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Biomedical subjects

I Elalamy

Publications and source records attributed to I Elalamy.

45 records · Page 3Linked to original sources
PubMed1995

[Resistance to activated protein C in venous thromboembolic complications. Incidence and clinical manifestations].

OBJECTIVES: The frequency of activated protein C resistance is not well established for patients with venous thromboembolic disease. We studied resistance to activated protein C in patients with a past history of deep vein or superficial vein thrombosis. METHODS: Activated protein C resistance was measured in 175 patients (37 males, 138 females; mean age 40.9 +/- 13.8 years; range 15-77) who had suffered a venous thromboembolic event more than one month earlier. Exclusion criteria were malignancy, known autoimmune disease or known coagulopathy. A control population of 50 healthy subjects were also tested to establish a normal lower limit (mean ratio minus 2 SD). RESULTS: The lower limit was established at 2.14. According to this definition, there were 29 thromboembolic patients who were resistant to activated C protein (17%). Two of the subjects considered healthy in the control group were also resistant (4%). There was no difference for age or sex between resistant and non-resistant subjects. Comparing our findings with those reported in the literature confirmed that 3 to 5% of healthy subjects and 15 to 25% of patients with history of venous thromboembolism are resistant to activated C protein. CONCLUSION: Resistance to activated C protein thus appears as a risk factor for thrombotic events which is comparatively more frequent than other causes of thrombotic disease.

Adolescent↗
PubMed1995

Prevalence and patient profile in activated protein C resistance.

Activated protein C resistance (APC-R) is a recently defined abnormality of the coagulation system predisposing to the development of a hypercoagulable state. The authors have attempted to evaluate the prevalence and clinical manifestation of APC-R by studying a population of 183 patients with a history of venous thromboembolic episodes. Laboratory evaluation of APC-R was performed using the test initially described by Dahlbäck and colleagues based on the activated partial thromboplastin time (APTT) with the Coatest APC resistance kit (Chromogenix, Sweden) on KC10 coagulometer (Amelung, Germany). These results showed a 13% prevalence of APC-R as demonstrated by an APC ratio below 2.0. The male-to-female ratio was 1:7. Most of the thrombotic episodes were deep venous thromboses (50%).

Adolescent↗
PubMed1995

Human anti-streptokinase antibodies induce platelet aggregation in an Fc receptor (CD32) dependent manner.

Exposure to streptokinase (SK) elicits anti-SK antibodies (Abs), which inhibit fibrinolysis and induce platelet aggregation. The mechanism of the latter is not fully understood, although it seems to involve platelet binding by a plasminogen streptokinase and anti-SK ternary complex. Anti-SK Abs were purified by affinity chromatography from serum of patients having received SK for acute myocardial infarction (AMI), and were shown to be of the IgG type. Their effects were studied with (i) human platelets in citrated plasma in the presence of SK or acetylated plasminogen-SK activator complex (APSAC), and (ii) in washed platelets, resuspended in Tyrode buffer after lowering the ionic strength, in the presence of APSAC (which provides both SK and plasminogen). An antibody concentration-response curve was obtained, showing a plateau in the presence of 0.1 mg/ml IgG. By increasing the concentration of APSAC, we obtained a unimodal response curve, the optimal concentration of APSAC being 0.05 U/ml. Aggregation was suppressed by chelating calcium with EDTA, blocking fibrinogen binding by the synthetic peptide Arg-Gly-Asp-Ser (RGDS), and raising intraplatelet cAMP with Iloprost (a prostacyclin analogue). Aggregation required the interaction of the anti-SK Ab Fc domain with the platelet Fc-gamma receptor type II, also known as CD32, since: (i) it was blocked by the monoclonal antibody IV-3 directed against CD32, (ii) it did not occur with F(ab)'2 fragments, which block the response to the intact IgG. The clinical relevance of these platelet-activating anti-SK antibodies remains to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMedDate not supplied

[Thrombosis of a cardiopulmonary bypass circuit despite recommended hypocoagulation with danaparoid during the acute phase of type II heparin-induced thrombocytopenia].

A 36-year-old patient was admitted to our hospital with ischaemic stroke. The initial assessment allowed the diagnosis of an antiphospholipid syndrome (APS) and an intracardiac mass suggestive of a heart tumour. The patient was treated with unfractionated heparin. Type II heparin-induced thrombopenia (HIT) was diagnosed on the 18th day of therapy. Given the risk of stroke recurrence it was decided to remove the cardiac tumour surgically. Cardiopulmonary bypass (CPB) was performed using danaparoid in a state of deep hypothermia, in accordance with the well-established protocol in use in our department. As the CPB and surgical procedure came to an end a massive thrombus began forming in the circuit, requiring immediate displacement of the CPB cannulae. The anti-Xa activity level obtained had been considered effective at an estimated 1.20 IU/ml, although, the level recommended by Magnani is between 1.50 and 2.0 IU/ml. There was no clinical consequence and postoperative recovery was uneventful. The discrepancy between the satisfactory level of anti-Xa activity and the thrombus formation in the CPB circuit raises the issue of the diversity of published anticoagulation protocols, the difficulty to extrapolate within a surgical team, the need for intensive laboratory monitoring within a narrow therapeutic range, as well as the patient profiles variability with concurrent disorders complicating their clinical management.

Adult↗
PubMedDate not supplied

[Influence of oral anticoagulant treatment on D-dimers levels].

The usefulness of D-dimers determination for the exclusion of deep vein thrombosis (DVT) has been extensively studied. The persistence of high levels of D-dimers has also been suggested as a marker of hypercoagulability in rare studies and might be used to identify patients at risk for recurrent DVT. We have studied the influence of oral anticoagulant treatment in 149 patients, 17 to 84 year-old, with a history of venous thromboembolism; 81 received oral anticoagulant treatment, 68 did not. Patients with known reasons for high level of D-dimers such as cancer were excluded. Thrombophilia was found in 84 patients. D-dimers measurements were performed by ELFA technique using Vidas (bioMérieux, France) analyzer. A significantly lower level of D-dimers was observed in patients under oral anticoagulant compared to patients without this treatment, 197 +/- 134 mug/L versus 399 +/- 239 mug/L, respectively (p < 0.001). A level upper the normal value (500 mug/L) was found in only 3 patients out of 81 receiving an oral anticoagulant treatment as compared with 21 of the 68 patients without treatment. This decrease of D-dimers in patients receiving oral anticoagulants was the same in the different age populations. There was no correlation between INR and D-dimers levels in this study. The clinician should be informed of the decrease of D-dimers in patients treated with anticoagulants. The decrease of D-dimers plasma level during oral anticoagulant treatment suggest that D-dimers concentration in plasma is an indirect marker of reduced clotting activity in vivo.

Administration, Oral↗