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Blood, Vol. 93 No. 4 (February 15), 1999:
pp. 1264-1270
Enhanced Endothelial Cell Apoptosis in Splenic Tissues of
Patients With Thrombotic Thrombocytopenic Purpura
Chau T. Dang,
Margret S. Magid,
Babette Weksler,
Amy Chadburn, and
Jeffrey Laurence
From the Laboratory for AIDS Virus Research, Division of
Hematology-Oncology, Department of Medicine, and Department of
Pathology, Cornell University Medical College, New York, NY.
Idiopathic thrombotic thrombocytopenic purpura (TTP) is a thrombotic
microangiopathy of obscure etiology. The fundamental pathologic lesion
is a hyaline thrombus composed of platelets and some fibrin accompanied
by endothelial cell proliferation and detachment, in the absence of an
inflammatory response. We have previously demonstrated that plasmas
from patients with both idiopathic TTP and a related disorder, sporadic
hemolytic-uremic syndrome (HUS), induce apoptosis and expression of the
apoptosis-associated molecule Fas (CD95) in vitro in those lineages of
microvascular endothelial cells (MVECs) that are affected
pathologically. We now demonstrate the presence of enhanced MVEC
apoptosis in splenic tissues from patients with TTP, documented by
terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling
(TUNEL) and morphology. This is accompanied by elevated Fas expression.
It contrasts with the absence of apoptosis in splenic tissues obtained
after splenectomy for trauma or immune thrombocytopenic purpura.
TUNEL-positive cells, identified by immunohistochemistry as MVECs or
macrophages, presumably engulfing apoptotic ECs, are noted in numerous
areas, including those apart from microthrombi. Thus, it is unlikely
that EC apoptosis is simply a sequela of thrombus formation. Based on
these data, we propose that MVEC apoptosis is of pathophysiologic
significance in idiopathic TTP/sporadic HUS.
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