Physiopathology of haemorrhagic syndrome related to ochratoxin A intoxication in rats.
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Biomedical subjects
Publications and source records attributed to B Boneu.
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Some particle counters give a routine determination of mean platelet volume. 272 determinations of this new parameter were performed on 107 hospitalized children in the hematology field. Giant platelets are a frequent sign in peripheral thrombocytopenia, and they are never observed in central thrombocytopenia. The determination of the mean platelet volume is of value in an emergency examination for thrombocytopenia, while awaiting the results of a myelogram, and in monitoring primary thrombocytopenic purpura. In this later condition, the persistance of an increased mean platelet volume in spite of an improvement in the number of platelets should lead to a suspicion of a relapse.
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Qualitative platelet parameters (volume, 5 hydroxy-tryptamine (5 HT) organelles studied by the mepacrine test, and density) were evaluated in 31 patients with acute leukaemia: 11 myelomonocytic (AML), 8 lymphoblastic (ALL), 12 granulocytic (AGL). Macrothrombocytosis was observed in most of the cases of AML, was rare in AGL and was never found in ALL. The 5 HT organelles/volume ratio was normal in AGL and ALL but was significantly decreased in AML. In contrast, platelet density distribution was always abnormal whatever the platelet volume and 5 HT organelle concentration. Thus, using simple new methods, convenient even in cases of thrombocytopenia, we demonstrate that qualitative platelet abnormalities are a constant feature in acue leukaemia and that they are more severe in AML.
Factor VIII complex was studied in patients presenting arterial hypertension. Visceral involvement was quantified using a clinical index calculated from ocular fundus, renal function and left ventricular hypertrophy data. A significant correlation was found between the mean arterial pressure, the visceral involvement and the level of complex VIII. Nevertheless, other data obtained in different patients (Conn's disease) suggest that the visceral involvement (and not the mean arterial pressure) is the main determining factor in the increase of factor VIII complex.
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After a brief survey of some physiologic properties of Von Willebrand factor activity (VIII r WF) the numerous clinical states with an increase of this activity are described. The authors report their own results concerning sepsis, chronic arteritis of lower limbs, diabetes, toxemia of pregnancy. In most cases the increase of VIII r WF activity appears as a sign of vascular injury and/or the consequence of tissular damage.
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In this paper the authors try to specify the leg ulcers physiopathology. They have first studied the vascular deficits, and they are able to conclude that this deficit is not the only factor responsible for the thrombosis. They try to rediscover the factors which could lead to the thrombosis, on the created local conditions (circulatory slackening, cooling, ischemia), by using clinical and biological "check-ups" as well as an exploration of the clotting. In many patients we find an anomaly such as: clotting "check-ups" disturbance, thrombocyte hyperaggregability, fibrinolysis deficit, antithrombin III deficit, cryoprecipitate, circulating immune complexes, hepatic "check-up" alteration. It is difficult to establish an accurate relation between these anomalies and a thrombosis but the frequent existence of such anomalies makes us think that they play a part in the ulcerations coming-up.
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