12th Congress of the European Hematology ... - Haematologica

without type 2 diabetes. Methods. This case-control study consisted of
100 CAD patients (55 males and 45 females) with angiograhically documented
coronary artery disease (at least 30% stenosis) which among
them 65 were diabetic patients with CAD, aged 57.6±8.4 and 35 were
CAD patients without type 2 diabetes, aged 53.3±9.1 and 59 (26 males
and 33 females) unrelated controls with angiographically normal coronary
and without diabetes, aged 54.3±3. All patients and controls were
from the Kermanshah province of Iran. Genotyping was done by PCR-
RFLP using Mnl I and Hind III for factor V Leiden and prothrombin
G20210A, respectively. Results. Heterozygous factor V Leiden mutation
was found in 3 out of 65 (4.6%) diabetic patients with CAD, 2 of 35
(5.7%) CAD patients without diabetes and 2 out of 59 (3.4%) control
subjects (p=0.6). Only 2 diabetic patients with CAD (around 3%) were
found to be heterozygous for both the 20210G and 20210A alleles of prothrombin
gene. No homozygous carrier for these mutations was found.
Summary/conclusions. The present results indicate that although the prevalence
of FV Leiden and the prothrombin 20210G:A are increased in CAD
patients compared to healthy individuals but these differences are not
significant. Neither FV Leiden nor prothrombin G20210A were associated
with type 2 diabetes mellitus or CAD.
0953
NEURAL CELL ADHESION MOLECULE (CD56) EXPRESSION ON PLASMA CELLS
IN MONOCLONAL GAMMOPATHIES
M. Kraj, U. Sokolowska, J. Kopec- Szlezak, R. Poglod, B. Kruk,
J. Wozniak, T. Szpila
Institute of Haematology, WARSAW, Poland
It was shown that absence of CD56 on malignant plasma cells (PCs)
is hallmark of plasma cell leukemia (PCL), special subset of multiple
myeloma (MM) (Leukemia 1998; 12: 1977) and may play role in pathogenesis
of central nervous system MM (Br J Haematol 2005; 129: 539).
There was also found that expression of CD56 correlates with presence
of osteolysis in MM and distinguishes MM from MGUS and lymphomas
with plasmacytoid differentiation (Am J Pathol 2002; 160: 1293). Aim of
this study was to evaluate intensity of CD56 expression on bone marrow
(BM) myelomatous PCs and to assess clinical correlations. The study
group consisted of 204 MM patients (112M 92F, median age 63, range
32-89yr ;30 at stage I, 50-II, 124 -III; 153 had osteolysis; monoclonal protein
IgG was in 128 patients, IgA-50, IgD-1, IgM-2, Bence Jones'20, NS-
3) and 26 PCL 8 IgM lymphoplasmacytic lymphoma and 14 MGUS
patients. Controls were 10 healthy subjects. Immunophenotyping was
done on freshly collected BM samples using triple staining combination
of CD138/CD56/CD38 monoclonal antibodies analysed by flow cytometry.
Plasma cells were identified as cells showing high-density expression
of CD38 and CD138 (syndecan-1). Antigen expression intensity
was calculated as relative fluorescence intensity (RFI) and for direct quantitative
analysis the QuantiBRITE test was applied. Mean channels of
phycoerythrin fluorescence were defined and antibody bounding capacity
(ABC) was then calculated using QuantiCALC software. Results. In
135 patients (66%) PCs showed CD56 expression. Out of all
CD38 ++ /CD138 + BM cells mean proportion of PCs with CD56 expression,
was 82±20%, median 91%. RFI values ranged from 7,6 to 27,4 in
particular patients (18,0±4,5, median 17,8) and the number of CD56
binding sites (ABC) on MM plasma cells ranged from 2255 to 58469
(14199±15038, median 8866). A correlation was found between RFI and
ABC values (r=0,76; p