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Biomedical subjects

M M Samama

Publications and source records attributed to M M Samama.

At least 109 records · Page 6Linked 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

Risk of thromboembolism in relation to an in-vitro fertilization programme: three case reports.

Severe thrombotic events following ovarian stimulation for in-vitro fertilization (IVF) procedures in three women are reported. None of these patients presented any concomitant clinical sign of ovarian hyperstimulation syndrome. Coagulation inhibitors were in the normal range but cardiovascular risk factors were present. It is postulated that early thrombosis could be favoured by high endogenous plasma oestrogen concentrations subsequent to ovarian stimulation when associated with another risk factor. Our data are discussed in relation to previous publications. It is suggested that risk factors must be considered individually before each IVF attempt. In patients at high risk, clinical management of the post-transfer period is recommended.

Adult↗
PubMed1995

[Current biological surveillance of oral anticoagulant treatment].

The prothrombin time is the coagulation time of citrated plasma in the presence of calcium and a tissue extract, thromboplastin, added in excess. The prothrombin time was historically the first method of evaluation and control of oral anticoagulation. Over the years, the different thromboplastins have changed, diversified, so affecting the result of the prothrombin ration established from the prothrombin time and a reference curve. In 1985, the International Committee on Thrombosis and Haemostasis requested that all the losts of thromboplastin have their international sensitivity index (ISI) indicated. This allowed uniformity of the results by the introduction of the INR (International Normalized Ratio) calculated by the formula: INR = (PTR)ISI, the PTR or prothrombin time ratio corresponding to the patients' prothrombin time divided by that of reference control plasma. It is, in fact, impossible to interpret the results of a prothrombin ration without knowing their expression in INR. The consequences of the absence of uniformity in the control of anticoagulant therapy are important and serious. The uncertainty concerning the degree of anticoagulation inherent in the use of a single prothrombin ratio may be the source of bleeding or thromboembolic complications. Curiously, the system based on the INR is neither generalised, nearly 10 years after its recommendation, nor adopted by the majority of practitioners. However, the stakes are high because the principal complication of oral anticoagulants remains bleeding, including the dramatic strokes. Moreover, the global mortality due to haemorrhagic complications is about 0.1 to 0.5% for treatments of short duration and much higher in prolonged therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

[Hemorrhagic complications of anti-vitamin K treatments].

Among iatrogenic complications of oral anticoagulation, hemorrhagic complications are the most frequent and potentially lethal. The major hemorrhagic risk is the intensity of anticoagulation. A decrease of this risk is obtained with tapering of INR. Age, sex, anticoagulant therapy, and other personal risk factors as duration of anticoagulation, are factors not admitted by all the authors. Our experience at Hôtel-Dieu University Hospital and the literature data provide evidence that patient follow-up in a specialized center should decrease the incidence of hemorrhagic complications.

Administration, Oral↗
PubMed1995

Red cell aggregability increases with the severity of venous insufficiency.

Several studies have suggested the presence of hemorheological abnormalities in venous insufficiency. The present prospective study was carried out to determine whether the increase in hemorheological disturbances parallels the evolution of the disease. Patients were recruited among ambulant outpatients and classified in 3 evolution stages of venous insufficiency according to the clinical and functional examination. Once a certain number of patients were included, the following successive inclusions were made in order to match for age and sex, in the other stages of venous insufficiency, the previously included patients. Since blood rheology is frequently altered in hypertension, diabetes and several other vascular pathologies, patients with those pathologies were not included. Sixty nine patients with venous insufficiency and 23 healthy subjects were tested, making up twenty three matching sets. Red blood cell (RBC) aggregation and disaggregation were assessed with the SEFAM erythroaggregameter on blood samples adjusted to 40% hematocrit. Statistical analysis showed a significant difference for the aggregation index (p = 0.0001), disaggregation shear rate (p = 0.0001) and fibrinogen (p = 0.006) between the 4 groups. Aggregability parameters increased gradually with the evolution of the disease, while the fibrinogen rise was significant only when varicose veins were present (stages 2 and 3). This progressive rise in RBC aggregability with the aggravation of venous insufficiency, by superimposing to the haemodynamic deficit, is likely to induce the formation of RBC aggregates in vivo, to perpetuate venous stasis and to contribute to the development of severe skin damages.

Blood Viscosity↗
PubMed1995

Laboratory monitoring of unfractionated heparin treatment.

Laboratory monitoring is indicated when unfractionated heparin is used in the treatment of established thromboses. Special problems may be encountered in patients with antithrombin III alteration, thrombocytopenia, heparin resistance, or with an increased risk of bleeding.

Drug Monitoring↗
PubMed1995

[Effects of thrombolysis on platelets and coagulation].

Rupture of an atherosclerotic plaque is often the trigger of the clotting process, via the activation of platelets which immediately adhere, aggregate and initiate coagulation on their surface. The final step of platelet aggregation involves membrane glycoprotein IIB-IIIA which has become available. Antibodies directed against this membrane receptor are currently under evaluation. They possess definite antithrombotic properties. Complex interactions between thrombolysis, leading to generation of plasmin, and platelet functions have been identified. Depending on its concentration and possibly successively, and according to in vitro experimental conditions, plasmin may be a platelet proaggregant or antiaggregant. Correlations have also been recently demonstrated between thrombolytic activity and coagulation, as, paradoxically, it has been shown that plasmin, the final step of thrombolysis, activates the intrinsic pathway of coagulation, predisposing to the formation of thrombin. This activation is involved in the efficacy of heparin therapy following intravenous thrombolysis during the acute phase of myocardial infarction. This paradoxical action of thrombolysis could also play a role in reocclusions after effective thrombolysis during the acute phase of myocardial infarction. A better understanding of the thrombolysis process and its interactions with platelets and coagulation is important in order to improve the results of this treatment, which are correlated with patient survival.

Blood Coagulation↗
PubMed1995

Changes in haemostatic variables induced by oral contraceptives containing 50 micrograms or 30 micrograms oestrogen: absence of dose-dependent effect on PAI-1 activity.

Several studies have suggested a dose-response relation between the oestrogen content of oral contraceptive (OC) and the risk of both venous thrombosis and arterial disease, when oestrogen doses were higher than 50 micrograms. However, there is no clear epidemiological evidence for a decrease in thrombotic risk with formulations containing less than 50 micrograms oestrogen. Therefore, we investigated haemostatic variables in users of OC containing either 30 micrograms (35 women) or 50 micrograms (29 women) ethinyl estradiol as compared with non users (64 women) matched for age and smoking status. Mean values of antithrombin activity were significantly lower in 30 micrograms or 50 micrograms oestrogen users than in non users (96% and 98% vs 105%, respectively, p < 0.001), but they were not significantly different between the two groups of OC users. There was a significant increase in mean values of factor VII antigen in women taking either 30 micrograms or 50 micrograms oestrogen as compared with non users (96% and 101% vs 85%, respectively, p < 0.005). Although the difference between both groups of OC users was not significant, a positive linear trend in factor VII levels was observed within the 0-50 micrograms oestrogen range (p < 0.001). Mean levels of fibrinogen were slightly higher in 30 micrograms or 50 micrograms oestrogen users than in non users (2.71, 2.66 g/l vs 2.55 g/l, respectively), but there was no significant difference between the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗
PubMed1995

[Variability of INR due to thromboplastin. Comparison of two recombinant thromboplastins and one rabbit thromboplastin].

We have compared the INR obtained with three different thromboplastin reagents: one rabbit and two recombinant tissue factor thromboplastins using the same coagulometer. A preliminary study has shown that freezing of plasmas at -80 degrees centigrade causes a 6% increase in INR. We did this experiment on 57 plasma samples from patients receiving oral anticoagulant therapy, none of them receiving heparin. Results show that global prothrombin activity expressed in percentage is significantly lower with recombinant tissue factors than with rabbit thromboplastin. ISI of one of the two recombinant thromboplastins did not seem to be appropriate to our coagulometer highpointing the variability of INR due to the coagulation analyzer. This underlines the necessity for each laboratory to assess the ISI value provided by the manufacturer according to its working conditions. This study suggests that the results of prothrombin time should be exclusively expressed in INR for patients treated with oral anticoagulants.

Animals↗
PubMed1995

Thrombolytic therapy: future issues.

A considerable amount of work has been devoted to thrombolytic therapy (about 3000 references from 1991 to 1995 in a Medline search). The most important and well established indication of thrombolytic treatment is acute myocardial infarction (MI). Megatrials have evidenced a significant 30 to 40% reduction in hospital mortality in the treated patients. However, lack of sufficient thrombolysis in approximately 25% of patients, reocclusion in 6 to 16% of patients and intracranial hemorrhage in about 0.5% of patients are the main concerns regarding thrombolysis. Three approaches should improve the results of thrombolytic therapy in acute MI: earlier medical treatment, use of more efficacious thrombolytic agents in combination with more active antithrombotic agents and reduction of severe bleeding with safer combination of drugs. An improved of laboratory monitoring may also reduce the incidence of severe hemorrhagic events. In acute pulmonary embolism (PE), a change of indication for treatment based on echocardiography and high probability ventilation-perfusion lung scan results (without requiring pulmonary angiography) could broaden the use of thrombolysis. However, thus far, there has not been a demonstration of a reduction in mortality in large controlled studies. Thrombolysis in acute ischemic stroke is an attractive treatment but thrombolytic treatment is still at an experimental stage. However, the successful use of rt-PA in acute MI has renewed the interest in thrombolysis for focal cerebro-vascular ischaemia. Large controlled studies with SK, rt-PA or UK locally or intravenously administered have been recently undertaken to evaluate the benefit/risk ratio of treatment which seems surprisingly variable in different subgroups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Ischemia↗