Blood.
`v. 102, no. 11, pt. 1 (Nov. 16 2003)
`General Collection
`Vii ;13L.C31
`2003.11 24 01:.51 •
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`3
`
`JOURNAL OF
`
`THE AMERICAN
`
`SOCIETY OF
`
`HEMATOLOGY
`
`VOLUME 102
`
`NUMBER 11
`
`NOVEMBER 16, 2003
`
`PART 1 OF 2 PARTS
`
`Forty-fifth annual
`
`meeting program
`and abstracts
`
`December 6-9, 2003
`
`San Diego, California
`
`0001
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`MYLAN - EXHIBIT 1006
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`

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`C O
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`T M°
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`JOURNAL OF
`
`THE AMERICAN
`
`SOCIETY OF
`
`HEMATOLOGY
`
`Blood, Journal of The American Society of Hen:mato
`(print ISSN 0006-4971, online ISSN 1528-0020), is
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`0002
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`117i
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`JOURNAL OF
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`THE AMERICAN
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`SOCIETY OF
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`HEMATOLOGY
`
`16 NOVEMBER 2003 • VOLUME 102, NUMBER 11 (PART 1 OF 2 PARTS)
`
`CONTENTS
`
`COVER FIGURE
`
`Skyline from Coronado, San Diego, California. Photo courtesy of Getty Images.
`
`INTRODUCTORY INFORMATION
`
`2 Leaders of the society since its founding
`
`3 Current society leadership
`
`4 Standing committees
`
`6
`
`Scientific subcommittees
`
`8 Recipients of awards
`
`9 Reviewers of abstracts
`
`10 Acknowledgements
`
`11
`
`Future annual meeting sites
`
`11 ASH headquarters office staff
`
`12 General information
`
`24
`
`San Diego Convention Center maps
`
`27 Master schedule
`
`INVITED SPEAKER
`SESSIONS
`
`35
`
`Special lectures
`
`PLENARY SESSION
`
`SIMULTANEOUS
`SESSIONS
`
`39 Saturday/Sunday schedule at a glance
`
`40 Education program
`
`60
`
`Scientific committee program
`
`85 Meet-the-expert breakfast sessions
`
`88
`
`2003 invited speaker index
`
`94
`
`2003 invited speaker disclosure index
`
`Sunday, December 7, 2003, 1:15 pm-3:30 pm
`Plenary session I
`
`103
`
`Sunday, December 7, 2003, 4:15 pm-5:45 pm
`The erythrocyte membrane and cytoskeleton
`Granulocytes, monocytes and macrophages I
`Vascular
`biology
`Molecular mechanisms of altered platelet production and function
`Cell biology and animal models
`New anticoagulant trials
`Signaling: in vivo hematopoiesis and lineage specification
`Hematopoietic microenvironment I
`Strategies for overcoming drug resistance
`Immature acute leukemia: the AML/ALL interface
`Molecular biology of acute myeloid leukemia
`Signaling pathway deregulation
`Ilodgkin lymphoma, treatment
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`110
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`Subiert US Ca delft I aws
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`CONTENTS (continued)
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`Chemotherapy/rituximab combinations and radioimmunotherapy
`Chronic myelogenous leukemia: new treatment strategies/molecular monitoring
`Myeloproliferative disorders: treatment
`CLL: ZAP-70/mutational status
`Genetics of multiple myeloma
`Experimental transplantation: engraftment
`Cell processing: mobilization I
`Immunotherapy
`Autologous transplantation: multiple myeloma
`
`Monday, December 8, 2003, 7:30 am-9:00 am
`Sickle cell disease: novel therapies
`Thalassemia and globin gene regulation I
`Granulocytes, monocytes and macrophages II
`Molecular mechanisms of lymphoid development
`Platelet adhesion
`Hemophilia
`Pathophysiology of thrombosis: experimental
`Thrombosis risk and management
`Transfusion medicine I
`Regulation of gene transcription I
`Hematopoietic microenvironment II
`Disordered gene expression in hematologic malignancy I
`Minimal residual disease and diagnostic markers in acute leukemia
`Acute leukemia: new agents
`Molecular cytogenetics and animal models
`Rituximab and biologic combinations
`Chronic myelogenous leukemia: resistance to imatinib
`CLL: therapy I
`Multiple myeloma: developmental therapeutics
`Experimental transplantation: regimens
`Nonmyeloablative transplantation
`Myeloablative matched related donor transplantation
`
`Monday, December 8, 2003, 11:00 am-12:30 pm
`Sickle hemoglobinopathies: cellular interactions and pathophysiology
`Granulocytes, monocytes and macrophages III
`T cell signaling
`Immune thrombocytopenias
`Factor V and factor VIII
`Von Willebrand disease
`Pathophysiology of thrombosis: mechanisms
`Transfusion medicine II
`Regulation of HSC self-renewal
`Molecular pharmacology and drug resistance of AML
`Diagnostic markers in AML
`Treatment and prognosis of acute myeloid leukemia
`Clinicopathologic and molecular factors impacting prognosis
`Non-Hodgkin lymphoma: treatment I
`Vaccine and dendritic cell-based therapies
`Myeloproliferative disorders: molecular pathogenesis
`CLL: therapy II
`Biology of multiple myeloma
`Experimental transplantation: basic biology
`Cell processing: mobilization II
`Secondary malignancy and ►ate complications after transplantation
`Autologous transplantation: amyloidosis and Hodgkin's disease
`
`Monday, December 8, 2003, 1:30 pm-3:00 pm
`Sickle cell disease: clinical correlations
`Thalassemia and globin gene regulation II
`Immunodeficiency, including HIV infection
`Tumor immunotherapy
`This material was copied
`at the NLM and may be
`subject US Copyright Laws
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`Acquired thrombocytopenias due to HIV, drugs and TTP
`Coagulation proteases
`Coagulation disorders
`Transcriptional regulators of hematopoietic stem cells
`Regulation of gene transcription II
`Signaling in hematopoietic cells
`Oncogenes and tumor suppressors in B cell malignancies
`Molecular pharmacology: drug resistance—novel agents and potential targets
`Advances in acute myeloid and lymphoblastic leukemias
`Acute promyelocytic leukemia
`Non-Hodgkin lymphoma: treatment II—adult and pediatric
`Myelodysplastic syndromes: biologic investigations
`Myeloproliferativc disorders: treatment and biology
`Novel approaches to multiple myeloma therapy
`GVHD biology
`Chronic gvhd and recurrent malignancy after transplantation
`Allogeneic mismatched or unrelated donor transplantation: KIR and graft manipulation
`Gene therapy: clinical results
`
`Monday, December 8, 2003, 3:30 pm-5:30 pm
`Iron and home metabolism
`Erythropoicsis I
`Platelet adhesion receptors
`Inhibitors of coagulation
`Antithrombotic therapy
`Hematopoietic development
`Signaling: survival and cycling
`Disordered gene expression in hematologic malignancy II
`Gene expression profiling in acute leukemia
`Acute myeloid leukemia
`Genomic and proteomic profiling
`Lymphoma: new agents
`Chronic myelogenous leukemia: imatinib. clinical results
`Myelodysplastic syndromes: clinical investigations
`CLL biology I
`Experimental therapy in multiple myeloma
`Modulation of GVHD and GVL/GVT effects
`Transplantation regimen toxicities and engraftment I
`Infections: complications
`Non-myeloablative matched related donor transplantation
`Gene transfer: biology and marking studies I
`Health services research: methodology
`
`Tuesday, December 9, 2003, 8:00 am-11:00 ani
`Erythropoiesis II
`Platelet activation and thrombus formation
`Pathophysiology of thrombosis: risk factors
`Signaling in stem and progenitor cells
`Stem cell plasticity
`Chromosomal rearrangements
`Disordered gene expression in hematologic malignancy III
`Mechanisms of letikemogencsis in AML
`Acute lymphoblastic leukemia I
`Acute lymphoblastic leukemia II
`Molecular pathogenesis of lymphoma
`Chronic myelogenous leukemia: signal transduction/gene expression
`CLL: biology II
`Myeloma microenvironment
`Therapeutics for plasma cell dyscrasia
`Cell processing: selection, expansion, purging and depletion
`Transplantation regimen toxicitics and engraftment II
`Graft-versus-host disease
`Allogeneic mismatched or unrelated donor transplantation: clinical outcomes
`Thismaterialwascopied
`atthe NLM and may be
`Subject US Copyright Laws
`
`0005
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`(continued)
`
`174
`175
`175
`
`Autologous transplantation: non-Hodgkin's lymphoma
`Gene transfer: biology and marking studies II
`Health services research: results
`
`POSTER SESSIONS
`
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`
`Saturday, December 6, 2003, 6:00 pm-7:30 pm
`Erythrocyte membrane, cytoskeleton, and enzymes
`Sickle hemoglobinopathies: basic and translational
`Thalassemia and globin gene regulation I
`Granulocytes, monocytes and macrophages I
`Hematologic complications of HIV infections
`Tumor immunotherapy
`Platelet adhesion and thrombosis
`Immune thrombocytopenias
`Coagulation and fibrinolytic proteases
`Von Willebrand's disease: women's health and rare bleeding disorders
`Genetic polymorphisms, other risk factors for thrombosis
`Antithrombotic therapy I
`Hematopoietic stem and progenitor biology I
`Stem cell plasticity
`Regulation of gene transcription I
`Cytokines and signal transduction I
`Apoptosis and cell cycle
`Mesenchymal stem cells
`Disordered gene expression in hematologic malignancy I
`Diagnostic and prognostic markers in leukemia I
`Acute lymphoblastic leukemia: pathophysiology, therapy and prognosis
`Acute leukemia: new agents I
`Clinicopathologic/molecular factors impacting prognosis I
`Lymphoma: treatment
`Radioimmunotherapy and rituximab combinations
`CML: molecular surveillance
`Myelodysplastic syndromes: clinical studies
`CLL: biology I
`CLL: therapy I
`Myeloma microenvironment and growth
`Therapeutics for plasma cell dyscrasia
`Experimental transplantation: regimens
`Stem cell mobilization and processing I
`Transplantation regimen toxicities and engraftment I
`Myeloablative matched related donor transplantation
`Allogeneic mismatched or unrelated donor transplantation: umbilical cord blood and
`reduced intensity transplants
`Allogeneic mismatched or unrelated donor transplantation: clinical outcomes
`Gene therapy: clinical results
`Health services research I
`
`Sunday, December 7, 2003, 5:45 pm-7:15 pm
`Erythropoiesis I
`Erythropoiesis II
`Thalassemia and globin gene regulation II
`Granulocytes, monocytes and macrophages II
`Lymphoid cell development
`Vascular wall biology
`Acquired thrombocytopenias: drugs, TFP and viral infections
`Factor V, factor VIII and von Willebrand factor
`DIC, fibrinolysis and thrombosis
`Coagulants and anticoagulants, cancer and thrombosis
`Transfusion medicine I
`Hematopoietic stem and progenitor biology II
`Regulation of gene transcription II
`Disordered gene expression in hematologic malignancy Il
`This material was copied
`atthe NLM and may be
`Subject US Copyright Laws
`
`0006
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`235
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`300
`301
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`306
`
`Oncogene signaling in hematological neoplasms
`Molecular pharmacology: drug resistance I
`Diagnostic and prognostic markers in leukemia II
`Acute myeloid leukemia: molecular biology and pathophysiology
`Acute myeloid leukemia
`Acute leukemia: new agents II
`Clinicopathologic/molecular factors impacting prognosis II
`Lymphoma: treatment and supportive care
`Lymphoma: new agents
`CML: biology and experimental therapies
`Myeloproliferative disorders: pathogenesis
`CLL biology and clinical correlations
`CLL therapy II
`Myeloma genetics and gene expression
`Novel approaches to multiple mycloma therapy
`Experimental transplantation: basic biology
`GVL/GVT effects: immunity
`Transplantation regimen toxicities and engraftment II
`GVHD
`Chronic GVHD: quality of life and recurrent malignancy after transplantation
`Non-myeloahlative matched related donor transplantation
`Autologous transplantation: leukemia/lymphoma
`Gene transfer: biology and marking studies I
`I lcalth services research II
`
`Monday, December 8, 2003, 5:30 pm-7:00 pm
`Iron and hone metabolism
`Sickle hemoglobinopathies: clinical
`Lymphoid cell signaling
`Platelet activation and secretion
`Platelet adhesion
`Platelet function disorders and congenital thrombocytopenias
`Regulation of coagulation and inflammation
`Hemophilia
`ADAMTS13, HIT. lupus. antiphospholipid syndrome, and microparticles
`Antithrombotic therapy II
`Transfusion medicine II
`Hematopoietic stem and progenitor biology III
`Hematopoietic stem and progenitor biology IV
`Cytokines and signal transduction II
`Hematopoietic microenvironment 111
`Chromosomal rearrangements
`Disordered gene expression in hematologic malignancy I❑
`Tumor suppressors
`Molecular pharmacology: drug resistance II
`Diagnostic and prognostic markers in leukemia III
`Acute myeloid leukemia: therapy and prognosis
`Acute lymphoblastic leukemia
`Genomic/proteomic studies and signaling pathways
`Molecular pathogenesis
`Immunotherapy and preclinical studies
`CML: clinical trials
`Myelodysplastic syndromes: biologic studies
`Myeloproli terative disorders: treatment
`CLL: biology II
`Myeloma biology
`Clinical studies in mycloma
`Experimental transplantation: engraftment
`GVHD biology: modulation of GVHD
`Stem cell mobilization and processing II
`Cell processing: selection, expansion, purging, and depletion
`Transplantation regimen toxicitics and engraftment 111
`This material was copied
`atthe NLM and may be
`Subject US Copyright Laws
`
`0007
`
`

`

`CONTENT' (continued)
`
`307
`308
`309
`310
`
`Infections: complications
`Secondary neoplasia and late complications after transplantation
`Autologous transplantation: clinical results
`Gene transfer: biology and marking studies II
`
`ABSTRACTS
`
`2a
`
`Index to abstracts
`
`4a Abstracts
`
`INDEXES
`
`998a Disclosure index
`
`999a Moderator disclosure index
`
`1004a Author index
`
`1093a
`
`Session index
`
`1099a Key word subject index
`
`CORPORATE FRIDAY
`
`1137a
`
`Symposium descriptions
`
`EXHIBITORS
`
`1146a Exhibitors
`
`1163a Exhibitor/product service directory
`
`This material was copied
`at the NLM and may be
`Subject US Copyright Laws
`
`0008
`
`

`

`This material may be protected by Copyright law (Title 17 U.S. Code)
`
`ANTITHROMBOTIC THERAPY II
`
`group (p<0.05 vs baseline); in comparison to the OPCAB group levels were 'Uglier at cud
`of surgery and 2 hrs post-op (p<0.05 vs OPCAB). IL-Il) was reduced in the CPB group
`relative to OPCA 13 patients at end of surgery until 24 hrs post-op (p<0.05). Platelet-
`leukocyte aggregate levels were increased relative to baseline at 30 min (p=0.0 I ) and at end
`of surgery (p<0.03) in the CPB group. Platelet P-selectin expression (p=0.04 and 0.002)
`and neutrophil CBI lb expression (p=0.01 and 0.02) were increased relative to baseline at
`30 min and at end of surgery in the CPB group. No change in these parameters was observed
`in the OPCAB group. Platelet counts (corrected for hematocrit) decreased from baseline in
`both groups through post-op day 4 but were nut different between groups. Summary: These
`data suggest that inflammation is up-regulated with the operative trauma of coronary artery
`revasculari zation regardless of surgical technique (IL-6 and CRP). This response, however,
`is enhanced by CPB as evidenced by increased IL-8, CRP, neutrophil CHI lb expression,
`and decreased IL-10. In addition, platelet activation measured as the formation of platelet-
`leukocyte complexes and platelet P-selcctin expression were observed only in the CPB
`group despite similar platelet count decreases in each group. As well, hemostatic activation
`measured as increased thrombomodulin levels was only observed in the CPB group.
`Conclusion: Inflammation and hemostatic activation (in particular platelets) measured by
`markers in the circulation are enhanced with CPB. These responses arc reduced with OPCAB:
`however, the inflammatory response remains significant. The differences in the platelet
`parameters observed between the CPU and OPCAB groups warrants further investigation
`to determine if this impacts on post-operative clinical outcomes.
`
`Poster Board #-Session:
`Abstract# 2987
`Thrombophilia and Chronic Thromboembolic Pulmonary
`Hypertension: High Prevalence of Antiphospholipid Antibodies
`and Possible Role in the Pathogenesis of the Disease. Franco Piovella,'
`Andrea D'Armini*,' Marisa Barone*,' Cristian Monterosso*,2 Luca Libre,'
`Chiara Piovella*,' Mario Vigano*.2 iServizio Malattie Tromboemboliche,
`I.R.C.C.S. Policlinic() San Malley, University of Pavia, Pavia, Italy:
`Policlinico San Matteo, University
`'Cattedra di Cardiochirurgia.
`of Pavia, Pavia, /hay.
`Chronic thromboembolic pulmonary hypertension (CTPH) is a rare disease which results
`from obstruction of the major pulmonary arteries by organized pulmonary emboli which
`have become incorporated into the pulmonary artery wall, causing an increase in pulmonary
`vascular resistances. Pulmonary ThromboEndarterectomy (PTE) is an effective surgical
`procedure tbr ('TPII. Approximately 45% of patients with CTEPI I demonstrate findings
`suggestive of previous venous thrombosis on lower extremity duplex ultrasound, supporting
`the hypothesis that in these cases CTEPII is a consequence of thromboembolic disease.
`Although CTEPI I likely has a thromboembolic origin, the role of thrombophilic factors is
`less clear. The presence of hereditary thrombotic risk factors has been shown to he increased
`in some studies, but no greater than control subjects in other studies. Anti-phospholipid
`antibodies (Al'I.A), however, are common, and have been reported in up to 20% to 50% of
`patients. APLA are strongly associated with thrombosis. Their presence constitutes the
`most common of the acquired blood protein defects, although the precise mechanisms
`whereby antiphospholipid antibodies alter hacmostasis to induce hypercoagulable state
`is not clear. Recently, we started in Pavia a program in which members ofa multidisciplinary
`team work in close interaction on the challenging problems these patients present in the
`evaluative, surgical, and post-operative phases of their care. Front May 1996 to August
`2003. 97 patients, all in New York Heart Association (NYHA) class III or IV were treated
`with PTE. Overall operative and pefi-operative mortality is 9.3% (9/97). At 3 months
`Ibllow-up, most surviving patients were in NYIIA class I or II. At 3 years. postoperative
`hemodynamic values were substantially maintained. All patients are maintained on chronic
`oral anticoagulant treatment. We assessed the presence of thrombophilia on 86/97 patients
`of our series. Phospholipid-dependent antibodies (antiphospholipid antibodies and lupus
`anticoagulant) were analysed by both immunological and clotting assays. Hereditary
`thrombotic risk thetors were also determined. Ant ithrombin, protein C and protein S activities
`were measured by functional assays. Mutations of factor V and factor II were identified by
`polymerase chain reaction. The rare deficiencies of natural coagulation inhibitors (AT, PC
`and PS) were detectable in less than 5% of patients. Factor V Leiden was present in 12%. and
`the prothrombin 20210A allele in 5% of our patients. Mild hyperhomocysteinemia associated
`with the homozygous C677T polymorphism in the MTHER gene was present in I I% of
`patients. The prevalence of anti-phospholipid antibodies (APLA), either isolated or in
`association with other coagulation defects, was strikingly elevated (38%). Monitoring
`oral anticoagulant treatment in patients with APLA may be extremely difficult, due to the
`possible interference of the antibody on Prothrombin Time (PT) which may result andlictually
`prolonged. 'rhisin some patients could he responsible of inadequate treatment, and be relevant
`to the pathogenesis and clinical course of this disease. An association has been described
`between the presence of APLA and the development of thrombocytopenia following exposure
`to heparin in (IPI I. A particular peri- and post-operative anticoagulant protocol utilizing
`sodium danaparoid was developed and successfully tested for patients at risk of developing
`heparin-induced thrombocytopenia 1111T).
`
`Poster Board #-Session: 208-111
`A bstract# 2988
`Does the Additional Presence of Lupus Anticoagulants in Patients
`with Increased Anticardiolipin Titers Increase the Risk of Clinical
`Manifestation? Wolfgang Micsbach*, Robert I I udeck*, Martina Boehm*,
`Birgit Putz*, Inge Schaffer. Interned Medicine, Goethe University, Frankhirt
`Germany.
`Both, anticardiolipin (a('L) antibodies and lupus anticoagulants (LA) arc established
`parameters to measure antiphospholipid antibodies but it is not clear if the additional
`presence of LA in patients with elevated aCL antibodies increase the risk of clinical
`manifestations of APS.
`
`807a
`
`Methods. We investigated retrospectively 300 patients with elevated aC'L antibodies.
`lei and IgM aC'L antibodies were tested by enzyme-linked immunosorbent assay ( EL ISA ).
`LA were tested by more than 2 different methods according to the proposed criteria of the
`SSC of the ISTH.
`Results. An increased titer of IgG aCL was found in 137 of 300 patients (46%). an
`increased titer of IgM aCL in 257 patients (86%). 98 patients had isolated increased IgG
`aCL titers. 182 patients had isolated increased IgM aCL titers. Lupus anticoagulants were
`additionally detected in 125/300 patients (42%).
`ith_LAAatLankaate to high aCL titers
`table 1.Clinical manifestations olpatictus
`Cl.
`LA
`LA -
`Patients with increased a
`125/100 02%)
`175/300 (W.)
`In total = 300)
`78/125 (63%)
`105/175 ((Aria
`Clinical manifestations
`LA *
`LA -
`Patients with highly increased aCL
`32/96 (33%)
`In = 96)
`64/96 (67%)
`45/64 (70%)
`23/32 (72 %)
`Its.
`Clinical manifestations
`The rate of clinical manifestations did not differ significantly between LA+ and LA-
`patients either in patients with elevated KT antibodies in total or in patients with highly.
`more than 10 times elevated aCL levels. In general, however the rate of clinical manifestation
`increased with increased aCL levels
`(73% vs. 57% in patients with moderate elevated aC'L levels. mr*0.11.5. OR 2.04; 95°'0C1
`I .13T- 3h. e6 ip)e.
`sence of LA was related significantly to the patients with highly increased aCL
`levels (64 of 96 patients, 67 % vs. 60 of 204 patients with moderate elevation of aC'L
`antibodies, 29 %; p<0.0005) and related to the IgG isotype (76 % of patients with highly
`elevated IgG aCL vs. 62 % of patients with highly elevated 1gM aCL; r0.05).
`Conclusion. The presence of LA is more common in patients with highly increased aC'L
`levels. While highly elevated aCL antibodies are related to frequent clinical manifestations
`of APS, the presence of LA did not show any additional influence on clinical manifestations
`of patients with aC'L antibodies.
`
`its.
`
`ANTITHROMBOTIC THERAPY II
`
`Poster Board #-Session: 209-111
`Abstract# 2989
`Validation of an Ideal Standard of Care for Patients with
`Documented Heparin Induced Thromhoeytopenia: A Quality-
`Control Study. Luc B. Dansereau*,' Marc E. Jolicoeur*,1 Diem-Quyen
`Nguyen*,' Harold J. Olney,' Denis Soulit'fres*."Infernal Medicine', Centre
`hospitalier de l'Universite de Montreal, Montreal, QC, Canada; 'Medicine
`and Hematology-Blood Bank, Centre hospitalier de 1•Universite de
`Montreal, Montreal, QC, Canada.
`Introduction. Three percent of patients exposed to heparin develop heparin induced
`thrombocytopenia (HIT). This syndrome is associated with a 30-day risk of clinical
`thrombosis greater than 50%. The management of 1111' remains controversial as little data
`exists regarding the efficacy of the currently proposed standard of care to prevent thrombosis.
`The aim of this quality-control study was to examine current practice in a teaching hospital
`and to assess the consequences of deviating from an ideal treatment strategy on the incidence
`of thrombotic events at 30 days. Patients and methods. Medlin literature was reviewed
`and a treatment algorithm was established according to recognized authorities and published
`guidelines. From this algorithm, 4 potential alternative management strategies were
`identified: I) heparin administration until diagnostic confirmation (anti-PF4 antibodies):
`2) delayed institution of alternative anticoagulation alter discontinuation of heparin: 3)
`length of anticoagulation less than I month: 4) accidental readministration of heparin. A
`chart review was undertaken on consecutive patients at a large teaching hospital (CI IUM)
`with a positive anti-PF4 antibody assay between January 2(11)2 and March 2003. In these
`patients, the diagnosis of HIT was considered confirmed if the platelet count dropped more
`than 50% and/or was less than I 00x I 05/L after any documented exposure to heparin. The
`prevalence of alternative management strategies was recorded. as was the development of
`thrombosis, bleeding and death during the 30 day follow up period. When necessary, a
`telephone interview was obtained at I month. Thromboses were confirmed by appropriate
`clinical investigation or autopsy, except in 5 cases of sudden death suspicious for thrombosis
`without autopsy data (considered probable thrombosis). Relative risk of thrombosis (95%
`confidence interval) was calculated fbr each of the 4 alternative management strategies.
`Results. Of 356 anti-PF4 antibody assays ordered, 57 were positive (16%). Four patients
`were considered false-positive (no heparin exposure, resolution of thrombocytopenia despite
`ongoing heparin therapy). Complete lidlow-up information was available for 52 of the 53
`remaining patients. These 53 patients had significant co-morbidities as 42 (79%) had an
`ICU admission and 32 (60%) had additional causes for thrombocytopenia. The most frequent
`indication for initial heparin administration was venous thromboembolism prophylaxis in
`23 pillions (.1.1"1.). A total of 22 patients (42.".,a) developed thrombosis. including sites ai
`(4), vcnou.17 ), both (6), or probable (5). The overall mortality in patients is Ith I II I ,m as 40"
`at one month (2) patients). The prevalence of alternative management .11
`and Met r
`relative risks of thrombosis are presented in table I. Conclusion. At our nisi] ninon. 1111 is
`associated with significant morbidity and mortality. A continued administration of heparin
`until diagnostic confirmation and a delay in the institution of altermark e anticoagulation
`such as lepirudin. argatroban or danaparoid were associated with :I
`increase in
`the risk of developing thrombosis.
`
`Alternative management strategies
`I leparin until diagnostic confirmation
`Delayed alternative anticoagulation
`Anticoagualtion less than I mont