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

to the presence of IVS1-6 mutation in the mother but an unknown pattern
at the 1st exon in the father. DNA sequencing showed a point mutation
G→T at CD7 of the β globin gene, confirmed also by ASO hybridisation,
which transforms codon 7 GAG (Glu) to a termination codon
TAG. This new allele causes β 0 Thalassaemia. Prenatal diagnosis has
been performed by Fetal Blood Sampling in the 20th week of gestation
as the couple presented late in pregnancy. The fetal sample has been
analysed both with DNA techniques and globin chain biosynthesis. The
fetus has inherited the CD7 mutation with biosynthetic ratio β/α=0,030
characteristic of heterozygous β 0 -thalassaemia. Conclusions. The identification
of new or rare mutations is indicative of the molecular heterogeneity
of β- thalassaemia in Albania. Moreover, it gives the possibility
for genetic counselling and prenatal diagnosis at 10- 12 weeks of gestation.
1396
THROMBOCYTOPENIA AND PSEUDOTHROMBOCYTOPENIA AFTER TREATMENT
WITH ABCIXIMAB. A PROSPECTIVE STUDY
E. Eduardo, J. Hurtado, A. García-Hernández, F. García-Candel,
J. Monserrat, M.J. Majado, A. Morales, J. Moraleda
Virgen Arrixaca Hospital, MURCIA, Spain
Background. Thrombocytopenia is a well-recognized adverse effect of
abciximab therapy (1-2% of patients). Abciximab is a glycoprotein
IIb/IIIa inhibitor widely used following coronary angioplasty to reduce
the incidence of thrombotic complications after revascularization. Abciximab
is a chimeric (human/mouse) monoclonal antibody that binds to
the fibrinogen binding site of the GP IIb/IIIa complex, inhibiting platelet
interactions and thrombus formation. Acute thrombocytopenia is a frequent
side effect of abciximab affecting 1% of patients after the first
exposure and 4% in subsequent exposures. This thrombocytopenia can
produce excessive bleeding increasing the risk of hemorrhagic complications
in coronary angioplasty and may require platelet transfusions
and discontinuation the abciximab infusion. Pseudothrombocytopenia
has also been described associated with abciximab treatment but much
more infrequently, and with no need of treatment modifications. Aims.
Our objective was to study whether the administration of abciximab had
any impact on the platelet count immediately after the administration
of the drug, and to detect any other platelet abnormalities. Methods and
results. From January 5th to February 5th 2007, we performed a prospective
study in 44 consecutive patients, 18 male and 9 female with a median
age of 69 (range 45-79), with acute ischemic myocardiopathy treated
with abciximab after coronary angioplasty. The patients received
abciximab at a dose of of 0.25 mg/kg i.v. bolus, followed by a 24 hours
infusion of 0,0625 mgr/kg/min. In addition the patients were treated
with sodium heparin (5000 IU, i.v. bolus), clopidogrel (75 mgr/day) and
oral acetylsalicylic acid (100 mg/day). Platelet counts were obtained prior
to and in the following 24hr following abciximab in 27 cases. Statistical
comparisons were made with the student-T test for paired data. The
median platelet count prior to abciximab was 189×109 /L (range 94-380).
We found a small but statistically significant decrease in the platelet
count post treatment with abciximab 177,5×109 /L (range 0-362),
(p=0,005). In addition we found one case of severe thrombocytopenia
that required platelet transfusion and one case of pseudothrombocytopenia
(Figure 1), in this series (4,5%).
Figure 1.
12 th Congress of the European Hematology Association
In the first case we excluded the existence of anti-PF4/heparin complex
antibodies (ID-PaGIA heparin/PF4 antibody test, DiaMed) prior
to the platelet transfusion. The patient with pseudothrombocytopenia
did not have any bleeding complications and did not required discontinuation
of abciximab treatment or intervention with platelet transfusions.
It has been proposed that clumping is due to antiplatelet antibodies
directed against the GP IIb/IIIa complex but the mechanism of
abciximab-associated thrombocytopenia is not clear. Evaluation of the
peripheral smear, to get the automated platelet count in citrate anticoagulated
blood samples, and the exclusion of PF4/heparin antibodies is
essential to make the differential diagnosis of these complications
with such a different management. Conclusions. Thrombocytopenia is
not uncommon after abciximab therapy and the medical community
should be aware of this complication. We have found a slight decrease
in the platelet number probably related with abciximab infusion, but
there was very mild and clinically irrelevant. The distinction of true
severe thrombocytopenia from pseudothrombocytopenia and from
heparin-induced thrombocytopenia in patients with acute coronary
syndromes treated with abciximab is highly suggested.
1397
DIVERGENT PATTERNS OF SERUM VASCLAR ENDOTHELIAL GROWTH FACTOR (VEGF)
IN PATIENTS WITH ACUTE LEUKEMIA AND LYMPHOMA
E. Elbaz, D. Aladle, M. El Awady, M. Waly
Faculty of medicine, MANSOURA, Egypt
VEGF has been implicated as the main endothelial pathway requied
for tumor neovasclariztion . Although most of the initial studies in
angigenesis were done on solid tumors, there were data suggesting the
importance of angiogenesis in hematological malignancies such as non-
Hodgkin’s lymphoma and acute leukemia .we detemined serum VEGF
by ELISA technique in patients with NHL(20 cases), acute lymphoblastic
leukemia (13 cases), and acute myeloblastic leukemia (14 cases) in
addition to 13 cases as a reference control group. Twenty five cases
were followed up afrter therapy (10 with NHL, 8 with ALL and 7with
AML).Signifcant high levels were only reported among patients with
AML (M±SD=345.7±227.3) and NHL (357±214.4) when compared to
controls control (189.2±70.5)(p< 0.05). On the contrary, a highly significant
reduction of serum VEGF was elicited in patients with ALL
(132.3±44.6) compared to controls (p< 0.01). Serum VEGF was significantly
reduced nearly to control level after therapy in NHL (M±SD
=142±47.9)and AML (210±69.5) as compared to the before therapy ,
while in ALL patients, serum VEGF was noticeably increased (168
±49.2) nearly to control level after therapy as compared to to that
before thrapy .We conclude that VEGF level in the serum may be used
be as a valuable angiogenic marker for identifying the clinical outcome
of patients with acute leukemias and NHL. Anti-angiogenesis is a
promising target for therapeutic interventions in lymphomas and acute
leukemias especially AML
1398
ACUTE MYELOID LEUKEMIA ASSOCIATED PLATELETS BEHAVIOR - FLOW CYTOMETRY
ANALYSIS IN CLINICAL CONTEXT
H. Bumbea, 1 A.M. Vladareanu, 1 S. Radesi, 1 V. Vasilache, 1 C. Ciufu, 1
A. Petre, 1 D. Casleanu, 1 I. Voican, 1 V. Popov, 2 M. Begu, 1
M. Dervesteanu, 1 M. Onisai, 1 C. Marinescu1 1 2 Emergency Universitary Hospital, BUCHAREST; County Hospital, PITESTI,
Romania
Background. Extensive bleeding is one of the most frequent causes of
death in acute myeloid leukemia (AML). Previous studies on platelet
behavior associated with this disease identified impaired activation
and aggregation processes. Aims. The aim of this study was to examine
platelet function in correlation with other haemorrhage risk factors
(fever, sepsis, recent bleeding, uremia, leucocytosys , hemathocrit value,
treatment). Methods. Whole blood flow cytometry analysis for
platelets surface proteins (Glycoprotein Ib-IX [CD42b, CD42a], Glycoprotein
IIb-IIIa [CD41, CD61], P-selectin [CD62P], granulophysin
[CD63]) was fulfilled in patients with acute myeloid leukemia in different
stages of diagnosis and therapy (n=22) in comparison with
healthy human controls (n=10). Results. Our results show a significant
decrease of fluorescence level associated with platelet activation markers
(CD63 [14.11% vs. 40.78% p