Platelet activation and thrombosis: Studies in a patient with essential thrombocythemia

Nurden, Paquita; Bihour, Claude; Smith, Michael R.; Raymond, J M; Nurden, Alan T.

doi:10.1002/(sici)1096-8652(199601)51:1<79::aid-ajh13>3.0.co;2-6

Cited by 31 publications

(7 citation statements)

References 18 publications

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“…Our results and the above‐mentioned studies document the therapeutic efficacy of aspirin in preventing further thrombotic events in patients with platelet hyperactivity. Additionally, Nurden et al (1996) documented platelet hyperaggregability due to platelet activation using specific monoclonal antibodies and flow cytometry in a patient with recurrent major venous thrombosis who was successfully treated with long‐term ticlopidine.…”

Section: Discussionmentioning

confidence: 99%

Thrombosis and bleeding in myeloproliferative disorders: identification of at‐risk patients with whole blood platelet aggregation studies

et al. 1999

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Summary.Seventy-five patients with chronic myeloproliferative disorders were studied to investigate platelet function by simultaneous measurement of platelet aggregation by the impedance method and ATP dense granule release using a whole blood platelet lumi-aggregometer, in an attempt to identify patients at risk for thrombosis and bleeding.Thirty-nine patients had at least one abnormal result indicating platelet hyperactivity (i.e. impedance or release with one agonist being above the reference range); 16 patients had platelet hypoactivity (i.e. at least one result was below the reference range), whilst 14 had co-existence of hyper-and hypoactivity. Six patients had normal results. 20/ 53 patients with platelet hyperactivity (alone or mixed) had a positive history of venous and/or arterial thrombosis; in comparison, only two of the other 22 patients had a positive history. During a median follow-up of 33 months, nine patients with and one patient without platelet hyperactivity respectively developed new thrombotic events before the addition of specific therapy. A total of 50 patients with and eight patients without platelet hyperactivity respectively received specific treatment including aspirin and/or cytotoxic therapy. All but one elderly patient with platelet hyperactivity have remained free of new thrombotic events on specific therapy. Two of the 17 patients with platelet hypoactivity had major clinical bleeding.These observations highlight the need to test platelets for hyper-as well as hypo-function and suggest a useful role for routine whole blood platelet aggregation studies to identify the patients at risk for thrombosis or bleeding.

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Section: Discussionmentioning

confidence: 99%

Thrombosis and bleeding in myeloproliferative disorders: identification of at‐risk patients with whole blood platelet aggregation studies

et al. 1999

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“…This must be of concern in the MPD patient population. Evidence exists for its benefit in patients with ongoing evidence of platelet activation whilst receiving aspirin (Nurden et al , 1996). These agents may be useful for patients with peptic ulcer disease or aspirin allergy.…”

Section: Management Of An Acute Thrombotic Event and Pharmacoprophylaxismentioning

confidence: 99%

Guidelines for the diagnosis, investigation and management of polycythaemia/erythrocytosis

et al. 2005

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“…The proportion of patients with ET and PV spontaneously (without stimulation by agonists) expressing activation-specific epitopes such as CD 62 (GMP 140, p-selectin), CD 63 (a lysosomal epitope), or thrombospondin, on the platelet surface is low in comparison to the percentage of patients with el evated plasma levels of platelet-specific proteins. 75 Re cently, Nurden et al 76 investigated platelet activation in a patient with ET using an antibody to a "receptor-in duced binding site" (RIBS) indicating bound fibrinogen through a conformational change of the activated recep tor. About 43% of the total platelet population of this patient expressed the RIBS epitope (normal subjects: 2.6%) but the percentage of platelets also expressing pselectin or CD 63 was much lower.…”

Section: Circulating Activated Plateletsmentioning

confidence: 99%

Relation of Platelet Abnormalities to Thrombosis and Hemorrhage in Chronic Myeloproliferative Disorders

Wehmeier¹,

Südhoff²,

Meierkord³

1997

Semin Thromb Hemost

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The chronic myeloproliferative disorders (MPD), predominantly polycythemia vera and essential thrombocythemia, are characterized by a high incidence of thromboembolic and, to a lesser degree, hemorrhagic complications. The disease process in chronic MPD affects a pluripotent progenitor cell and results in trilineage hematopoietic proliferation. Clonal involvement of megakaryocytopoiesis is regarded as the main origin of thromboembolism in MPD and results in abnormal platelet production. These platelets show increased size heterogeneity and ultrastructural abnormalities, and their function in vitro is in many ways impaired with a high degree of individual variability. Elevated levels of platelet-specific proteins, increased thromboxane generation, and expression of activation-dependent epitopes on the platelet surface are common on chronic MPD, and may reflect an inappropriate state of platelet activation. Although a variety of platelet receptor deficiencies and some defects of intracellular signaling pathways have been identified, the different platelet defects in MPD could not be traced back to an underlying general pathogenetic mechanism. On progression of chronic MPD to more advanced stages of the disease, the number of platelet abnormalities tend to increase. Cytoreductive drugs may partly improve platelet dysfunction, and platelet inhibitory agents reduce symptoms of platelet activation. However, neither of these therapeutic principles is able to normalize platelet function in MPD. As an alternative to conventional treatment, specific suppression of clonal megakaryocyte growth and recovery of polyclonal hematopoiesis may be achieved by biologic agents such as interferon alpha. Such treatment strategies may prevent thromboembolic complications together with hematologic symptoms and progression of the disease and should be further evaluated in prospective studies.

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Platelet activation and thrombosis: Studies in a patient with essential thrombocythemia

Cited by 31 publications

References 18 publications

Thrombosis and bleeding in myeloproliferative disorders: identification of at‐risk patients with whole blood platelet aggregation studies

Thrombosis and bleeding in myeloproliferative disorders: identification of at‐risk patients with whole blood platelet aggregation studies

Guidelines for the diagnosis, investigation and management of polycythaemia/erythrocytosis

Relation of Platelet Abnormalities to Thrombosis and Hemorrhage in Chronic Myeloproliferative Disorders

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