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12 th Congress of the European Hematology Association Bleeding disorders 0082 ACQUIRED HEMOPHILIA IN URUGUAY (1977–2007) IN MEMORIAM PROF. ROBERTO DE BELLIS J. Novoa, R. De Bellis Ministry of Health, MONTEVIDEO, Uruguay Background. acquired factor VIII inhibitor in a non-hemophiliac patient (acquired hemophilia A), is a rare life-threatening bleeding disorder. Treatment is an emergency and must control hemorrhagic manifestations and ultimate suppression of antibody production. Current management is challenging with the availability of novel agents, but immunosupression could lead the patient to fatal infectious complications. The experience of thirty years in the diagnosis and treatment of this patients in Uruguay is presented. Methods. 21 patients were studied from 1977 to 2007 in three medical institutions in Uruguay. Gender: 12 women and 9 men. Age: from 18 to 87 years old (median age 78). To dosage of factor VIII inhibitors we employed in the first years Carol Kasper’s tecnique and in the last three years Nijmejen & Kasper technique. Results. the underlying condition in these cases were: idiopathic 9, lymphoproliferative disorders (non Hodgkin’s lymphoma, chronic lymphoid leukemia, multiple myeloma) 4, PAR 2, puerperal conditions 2, hepatic transplantation 1, lupus erithematosus 2 and metastatic cáncer 1 patient. All of them presented with severe spontaneous haemorrhage. The main areas of bleeding were: central nervous system, calf haematoma, gastrointestinal, cellular subcutaneous, hematuria and oropharinx. Prolonged APTT, and reduced factor VIII:C level was detected. The factor VIII inhibitor titre ranged from 4,5 to 160 Bethesda Units (BU). All received high dose steroids and factor VIII concentrates (cryoprecipitate or recombinant human factor VIII). 7 patients received cyclofosfamide intravenous, and 14 of them intravenous immunoglobulin. One patient received rituximab 375 mg/m2 during 4 weeks with excelent outcome. Other patient received factor rVII in two oportunities, with very good outcome too. 9 patients died of bleeding complications and 1 ot them of septic shock with normal values of factor VIII: C, in remission. Conclusions. Our experience confirms that significant clinical bleeding is the major presenting symptom of acquired hemophilia A. On this serie the most frecquent condition was idiopathic, affecting mainly elderly patients and associated with high mortality due to bleeding or immunosupression. Factor rVII and rituximab were two new options for succesfull treatment but have a very high cost. Treatment must be individualiced in order to obtain the fastest resolution of bleeding but avoiding the consequences of immunosupression that can lead the patient to fatal infections. 0083 EXCLUSION OF HAEMOPHILIA A BY DIRECT MUTATION DETECTION IN TRIGEMINI PREGNANCY A. Bors, H. Andrikovics, K. Hajdu, J. Bátorfi, M. Török, L. Nemes, A. Tordai National Medical Center, BUDAPEST, Hungary Haemophilia A (HA) and haemophilia B (HB) are common X-linked bleeding disorders resulting from the inherited deficiency of coagulation factors VIII (fVIII) and IX (fIX), respectively. Female relatives of patients with haemophilia may be carriers and many of them request carrier status determination and prenatal diagnosis. In the framework of the molecular diagnostics service for haemophiliacs as a tertiary national referral center, since 1998, prenatal diagnostics was required in 42 cases out of 153 HA and 2 cases out of 31 HB affected families (28 male and 16 female fetuses). In cases of male fetuses, cycle sequencing or large gene inversion detection as direct mutation analysis, (in 2 and 12 cases respectively) and linkage analysis using intragenic polymorphisms in 14 cases was used as a method for prenatal diagnosis. Overall, 19 healthy and 9 haemophilia affected male fetuses were diagnosed. Furthermore, we hereby report an unusual case, a 33-year-old obligate HA-carrier woman (fVIII gene, intron 22 inversion carrier) who conceived three embryos during an in vitro fertilisation procedure and requested prenatal diagnosis. Transabdominal chorion-villus sampling was performed on the 9th week of pregnancy with successful sample acquisition form all three embryos. Long-distance PCR for intron 22 inversion detection indicated two healthy boys and one carrier girl. Knowing that all of the fetuses are free of HA-manifestation, the couple desisted from reduction. On the 35th week of pregnancy a caesarean section was performed on the bases 30 | haematologica/the hematology journal | 2007; 92(s1) of comlex indications and a 1950 g and a 2200 g boy and a 2350g premature girl were born. Our results further confirm, that molecular genetic investigations play an important role in haemophilia prenatal diagnostics. 0084 HAEMOSTATIC THERAPY DURING SURGICAL OPERATIONS TO HAEMOPHILIA PATIENTS WITH INHIBITOR T. Polyanskaya, Y. Zorenko, E. Karpov Hematological Scientific Center, MOSCOW, Russian Federation Introduction. We present our experience surgical treatments of haemophilia patients with inhibitor. Haemostatic therapy is one of the leading problems in treatment of haemophilia patients with inhibitor. Patients and Methods. In total in our department there were 67 surgical operations to patients with inhibitor. All patients were with sever haemophilia. 68% of them were patients with high responding inhibitors, usually greater than 10 BU. All of them were HCV + . The majority of surgical operations were a high degree of risk, there were: total knee and hip replacement (6), extirpation of pseudotumour (10), osteosynthesis (6), synovectomy (16), ectomy of iliopsoas hematomas with intra-abdominal bleeding (3) and others. To all patients with a high titer before operation carried out plasmapheresis for decrease until inhibitor was not reduced up to 2 BU or lower. We used different hemostatic treatment. The last 3 years haemostatic therapy during the operation realized by preparation Novo Seven - from 120 mkg/kg each two hours per day of operation up to 90 mkg/kg each 4 hours for 9 day, then FEIBA 50 U/kg 2 times day till 14 days. Results. In 75% of cases there were good results (positive functional and anatomic results). 12% of cases have become complicated by bleedings. Most of them have been connected with insufficient hemostatic treatment and the expressed local inflammation. Fatal outcomes were not. The best results were when the hemostatic treatment was carried out by recombinant activated factor VII (rFVIIa-NovoSeven) during the operation and the first days after and then by activated protrombin complex concentrate (FEIBA). Conclusions. Modern hemostatic therapy in a complex with additional methods allows carrying out the haemophilia patients with inhibitor of surgical operations of any complexity. It is necessary to provide a good hemostasis both during operation, and in the first days after operation. At operative interventions of a high degree of risk hemostatic therapy is better for carrying out NovoSeven or FEIBA. 0085 MANAGEMENT OF HEMOPHILIA IN THREE PREMATURE NEONATES P. Brons, 1 K. Kraft, 2 R. Verlaak, 3 A. van Heijst1 1 Radboud Univ. Nijmegen Medical Centre, NIJMEGEN; 2 Rijnstate Hospital, ARNHEM; 3 Canisius Wilhelmina Hospital, NIJMEGEN, Netherlands We describe the management and outcome of hemophilia in three premature infants. Only 3 other patients have been described in literature thus far. Two twins born at 33 weeks of gestation with moderate hemophilia A (factor VIII activity of 2%) were treated with prophylactic factor VIII replacement because of prematurity and the associated increased risk of intracranial hemorrhage. We preferred minimal blood sampling to avoid the insertion of a central venous catheter (CVC). The first born twin received a CVC for only two days for temporary difficult venous access during a clinical suspicious but non proven infection at day 9. He received prohylactic treatment for 17 days and no bleeding complications were observed. Recovery of factor VIII was 94%. No presence of factor VIII inhibitors were found for up the age of 18 months. The second twin developed respiratory distress and an infection with staphylococcus aureus. No bleeding episodes and no cranial hemorrhage were observed until day 7. On day 8 the infant became septic with bacteremia caused by enterobacter cloacae with rapid deteoriation. In the final phase of the septic shock a pulmonary bleeding occurred and a cranial ultrasound showed a intraventricular bleeding. He died on day 8. The third child was a premature infant born at 31 weeks of gestation with prolonged bleeding form a scalp pH-measurement. He was diagnosed with hemophilia B and started with prophylactic factor IX replacement 17 hours after birth. A grade II intraventricular bleeding was found on day 2 and he received intensive replacement therapy to achieve a through factor IX level of 70% for 17 days. A central venous catheter was inserted to avoid continuous access. The mean recovery of factor IX was 46% (range 28%-69%) and the half life time was 5,8 hours. A cerebral ultrasound on day 17 showed no signs of intracerebral hemorrhage and he was discharged at our hospital at day 28. No presence of factor VIII inhibitors were found for up the age of 16 months.
0086 THROMBELASTOGRAPHIC CHART RELIABLE REFLECTION OF HEMOSTATIC IMPACT OF ITP IN CHILDREN M. Serban, 1 S. Arghirescu, 1 M. Bataneant, 1 M. Lelik, 2 C. Jinca, 1 E. Boeriu, 1 L. Stana, 1 A. Oprisoni 1 1 University of Medicine and Pharmacy, TIMISOARA; 2 Spitalul Clinic de Urgenta pt Copii, TIMISOARA, Romania Background. Immune Thrombocytopenic Purpura (ITP) in children continues to be confronted with life threatening bleedings despite its generally accepted benign evolution. This risk is dependent primarily on the hemostatic efficiency of platelets, rather than the platelet count. Aims. Therefore, looking for a supplementary information about hemostatic consequence of thrombocytopenia and taking into account the multiple targets of platelets, we aimed a bedside evaluation of the whole dynamic process of hemostasis by means of thrombelastography (TEG) in ITP patients. Method. Our study included 34 patients: 35,29% with severe, 26,47% with moderate, and 14,70% with mild ITP. We analyzed TEG parameters: r (reaction time), k (clot kinetics to reach 20 mm amplitude), Angle α (clot strengthening), MA (maximum aplitude), G (clot strength) in correlation with platelet count and some hemostatic explorations: bleeding time (BT), clot retraction rate (CRR), prothrombin consumption ratio (PCR) and APTT. Results. In our study, we assessed the following hemostatic abnormalities ascribed to thrombocytopenia: PCR (p
Page 1 and 2: haematologica the hematology journa
Page 3 and 4: Information for readers, authors an
Page 5 and 6: EHA Executive Board E. Hellström-L
Page 7 and 8: Poster session I POSTER SESSION POS
Page 9 and 10: 12 th Congress of the European Hema
Page 11 and 12: dasatinib. Methods. We studied Ikar
Page 13 and 14: Expression of the oncogene H-Ras an
Page 15 and 16: is the gene for the erythropoietin
Page 17 and 18: safety of a slow-release liposomal
Page 19 and 20: 0029 OUTCOME OF THE TREATMENT OF AD
Page 21 and 22: drug-induced apoptotic response of
Page 23 and 24: 41% in the PI3K- group (p=0.001). I
Page 25 and 26: Acute myeloid leukemia - Clinical I
Page 27 and 28: to 60 years (n=116, or 72%) receive
Page 29 and 30: 0056 PROGNOSTIC SIGNIFICANCE OF FLT
Page 31 and 32: Anemia and Bone marrow failure 0061
Page 33 and 34: tified with the current protocol. S
Page 35 and 36: new cases of lead poisoning due to
Page 37: icance, from baseline to week 6 (p
Page 41 and 42: trials. The aim of this retrospecti
Page 43 and 44: tant function in this disease, nega
Page 45 and 46: ed to a favorable outcome. Bialleli
Page 47 and 48: stronger levels of p21 in the cell
Page 49 and 50: hematological centers in one countr
Page 51 and 52: ure 1). Conclusions. Results for re
Page 53 and 54: patients. After a median follow-up
Page 55 and 56: Cytogenetics and Molecular diagnost
Page 57 and 58: 0135 ROUTINE DETECTION OF CYTOGENET
Page 59 and 60: (MMolR, defined as a BCR-ABL x 100
Page 61 and 62: 0146 ARSENIC TRIOXIDE INDUCES ACCUM
Page 63 and 64: tinguish between genotypic B-cell l
Page 65 and 66: Genomics and proteomics 0158 PLASMA
Page 67 and 68: 0164 EVALUATION OF MULTIPLEX LIGATI
Page 69 and 70: each patient’s replicate conditio
Page 71 and 72: 0174 RELATION BETWEEN LOW PML-RARα
Page 73 and 74: 0179 ESHAP VS GIN AS SALVAGE AND MO
Page 75 and 76: Immunology and gene therapy 0184 EA
Page 77 and 78: Cell viability was not affected by
Page 79 and 80: month is not relevant to chronic Gv
Page 81 and 82: Infection and supportive care I 020
Page 83 and 84: 0206 POTENTIAL ROLE OF CMV IN THE O
Page 85 and 86: 3H-thymidine uptake in cell culture
Page 87 and 88: 0217 TUBERCULOSIS AMONG A COHORT OF
Page 89 and 90:
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
Page 113 and 114:
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
Page 257 and 258:
induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
Page 341 and 342:
0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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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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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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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
Page 385 and 386:
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
Page 417 and 418:
1110 CONSTITUTIVE ACTIVATION OF STA
Page 419 and 420:
efficacy results with a well-tolera
Page 421 and 422:
unmutated VH genes, and high and lo
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Aims. Aim of this study was to pred
Page 425 and 426:
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
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
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to-pelvic or perineal trauma. No me
Page 437 and 438:
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
Page 443 and 444:
egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
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admitted to ICU were discharged des
Page 449 and 450:
events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
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
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
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mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
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
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(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
Page 505 and 506:
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
Page 511 and 512:
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
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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
Page 529 and 530:
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
Page 541 and 542:
immune globulin was administered at
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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,
Page 559 and 560:
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.,
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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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12 th Congress of the European Hema
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12th Congress of the European Hematology ... - Haematologica

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