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Biomedical subjects

M Samama

Publications and source records attributed to M Samama.

At least 217 records · Page 12Linked to original sources
PubMed1982

[Measurement of platelet volume: methodologic approach and application in diabetes].

A comparative study of platelet count and platelet volume distribution was performed on whole blood (Coulter counter S+) or platelet rich plasma (Thrombo Coulter and Coulter ZBI + Channelyser C 1 000). With the exception of severe thrombocytopenia the results of platelet counts obtained with the coulter S + were very reproducible (CV less than 4%) and a good correlation was observed between results obtained on whole blood and on platelet rich plasma (PRP). The mean platelet volume (MPV) was significantly higher in whole blood than in PRP, but the difference was very slight, suggesting that platelet volume distribution in PRP and in whole blood are similar. In whole blood collected in EDTA MPV increased significantly during the 2 hours after blood collection and then reached a plateau. This finding underlines the need for a standard technique. Preliminary results obtained with the Coulter S + in 86 diabetic patients and in 73 unselected control subjects demonstrated a significant increase of MPV and of the index of platelet distribution (IDP) given by the apparatus, without modification of platelet count in diabetics. These results could suggest a compensated increased platelet consumption in the circulating blood.

Blood Platelets↗
PubMed1982

[Study of coagulation and fibrinolysis in 131 cases of recurrent deep vein thrombosis].

The study concerns 131 patients with a history of recurrent deep vein thrombosis. The predisposing and triggering factors of thrombosis have been carefully recorded and a study of hemostasis parameters has been performed, including AT III determination, fibrinolytic activity before and after venous occlusion, plasminogen, alpha 2-antiplasmin and histidine-rich glycoprotein determination. A congenital AT III deficiency was detected in six patients (4.4%). The most frequent finding was a decrease in fibrinolytic activity after venous occlusion. If one accounts for patients with a disease predisposing to thrombosis: Behçet's disease, cancer, hiatus hernia, Cockett's syndrome (14 patients), or a biological anomaly such as: deficiency in AT III, decrease in fibrinolytic activity. circulating anticoagulant, increase in lipids or uric acid, decrease in plasminogen or increase in alpha 2-antiplasmin (57 patients), there are still 60 patients (45% of the cases) in whom thromboses remain unexplained.

Adolescent↗
PubMed1982

[Thrombopenia caused by heparin. Review of the literature apropos of a personal case].

Following operation for bladder papilloma and subcutaneous heparin therapy, a patient developed severe thrombopenia with biological signs of disseminated intravascular coagulation (D. I. C.). Heparin therapy was discontinued and the platelet count became normal, no further signs of (D. I. C.) being apparent. Histological examination of the excised tumor showed that it was non-malignant, the thrombopenia being directly related to the heparin treatment. A review of the published literature demonstrated variations in the frequency of this complication reported, with an apparently higher incidence in the USA than in France. This could possibly depend upon whether the heparin was prepared from pulmonary or intestinal tissue. The thrombopenia may be severe (platelet count less than 100,000/mm3) with resulting hemorrhages or more commonly thromboses, or moderate without clinical expression. The dose or mode of administration of the heparin does not appear to be a factor in the development of the thrombopenia, its mechanism not being clearly elucidated. From the practical point of view, a platelet count should be performed before heparin treatment, and this should be repeated if the treatment is continued for more than four days.

Aged↗
PubMed1981

[Acquired Willebrand factor deficiency associated with monoclonal IgG kappa gammapathy. Presence of an inhibitor of ristocetin co-factor (author's transl)].

An 85-year-old woman without personal history of haemorrhages was found to have qualitative and quantitative deficiency of Factor VIII persisting at least 6 months. Asymptomatic monoclonal IgG kappa gammopathy was also discovered in the same patient, together with a circulating inhibitor of ristocetin co-factor. The fact that the inhibitory effect was reduced after the patient's serum IgG's were bound to staphylococcal protein A suggests that the inhibitor belonged to that category of immunoglobulins, although the authors were unable to detect it after elution.

Aged↗
PubMed1981

[Changes in serum beta-thromboglobulin levels during oral contraception, cardiac valve disease and pulmonary embolism (author's transl)].

beta-thromboglobulin (beta TG), a platelet-specific protein, was measured in the plasma of 53 healthy subjects (20 men and 33 women), 53 women using estrogen-progestogen contraceptives, 31 patients with cardiac valve disease (including 19 with prosthesis) and 71 patients about to undergo scintigraphy for suspected pulmonary embolism. Compared with levels in healthy subjects, beta TG levels were significantly increased in oral contraceptive users and in cardiac patients with or without prosthesis. High beta TG levels were also found in 20 out of 28 patients with pulmonary embolism confirmed by scintigraphy, but also in some of the .9 lung patients with chronic bronchopulmonary disease. Cardiac patients treated with heparin had higher beta TG levels than non heparin-treated patients, which raises queries about a possible influence of heparin on this particular blood protein.

Adult↗
PubMed1981

Study of platelet diameter distribution in patients with valvular heart disease and with prosthetic heart valve replacement.

We have studied the platelet count and the megathrombocyte index (MI), or percentage of platelets that have a diameter greater than 2.9 micrometers, in 100 patients with valvular heart disease. The mean platelet count is significantly lower than in controls (p less than 0.0005) and the MI is significantly increased (p less than 0.01). No difference was observed in these two parameters according to the variety of the valvular heart disease. 45 of the same patients were studied after prosthetic heart valve replacement. Our results show a significant elevation of platelet count and a significant decrease of MI compared with the presurgical values in all groups except in the mitral one in which MI remains increased. This work demonstrates the presence of platelet abnormalities which reveal a compensated thrombocytolytic state in patients with valvular heart disease and its partial correction after aortic, but not mitral, valve replacement.

Adolescent↗
PubMed1981

Low-dose heparin in gynecologic surgery: effect on blood coagulation tests.

The laboratory control of low-dose heparin therapy is generally regarded as unnecessary. A laboratory study of the effects of low-dose heparin was performed using different methods: an amidolytic method and a method involving the inhibition of factor Xa in a coagulation test. Variations in partial thromboplastin time, recalcification clotting time, thrombin time and the plasma antithrombin III levels were also studied. These tests were repeated (days 0, 1, 3, 8) in 27 women between the ages of 27 and 62 years who were undergoing gynecological surgery. They received 5,000 IU of heparin either twice or thrice daily. There was no correlation between heparin levels in the blood and global clotting tests simultaneously performed. The plasma heparin levels varied between 0 and 0.15 IU/ml with both methods. A detectable heparin concentration on days 1, 3 and 8 was present in only half of the cases receiving the twice daily regimen. The plasma antithrombin III activity and concentration were not modified during treatment.

Adult↗
PubMed1981

Constitutional thrombocytopathy with subnormal response to thromboxane A2.

A new type of congenital platelet dysfunction was found in a young woman presenting a life-long bleeding disorder. The known types of thrombopathia and von Willebrand's disease were excluded by appropriate investigations. The platelets were morphologically normal, underwent normal shape change and contraction and synthesized thromboxane A2 (TXA2) normally. The release reaction was abnormal and the aggregation response to ADP, adrenalin, collagen, thrombin, sodium arachidonate and vasopressin was depressed due to decreased sensitivity of the platelets to prostaglandin endoperoxides and TXA2. Platelet cAMP content was increased.

Adolescent↗
PubMed1981

[Estimation of Stuart factor using a synthetic substitute during oral anticoagulant treatment. Preliminary results (author's transl)].

The estimation of Stuart Factor (Factor X) with a new synthetic substrate S-2337, and the prothrombin time were compared in 91 patients treated with oral anticoagulants for more than one month. There was a good correlation between the two tests (r = 0.79 and 0.81 depending on the thromboplastin used). The results of out short study suggest a therapeutic zone between 20 p cent and 32 p cent of factor X but these values require confirmation. This method may constitute a progress in the laboratory supervision of treatment with coumarin derivatives for it permits better standardisation of the results and may easily be adapted to an autoanalyser.

Administration, Oral↗
PubMed1981

[Laboratory control of anticoagulant treatments (author's transl)].

Laboratory control of anticoagulant treatments is still unclear, in spite of 25 years experience, better knowledge of the mechanisms of action of the different drugs, and the new techniques available. In general, laboratory control includes a test specific for the action of the drug involved, associated or not with a test that reflects global coagulability. During heparin treatment, the association of recalcification time or activated partial thromboplastin time with heparin levels is recommended. A weekly platelet count can eliminate heparin-induced thrombocytopenia. During oral anticoagulant treatment, the association of thromboplastin time or Owren's thrombotest with activated partial thromboplastin time is indicated. The therapeutic ranges for thromboplastin times are different according to the reagents used and should be specified by the laboratory since present methods of standardization are not yet satisfactory.

Anticoagulants↗
PubMed1981

Ultrastructure of a model of thrombogenesis induced by mechanical injury.

Injured cortical arteries were observed by electron microscopy. Haemostasis was brought about by both platelets and fibrin, but the intravascular thrombus contained only platelets. Some platelets adhered to the exposed subendothelium but did not form a continuous layer. Such platelet adhesion does not provoke a thrombus, which appears only at the opening in the artery. There was a gap of 7 micrometers between the thrombus and the intact arterial wall. The thrombus was built up progressively by concentric accumulation around the main injury. Central platelets were closely packed and the more distal ones loosely gathered but not touching and not activated. This structure was very different from that observed in in vitro aggregates which formed rapidly and whose platelets are all at the same stage of development and disposed radially. This implies a different sequence in the physiological evolution of platelets submitted to either mode of activation. The results obtained with the present model differ in several respects from those obtained with other models.

Animals↗