Platelet‐derived growth factor (PDGF) is thought to play some role in the genesis of fibrosis associated with myeloproliferative disorders. In addition, transforming growth factor‐β (TGF‐β) has been confirmed to promote fibrotic process. Both PDGF and TGF‐β have been shown to cooperate with epidermal growth factor (EGF) in regulating the growth of human marrow fibroblasts. All three are contained in platelet α‐granules.

We report the results of a study in patients with myelofibrosis with myeloid metaplasia (MMM). We evaluated PDGF, TGF‐β and EGF‐like activities in circulating platelets from patients compared to healthy subjects. In contrast to EGF‐like intraplatelet levels which were similar in patients and in normal donors (1‐4 ng/10⁹ platelets), we found constantly higher values for both PDGF and TGF‐β in MMM patients. In both radioimmunoassay (RIA) and assay for mitogenic activity on human bone marrow fibroblasts, PDGF levels were increased on the average 2‐3·5‐fold over the levels found in normal donors (P<0·01 and P<0·001, respectively). PDGF serum levels in patients were consistent with those found in platelets. In platelet‐poor plasma (PPP), PDGF concentrations were undetectable or ≃ 2 ng/ml in patients and in control donors as well. The total TGF‐β activity in platelet lysates, determined using a competitive radioreceptor binding assay on Swiss 3T3 mouse cells and an inhibition growth assay on CCL64 cells, was found 2‐3‐fold increased in patients with MMM as compared to control subjects (P<0·003).

These results emphasize that, not only PDGF, but also TGF‐β are implicated in the myelofibrosis with myeloid metaplasia.