PF 4 versus βTG as evidence for platelet activation in myeloproliferative disorders

G. Luzzatto, F. Fabris, M. Mazzucato, A. Girolami

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

19 patients with MPD have been studied. As described in normals, and age-related increase in β-thromboglobulin (βTG) release is observed. Such release, however, is greater in patients with myeloproliferative disorders (MPD). MPD seem therefore to cause platelet activation, allowing an earlier and more evident manifestation of physiologic ageing phenomena. PF 4 levels are near zero both in controls and patients, regardless of platelet number. This suggests that increased levels of PF 4 represent only a laboratory artifact, caused by platelet activation in vitro. Mean ability in producing thromboxane B2 (TxB2) is increased, but is perfectly normal in patients with normal platelet count and decreased in 3 thrombocythaemic patients, who seem to present an increased thrombotic risk. TxB2 is reduced almost to zero by the administration of aspirine plus dipyridamole; contrarily, all other parameters were unaffected, either by such drugs or by AD 6, a new coumarin derivative with antiplatelet properties.

Original languageEnglish
Pages (from-to)299-304
Number of pages6
JournalScandinavian Journal of Haematology
Volume35
Issue number3
Publication statusPublished - 1985

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Myeloproliferative Disorders
Platelet Activation
Thromboxane B2
Platelet Count
Coumarins
Dipyridamole
Artifacts
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Hematology

Cite this

PF 4 versus βTG as evidence for platelet activation in myeloproliferative disorders. / Luzzatto, G.; Fabris, F.; Mazzucato, M.; Girolami, A.

In: Scandinavian Journal of Haematology, Vol. 35, No. 3, 1985, p. 299-304.

Research output: Contribution to journalArticle

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AB - 19 patients with MPD have been studied. As described in normals, and age-related increase in β-thromboglobulin (βTG) release is observed. Such release, however, is greater in patients with myeloproliferative disorders (MPD). MPD seem therefore to cause platelet activation, allowing an earlier and more evident manifestation of physiologic ageing phenomena. PF 4 levels are near zero both in controls and patients, regardless of platelet number. This suggests that increased levels of PF 4 represent only a laboratory artifact, caused by platelet activation in vitro. Mean ability in producing thromboxane B2 (TxB2) is increased, but is perfectly normal in patients with normal platelet count and decreased in 3 thrombocythaemic patients, who seem to present an increased thrombotic risk. TxB2 is reduced almost to zero by the administration of aspirine plus dipyridamole; contrarily, all other parameters were unaffected, either by such drugs or by AD 6, a new coumarin derivative with antiplatelet properties.

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