Blood Journal
Leading the way in experimental and clinical research in hematology

Studies on Platelets

  1. ANTHONY V. PISCIOTTA, M.D.,
  2. MARIO STEFANINI, M.D., and
  3. WILLIAM DAMESHEK, M.D.
  1. Ziskind Laboratories (Hematology Section) of the New England Center Hospital and Pratt Diagnostic Clinic, and the Department of Medicine, Tufts College Medical School, Boston, Mass.

Abstract

1. The morphologic characteristics of the megakaryocytes were studied in fourteen normal or nonthrombocytopenic individuals, in nine patients with idiopathic thrombocytopenic purpura (I.T.P.), in two individuals with pernicious anemia, and in two normal individuals in whom thrombocytopenia was temporarily induced by the administration of plasma from a patient with a circulating high-titer platelet agglutinin. Phase contrast microscopy was used on unfixed, unstained materials.

2. The characteristics observed in normal megakaryocytes and in those from patients with I.T.P. confirmed data previously obtained with the use of fixed and stained material. In I.T.P. the bone marrow megakaryocytic series presented the following significant findings: (a) an increase in the number of the megakaryocytes, particularly of the younger forms. Young forms were particularly prominent in I.T.P. of the "acute" variety. (b) Production of platelets by promegakaryocytes, the platelets appearing large and bizarre. (c) Lack of platelet formation at the periphery of the cell and lack of granularity in the outer layer of the mature megakaryocyte. (d) Presensce of marked degenerative changes in the nucleus and cytoplasm of the megakaryocytes. The abnormalities observed suggested the possibility of a double mechanism: one in which the circulating platelets were injured, the other in which the megakaryocyte itself was attacked.

3. In a patient with a high-titer circulating platelet agglutinin the alterations of the megakaryocytes were fundamentally similar, although the granularity of the cytoplasm appeared to be less affected and the degenerative changes more pronounced. Similar abnormalities could be reproduced in the normal individuals receiving the patient's plasma. These results again suggested that, at least in those cases of I.T.P. in which the thrombocytopenia was due to a circulating antiplatelet factor, this acted by: (a) attacking the platelets being discharged from the megakaryocyte; (b) preventing the normal formation of platelets; (c) preventing the normal development of the megakaryocyte from younger to more mature forms.