Platelet factor-4 excretion in myeloproliferative disease: implications for the aetiology of myelofibrosis |
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| Authors: | Samuel A.,Burstein ,Thomas W.,Malpass,Esther,Yee,Marshall,Kadin,Malcolm,Brigden&dagger ,John W.,Adamson Laurence A.,Harker |
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| Affiliation: | Scripps Clinic and Research Foundation, Department of Basic and Clinical Research, La Jolla, California;Division of Hematology, Department of Medicine, and Department of Laboratory Medicine, University of Washington School of Medicine, Seattle, Washington;Island Medical Laboratories, Victoria, British Columbia |
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| Abstract: | S ummary. Experimental evidence suggests that the fibroblastic proliferation often associated with the myeloproliferative disorders is not part of the neoplastic process, but is secondary to an unknown stimulus. This stimulus may be a factor derived from platelets which promotes the proliferation of fibroblasts in vitro (PDGF). Plateletderived growth factor is localized to platelet α-granules together with PF4 and β-TG. As an indicator of α-granule release, we have measured PF4 levels in plasma. platelets and urine in 46 normal subjects and 49 patients with myeloproliferative disorders, secondary thrombocytosis and miscellaneous malignancies. All 11 patients with elevated urinary PF4 excretion exhibited myelofibrosis, whereas 11 of 22 patients with documented myelofibrosis had urinary PF4 excretion in the normal range. No correlation was seen between marrow fibrosis and plasma levels or the platelet content of PF4. The data are consistent with the possibility that release of mitogen(s) from platelet or megakaryocyte α-granules in some patients with myeloproliferative disorders is pathogenetically related to the development of marrow fibrosis. |
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