Platelets in idiopathic thrombocytopenic purpura are increased in size but are of normal density

Illes, I.; Pfueller, Sharron L.; Hussein, Sonay; Chesterman, Colin N.; Martin, John F.

doi:10.1111/j.1365-2141.1987.tb02322.x

Cited by 22 publications

(12 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Large platelets are an often cited feature of idiopathic thrombocytopenic purpura (ITP) (Illes et al, 1987), although they do not reach the size or abundance seen in the present work. Interestingly, several patients described in the literature, including the patient described by Moll et al (1998) and patient 3 of our study, were first suspected of having ITP before type 2B VWD was diagnosed.…”

Section: Discussioncontrasting

confidence: 82%

Platelet ultrastructural abnormalities in three patients with type 2B von Willebrand disease

et al. 2000

View full text Add to dashboard Cite

Summary. Several reports have described the presence of giant platelets in patients with type 2B von Willebrand disease (VWD). We have now characterized the ultrastructural changes in platelets from three unrelated patients with type 2B VWD and different mutations within exon 28 of the von Willebrand factor (VWF) gene. Electron microscopy showed that each of these subjects had an increased proportion of large platelets when compared with those of a patient with type 2A VWD or control subjects. Immunogold labelling for VWF was performed. Large masses detected by anti-VWF antibody were seen not only on the platelet surface, but also inside the platelet surfaceconnected canalicular system (SCCS) when ultrathin sections were labelled. This suggested translocation of the abnormally bound VWF from the platelet surface. Labelling of the a-granules was eccentric as for normal platelets. Labelling for glycoprotein (GP) Ib was seen on the surface and within the SCCS, suggesting co-localization with the bound VWF. However, there was no evidence for VWF in endosomes or other endocytic vesicles. The presence of platelet-bound VWF was not accompanied by high levels of platelet activation, as detected by electron microscopy, or by using monoclonal antibodies against P-selectin or activation-dependent determinants on GP IIb-IIIa in flow cytometry. Intriguingly, platelet ultrastructure often resembled that seen in patients with congenital thrombocytopathies characteristic of giant platelet syndromes.

show abstract

Section: Discussioncontrasting

confidence: 82%

Platelet ultrastructural abnormalities in three patients with type 2B von Willebrand disease

et al. 2000

View full text Add to dashboard Cite

show abstract

“…Recovery of platelet numbers following consumption has also been associated with an increase in platelet volume, which normalizes as platelet count returns to normal [103][104][105]. In addition to increased platelet size and thus greater platelet surface area for platelet interactions, the newly formed reticulated platelets are also hemostatically more active [106].…”

Section: A -Thrombocytopeniamentioning

confidence: 99%

Platelet Turnover in Atherothrombotic Disease

Lordkipanidzé

2012

CPD

View full text Add to dashboard Cite

Platelets play a pivotal role in primary hemostasis where their rapid response to vascular injury prevents excessive bleeding. To accomplish this, platelets are enriched in membrane receptors and cytoplasmic enzymes with often redundant and self-amplifying functions leading to platelet activation, release into the bloodstream of hemostatically active compounds and culminating with thrombus formation. However, the same process in the pathological state of atherosclerosis can lead to thrombotic complications such as an acute coronary syndrome or stroke. The role of platelets in this process is more extensive than previously believed. Several lines of evidence suggest that platelets contribute not only to the acute thrombotic events in atherosclerosis, but also to disease initiation and progression. This review focuses on the role of platelet heterogeneity and turnover in atherothrombotic disease. Specifically, this article covers (a) the regulation of platelet formation; (b) the role of the heterogeneity of platelets in atherothrombotic diseases; (c) the disease-modifying effect of platelets on the development of atherosclerosis; and (d) the modifying effect of atherosclerotic disease on platelet production and function; (e) the platelet indices influencing platelet responsiveness to antiplatelet therapies; and finally (f) the potential novel therapeutic modalities that could be applied in atherothrombosis.

show abstract

“…This is supported by studies of thrombocytopenia in humans. 69,70 Changes in the Volume of Platelets in Acute Coronary Syndromes…”

Section: The Relationship Between Megakaryocytes and Platelet Volumementioning

confidence: 99%

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Loo

Martin

1999

ATVB

Self Cite

124

View full text Add to dashboard Cite

Abstract-Platelets are heterogeneous with respect to their size, density, and reactivity. Large platelets are more active hemostatically, and platelet volume has been found to be increased both in patients with unstable angina and with myocardial infarction. Furthermore, platelet volume is a predictor of a further ischemic event and death when measured after myocardial infarction. Platelets which are anucleate cells with no DNA are derived from their precursor, the megakaryocyte. Therefore, it is suggested that changes in platelet size are determined at thrombopoiesis in the megakaryocyte and that those changes might precede acute cardiac events. Understanding of the signaling system that controls platelet production may also further elucidate the cascade of events leading to acute vascular occlusion in some patients. (Arterioscler Thromb Vasc Biol. 1999;19:672-679.)Key Words: platelets Ⅲ myocardial infarction Ⅲ unstable angina Ⅲ coronary heart disease Ⅲ thrombosis T he biological events that occur in the coronary artery that immediately precede acute coronary syndromes are still not clear. However, platelets are involved, and changes in platelets may be a causal factor in producing a thrombus in the coronary artery.Aspirin is the most widely used antiplatelet drug. As platelets have no nucleus and are therefore unable to synthesize protein de novo, an aspirin-induced functional defect lasts for the whole life span of the platelets (8 to 10 days). 1 The results of large trials 2-4 of the beneficial effect of aspirin treatment in patients with unstable angina are consistent with the hypothesis that platelet activity is causally related to acute coronary syndromes. Both the medium-(12 weeks) 2 and long-term (2 years) 3 risk of cardiac death and myocardial infarction (MI) in patients with unstable angina is reduced. More recently, the significant benefit of antiplatelet therapy with aspirin in protection against acute cardiovascular syndromes and death was further supported in an overview of 145 randomized trials by the Antiplatelet Trialists' Collaboration. 5 Given the known effects of aspirin as an inhibitor of platelet function, these trials are strong evidence that platelets may contribute to the pathophysiology of the acute complications of coronary artery disease. Aspirin is an inhibitor of only one of several specific pathways leading to platelet activation and aggregation. 1 Inhibition of the glycoprotein (GP) IIb/IIIa receptor blocks the binding of fibrinogen, which is the final common pathway of platelet aggregation. 6 Integrelin, which is a GP IIb/IIIa receptor inhibitor, was evaluated in 227 patients with unstable angina and reduced significantly the number and duration of Holter-recorded ischemia compared with aspirin therapy. 7 These recent data are further strong support for the pivotal role of platelets in patients with unstable angina.Circulating platelets are heterogeneous in size, density, and reactivity. 8,9 Changes in these variables may be causal in acute coronary syndromes. 10 Initial plaque ...

show abstract

Platelets in idiopathic thrombocytopenic purpura are increased in size but are of normal density

Cited by 22 publications

References 17 publications

Platelet ultrastructural abnormalities in three patients with type 2B von Willebrand disease

Platelet ultrastructural abnormalities in three patients with type 2B von Willebrand disease

Platelet Turnover in Atherothrombotic Disease

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Contact Info

Product

Resources

About