids].

PURPOSE: The purpose of the present study was to compare the results obtained with a human recombinant thromboplastin (Innovin, Baxter) (IN) and a high-sensitivity rabbit brain reagent (Thromboplastin IS, Baxter) (IS), on the performance of prothrombin time (PT) test and the functional assay of factors included in the extrinsic coagulation system, in order to establish possible differences on imprecision, diagnostic accuracy and sensitivity to the oral anticoagulant defect, between the two products. MATERIAL AND METHODS: Six Spanish hospital took part in the study. Plasma samples from 221 healthy subjects, 100 patients with severe liver disease, 27 with dysfibrinogenaemia, 10 with lupus anticoagulant and from 13 individuals propositus and their relatives with congenital deficiencies of the extrinsic coagulation pathway, and their relatives were studied; 188 patients stabilized on oral anticoagulant therapy and 82 on heparin therapy were also included. The in vitro effect of heparin was tested by addition of increasing amounts of heparin (0.3 to 10.0 IU/mL) to aliquots of normal plasma. RESULTS: Both in the intra-assay and in the inter-assay imprecision study, a better coefficient of variation was obtained with IN when the PT was performed on abnormal samples. Prothrombin time ratio from patients with liver disease had significantly higher values with IS. On the contrary, IN had a higher sensitivity in samples from patients with dysfibrinogenaemia or from those stabilized on oral anticoagulant therapy. In showed a very low sensitivity to heparin at concentrations corresponding to the therapeutic range. CONCLUSIONS: The results of this field study indicate that IN, compared with a high-sensitivity rabbit brain thromboplastin, is a suitable reagent for PT determination in normal subjects, patients with liver disease or with congenital deficiencies of clotting factors. It shows a higher sensitivity in cases of dysfibrinogenaemia and in patients on oral anticoagulant therapy. In addition, the recombinant reagent had better reproducibility when the PT was performed on abnormal samples, and it was hardly affected by heparin within the therapeutic range.

Afibrinogenemia↗
PubMed1993

Effects of linoleic and oleic acid anilides on prostacyclin synthesis and fibrinolytic profile of human endothelial cells in culture: relevance to the toxic oil syndrome.

We evaluated the effects of fatty-acid anilides (FAA) on prostacyclin (PGI2) synthesis and on the fibrinolytic properties of human umbilical vein endothelial cells. Preincubation of endothelial cells with oleic- and linoleic-anilides (OAA and LAA, respectively) resulted in a time- and concentration-dependent inhibition of ionophore A23187- and thrombin-induced PGI2 synthesis. However, no significant effects of FAA on arachidonic acid-induced PGI2 synthesis were found, except with 1000 microM LAA which inhibited cyclooxygenase activity after 24 h. In general terms, OAA showed similar inhibitory effects on PGI2 production as did LAA, but with a shifted time course, since the production of PGI2 at 24 h for OAA was similar to that observed for LAA at 2 h. The release of labeled arachidonic acid from cell membranes was significantly reduced (75-85%), after 24 h, with both FAA. The effect of 100 microM LAA on thrombin-induced PGI2 production was rapid (within 15 min) and irreversible after 60 min. The recovery of PGI2 synthesis after LAA treatment was blocked by cycloheximide, suggesting a decrease of phospholipase(s) activity or cessation of enzyme synthesis. Moreover, this reduced PGI2 synthesis was not associated with [3H]adenine release. Our data indicate that FAA induce a significant impairment of stimulated PGI2 synthesis and arachidonic acid release in endothelial cells, acting primarily as inhibitors of phospholipase(s) rather than of cyclooxygenase. Finally, both LAA and OAA induce an anti-fibrinolytic activity in these cells where major changes are observed in the plasminogen activator inhibitor and the urine-type plasminogen activator.

Anilides↗
PubMed1993

[Pregnancy and thrombophilia in women with congenital deficit of antithrombin III, protein C, protein S or plasminogen: analysis of 39 cases].

BACKGROUND: Pregnancy, delivery and puerperium are situations which increment the risk of thromboembolic complications in women who are carriers of congenital heterozygotic deficits of type I antithrombin III (ATIII), protein C (PC) or protein S (PS). The aim of this study was to analyze the experience of the authors and propose therapeutic conduct in each case. Furthermore, the spontaneous losses of pregnancy related with these deficits were studied. METHODS: Thirty-nine women, seventeen with ATIII deficit, fifteen with PC deficit and four with a deficit of PS and three with a plasminogen (Pg) deficit totalling 79 pregnancies and 51 thrombotic episodes sixteen of which were related with the pregnancy, delivery or puerperium were studied. The antigenic and functional activity of ATIII, PC, PS and Pg were determined. RESULTS: The incidence of thrombosis for the ATIII deficit during pregnancy was 39%, which was greater, of statistical significance (p = 0.046), than the 15% observed during puerperium. In women with a deficit of PC, the incidence of thrombosis was 4.5% during pregnancy and 14% during puerperium with no significant difference between the two situations. The incidence of thrombosis during pregnancy and postpartum in the deficit of ATIII was significantly higher (p < 0.025) than that observed for the deficit of PC. For women with a deficit of PS and Pg the incidence of thrombosis was nul in pregnancy and puerperium. CONCLUSIONS: Pregnancy and puerperium are situations which trigger thrombotic phenomena and increase the risk of the same in women with a deficit of antithrombin III and protein C and, to a lesser degree, the deficit of protein S or plasminogen. A strict control of these situations and individualized treatment is required according to the type of deficit, presence of previous thromboembolic history and anticoagulant history at the time of pregnancy. No increase in the risk of loss of pregnancy in any of the deficits studied was observed.

Adult↗
PubMed1993

Acceptor splice site mutation in the invariant AG of intron 5 of the protein C gene, causing type I protein C deficiency.

An acceptor splice-site mutation (3318, A-->G) in the invariant AG of intron 5 of the human protein C gene has been identified in a Spanish family with heterozygous type I protein C (PC) deficiency and thromboembolic disease. Family studies confirmed cosegregation of the mutation with type I PC deficiency. Computer analysis of the mutated sequence predicted the normal splicing site to be abolished by this mutation, whereas a cryptic splice site located two nucleotides downstream, in exon 6, is probably activated. According to this, 3318, A-->G should result in a frameshift with a stop at codon 119, in agreement with the presence of a type I or quantitative PC deficient phenotype in the affected members of the family.

Adult↗
PubMed1993

Acquired factor VIII inhibitor preceding chronic lymphocytic leukemia.

An acquired factor VIII inhibitor was found in an 82-year-old woman who presented with numerous spontaneously appearing ecchymoses. Coagulation studies revealed the presence of a prolonged activated partial thromboplastin time that was not corrected by 1:1 mixture with normal fresh plasma after a 2-h incubation. Factor VIII:C was 4%, and the titer for factor VIII inhibitor was 9 Bethesda units. Three months later, after a retroperitoneal hemorrhage, a lymphocytosis was found in her peripheral blood with morphological and surface immunophenotype characteristics of B-cell chronic lymphocytic leukemia, later confirmed by bone marrow morphological and immunocytochemical examinations. To our knowledge, this is the first report of an autoimmune factor VIII inhibitor associated with chronic lymphocytic leukemia.

Aged↗
PubMed1993

Lack of effect of influenza vaccine on anticoagulation by acenocoumarol.

OBJECTIVE: To analyze the effects of influenza vaccine on patients receiving chronic anticoagulant therapy with acenocoumarol. DESIGN: A prospective trial. SETTING: Hospital de la Santa Creu i Sant Pau, Barcelona. PATIENTS: Forty-three patients who received acenocoumarol, had stable levels of International Normalized Ratio (INR), and did not need dosage modification for four months before entering the study. INTERVENTION: A study of anticoagulation levels measured by INR at 7, 15, and 30 days from administration of the trivalent vaccine from the 91-92 campaign was conducted. MAIN OUTCOME MEASURES: Comparison was made between basal values (day 0) and anticoagulation levels at 7, 15, and 30 days from vaccine administration by means of a repeated-measures ANOVA. RESULTS: Nine patients (21 percent) had INR levels out of the therapeutic range during the study period. INR increased in three of these patients and decreased in six. There were no significant intraindividual changes in INR values during the time period analyzed (p = 0.125). No hemorrhagic or thrombotic manifestations occurred and no significant changes in renal or hepatic biochemistry were observed. CONCLUSIONS: Influenza vaccine does not modify acenocoumarol activity in patients receiving long-term anticoagulant therapy.

Acenocoumarol↗