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Biomedical subjects

C Lecrubier

Publications and source records attributed to C Lecrubier.

At least 37 records · Page 2Linked 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

[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↗
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↗
PubMed1980

Platelet aggregation related to age in diabetes mellitus.

Platelet aggregation induced by ADP and collagen was studied in 174 diabetic patients before entering a controlled clinical trial. The clinical characteristics have been precisely defined. The degree of retinal abnormality was assessed by fundus angiofluorography in every patient. Most patients had background retinopathy; the remainder were normal. All results were computer analysed. The only significant relationship observed was between platelet sensitivity to ADP which increases regularly in relation to age in both insulin- and non-insulin-treated diabetic patients with or without background retinopathy. Spontaneous platelet aggregation was observed in 13 subjects and was not correlated to the existence of a neuropathy or any other clinical characteristics.

Adenosine Diphosphate↗
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↗
PubMed1976

[Quantitative determination of Willebrand factor activity in Willebrand's disease].

Certain new data about the nature of Willebrand factors are discussed, its activity being considered as part of the activity of the antihemolytic factor VIII. An one-stage method for its determination is described based on the absence of thrombocytic aggregation in the presence of ristocetin in the patients with Willebrand disease as well as the illustration of one case.

Adult↗
PubMed1975

Increased sensitivity of platelets to adrenaline in human myotonic dystrophy.

Platelets from patients with myotonic dystrophy showed a normal pattern of aggregation in response to adenosine diphosphate (A.D.P.) and collagen but were unusually sensitive to adrenaline, aggregation being detectable with adrenaline concentrations as low as 0.041 mumol per litre. In other diseases in which such sensitivity has been reported this has been accompanied by a similarly altered response to A.D.P. The increased platelet aggregation could be due to increased uptake of Ca++ by platelets or to a decrease in phosphorylation of the platelet membrane.

Adenosine Diphosphate↗