The purpose of this study is to examine how ANA affects
platelet endothelial activation and FGF-2 release. Myelofibrosis is one of the
normal outcomes of essential thrombocythemia. The myelosuppressive medicine
used by ET itself may increase the risk of myelofibrosis development. A major
challenge in treating ET is minimizing this risk. It is believed that
fibroblast growth factor-2 is released by activated thrombocythemic platelets
(FGF-2). The myelosuppressive drug anagrelide (ANA) inhibits platelet activity.
The main worry with ANA is that it can raise the potential risk of developing
myelofibrosis. In this study, we provide the outcomes of a randomized group of
ET patients receiving ANA therapy who, after a 5-year follow-up, demonstrated a
decrease in myelofibrosis. The fact that ANA has a wider action that also
impacts platelet function is a likely reason for this finding. In the current
study, we found that ANA normalizes FGF-2 levels by preventing platelet
endothelial activation, which improves the myeloproliferation and fibrosis
outcomes for ET patients.
Author(s) Details:
Rossella Cacciola,
Department of Clinical and Experimental Medicine, Haemostasis Unit,
University of Catania, Italy.
Elio Gentilini Cacciola,
Department of Clinical and Experimental Medicine, Haemostasis Unit,
University of Catania, Italy.
Emma Cacciola,
Department of Medical, Surgical and Advanced Technologies Sciences
“G.F. Ingrassia”, Unit of Haemostasis, University of Catania, Italy.
Please see the link here: https://stm.bookpi.org/CPMS-V5/article/view/7661
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