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Biomedical subjects

J Conard

Publications and source records attributed to J Conard.

At least 181 records · Page 10Linked to original sources
PubMed1981

[Chronic disseminated intravascular coagulation in a case of ventricular aneurysm. Correction by low-dose heparin].

A case of intravascular coagulation in a patient with a very large ventricular aneurysm is reported. Biological signs of defibrination with a low serum fibrin of 0,80 g/1, thrombocytopaenia of 80,000/mm3 and the presence of soluble complexes and FDPs were detected after recurrent haematuria. Low dose heparin (0,15 to 0,20 ml x 2/day by subcutaneous injection) led to normalisation of the fibrinogen levels, increased the platelet count and reversed the consumptive coagulopathy. Each withdrawal of heparin (5 attempts over 16 months) led to a biological relapse. At the final withdrawal of therapy, the biological abnormalities remained minor; the consumption of fibrinogen and platelets was well compensated. Similar cases have been published in aortic aneurysms with and without dissection, but the association with a cardiac aneurysm has not been reported previously. The physiopathological mechanism of the coagulopathy is discussed and the authors suggest routine study of the coagulation system in all patients with cardiac aneurysms. This case illustrates the efficacity of moderate doses of heparin in a patient with "biological hypercoagulability" well documented by laboratory investigations.

Chronic Disease↗
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↗
PubMed1980

[Migraine or transient ischemic attacks in a patient with essential thrombocythaemia. Treatment with ticlopidine (author's transl)].

Ischemic cerebrovascular symptoms occuring in patients with essential thrombocythaemia are usually attributed to platelet or platelet-fibrin emboli. A patient is described in whom transient ischemic attacks (TIA) had some features - namely the presence of headache and the progressive onset of symptoms - unusual for an embolic phenomenon but suggestive of a migrainous event. No further attack occured when the patient was treated by an antiplatelet drug ticlopidine, though platelet count was unchanged. The relationship between platelets, TIA and migraine are discussed.

Blood Platelets↗
PubMed1979

[Haemorrhagic complications using streptokinase during 98 treatments. Place of the biological surveillance (author's transl)].

Streptokinase was administered to 98 patients, 75 of them with arterial occlusion of the limbs, in accordance with the classical protocol of high and continuous doses (150,000 international units per hour for 48 to 78 hours after an initial standard dose of 500,000 units). There were a total of 15 haemorrhagic complications: --related to a non-respected contraindication (1 case) --traumatic (4 cases) --spontaneous (10 cases), responsible for or contributing to a fatal outcome in 4 instances. In addition, there were 13 spontaneous or provoked haemorrhagic side effects. Retrospective analysis of laboratory results shows that it is difficult to predict haemorrhage: the degree of fibrinopaenia and fibrin breackdown product levels are not closely related to the onset of bleeding. Nevertheless, the combination of a residual fibrin level of less than 1.50 g/l approximately with an amount of fibrinogen broken down (difference between fibrinogen levels before treatment and during treatment) of more than 3 grams was present in the great majority of patients in whom complications developed. The absence of bleeding seen when plasma thrombolytic activity, assessed by the Blix test, is inadequate, suggests the existence of a relationship between biological effectiveness and the risk of haemorrhage. In practice, apart from strict observation of contraindications, the risk of haemorrhage must be born in mind when the therapeutic decision is made. Careful clinical surveillance is today more important than laboratory studies in the prevention of haemorrhagic complications, the price which must be paid for the thrombolytic activity of streptokinase. The latter is capable of acting not only upon the vascular obstruction but also upon haemostatic clots.

Adolescent↗