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12 th Congress of the European Hematology Association 0817 THROMBOPHILIC RISK FACTORS AMONG 16 LEBANESE PATIENTS WITH CEREBRAL VENOUS AND SINUS THROMBOSIS Z. Otrock, A. Taher, W. Shamseddeen, R. Mahfouz American University of Beirut Medical Ct, BEIRUT, Lebanon Background. Cerebral venous and sinus thrombosis (CVST) is a multifaceted disorder. It has multiple predisposing factors including pregnancy and postpartum state, surgery, head trauma, arterio-venous malformations, infection, paraneoplastic and autoimmune disease, and particularly the use of oral contraceptives. In addition, inherited blood coagulation disorders play an important role in the development of CVST. Aims. In the present study, the frequency of inherited thrombophilic risk factors among 16 CVST patients has been evaluated. Methods. Sixteen patients, diagnosed with CVST at the American University of Beirut Medical Center, were identified by medical chart review and thrombophilia screening. We have tested these patients for the prothrombotic mutations G20210A of the Factor II gene and G1691A of the factor V Leiden gene, and the C677T methylenetetrahydrofolate reductase (MTHFR) gene. We also assessed the presence of acquires thrombophilia (lupus anticoagulant and anticardiolipin antibodies) and other risk factors (pregnancy and postpartum state, surgery, paraneoplastic disease, and the use of oral contraceptives). Results. Of the 16 CVST patients, half were female and the mean age was 22.9 years (range: 1-46 years). Five out of the 16 CVST patients (31.2%) showed the G1691A mutation of factor V (4 were heterozygous and 1 was homozygous). The frequency of the C677T MTHFR genotype was 50% (8/16) in patients (2 of them were homozygous). Four of the patients (25%) had both factor V Leiden and MTHFR mutation. None of the patients expressed the G20210A Factor II allele variant. Three of the patients had positive antiphospholipid antibodies; one of them was heterozygous for factor V Leiden and MTHFR mutations. At the time of CVST, 2 females were taking oral contraceptives; one of them was homozygous for factor V Leiden (this was the only patient in this series to have a positive family history of venous thromboembolism). Four patients were known to have a malignancy; 2 had non-Hodgkin’s lymphoma, 1 had acute lymphoblastic leukemia and the last had breast cancer. Conclusions. Despite the limitation of sample size, we identified an inherited coagulopathy at high rate in our patients. Combined inherited thrombophilia was also present in 25% of patients. In addition, the prevalence of acquired thrombophilia and other contributing factors was also high. This finding supports the impression of a multifactorial process leading to CVST in Lebanese patients. 0818 GENETIC POLYMORPHISM OF HEMOCOAGULATION FACTORS IN PATIENTS WITH PORTAL THROMBOSIS E. Sysoeva, 1 E. Lukina, 1 G. Sukhanova, 1 E. Voronkova, 1 N. Khoroshko, 1 S. Vasiljev, 1 E. Kitsenko, 2 E. Lyubiviy, 2 A. Eramishantsev2 1 National Research Center for Hematology, MOSCOW; 2 National Research Center for Surgery, MOSCOW, Russian Federation Background. the prehepatic portal hypertension due to portal thrombosis was belived to be a rare condition (about 10% of all cases of portal hypertension). Chronic myeloproliferative disorders (MPD) were considered to be the main cause of thrombotic complications in adult patients (pts), and thrombophilia - to be a predisposing factor. Aims. To study genetic polymorphism of hemocoagulation factors in patients with portal thrombosis. Materials and Methods. 54 patients (21 males, 33 females, Median age - 43 years) with portal thrombosis confirmed by Doppler sonography were included into this study. The period from the first manifestation of portal hypertension (splenomegaly, varicose dilatation of esophageal veins) to examination in our Center varied from 4 to 480 months (Median 60 months). Only 25 (46%) patients had bone marrow morphology of myeloproliferative disorders. The other patients had normal pattern of bone marrow, normal blood picture or cytopenias. All patients were screened for polymorphism of 10 genes of hemocoagulation system. Results. Polymorphisms of genes hemocoagulation system were found in 67% pts, including mutation in genes of methylenetetrahydrofolatereductase in 26 (48%) pts (5 - homozygous), plasminogen activator inhibitor-1 (PAI-1) in 22 (41%) pts (8 -homozygous), β-Fibrinogen-455 G-A heterozygous - in 12 (22%) pts, integrin α II - in 14 (26%) pts (3 - homozygous). Heterozygous mutations in genes factor V Leiden were found in 2 cases, prothrombin - in 1 pt., factor VII - 4 pts, P-selectin (CD 162) - in 4 pts. The majority of patients (35%) had combination of 3 and more polymorphisms. Combination of MPD and polymorphisms of genes hemocoagulation system was found in 23 306 | haematologica/the hematology journal | 2007; 92(s1) (43%) pts. Conclusions. The use of molecular diagnostic methods reveals the high frequency of genetic polymorphism of hemocoagulation factors in patients with portal thrombosis The presence of the hereditary thrombophilia proves the necessity of prescribing anticoagulant/antiaggregant therapy in patients with portal thrombosis. 0819 PROTHROMBOTIC RISK FACTORS IN CHILDREN WITH HENOCH-SCHONLEIN PURPURA E. Kurekci, 1 S. Kalman2, A.A. Atay, 1 B. Hachiamdioglu, 2 H.I. Aydin, 2 Y. Egin3, C. Beyan, 1 F. Gok, 2 N. Akar, 4 O. Ozcan1 1 Gulhane Military Medical Academy, ANKARA; 2 Department of Pediatrics, ANKARA; 3 Department of Molecular Hematology, ANKARA; 4 Ankara University School of Medicine, ANKARA, Turkey Background. Henoch-Shönlein purpura (HSP) is an acute immunoglobulin A (IgA)'mediated leukocytoclastic vasculitis that affects primarily children. The dominant clinical features of HSP are cutaneous purpura, arthritis, abdominal pain, gastrointestinal (GI) bleeding due to bowel infarction with or without perforation, orchitis, and nephritis. Stroke may occur in some of the cases. The precise etiology of the disease is not clear, but HSP typically follows an upper respiratory tract infection. Yilmaz et al. (2005) reported that in patients with HSP, fibrinogen, Ddimer, TAT complex, PF-1, PF-2, vWAg, and RiC of levels were significantly higher during the acute phase were than during recovery phase and significantly higher than those of control subjects. The severity of disease was significantly correlated with TAT, PF-1, PF-2, vWAg, and Ddimer levels. These factors may be risks for thrombosis seen in vasculitis. Several hereditary factors have been associated with increased risk of thrombosis. Of these, protein C (PC), protein S (PS), anti-thrombin (AT) and thrombophilic gene mutations [factor V Leiden (FVL), prothrombin G20210A, and C677T variant of methlenetetrahydrofolate reductase (MTHFR)] were well described risk factors for thrombosis. Herein, we report the results of prothrombotic risk factor analysis of patients with HSP. Methods. Twenty-four patients (16 girls, 8 boys) with HSP and 48 (32 girls and 16 boys) healthy age- and sex-matched children were investigated for risk factors for thrombosis (PC, PS, AT, factor VIII, factor IX, vWF, FVL, prothrombin 20210A, and MTHFR C677T) and its relation with clinical signs. Blood samples were drawn minimum three months elapsed from the diagnosis. Results. The rates for skin, joint, GI, and renal involvement were 100%, 50%, 8%, and 4,1%, respectively. Plasma PC, PS, AT, factor VIII, factor IX, and vWF levels were within normal limits. The percentages of FVL and MTHFR mutations were 4.1% and 54.1%, respectively. Factor V Leiden was found in 10.4% and MTH- FR mutation in 54.1% of the controls. Prothrombin 20210A was not found in the patient group whereas it was shown in 2% of the controls. There was no relationship between the prothrombotic risk factors and clinical manifestations. Conclusions. Well-known prothrombotic risk factors possibly do not play a role in clinical manifestations of Henoch- Schonlein purpura. 0820 THE IG.G ANTI-PROTHROMBIN ANTIBODIES ASSOCIATE WITH THE VENOUS THROMBOEMBOLISM IN WOMEN J. Gonzalez-Ordonez, 1 M. Moran-Alcala, 1 C. Fernandez-Canal, 2 M.E. Gonzalez, 2 C. Fernandez-Alvarez, 2 D. Macias, 1 M Peliz1 1 Hospital San Agustin, AVILES; 2 Hospital de Cabueñes, GIJON, Spain Background. The association of antiphospholipid antibodies with either vascular thrombosis or fetal morbidity is known as the antiphospholipid syndrome (APS). Although the pathogenic role in the thrombotic complications of the APS seems clear for the lupus anticoagulant the association between thrombosis and other related auto-antibodies is not obvious. Data of the clinical association between the venous thromboembolism (VTE) and anti-prothrombin (aPT) antibodies are scarce and inconclusive. We aim to know any possible association between these antibodies (using methods for both isotypes) and the VTE. Population and methods. We studied 79 unrelated patients with an episode of VTE (objectively diagnosed) and 79 healthy controls of similar gender and age [in overall 62.0 (12.8) y, 48.7% males]. Among the patients, 25 (32%) have suffered a pulmonary embolism (PE) with or without a related DVT and 24 (30%) a recurrent episode of VTE. We performed a commercial enzyme linked immunoassay (ELISA) for both isotypes (IgG and IgM) of the aPT antibodies in serum seven months after the acute thrombotic episode. Results. We tested several arbitraries and statistical cut-off values obtaining a weak positive association with
the 97.5th percentile (5.2 U/mL) generating an OR=4.3 (1.0-18.7) (p
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
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(MMolR, defined as a BCR-ABL x 100
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0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
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0250 INACTIVATION OF SUPPRESSOR OF
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Bortezomib 1.3 mg/m 2 days 1,4,8,11
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Response was defined according to E
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G-CSF can be used in neutropenic pa
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ence and functional activity of CD8
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itating tumor development, or engag
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phoma and SNT-13, -15 were establis
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usage (2/20 ie 10%) were observed.
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0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
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(range, 1-6) and 11 treatment cycle
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0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
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functional activity was confirmed b
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No major toxicity, neither hematolo
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enewal potential of X-RAR-positive
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(50-99) respectively. Serial analys
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cell-interaction, adhesion and acti
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0340 ALTERED FIBRIN CLOT STRUCTURE
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Conclusions. This study demonstrate
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0354 FACTOR V LEIDEN HOMOZYGOUS GEN
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Results. From July 2005 through Mar
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0364 CLINICAL EFFICACY OF OXALIPLAT
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one marrow and peripheral blood ste
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ecently suggested (Boissel et al.,
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0378 SAFETY AND EFFICACY OF THE TER
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Cytogenetics and molecular diagnost
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0385 CYTOPLASMIC MUTATED NUCLEOPHOS
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0390 ELTROMBOPAG RAISES PLATELET CO
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factor for the achievement of CR wa
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The cases of RAS showed two peaks o
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is 85%. Seven out of the 25 relapse
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0409 FRACTIONATED RADIOIMMUNOTHERAP
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0414 COMPARATIVE ANALYSIS OF THE CO
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successfully managed with GM-CSF di
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49% for PCR positive patients (95%
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+8 (1 PR+1 HI) and 14/24 pts with c
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(e.g. bcr-abl leading to CML). CSC
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0438 TERC MUTATIONS ANALYSIS IN PAT
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observed in all mice. Analysis of l
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ex-vivo expansion of HUCB-derived H
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ic kidney disease in univariate or
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One hundred eleven CN AML patients,
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to asses intestinal epithelial dama
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genesis of acute myeloid leukaemia
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polymorphism at nucleotide 4889 of
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expression along with a decreased C
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0487 MUTATIONAL STATUS OF NUCLEOPHO
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previously reported, a single cours
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0497 SINGLE AGENT CLORETAZINE (VNP4
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ly received melphalan-based chemoth
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were similar among the 3 groups. Ho
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Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
Page 263 and 264: er patient does not indicate such t
Page 265 and 266: Myeloma and other monoclonal gammop
Page 267 and 268: secutive patients with MM, referred
Page 269 and 270: whether gene expression values may
Page 271 and 272: 0705 THE SHIFT OF TREATMENT FOR NAS
Page 273 and 274: 0710 CLINICO-PATHOLOGICAL FEATURES,
Page 275 and 276: patients presented a stage IV disea
Page 277 and 278: plete remission or recurrent diseas
Page 279 and 280: known at NHL diagnosis, were includ
Page 281 and 282: 0731 THE IMPACT OF HIV ON NON-HODGK
Page 283 and 284: patients had died of their underlyi
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Page 287 and 288: modulated after 24 h (37 up- and 59
Page 289 and 290: 0753 A SUSTAINED REMISSION OF IDIOP
Page 291 and 292: and treatment, has rarely been syst
Page 293 and 294: uncontrolled massive bleeding affec
Page 295 and 296: Results. A total of 396 patients we
Page 297 and 298: C30 questionnaire, and the correspo
Page 299 and 300: wave length of light of reflected r
Page 301 and 302: 0783 PREVALENCE OF MEMBRANE PROTEIN
Page 303 and 304: erozygous mother has a more severe
Page 305 and 306: 0794 CARDIAC MANIFESTATIONS IN A BR
Page 307 and 308: 0799 INEFFECTIVE ERYTHROPOIESIS IN
Page 309 and 310: p=0.014 and p=0.003, respectively).
Page 311 and 312: 0809 CURRENT APPROACH TO CHELATION
Page 313: Thrombosis II 0814 UNSUSPECTED PULM
Page 317 and 318: symptoms of DVT, 3 (7.89%) previous
Page 319 and 320: Transfusion medicine and vascular b
Page 321 and 322: tions (most bacterial, 2 malaria, 6
Page 323 and 324: 0844 INCREASED LEUKOCYTE-PLATELET I
Page 325 and 326: 0851 CORD BLOOD DERIVED MESENCHYMAL
Page 327 and 328: SIMULTANEOUS SESSION II Chronic mye
Page 329 and 330: 0862 COMPARISON OF DASATINIB TO HIG
Page 331 and 332: 0867 COMPREHENSIVE GERIATRIC ASSESS
Page 333 and 334: 0872 MN1 INDUCES LEUKEMIA IN MICE A
Page 335 and 336: 0877 PAX5/TEL TRANSDUCED PRE-BI CEL
Page 337 and 338: 0882 CISPLATIN INDUCES THROMBIN GEN
Page 339 and 340: have an early manifestation of typi
Page 341 and 342: 0892 INTEGRATION OF GENOME WIDE SNP
Page 343 and 344: 0897 THE PHENOTYPE OF JAK2V617F MUT
Page 345 and 346: gest diverse sequences of NPM mutan
Page 347 and 348: 2004 to January, 2006. At enrollmen
Page 349 and 350: with a p value of ≥ 0.10. Sets of
Page 351 and 352: BRIC 126 and 4N1K) in cells lacking
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Page 355 and 356: 0927 MK-0457, A NOVEL MULTIKINASE I
Page 357 and 358: Publication Only 0933 CLINICAL FEAT
Page 359 and 360: HSCT from the available Asian as we
Page 361 and 362: that the incidence of JAK2 mutation
Page 363 and 364: without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
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0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
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survival of five years. This dismal
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1011 FLOW CYTOMETRIC DNA INDEX AND
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1018 THE EFFECT OF THE SUGARBAKER P
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1024 KIR/HLA CLASS I MISMATCHING AN
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ment details and thrombotic histori
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1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
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1063 ABNORMAL METHYLATION STATUS OF
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1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
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1099 ALTERATIONS IN THE NATURAL KIL
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1105 CYTOGENETIC ABNORMALITIES IN 3
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1110 CONSTITUTIVE ACTIVATION OF STA
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efficacy results with a well-tolera
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unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
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tested across a wide range of human
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were incidentally diagnosed (52%).
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ß2GP1 may be considered as determi
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characterized in 198 β thalassaemi
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1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
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of the drug is crucial to allow lon
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egarding cost analysis of ASCT in G
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ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
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events -Postoperative states: 9,19%
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efficacy and decreased atherosclero
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1217 INCIDENCE OF EARLY STAGE IDIOP
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1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
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posed, was: DF = (CD43%+FMC7%+CD79b
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treatment of acute promyelocityc le
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loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
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1265 POSACONAZOLE THERAPY IN REFRAC
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ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
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disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
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phamide 750 mg/m 2 on day 1, vincri
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nomenon is unclear. It has been sug
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oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
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Results. Though there was no recogn
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2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
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median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
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to the presence of IVS1-6 mutation
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fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
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agents. They involve primarily the
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voriconazole for 2 months followed
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typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
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with development of BC/AP. 2. EVI-1
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1447 THE IMPACT OF DISPARITY IN SHO
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three had visual field defects, two
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acquired mutation most prone to cau
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1466 ROS GENERATION AND APOPTOSIS I
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1473 DIARRHEIC SYNDROME, A CLINICAL
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gene fusion is an independent progn
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1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
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immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
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Hodgkin’s disease is well known,
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gram provided a unique chance to de
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even when ADP-induced plt activatio
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medullary involvement of multiple m
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1540 ADMINISTRATION OF G-CSF AND CH
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1548 QUALITY ANALYSIS OF THE MULTID
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Index of authors A Aapro, M., 0377,
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Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
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Vincenzi, C., 1060 Viniou, N.-A., 0
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Zouabi, H., 0503, 0999 Zoumbos, N.C
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12th Congress of the European Hematology ... - Haematologica

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