Platelet Glycoprotein IIb/IIIa Receptors and Glanzmann’s Thrombasthenia

French, Deborah L.; Seligsohn, Uri

doi:10.1161/01.atv.20.3.607

Cited by 72 publications

(55 citation statements)

References 44 publications

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“…111 The most common polymorphism is the C1565T mutation in the IIIa subunit, which results in a wild-type allele designated PL A1 with leucine at amino acid 33 and a PL A2 allele with proline at position 33. Among individuals of European ancestry, the PL A1 and PL A2 alleles occur at a frequency of Ϸ85% and 15%, respectively.…”

Section: Platelet Hyper-reactivitymentioning

confidence: 99%

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Feinbloom

Bauer

2005

ATVB

108

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Abstract-Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired hemostatic risk factors have been described in the pathophysiology of venous thrombosis, the degree and type of abnormalities that contribute to arterial thrombosis are less well understood. Endothelial cell injury with the elaboration of proinflammatory mediators stimulates the process of arterial thrombosis. Although this is most often the result of endovascular injury attributable to atherosclerotic disease, other disease states can elicit a similar response as well. Similarly, once thrombosis has been initiated, variations in the activity of coagulation proteins and endogenous anticoagulants, as well as the kinetics of platelet aggregation, may alter the effectiveness of thrombus formation. Epidemiological studies have identified several acquired or inherited states that may result in endothelial damage or altered hemostatic equilibrium, thereby predisposing patients to arterial thrombosis. These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, elevated fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), hereditary thrombophilias, and platelet hyper-reactivity. This review explores our present understanding of these risk factors in the development of arterial thrombotic events. At present, the literature supports a role for hyperhomocysteinemia, elevated C-reactive protein, and elevated fibrinogen as risk factors for arterial thrombosis. Similarly, the literature suggests that lupus anticoagulants and, to a lesser extent, elevated titers of cardiolipin IgG antibodies predispose to arterial vascular events. In certain subsets of patients, including those with concomitant cardiac risk factors, Ͻ55 years of age, and women, hereditary thrombophilias such as carriership of the factor V Leiden and the prothrombin G20210A mutations may confer a higher risk of arterial thrombosis. However, the data on Factor VII, PAI-1, and platelet receptor polymorphisms are contradictory or lacking.

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Section: Platelet Hyper-reactivitymentioning

confidence: 99%

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Feinbloom

Bauer

2005

ATVB

108

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“…1 Soon after their production in megakaryocytes, GPIIb (␣ IIb ) and GPIIIa (␤ 3 ) are introduced into the endoplasmic reticulum (ER), where they form a complex, undergo N-linked glycosylation, and form disulfide bonds. The complex is transported to the Golgi apparatus for final oligosaccharide processing and then to the open canalicular system, ␣ granules, and plasma membrane.…”

Section: Introductionmentioning

confidence: 99%

Identification of a region in glycoprotein IIIa involved in subunit association with glycoprotein IIb: further lessons from Iraqi-Jewish Glanzmann thrombasthenia

Yatuv

Rosenberg

Zivelin

et al. 2001

Blood

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“…Many patients with identified mutations are compound heterozygotes being higher where consanguinity is common. At the present time, 38 mutations in GPIIb The molecular characterization of Glanzmann's thrombasthenia in patients and their families has permitted DNA-based carrier detection and prenatal diagnoses to be performed [4]. Acquired thrombasthenia due to glycoprotein IIb-IIIa platelet antibodies has also been defined in several conditions [5].…”

Section: Discussionmentioning

confidence: 99%

Glanzmann’s Thrombasthenia Complicating Pregnancy

Magudapathi¹

2012

J Clin Case Rep

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Glanzmann's thrombasthenia is a rare autosomal recessive hemorrhagic disorder caused by abnormal platelet glycoprotein complex (GP IIb-IIIa) presenting with hemorrhagic symptoms. Pregnancy is not uncommon because fertility is not affected but an association is rare. Also delivery often results in haemorrhage. Newborn thrombocytopenia is occasionally severe, but is always transitory. We report a 21-year old primigravida, who underwent vaginal delivery at term with IUGR and Oligohydramnios. Glannzmann's thrombasthenia was characterized by aggregation and this patient went undiagnosed till adolescence until evaluated for puberty menorrhagia which is uncommon. She received single donor platelet transfusion during the intrapartum period along with tranexemic acid. Platelet transfusion may result in alloimmunization and make successive transfusions less effective. We did not use Factor VII in the intrapartum period due to cost and suspected fetal effects. Postnatally she had hematuria settled on the 2 nd day with conservative management. We present this case because of association of Glanzmann's thrombasthenia with IUGR and oligoamnios the only reported case so far.

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Platelet Glycoprotein IIb/IIIa Receptors and Glanzmann’s Thrombasthenia

Cited by 72 publications

References 44 publications

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Identification of a region in glycoprotein IIIa involved in subunit association with glycoprotein IIb: further lessons from Iraqi-Jewish Glanzmann thrombasthenia

Glanzmann’s Thrombasthenia Complicating Pregnancy

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