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Blood, 1953, Vol. 8, No. 8, pp. 703-723.
© 1953 American Society of Hematology, Inc.
Studies on Platelets
X. Morphologic Characteristics of Megakaryocytes by Phase
Contrast Microscopy in Normals and in Patients with
Idiopathic Thrombocytopenic Purpura
ANTHONY V. PISCIOTTA M.D.1,
MARIO STEFANINI M.D.1, and
WILLIAM DAMESHEK M.D.1
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.
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.
Submitted on January 6, 1953
Accepted on February 17, 1953
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