Changes in splenic microcirculatory pathways in chronic idiopathic
thrombocytopenic purpura
EE Schmidt, IC MacDonald and AC Groom
Department of Medical Biophysics, University of Western Ontario, London,
Canada.
The spleen plays a central role in the pathogenesis of chronic idiopathic
thrombocytopenic purpura (ITP); it produces massive quantities of
antiplatelet antibodies, leading to accelerated phagocytosis of platelets.
Lymphoid hyperplasia typically occurs in the spleen, characterized by large
numbers of lymphatic nodules with active germinal centers. Whether changes
in splenic microcirculatory pathways also occur is not known. We have
studied this question by scanning electron microscopy of corrosion casts,
comparing spleens removed from patients with ITP with normal spleens
obtained from organ transplant donors. The casts demonstrate two major
changes in microcirculatory pathways in ITP. Firstly, a striking
proliferation of arterioles and capillaries is found in the white pulp and
marginal zone (MZ), seen as extensive vascularization in 92.3% of lymphatic
nodules (n = 191) versus 0.6% (n = 224) in normal spleens. Secondly, the
marginal sinus, a series of flattened, anastomosing vascular spaces between
the white pulp and MZ, is absent in 89.4% of lymphatic nodules versus 4.9%
in normal spleens. The cause of these microcirculatory changes, which may
not be exclusive to ITP, is presently unknown. Absence of the marginal
sinus may affect distribution of blood flow through the MZ such that
platelets spend increased amounts of time in the proximity of macrophages.
In the presence of antiplatelet antibodies found in ITP spleens, this
delayed transit would lead to greatly increased platelet destruction.
Volume 78,
Issue 6,
pp. 1485-1489,
09/15/1991
Copyright © 1991 by The American Society of Hematology
