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Prepublished online as a Blood First Edition Paper on August 22, 2002; DOI 10.1182/blood-2002-05-1496.
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Blood, 15 December 2002, Vol. 100, No. 13, pp. 4358-4366
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Invasive aspergillosis in allogeneic stem cell transplant
recipients: changes in epidemiology and risk factors
Kieren A. Marr,
Rachel A. Carter,
Michael Boeckh,
Paul Martin, and
Lawrence Corey
From the Fred Hutchinson Cancer Research Center
Programs in Infectious Diseases and Long-term Follow-up, Seattle, WA,
and the University of Washington Department of Medicine and Laboratory
Medicine, Seattle.
The incidence of postengraftment invasive aspergillosis (IA) in
hematopoietic stem cell transplant (HSCT) recipients increased during
the 1990s. We determined risks for IA and outcomes among 1682 patients
who received HSCTs between January 1993 and December 1998. Risk
factors included host variables (age, underlying disease), transplant
variables (stem cell source), and late complications (acute and chronic
graft-versus-host disease [GVHD], receipt of corticosteroids,
secondary neutropenia, cytomegalovirus [CMV] disease, and
respiratory virus infection). We identified risk factors associated
with IA early after transplantation ( 40 days) and after engraftment
(41-180 days). Older patient age was associated with an increased risk
during both periods. Chronic myelogenous leukemia (CML) in
chronic phase was associated with low risk for early IA compared with
other hematologic malignancies, aplastic anemia, and myelodysplastic
syndrome. Multiple myeloma was associated with an increased risk for
postengraftment IA. Use of human leukocyte antigen
(HLA)-matched related (MR) peripheral blood stem cells conferred
protection against early IA compared with use of MR bone marrow, but
use of cord blood increased the risk of IA early after transplantation.
Factors that increased risks for IA after engraftment included receipt
of T cell-depleted or CD34-selected stem cell products, receipt of
corticosteroids, neutropenia, lymphopenia, GVHD, CMV disease, and
respiratory virus infections. Very late IA (> 6 months after
transplantation) was associated with chronic GVHD and CMV disease.
These results emphasize the postengraftment timing of IA; risk factor
analyses verify previously recognized risk factors (GVHD, receipt of
corticosteroids, and neutropenia) and uncover the roles of lymphopenia
and viral infections in increasing the incidence of postengraftment IA
in the 1990s.

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