thrombasthenia


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thrombasthenia

 [throm″bas-the´ne-ah]
1. decreased platelet function; called also thromboasthenia.
Glanzmann thrombasthenia a hereditary platelet abnormality characterized by defective clot retraction, prolonged bleeding time, and related symptoms such as epistaxis and inappropriate bleeding. Clinically there is abnormal glass adhesion and impaired aggregation to ADP, collagen, and thrombin. Called also thrombasthenia and Glanzmann's disease.

throm·bas·the·ni·a

(throm'bas-thē'nē-ă),
An abnormality of platelets characteristic of Glanzmann thrombasthenia.
See also: Bernard-Soulier syndrome.
Synonym(s): thromboasthenia
[thromb- + G. astheneia, weakness]

thrombasthenia

/throm·bas·the·nia/ (throm″bas-the´ne-ah) a platelet abnormality characterized by defective clot retraction and impaired ADP-induced platelet aggregation; clinically manifested by epistaxis, inappropriate bruising, and excessive posttraumatic bleeding.
Glanzmann thrombasthenia  thrombasthenia.

thrombasthenia

[throm′basthē′nē·ə]
Etymology: Gk, thrombos, lump, a + sthenos, not strength
decreased platelet function. See Glanzmann thrombasthenia.

thrombasthenia

Glanzmann's disease, see there.

throm·bas·the·ni·a

(throm'bas-thē'nē-ă)
An abnormality of platelets; to date, several varieties have been categorized; often finding characteristics of Glanzmann thrombasthenia.
Synonym(s): thrombo-aesthenia.
[thromb- + G. astheneia, weakness]

thrombasthenia

An obsolescent term for the condition in which blood platelets are present in normal numbers but do not function normally in their role in blood clotting. The condition may be inherited but is more commonly acquired. With the rapid growth in understanding of platelet function this term is likely to disappear.

throm·bas·the·ni·a

(throm'bas-thē'nē-ă)
Abnormality of platelets.
Synonym(s): thromboasthenia.
[thromb- + G. astheneia, weakness]

thrombasthenia (throm´basthē´nēə),

n a hemorrhagic diathesis associated with qualitative abnormalities of the platelets.

thrombasthenia

a platelet abnormality characterized by defective clot retraction and impaired ADP-induced platelet aggregation. There are mild bleeding tendencies. Inherited as an autosomal recessive disorder in Otterhounds. Called also Glanzmann's disease, Glanzmann-Naegeli syndrome.
References in periodicals archive ?
FVII defciency, * FVII leve was 20%, ND: Not done, VWD: Von Willebrand disease, VWF: Von Wolebrand factor, BSS: Bernard-Soulier syndrome, GT: Glanzmann thrombasthenia
Defects in Glanzmann thrombasthenia and LAD-III (LAD-1/v) syndrome: the role of integrin [beta]1 and [beta]3 in platelet adhesion to collagen.
Molecular study of Glanzmann thrombasthenia in 3 patients issued from 2 different families.
Describing Prof Caen as a man "who has dedicated his life to the study of Glanzmann's Thrombasthenia, " Mr Justice Astill said his evidence suggested that Mrs Wood could have survived.
This report highlights the case of a 3-year-old girl affected by Glanzmann thrombasthenia, an inherited platelet function disorder (PFD), characterized by abnormalities of glycoprotein complex IIb/IIIa (integrin [[alpha].
Since Glanzmann thrombasthenia is a disease caused by platelet dysfunction, there is defect in primary clot formation and mucosal bleedings are observed frequently.
Glanzmann thrombasthenia, a membrane defect characterized by dysfunction or loss of the GP IIb/IIIa receptor site, may be diagnosed by its characteristically diminished secretion and aggregation responses to all agonists with the exception of a modest response to arachidonic acid.
It has been used to detect the absence of glycoprotein IIb/IIIa receptors in patients with Glanzmann thrombasthenia and has been used to study deficiencies of glycoprotein Ia, Ib, IIb, IV, and IX.
Platelet transfusion in a patient affected by Glanzmann's thrombasthenia with antibodies against GPIIb-IIIa.
Glanzmann thrombasthenia is an autosomal recessive disorder seen most frequently in consanguinity.
The pathogenesis and molecular defects of many primary thrombocytopathies are well known and relate to defects in structural or functional glycoproteins, such as the abnormal expression of gpIIb/IIIa in Glanzmann thrombasthenia and gpIb in Bernard-Soulier disease (8994).
Patients with afibrinogenemia or Glanzmann thrombasthenia (abnormalities of the GP Iib-IIIa receptor) lack both primary and secondary responses to various platelet agonists (27).