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Biomedical subjects

M Samama

Publications and source records attributed to M Samama.

At least 163 records · Page 9Linked to original sources
PubMed1986

[Thrombolytic treatment in the acute phase of myocardial infarction. Evaluation in 1986].

Fibrinolytic therapy is effective in reducing the extent of myocardial infarction by lysing intracoronary clots. An overview of twelve trials of prolonged intravenous infusion of SK showed a highly significant reduction in short term mortality. Intra coronary SK infusion achieved reperfusion of the coronary artery in 60 to 90 p. 100 of patients and improvement of left ventricular function was reported. Mortality was also significantly reduced at 6 months. The frequency of bleeding was relatively low and ventricular arrhythmias were not a serious problem. High dose brief duration intravenous SK therapy achieved reperfusion of the occluded coronary artery in 44 to 60 p. 100 of patients. Left ventricular function was also improved. An Italian multicentre trial has shown a significant decrease in the overall hospital mortality of a randomized population. There is no evidence that UK was more effective than SK. New fibrinolytic agents (T-PA, acylated SK-plasminogen activator), with more fibrin specific activity, were successful in inducing coronary thrombolysis in patients with acute myocardial infarction. The rate of reocclusion was about 20 p. 100 and additional stabilising procedure (percutaneous transluminal coronary angioplasty) was necessary in many patients.

Fibrinolytic Agents↗
PubMed1986

Comparison of antithrombotic activity of two heparin fragments PK 10169 (mol. wt. 5,000) and EMT 680 (mol. wt. 2,500) and unfractionated heparin in a rabbit experimental thrombosis model: relative importance of systemic anti-Xa and anti-IIa activities.

Two fragments obtained by chemical depolymerization of heparin from porcine mucosal origin PK 10169 (mol. wt. 5,000) and EMT 680 (mol. wt. 2,500) were compared to the original heparin in a rabbit experimental thrombosis model. Thrombosis was induced either by human serum or by bovine Xa. Various doses of heparins (6 animals per dose and per inducer) were injected in order to find the lowest systemic levels of anti-Xa and anti-IIa activities able to inhibit venous-induced thrombogenesis. The systemic activities associated with an inhibition of 50% of the generated thrombi were as follows: 0.17 +/- 0.02 anti-Xa and 0.16 +/- 0.03 anti-IIa units obtained after injection of 97 micrograms/kg (14 anti-Xa and anti-IIa units/kg) of unfractionated heparin, 0.28 +/- 0.04 anti-Xa and 0.14 +/- 0.03 anti-IIa units obtained after injection of 250 micrograms/kg (15 anti-Xa and 7.5 anti-IIa units/kg of PK 10169, and 2.6 +/- 0.2 anti-Xa and 0.06 +/- 0.01 anti-IIa units obtained after injection of 5000 micrograms/kg (260 anti-Xa and 5 anti-IIa units/kg) of EMT 680. These results suggest that the presence of an anti-IIa activity associated with the anti-Xa activity strongly increases the thrombogenesis inhibition in the serum and Xa-induced thrombosis for the heparin fragments of low and very low molecular weight used in this study.

Animals↗
PubMed1986

[Uterine rupture causing acute defibrination syndrome. Apropos of 3 cases].

The authors report three cases of rupture of the uterus during delivery, complicated by an acute defibrination syndrome. Death resulted in two cases. The sequence of rupture of the uterus----shock----pathological condition of coagulation----great increase in the shock occurred in all three patients. This sequence could only be arrested in one of the three patients who had a total hysterectomy. Partial hysterectomy in the other two was ineffective. These three case histories suggest that total hysterectomy after even partial correction of the haemorrhagic state can be the best treatment in this very serious condition.

Adult↗
PubMed1986

[Resistance to vitamin K antagonists. 6 cases].

Haemorrhage is the most frequent complication of oral anticoagulant therapy (OAT) and a resistance to these drugs is rarely reported. The following classification of OAT resistance is proposed: primary or secondary resistance according to the delay of onset (at the initiation of therapy or later); selective or generalized according to the number of drugs involved (only one or several); absolute or relative as judged by the prolongation of the prothrombin time (absent or moderate). Six cases are reported and the mechanisms of resistance are discussed: no intake, variations in the vitamin K availability (diet, intestinal absorption and synthesis of vitamin K), variations in the pharmacokinetics of oral anticoagulants (drug interactions, abnormal hepatic metabolism) and variations in the receptor affinity (hereditary resistance). Resistance is often overcome by progressive increase of the doses of oral coagulant, or by changing drugs, to warfarin or coumadin (long acting drugs).

Adult↗
PubMed1986

[Constitutional protein C deficiency in 57 patients from 22 non-related families].

A congenital deficiency in protein C (physiological inhibitor of coagulation) was identified in 57 patients: the deficiency was quantitative (type I) in 20 families, qualitative (type II) in two families. The transmission was autosomal dominant in 21 families but was suspected to be recessive in one family: the 18 years old homozygous propositus has a severe deficiency (protein C = 16 p. 100): both parents are heterozygous (consanguinity was present) and 5 other family members with heterozygous deficiency are asymptomatic. In the 49 patients (25 women, 24 men) belonging to the 21 other families, 9 men and 4 women (27 p.100) are asymptomatic although precipitating factors had existed in 5 patients. In the remaining 36 symptomatic patients, a deep venous thrombosis was observed in 34, a pulmonary embolism in 18. Recurrent arterial thromboses were diagnosed in 3 patients. The first thrombotic episode was observed at the mean age of 27 +/- 11 years and a triggering factor was found in 26 patients (72 p. 100). Thrombosis was recurrent in 21 (60 p. 100). In the patients without oral anticoagulant treatment, mean protein C antigen concentrations were 47 +/- 9 p. 100 and mean protein C activity was 46 +/- 10 p. 100. In 4 patients with type II deficiency, protein C antigen levels were normal (113 +/- 15 p. 100), contrasting with decreased protein C activity (43 +/- 6 p. 100). Thirty-eight patients have been treated with oral anticoagulants and a skin necrosis developed in the homozygous patients only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Treatment of deep venous thromboses with heparin. Therapeutic management and biological monitoring].

Heparin may be administered either prophylactically (to prevent postoperative thromboembolic complications) or therapeutically (when thrombosis has occurred) and the dosages are very different. In addition, low molecular weight heparins are now available, and usually reserved only for prevention of thrombosis. The biological monitoring of these different therapies has evolved, and in addition to the classical tests like the recalcified plasma clotting time or the APTT, it is now possible to use more specific tests like the amidolytic activity of anti-IIa or anti-Xa. None of the simple tests alone is satisfactory for the verification of the efficacy of the treatment on a formed thrombosis or for detecting patients at high risk of haemorrhage. At this present state of our knowledge, the association of two of the preceding tests is recommended as any discrepancy could lead to the detection of an associated, unrecognised abnormality such as a circulating anticoagulant factor or thrombocytopaenia. The monitoring of classical prophylactic treatment generally only requires a very limited monitoring.

Acute Disease↗
PubMed1985

Questions and answers on prothrombin time standardisation in oral anticoagulant control.

One of the reasons why oral anticoagulants fell into disrepute is the absence of internationally accepted standardised procedures for controlling the level of anticoagulation. This deplorable situation resulted in over- and under-coagulation and uncertainty in the therapeutic range. International conformity can now be obtained by using an International Normalised Ratio (INR) which is derived from the individual result obtained in a given plasma sample and the International Sensitivity Index (ISI) of the tissue thromboplastin reagent used. Any thromboplastin reagent can be calibrated against an international primary or secondary W. H. O. reference preparation, so as to obtain its International Sensitivity Index. The new system of reporting the level of anticoagulation was designed and can only safely be applied in patients taking oral anticoagulants.

Administration, Oral↗
PubMed1985

Severe protein C deficiency in congenital thrombotic disease--description of an immunoenzymological assay for protein C determination.

An immunoenzymatic assay (ELISA) is described for the quantitative assay of protein C in plasma. This technique allows a safe, reliable, and sensitive assay of protein C, and is easily used for routine investigation. Using this technique, a protein C deficiency (0.16 U/ml) was discovered in a 16 year old patient with a history of very severe thrombotic disease. Protein C deficiency was also discovered in his mother (0.62 U/ml) and father (0.50 U/ml). We therefore suggest that this case could represent a homozygous deficiency of protein C.

Adolescent↗
PubMed1985

[Trial treatment of severe Raynaud's phenomenon with prostacyclin (PGI2)].

Severe forms of Raynaud's phenomenon are very disabling. In a randomized, single-blind trial, we have evaluated the effects of PGI2, a natural compound with strong vasodilator and anti-platelet activities, in 14 patients presenting with Raynaud's phenomenon. The patients received a 24-hour infusion of either PGI2 in doses of 10 mg/kg.min, or only the solvent (glycine buffer). All patients recorded the frequency and severity of the attacks before and after treatment, and 7 of the 8 patients who received the solvent benefited from a PGI2 infusion 30 to 60 days later. Among the 14 patients (6 men, 8 women), 10 had underlying collagen disease. The number of attacks per week was initially 15.9 +/- 5.3 (mean +/- s.e.). The resulting impairment was pronounced (+ + on a + to + + + scale). Radioimmunoassays of prostaglandins showed a strong increase in 6-keto PGF1 alpha levels during the infusion, without changes in thromboxane levels. A significant (p less than 0.05) reduction was observed in the number of attacks (2.6 +/- 2.5 per week) and in impairment (+ on average after PGI2 but not after the buffer). Improvement after PGI2 lasted from 0.5 to 12 months, and all but one patient regarded the treatment as effective in long-term, despite undesirable side-effects (flush, hypotension) which occurred regularly during PGI2 infusion. In all patients with ulcerations of the finger tips, these healed more rapidly after PGI2. It is concluded that in spite of immediate discomfort, PGI2 in 24-hour infusions seems to be of value in the treatment of severe Raynaud's phenomenon.

Drug Evaluation↗
PubMed1985

Episodes of increased fibronectin level observed in a patient suffering from recurrent thrombosis related to congenital hypodysfibrinogenaemia (fibrinogen Malmoe).

A study has been conducted in a Swedish patient with severe thrombotic disease and repeated miscarriages related to a hypodysfibrinogenaemia with defective thrombin binding to the abnormal fibrin. The hypodysfibrinogenaemia was found in several members of the family. The patient also had an increased concentration of fibronectin in her plasma at two different occasions. This would appear to be unrelated to the abnormal fibrinogen since a normal concentration of fibronectin has been found in her relatives presenting the same fibrinogen anomaly, and in the patient at two other times. In conclusion, the thrombotic disorder in this patient presenting a congenital hypodysfibrinogenaemia may be explained by the defective thrombin binding to fibrin.

Adult↗