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Biomedical subjects

J Conard

Publications and source records attributed to J Conard.

At least 163 records · Page 9Linked to original sources
PubMed1983

Familial and constitutional bleeding disorder due to platelet cyclo-oxygenase deficiency.

Three family members from two successive generations had a bleeding tendency. Their template bleeding time was prolonged and platelet aggregation induced by ADP and adrenaline showed no second wave; collagen at low to moderate concentrations failed to aggregate and release ATP, whereas higher amounts aggregated and released. Aggregation and release due to thrombin, ristocetin, and synthetic epoxy derivatives (U 44069 and U 46619) were normal. Arachidonate (AA) was inactive, and was not converted either in thromboxane (TX) A2 activity evaluated on the rabbit aorta strip, nor in TXB2 evaluated by radioimmunoassay and by radiochromatography. The parallel impairment of TXB2 and PGE2 formation by the patient's platelets are compatible with a platelet cyclo-oxygenase deficiency. This study suggests that transmission is autosomal dominant, and confirms that cyclo-oxygenase is not needed for aggregation and ATP release by high amounts of collagen.

Adolescent↗
PubMed1983

Study of platelet aggregation induced by platelet activating factor (PAF) after administration of ticlopidine or aspirin.

Platelet aggregation induced by platelet activating factor (PAF) was studied in 95 subjects: 39 controls, 23 patients receiving aspirin and 33 receiving ticlopidine. Potentiation of aggregation by concentrations of adrenaline unable to induce aggregation when used alone was also assessed. The 33 patients treated with ticlopidine showed a highly significant fall of platelet aggregation (p less than 0.001) at the three concentrations of PAF used. The 23 subjects receiving aspirin showed a diminution of platelet aggregation induced by PAF due to inhibition of ADP release. In these last two groups, adrenaline often potentiated platelet aggregation. However, this phenomenon was absent in subjects having taken aspirin in the hours before blood was drawn. This study demonstrates ticlopidine's inhibitory action on PAF-induced aggregation and confirms ticlopidine's role in reducing platelet aggregation by ADP, which has previously been demonstrated.

Adult↗
PubMed1983

Molar antithrombin concentration in normal human plasma.

Crude, commercial thrombin preparations and purified bovine thrombin were incubated with normal human reference plasma and the amount of thrombin inactivated was calculated. 1 ml of human plasma inactivated 140-193 NIH U of the various crude thrombin preparations. In the presence of heparin, a lower thrombin-inactivating capacity of plasma was confirmed using crude thrombin, but this phenomenon was less pronounced with the purified thrombin preparation. The molar concentration of the purified bovine thrombin was determined by active site titration. Comparing with protein concentration (A280), this preparation was 92% pure. 1 ml of human plasma inactivated 2.57 mumol of thrombin in the absence of heparin, and 2.50 mumol with heparin. Assuming 1:1 stoichiometry in the thrombin-antithrombin reaction, these results suggest that the concentration of antithrombin in the pooled reference plasma is approximately 2.57 mumol/l or 0.15 g/l.

Animals↗
PubMed1983

[Determination of the factor VIII ristocetin cofactor (Willebrand factor) using a semi-quantitative slide test. Preliminary results].

The assay of factor VIII, co-factor of Ristocetin (VIIIR:Co) is a relatively delicate procedure which is presently reserved to specialized laboratories. It requires the use of an aggregometer and a long and difficult preparation of human platelets. In parallel with this classical method, we have used a new, rapid, semi-quantitative slide test whose advantages are: simple technique and rapid answer (2 minutes), small volume of plasma required for the test (50 microliters) and the possibility of using citrated or heparinized plasma taken form a venous or capillary blood sample. Using this test, we have assayed factor VIII co-factor of ristocetin: in 31 hospitalized adults patients with no previous history of bleeding and no disturbance of haemostasis and in 18 patients with Willebrand's factor deficiency in comparison with the standard technique using aggregometry (Allain's method); - in 28 normal neonates, in comparison with the VIIIR:Ag factor assay (Laurell's technique), only because of the small sample volume available; - in 17 patients with various disease associated with an abnormality of the VIII complex in comparison with the assay of VIIIR:Ag and VIIIC. The results obtained in the normal adults show a satisfactory correlation between the two methods. The mean level of factor VIII:Co is 100 +/- 10 per cent (M +/- SD) with the semi-quantitative slide test and 109 +/- 20 per cent (M +/- SD) with the method taken as the reference. The correlation is also satisfactory for patients with a deficit of Willebrand's factor. The test performed on the neonates gives a mean value of 101 +/- 37 per cent (M +/- SD) with good correlation between the factor VIIIR:Ag and the factor VIIIR:Co.

Adult↗
PubMed1983

[4 cases of acquired Willebrand factor deficiency associated with monoclonal dysglobulinemia].

Acquired von Willebrand syndrome is reported in four patients with monoclonal IgG: benign gammapathy in three cases, multiple myeloma in one case; to our knowledge, this last association has not been previously reported. Coagulation abnormalities included a borderline bleeding time, a low platelet retention on glass beads, decreased levels of factor VIII coagulant activity (VIII: C), factor VIII related-antigen (VIII R: Ag) and ristocetin induced agglutination cofactor (VIII R: RC). The late clinical onset, the negative family history and the immunological abnormality suggest an acquired von Willebrand syndrome. After cryoprecipitate infusion the patients did not show the expected rise and there was no secondary increment in factor VIII: C. Time-dependent inhibition of factor VIII R: RC and factor VIII: C was found in one case only and was associated with qualitative abnormality of factor VIII R: Ag demonstrated by crossed-immunoelectrophoresis. It was not possible to interpret this last test in the other cases, due to the very low level of factor VIII R: Ag. The factor VIII abnormalities might be related to the binding and/or destruction of factor VIII by a circulating antibody, or to the adsorption of this factor on the malignant lymphocytes.

Adult↗
PubMed1983

[Demonstration of spontaneous platelet aggregation and research on circulating platelet aggregates: methodology, results and significance].

136 control subjects and 131 patients, consisting of 23 diabetics with severe retinopathy, 43 cases of valvular disease with or without a prosthesis and 65 patients who had a cerebral vascular accident, were systematically investigated for the presence of spontaneous platelet aggregation 31 controls and 108 patients were examined for reversible circulating platelet aggregates using the technique of Wu and Hoak. Frank spontaneous aggregation was observed in 6 of the 136 control subjects, 6 of the 21 patients without a valvular prosthesis and 2 of the 22 patients with such a valvular prosthesis and 2 of the 22 patients with such a prosthesis, only 1 of the 23 diabetics and 5 of the 65 patients with old or recent cerebral vascular accidents. The incidence of spontaneous aggregation seems to be directly related to certain operative conditions: the type of machine used, the number of platelets, and to the treatment administered, the Wu and Hoak test. No statistically significant correlation was demonstrated between spontaneous aggregation and the Wu and Hoak test. The exact clinical significance of the presence of spontaneous aggregation is still disputed. However, the examination for this abnormality should be routine as its presence can alter the interpretation of the results of aggregation induced by various aggregating agents.

Blood Platelets↗
PubMed1982

[Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system and major fibrinopenia (author's transl)].

A 32-year-old patient without previous medical history died within three weeks of acute Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system. No definite cause could be elicited. The course of the disease was complicated by anuria attributed to hepotorenal syndrome. Laboratory tests demonstrated major fibrinopenia. Detailed study of the haemostatic system was suggestive of hepatic failure associated with consumption coagulopathy of obscure origin.

Adult↗
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

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↗