Case Report
Acta Haematol 2003;110:193–196
DOI: 10.1159/000074224
Splenectomy for Massive Splenic
Infarction Unmasks Paroxysmal
Nocturnal Hemoglobinuria
Costas Tsatalas
a
Dimitris Margaritis
a
Despina Pantelidou
a
Ioannis Kotsianidis
a
Anastasios J. Karayiannakis
b
Emanuel Spanoudakis
a
Zafiris Kartasis
a
Vasiliki Kaloutsi
d
Alexandros Polychronidis
b
Ioannis Manavis
c
George Bourikas
a
a
Department of Hematology,
b
Second Surgical Department and
c
Department of Radiology, School of Medicine,
Democritus University of Thrace, Alexandroupolis, and
d
Department of Pathology, School of Medicine,
Aristotle University of Thessaloniki, Thessaloniki, Greece
Received: March 25, 2003
Accepted after revision: July 14, 2003
C. Tsatalas, MD
Department of Hematology, School of Medicine
Democritus University of Thrace, Ioakim Kaviri 6
GR–68100 Alexandroupolis (Greece)
Tel. +32 5510 76152, Fax +32 5510 76154, E-Mail ktsatala@med.duth.gr
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© 2003 S. Karger AG, Basel
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Key Words
Paroxysmal nocturnal hemoglobinuria W Splenic
infarction W Splenic vein thrombosis W Splenectomy
Abstract
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare
disorder characterized by pancytopenia, hemolysis, and
thrombosis. Abdominal vein thrombosis is a life-threat-
ening manifestation of this disease. We present a patient
with complete spleen necrosis due to thrombosis of the
splenic vessels. After splenectomy, other causes of
thrombophilia were excluded and the diagnosis of PNH
was established. The patient was put on anticoagulation
but despite the prophylactic international normalized
ratio maintained over the last 18 months of follow-up, he
had another episode of intrahepatic thrombosis which
was treated with tissue plasminogen activator thrombo-
lysis.
Copyright © 2003 S. Karger AG, Basel
Introduction
Paroxysmal nocturnal hemoglobinuria (PNH) is an
acquired clonal disorder of the hematopoietic stem cell
that results in the production of abnormal blood cells.
These cells are deficient in all surface proteins which are
normally attached to the cell membrane by a glycosyl-
phosphatidylinositol (GPI) anchor. The abnormal GPI
molecules in PNH are the result of a somatic mutation of
the PIG-A gene which encodes a protein necessary for
their biosynthesis. The disease presents with various clini-
cal manifestations depending on the size of the abnormal
clone and the most affected blood cells. PNH is mainly
characterized by intravascular hemolysis with hemoglo-
binuria and life-threatening thrombosis [1]. Although ve-
nous thrombosis is a frequent complication in PNH
patients, arterial thrombosis is rare and only a few cases
have been reported [2, 3]. Here, we report a patient in
whom the diagnosis of PNH was made after total splenic
parenchymal necrosis due to thrombosis of the splenic
vessels.