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october 7-9, 2012 • NEW ORLEANS, LA
based gating, ranging from 0.02% to 83.23%. No patients
showed GPI-deficient monocytes by one but not the other
gating strategy. The presence of blasts in acute leukemias
resulted in abnormal clustering patterns by both gating
techniques.
Conclusions:
CD64 is strongly expressed in all
monocytes, does not have a bridge of CD64-dim events, and
shows a distinct cluster, allowing for more objective gating.
Acknowledgements:
This study was supported by an
unrestricted educational grant from Alexion Pharmaceuticals.
P13
CLINICAL AND IMMUNOPHENOTYPIC PROFILE OF
PATIENTS WITH GPI-DEFICIENT CELLS USING 2010
CONSENSUS TESTING METHOD: BRITISH COLUMBIA
EXPERIENCE
Bakul I Dalal, Nikisha S Khare, Steven Pi
Flow Cytometry Service, Division of Laboratory Hematology,
Vancouver General Hospital
Background:
Cells lacking glycosyl phosphatidyl inositol
(GPI)-associated antigens are seen in paroxysmal nocturnal
hemoglobinuria (PNH) and certain bone marrow failure
states. Precise quantitation of GPI-deficient cells and
indications for testing have recently been standardized
(Parker, 2005; Borowitz, 2010). We report here our
experience of testing patients for GPI-deficient cells based
on the recommended indications and using the Borowitz
2010 protocol.
Methods:
300 tests were done on 281
patients over a 16 month period. A 7-color panel consisting
of CD45, CD15, CD33, CD64, CD14, CD24 and FLAER
was used for granulocytes and monocytes, while a 2-color
panel consisting of CD235 and CD59 was used for RBCs.
Minimum 25 events were necessary to consider a specimen
positive. Indications for testing were verified by chart
review, CBC, bone marrow examination, cytogenetics, and
laboratory tests for hemolysis.
Results:
GPI-deficienct cells
were seen in 45/300 (15%) tests in 36/281 patients. The
clone size varied from 0.01% to 95.09%. The difference
between the number of GPI-deficient granulocytes and
monocytes ranged from -47.1% to +11.96%. In 27/45
cases, monocytes returned a higher number of GPI-
deficient cells than granulocytes. Frequency of GPI-deficient
cells under various indications (table-1) were: 1. known
PNH (6/8), hemolysis (6/22), thrombosis (1/43), aplastic
anemia (16/29), myelodysplastic state (4/16), unexplained
cytopenias (13/142), and others (4/54). Among patients with
cytopenias, those with pancytopenia had higher incidence
of GPI-deficient cells (8/36) than those with mono- (1/62)
or bi-cytopenias (4/42).
Acknowledgments
: This study was
supported by an unrestricted educational grant from Alexion
Pharmaceuticals.
P14
IMMUNOGLOBULIN HEAVY CHAIN ISOTYPE
EXPRESSION IN CHRONIC LYMPHOCYTIC LEUKEMIA:
LACK OF CORRELATION WITH KARYOTYPIC
ABNORMALITIES
Adriana Doldan-Silvero
1
, Laila Mnayer
1,2
, Joseph A.
DiGiuseppe
1
1
Dept. of Pathology Hartford Hospital,
2
Clinical Laboratory
Partners
Immunoglobulin heavy chain expression in chronic
lymphocytic leukemia (CLL) has been shown to correlate
with a number of prognostic clinical and laboratory variables.
Karyotypic abnormalities as determined by interphase
fluorescence in situ hybridization (FISH) have also been
shown to have prognostic value in CLL. In this study, we
sought to determine whether immunoglobulin heavy chain
expression correlates with karyotypic abnormalities in a
POSTER ABSTRACTS