ABSTRACT BOOK 2017 Annual Scientific Meeting 29 October – 1 November Sydney International Convention Centre www.haa2017.com Abstract Numbers Oration Presentations 001 – 003 ……………………………………………………………………………………… ………………… Presidential Presentations: 004 – 014 ……………………………………………………………………………………… …………………. Opening Symposium: 015 – 017 ……………………………………………………………………………………… ………………… Closing Symposium: 018 – 020 ……………………………………………………………………………………… ………………… Combined Symposium HSANZ/BMTSAA 024 – 025 ……………………………………………………………………………………… ………………… HSANZ Oral Presentations: 026 – 101 ……………………………………………………………………………………… ………………… HSANZ Mini Oral 105 – 112 ……………………………………………………………………………………… ………………… HSANZ Poster Presentations ……………………………………………………………………………………… ………………… Acute Leuk: (P001 – P024) 114 - 136 ……………………………………………………………………………………… ………………… BMT: (P025 – P046) 137 - 157 ……………………………………………………………………………………… ………………… CLL: (P047 – P054) 158 - 166 ……………………………………………………………………………………… ………………… CML: (P055 – P061) 167 - 173 ……………………………………………………………………………………… ………………… Lymphoma: (P062 – P088) 174 - 200 ……………………………………………………………………………………… ………………… MDS: (P089 – P090) 201 - 204 ……………………………………………………………………………………… ………………… MPD: (P091 – P099) 205 - 213 ……………………………………………………………………………………… ………………… Myeloma: (P100 – P129) 214 - 242 ……………………………………………………………………………………… ………………… Non-Malig: (P130 – P143) 243 - 258 ……………………………………………………………………………………… ………………… Supptve Care: (P144 – P158) 259 – 273 ……………………………………………………………………………………… ………………… ANZSBT Oral Presentations: 274 – 314 ……………………………………………………………………………………… ………………… ANZSBT Mini Orals Presentations: 318 - 323 ……………………………………………………………………………………… ………………… ANZSBT Poster Presentations: (P159 – P224) 324 – 396 ……………………………………………………………………………………… ………………… THANZ Oral Presentations: 397 – 429 ……………………………………………………………………………………… ………………… THANZ Mini Oral Presentations: 433 - 438 ……………………………………………………………………………………… ………………… THANZ Poster Presentations: (P225 – P292) 439 – 509 ……………………………………………………………………………………… ………………… Nursing Oral Presentations: 510 – 542 ….………………………………………………………………………………… ………………… Nursing Mini Oral Presentations: 546 - 549 ….………………………………………………………………………………… ………………… Nursing Poster Presentations: (P293 – P302) 550 – 557 ……………………………………………………………………………………… ………………… BMTSAA Oral Presentations: 558 – 566 ……………………………………………………………………………………… ………………… BMTSAA Poster Presentations: (P303 – P305) 567 - 570 001. Barry Firkin Oration: Well within 6 degrees of separation: From ristocetin to collagen binding and beyond. Favaloro E NSW Health Pathology, Westmead Hospital Barry Firkin was an esteemed and respected scientist in the field of haematology with a broad clinical and academic interest. One of his most marked achievements, however, was the discovery that ristocetin promoted platelet aggregation in a von Willebrand factor (VWF) dependent manner, paving the way for the development of several diagnostic assays based on this finding. Undeniably, the ristocetin induced platelet aggregation (RIPA) and VWF ristocetin cofactor (VWF:RCo) assays are now part of the standard repertoire of laboratory tests for identification or exclusion of von Willebrand disease (VWD), in turn the most common bleeding disorder (arising from defects or deficiency of VWF). Indeed, VWF:RCo is still today considered the surrogate gold standard ‘functional’ or VWF ‘activity’ assay in VWD diagnostics. This presentation will explore VWD diagnostics, in part as a historical journey, and reflect on the many milestones and changes over recent decades. One milestone along this journey, for example, was the development of the VWF collagen binding (VWF:CB) assay as a second ‘functional’ or VWF activity assay in VWD diagnostics. Rather than being a replacement for VWF:RCo, the VWF:CB is seen as a supplementary assay that reflects a surrogate of one function of VWF, namely subendothelial matrix adhesion, as part of the process of attaching platelets to damaged tissue, and subsequent thrombus formation. The VWF:RCo, in turn, reflecting a surrogate of a complementary function of VWF, being platelet adhesion, as part of the process of facilitating platelets to attach to each other and to damaged tissue, and thus also aiding subsequent thrombus formation. More recently, this functional surrogate of VWF binding to platelets, aka the classical VWF:RCo assay, has been morphed into a variety of ‘glycoprotein Ib (GPIb) – binding assays’, and has even spawned a new ISTH SSC recommended nomenclature, including terms such as VWF:GPIbR and VWF:GPIbM. These are assays that may or may not use ristocetin, and generally do not even use platelets. 002. Ruth Sanger Oration: Reflections of a Journeyman Transfusionist Flanagan P New Zealand Blood Service In May 1975 the World Health Assembly endorsed a resolution (WHA 28.72) urging member states to promote the development of national blood services based on the principle of voluntary non remunerated donation and in doing so requested further study into ethics and safety of commercial plasmapheresis. 35 years later a further resolution was endorsed (WHA 63.12) requesting member states to take all necessary steps to establish, implement and support the development of nationally co-ordinated BTSs with the aim of achieving self-sufficiency. During the intervening period dependency on plasma products derived from paid donor plasma increased significantly. Indeed in 2016 over 60% of the plasma products used globally were derived from this source raising questions as to whether plasma should now be considered as a strategic resource. This presentation will review the principles underpinning the concepts of voluntary non remunerated donation and self-sufficiency and in doing so consider whether they continue to be relevant in the 21st century. 003. Carl de Gruchy Oration: Chemotherapy, radiotherapy, immunotherapy, cellular therapy: the shifting sands of stem cell transplantation Gottlieb D University of Sydney The last decade has seen an explosion in interest in the role of the immune system in curing cancer. For most physicians, immunotherapy has meant using monoclonal antibodies targeting antigens on the surface of cancer cells or more recently targeting inhibitory proteins on lymphocytes. More recently, the use of immune system cells as therapies themselves, principally in the form of genetically modified T-cells bearing artificial antigen receptors, has garnered intense attention. T-cell therapy has a longer history than is generally recognised. It is inherently bound to allogeneic stem cell transplantation, a procedure that exerts the majority of its therapeutic (and much of its negative iatrogenic) effect through T-cell activity. The role of T-cells in allogeneic transplantation became apparent well after the birth of transplantation itself and the potential therapeutic effects of T-cells were recognised even later. Stem cell donor-derived lymphocytes, first unmanipulated, then as purified antigen-specific cells were identified initially for their value as therapies in patients with refractory opportunistic infection. The herpes viruses EBV and CMV were the initial targets, but a gradual awareness that specific T-cells may play a role in a wide range of viral and fungal infections has emerged. A major inhibition has been the need to generate a specific T-cell product for each recipient, rendering T-cell therapy complex and expensive. The recognition that partially HLA matched 3rd party cryopreserved antigen-specific T-cells also have beneficial therapeutic effects largely circumvents this problem. With the advent of T-cell therapies utilising artificial chimeric antigen receptors directed towards CD19, a new era was born. The recent FDA approval of autologous CD19 CAR T-cells for younger patients with refractory acute lymphoblastic leukaemia (albeit at a phenomenal price) has thrust T-cell therapy into the spotlight. CAR T-cells are being developed for a range of other indications. Within the context of allogeneic stem cell transplantation, integration of specific T-cells directed at both infection and malignancy has the potential to be combined with removal of non-specific or alloreactive T-cells making a path towards a GVHD free, and infection and relapse reduced outcome clearer. Better specificity means better transplants. Less chemotherapy and radiotherapy, more immunotherapy and cellular therapy seems the way of the future. 004. What a headache, paediatric experience with Intragam 10. Crighton G1,2,3, Kinmonth A1, Savoia H1,3 1Royal Children's Hospital, Melbourne, Australia, 2Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia, 3Royal Women's Hospital, Melbourne, Australia In March 2017, domestically supplied Intravenous Immunoglobulin (IVIg) Intragam P (CSL Behring) was replaced with Intragam 10 (CSL Behring). Intragam 10 is a more concentrated immunoglobulin product (10% versus 6%) and uses a different stabilising agent. Intragam 10 was introduced on the basis of two small cohort studies performed in adults, with no evidence to support its safety and efficacy in paediatric patients. Aim To review the safety profile and any adverse events associated with Intragam 10 at the Royal Children’s Hospital, Melbourne. Methods A retrospective study of all Intragam 10 infusions from March to June 2017. Data collected included: demographics, dose, patient weight, indication, rates of infusion, patient vital signs, clinical assessments, re-presentation to hospital or correspondence with clinicians. Phone review was performed in the first month to determine if