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Results for “THROMBOCYTOPATHY”

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At least 37 records · Page 2Linked to original sources
PubMed1975

[Primary disaggregational thrombocytopathies].

The authors present the results of clinico-laboratory examination of 30 patients with a congenital (hereditary) hemorrhagic tendency associated with an isolated disturbance of the adhesive-aggregation platelet function. Several variants of disaggregational thrombocytopathies were distinguished. Characteristics of hemorrhagic phenomena in the patients is given; a tendency to hemorrhages in them was more frequently detected with the aid of Borchgrevink's test they in determination of bleeding time after Duke.

Adolescent↗
PubMed1989

[Constitutional thrombocytopathies and thrombocytopenias].

Inherited thrombocytopathies and thrombocytopenias are very rare diseases but they constitute a model for exploring platelet physiology. These congenital platelet disorders concern adhesion, activation and release, aggregation. The diagnosis is based on specialized biological investigations. The treatment of hemorragic episodes involves platelet infusions.

Blood Platelet Disorders↗
PubMed1979

[Aspirin-like defect - a hereditary thrombocytopathy due to impaired release of platelet adenosine diphosphate].

This report presents the case of a 36 year old woman with an inborn haemorrhagic syndrome, who exhibited a lifelong history of spontaneous bruising, nose bleeding, prolonged bleeding after tooth extraction, and menometrorrhagia. The routine tests of haemostasis were consistent with impaired platelet functions. The diagnosis of the "Aspirin-like defect" was made on the basis of the following findings: the bleeding time was prolonged, whereas the platelet count and morphology were normal; platelet retention in glass bead filters was unmeasurable. ADP-induced platelet aggregation was normal, while it was markedly reduced with collagen and epinephrine. The platelet ADP and ATP content, as well as the ATP/ADP ratio were within normal limits. Aggregation of platelets pre-incubated with aspirin was only slightly reduced when induced by ADP, collagen, or epinephrine. These findings suggest that the thrombocytopathy in our patient is due to an impaired ADP release from the platelet granules containing normal quantities of adenine nucleotides. A similar disorder is observed in normal subjects after aspirin ingestion, and therefore the defect described in this paper is referred to as the "Aspirin-like" defect.

Adenosine Diphosphate↗
PubMed1988

[The effectiveness of the combined treatment of thrombocytic hemorrhagic diathesis of dogs with prednisolone and blood transfusion in the model of an aspirin-produced thrombocytopathy].

The administration of 20 mg/kg of acetylsalicylic acid in 18 clinically healthy dogs resulted in a thrombocytopathy with lengthened capillary bleeding time and irreversible aggregation inhibition. Through the set up of individual dilution series, one could conclude the proportional percentage of aggregation functional transfused thrombocytes. The capillary bleeding time was shortened after the intravenous injection of prednisolone (5 mg/kg) without measurable influence on the thrombocytes. Compared to the singular use of cortisone or blood transfusion alone, the effect on capillary bleeding time became magnified when one combined transfusion and corticosteroids. The fresh blood conserves (12 hours) were, with respect to the haemostyptical properties, superior to blood stored for 5 days. The component of aggregation-functional thrombocytes was, due to the prophylactic cortisone application prior to transfusion, not increased.

Animals↗
PubMedDate not supplied

[Hereditary thrombocytopenia-thrombocytopathy with myelofibrosis (author's transl)].

A case of hereditary autosomal recessive thrombocytopenia is reported. Thrombocytopathy is associated with the thrombocytopenia. There is a contrast between the cytologic aspect of poor bone-marrow without any megakaryocyte and the histologic aspect of dense bone-marrow with a normal number of megakaryocytes. Myelofibrosis can explain this discrepancy. The life time of platelets being just a little shortened, the disease is probably due to a lack of bone-marrow production.

Adolescent↗
PubMed1982

Bronchogenic carcinoma, leukemoid reaction, marantic endocarditis, and consumptive thrombocytopathy.

This paper details the simultaneous occurrence of a severe leukemoid reaction, non-bacterial thrombotic endocarditis (NBTE) (marantic endocarditis), and a consumptive thrombocytopathy without signs of micro-angiopathic hemolysis on peripheral blood smear in a patient with terminal metastatic, undifferentiated, large cell bronchogenic carcinoma. The case is presented and the condition is discussed in detail.

Blood Platelet Disorders↗
PubMedDate not supplied

[Endotoxinemia as a factor in the pathogenesis of thrombocytopathies in patients with acute infectious destruction of the lungs].

Laboratory studies of the influence of the staphylococcal endotoxin on functional properties of thrombocytes and clinical observations of patients with a pronounced syndrome of endotoxicosis have shown an important role of endotoxinemia in pathogenesis of the arising thrombocytopathies. Possibilities of the medicamentous protection of blood plates from the damaging action of endotoxinemia are considered.

Acute Disease↗
PubMedDate not supplied

[Electro-optic method of recording antigen-antibody interactions in detection of antiplatelet antibodies in hemorrhagic thrombocytopathies].

A new electrooptic method was used to study the antiplatelet autoimmune process. Antiplatelet antibodies were assessed in 60 patients with idiopathic thrombocytopenic purpura and 60 ones with acquired hemorrhagic thrombocytopathies. The reference group consisted of 50 donors. The relationship between the autoimmune process intensity and the disease severity, as well as blood platelet counts over the course of corticosteroid therapy was studied.

Adolescent↗
PubMed1990

Malondialdehyde formation by blood platelets: a diagnostic test to assess acetylsalicylic acid induced thrombocytopathy?

We investigated whether the measurement of N-ethylmaleimide stimulated malondialdehyde (MDA) formation by blood platelets from normal subjects is equally sensitive to acetylsalicylic acid intake as are platelet aggregation studies. MDA production and platelet aggregation by collagen and arachidonate were assayed in ten healthy volunteers before and up to ten days after a single oral dose of 500 mg aspirin. Discordant results of the two tests were seen in several subjects 4 to 6 days after aspirin intake. In three cases with still suppressed MDA values on day 4, collagen or arachidonate induced aggregation was normalized. However, on day 6, when MDA was normalized in all subjects, the aggregation response to arachidonate was still pathologic in 5 of the ten volunteers. In case of a patient with abnormal aggregation response to arachidonate and/or collagen, therefore, a normal MDA value does not permit to exclude aspirin as the cause of the platelet dysfunction.

Adult↗