Variation of PDGF, TGFβ, and bFGF levels in essential thrombocythemia patients treated with anagrelide

We studied 15 patients with essential thrombocythemia (ET) before treatment and after normalization of platelet count by anagrelide. Significantly increased plasma levels of PDGF, TGFβ, and bFGF were found. Patients with mild reticulin fibrosis in bone marrow had higher PDGF levels. During treatment...

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Bibliographic Details
Published in:American journal of hematology Vol. 70; no. 2; pp. 85 - 91
Main Authors: Lev, P.R., Marta, R.F., Vassallu, P., Molinas, F.C.
Format: Journal Article
Language:English
Published: New York Wiley Subscription Services, Inc., A Wiley Company 01-06-2002
Wiley-Liss
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Summary:We studied 15 patients with essential thrombocythemia (ET) before treatment and after normalization of platelet count by anagrelide. Significantly increased plasma levels of PDGF, TGFβ, and bFGF were found. Patients with mild reticulin fibrosis in bone marrow had higher PDGF levels. During treatment, plasma TGFβ and bFGF levels remained elevated in most patients (P < 0.0001 and P < 0.01, respectively). Intraplatelet PDGF levels were low before treatment (P < 0.006) and normal on hematological remission, without relation with the presence or absence of reticulin fibrosis in bone marrow. Intraplatelet TGFβ levels were normal regardless of the platelet count. Intraplatelet bFGF levels were raised before (P < 0.001) and during treatment (P < 0.01). By immunostaining, TGFβ and bFGF were seen in megakaryocytes and lymphocytes with a similar pattern of intensity in patients and controls, suggesting that other cells might also contribute to the raised plasma values. We believe that the plasma increment of these cytokines suggests that they play a role in the pathogenesis of ET. The normal PDGF plasma level found during treatment may be in relation with the platelet count. However, the persistent increase of TGF‐β in plasma and bFGF both in plasma and platelets may indicate dysregulation of cytokine synthesis in TE. Am. J. Hematol. 70:85–91, 2002. © 2002 Wiley‐Liss, Inc.
ISSN:0361-8609
1096-8652
DOI:10.1002/ajh.10091