Elevated vascular endothelial growth factor (VEGF) serum levels in idiopathic myelofibrosis

F Di Raimondo1, M P Azzaro, G A Palumbo

  • 1Division of Hematology, University of Catania, Ospedale Ferrarotto, Catania, Italy.

Leukemia
|June 22, 2001
PubMed

Insights

Patients with idiopathic myelofibrosis with myeloid metaplasia (MMM) show significantly higher vascular endothelial growth factor (VEGF) levels. Platelets are a major source of this angiogenic factor in MMM.

Area of Science:

  • Hematology
  • Oncology
  • Angiogenesis Research

Background:

  • Idiopathic myelofibrosis with myeloid metaplasia (MMM) is associated with increased angiogenesis.
  • Previous studies indicate elevated microvessel density in MMM.
  • Circulating angiogenic factor levels in MMM remain incompletely understood.

Purpose of the Study:

  • To evaluate serum levels of vascular endothelial growth factor (VEGF) in patients with MMM.
  • To correlate VEGF levels with clinical and laboratory features of MMM.
  • To investigate the role of platelets as a source of VEGF in MMM.

Main Methods:

  • Serum VEGF levels were measured in 31 MMM patients and 12 healthy controls.
  • VEGF was correlated with clinical parameters (Hb, WBC, PLT, LDH, creatinine) and disease features (cellularity, fibrosis, organomegaly, therapy).
  • VEGF levels in platelet-rich and platelet-poor plasma were compared.

Main Results:

  • MMM patients exhibited significantly higher serum VEGF concentrations compared to controls (Median 1208 ng/ml vs 138 ng/ml, P < 0.0001).
  • No significant correlation was found between VEGF and most clinical/laboratory parameters, except for a subgroup with normal/low VEGF.
  • Platelet-rich plasma showed higher VEGF, and MMM platelets contained four times more VEGF than controls, suggesting platelets are a key VEGF source.

Conclusions:

  • VEGF is overproduced in idiopathic myelofibrosis with myeloid metaplasia, supporting increased angiogenic activity.
  • Platelets are identified as a significant, but not exclusive, source of VEGF in MMM patients.
  • Further research into VEGF's role in MMM pathogenesis and potential therapeutic targeting is warranted.