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J Fontcuberta

Publications and source records attributed to J Fontcuberta.

At least 91 records · Page 5Linked to original sources
PubMed1995

Adverse reaction to streptokinase with multiple systemic manifestations.

We report the case of a 47-year-old woman with a history of mitral valve replacement with a mechanical prosthesis who was admitted to the hospital with a 3-month history of progressive exertional dyspnoea and was diagnosed as suffering from prosthetic valve thrombosis. Two consecutive courses of streptokinase were given as an intravenous infusion over 90 min at a dose of 1,500,000 IU each. Twenty minutes after the start of the second infusion (3 h and 20 min after the first one) she developed chills, fever, tachycardia and hypotension: symptomatic treatment was given and the infusion was completed. Two days later jaundice and choluria appeared with laboratory findings of hepatic cytolysis and cholestasis and renal insufficiency. The results of extensive microbiological and immunological investigations were not revealing. All the laboratory values spontaneously returned to baseline levels over the next 4 weeks. These abnormalities were attributed to an allergic reaction to streptokinase, although the exact pathogenic mechanisms involved are not known. We believe that further studies to elucidate the mechanism involved in the production of these effects are warranted in view of their potential clinical severity.

Female↗
PubMed1995

Bioavailability and pharmacokinetics of a new low molecular weight heparin (RO-11)--a three way cross-over study in healthy volunteers.

This study reports on the bioavailability and pharmaco kinetics of a new low molecular weight heparin (RO-11), with a mean molecular weight of 3,600-3,800 daltons. It was administered to 12 healthy individuals in an open, cross-over study. Each subject was randomly assigned to three experimental treatments: a) 30 mg by subcutaneous route, b) 60 mg subcutaneously and c) 60 mg intravenously, leaving a wash-out period of one week between treatments. The pharmacokinetic profile was calculated by means of the anti-FXa effect, measured on serial samples taken before and during the 24 h period after each treatment. The effects of the drug on global coagulation tests, Antithrombin-III levels, tissue-factor pathway inhibitor activity and anti-FIIa activity were also assessed. After the intravenous injection, a maximal anti-FXa effect of 1.30 +/- 0.18 IU/ml was measured at 0.05 h and was not measurable after 12 h. After the subcutaneous injection of 30 and 60 mg, the maximal anti-FXa effect (0.34 +/- 0.08 IU/ml and 0.54 +/- 0.06 IU/ml) was reached after 2-4 h, and was not measurable after 12-18 h. The magnitude of this effect was dose-dependent and the absorption and elimination processes followed a first-order pattern for every dose and route. RO-11 showed a biological half-life of about 5 h and a high subcutaneous bioavailability (96%).

Adult↗
PubMed1995

Prothrombotic state and signs of endothelial lesion in plasma of patients with inflammatory bowel disease.

Recent investigations suggest that microthrombi formation in bowel capillaries could be a determinant factor in inflammatory bowel disease (IBD) pathogenesis. To evaluate the implication of the hemostatic system during these thrombotic events, we analyzed plasmatic values of prothrombotic state markers, physiologic inhibitors of coagulation, and endothelial lesion markers in 112 IBD patients. We found an increase in thrombin-antithrombin complexes and a decrease in antithrombin III, probably due to consumption, demonstrating an increase in thrombin generation. High levels of D-dimer reflect increased fibrin formation, but there is no correlation between thrombin generation markers and D-dimer, possibly suggesting the presence of inadequate fibrinolysis. Levels of tissue factor pathway inhibitor were higher in patients than in controls. Nine patients with Crohn's disease (35% of our sample) had levels of this marker under 70% (range 37-69%). Von Willebrand factor values were increased and those of thrombomodulin only in active patients. Most of the changes were detected in patients with inflammatory activity, and there were no differences between ulcerative colitis and Crohn's disease. In conclusion, these results support the hypothesis that there is an endothelial lesion with sustained coagulation activation in IBD patients.

Adult↗
PubMed1995

Heparin-induced thrombocytopenia and heart operation: management with tedelparin.

Anticoagulation for cardiopulmonary bypass in the infrequent clinical setting of thrombocytopenia associated with the use of unfractionated heparin is a very serious problem. We describe a case in which a low-molecular-weight heparin (tedelparin) was selected for this purpose based on a platelet aggregation test, permitting adequate anticoagulation during cardiopulmonary bypass for valve replacement. This case report might help establish an adequate anticoagulation protocol when faced with a patient suffering from this condition.

Cardiopulmonary Bypass↗
PubMed1995

Aprotinin versus desmopressin for patients undergoing operations with cardiopulmonary bypass. A double-blind placebo-controlled study.

BACKGROUND: Aprotinin reduces blood loss in operations done with cardiopulmonary bypass, whereas the use of desmopressin remains controversial. We compared aprotinin, desmopressin, and placebo in a double-blind, randomized trial to evaluate bleeding and transfusion requirements. METHODS AND RESULTS: One hundred forty-nine patients (48 received aprotinin, 50 desmopressin, 51 placebo) were included. Blood loss and transfusion requirements were recorded and levels of Factor VIII coagulant activity, von Willebrand's factor, thrombin-antithrombin complexes, and D-dimer were measured. Overall blood loss was 195 +/- 146 ml/m2 in the aprotinin group, 400 +/- 192 ml/m2 in the desmopressin group, and 489 +/- 361 ml/m2 in the placebo group (95% confidence intervals: difference between desmopressin and aprotinin 98 to 312 ml/m2, p < 0.001; difference between placebo and aprotinin 190 to 398 ml/m2, p < 0.001). Twenty-six percent of patients treated with aprotinin, 66% of those treated with desmopressin, and 56% of those treated with placebo were given transfusion (95% confidence intervals: difference between aprotinin versus placebo plus desmopressin 51% to 71%, p < 0.001). Fibrinolytic activation throughout cardiopulmonary bypass was markedly higher with placebo or desmopressin administration. D-dimer level correlated with overall blood loss in patients receiving desmopressin or placebo, but not in those receiving aprotinin. CONCLUSION: Aprotinin administration reduces blood loss and transfusion requirements in cardiopulmonary bypass. This benefit may be explained by a lower activation of fibrinolysis.

Antithrombin III↗
PubMed1995

Presentation of an acquired factor VIII inhibitor with a muscular haematoma mimicking a deep venous thrombosis in a patient with breast cancer.

Acquired haemophilia is a rare disorder that it is associated with several diseases. Patients may present with spontaneous haematomas in different places which can sometimes be fatal. We present a 69-year-old woman with breast carcinoma who developed a factor VIII inhibitor. The initial haemorrhagic event was a spontaneous deep muscular haematoma in the right leg mimicking a deep venous thrombosis. She was successfully treated with prednisone.

Aged↗
PubMed1995

The effect of endogenous oestradiol levels on protein S concentration during a menstrual cycle and after GnRH analogues and gonadotropin therapy.

We studied two groups of females to investigate the effect of endogenous oestradiol levels on total and free protein S (tPS, fPS) plasma concentrations. One group (group I) consisted of 12 healthy volunteers who were studied throughout one menstrual cycle; the other group (group II) consisted of 16 young women who were treated with GnRH analogues and gonadotropins before undergoing in vitro fertilization. Neither tPS nor fPS varied significantly with respect to the physiological changes of oestradiol or to the very low and high levels of oestradiol, achieved after GnRH analogues suppression and gonadotropin stimulation. These results indicate that endogenous oestradiol does not affect PS concentration.

Adolescent↗
PubMed1995

Hemostatic disturbances in acute ischemic stroke: a study of 86 patients.

The relevance of coagulation abnormalities in ischemic stroke remains uncertain. The purpose of this study was to identify abnormal patterns of coagulation in established ischemic stroke. We measured coagulation parameters in 86 patients with acute ischemic stroke: 10 lacunar, 55 atherothrombotic and 21 cardioembolic. Statistical comparisons were made between different stroke groups and between all stroke patients and 60 healthy controls. A decrease in functional antithrombin III and plasminogen and an increase in thrombin-antithrombin III complexes, total protein S, tissue plasminogen activator, plasminogen activator inhibitor and D-dimer were observed in the stroke group (p < 0.05). A positive correlation was found between tissue plasminogen activator and thrombin-antithrombin III levels in cardioembolic stroke (p < 0.05). Protein C levels showed significant differences between the three groups, and in the cardioembolic group they were lower than in controls (p < 0.05). Antiphospholipid antibodies were positive in two cases. We conclude that activation of coagulation and fibrinolytic pathways was observed during the acute phase of ischemic stroke. Protein C activity is different in the three types of strokes analyzed, and higher levels seem to be associated with lacunar lesions. Antiphospholipid antibodies do not seem to play an important role in the pathogenesis of stroke in a nonselected population.

Aged↗
PubMed1994

Severe homozygous protein C deficiency: identification of a splice site missense mutation (184, Q-->H) in exon 7 of the protein C gene.

Single strand conformation polymorphism (SSCP) analysis of exon 7 of the protein C gene has identified a novel splice site missense mutation (184, Q-->H), in a newborn child with purpura fulminans and undetectable protein C levels. The mutations, seen in the homozygous state in the child and in the heterozygous state in her mother, was characterized and found to be a G to C nucleotide substitution at the -1 position of the donor splice site of intron 7 of the protein C gene, which changes histidine 184 for glutamine (184, Q-->H). According to analysis of the normal and mutated sequences, this mutation should also abolish the function of the donor splice site of intron 7 of the protein C gene. Since such a mutation is compatible with the absence of gene product in plasma and since DNA sequencing of all protein C gene exons in this patient did not reveal any other mutation, we postulate that mutation 184, Q-->H results in the absence of protein C gene product in plasma, which could be the cause of the severe phenotype observed in this patient.

Base Sequence↗