5^th World Hematologists Congress August 18-19, 2016 London, UK

Biography:

Shaoying Li has received her MD from Beijing Medical University (Current name: Peking University Health Science Center). She is an Assistant Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. She is board certified in Anatomic Pathology, Clinical Pathology and Hematology. In addition to clinical responsibilities on lymphoma, leukemia and flow cytometry services, she has been actively participating in multiple research projects in lymphoma and leukemia, which has led to 50 research papers and multiple book chapters. She also serves as Member of Editorial Boards and ad hoc Reviewer for multiple journals. Her major research interests include molecular cytogenetic risk stratification of DLBCL with a focus on “double hit” lymphoma and clinicopathologic and molecular study of mantle cell lymphoma.

Abstract:

Double-hit lymphoma (DHL) has been defined by 2008 WHO as a B-cell lymphoma with MYC/8q24 rearrangement in combination with a translocation involving another gene such as BCL2 or BCL6. The most common form of DHL has translocations involving MYC and BCL2, also known as MYC/BCL2 DHL. In the past few years, numerous case series of MYC/BCL2 DHL have been reported in the literature. Most cases of MYC/BCL2 DHL morphologically resemble diffuse large B-cell lymphoma (DLBCL) or high grade B-cell lymphoma, not otherwise specified (previous name in 2008 WHO: B-cell lymphoma, unclassifiable with features intermediate between DLBCL and Burkitt lymphoma). These tumors have a germinal center B-cell immunophenotype but an aggressive clinical course characterized by a high proliferation rate, advanced-stage disease, extranodal involvement, high International Prognostic Index score and high serum lactate dehydrogenase levels. All tumors have a complex karyotype. Despite a variety of therapeutic approaches that have been used to date, patients with DHL have a poor prognosis. Here we will discuss the clinicopathologic, immunophenotypic, cytogenetic and prognostic features of MYC/BCL2 DHL and some remaining issues.

Biography:

John Batchelor is currently a Consultant in Emergency Medicine at Central Manchester Foundation Trust, UK. He is also Honorary Lecturer at Manchester Metropolitan University. He was graduated from Leeds University England in 1982. He is a Fellow of the Royal College of Surgeons of Ireland and Fellow of the Faculty of Emergency Medicine of England. He undertook his MD training at University College London, UK. He has written extensively on the subject of minor head injuries. He has presented a paper in Paris in 2012 on meta-analysis looking at the relationship between cerebral microbleeds and anitiplatelet agents. He has also recently published a meta-analysis on the effect on mortality of platelet transfusions in adults with spontaneous or traumatic antiplatelet associated intracranial hemorrhage. His current research interest lies in the area of risk factors for intracranial hemorrhage in both adults and pediatrics secondary to coagulopathy and thrombocytopenia.

Abstract:

With an ever increasing elderly population, falls in the elderly is a common condition presenting on a daily basis to Emergency departments. Many of these elderly fallers will have head injuries and will be taking antiplatelet agents, notably aspirin. The risk of traumatic intracranial hemorrhage is increased in patients taking antiplatelet agents although the risk is less than that of warfarin (odds ratio of 2.5 versus 1.5). The risk of mortality in patients’ taking aspirin with traumatic brain injury is slightly increased in patients on antiplatelet agents in contrast to warfarin where the mortality is doubled. On the basis of this level of evidence some clinicians advocate the use of a platelet transfusion in patients with traumatic brain hemorrhage who are on antiplatelet agents. The evidence for this will be reviewed. Desmopressin is an alternative agent which might have a potential role in this area. Finally the role of platelet function assays will be reviewed based upon the current research evidence in this area.

Biography:

C Cameron Yin has received her MD degree from Beijing Medical University and PhD from the University of Wisconsin-Madison. She is currently an Associate Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. In addition to clinical responsibilities on the Leukemia, Lymphoma and Molecular Diagnostic services, she has been actively participating in multiple research projects in the molecular genetic abnormalities in leukemia and lymphoma, which has led to over 100 research papers and over 20 book chapters.

Abstract:

It has been assumed that immunoglobulin (Ig) can only be produced by B-cells and plasma cells. Recently, we have reported that Ig can be expressed by other types of cells such as epithelial cancer cells. In this study, we studied Ig expression in acute myeloid leukemia (AML). We found that Ig was expressed at a high frequency and level in AML cell lines and primary myeloblasts, but not in monocytes or neutrophils from healthy controls by RT-PCR, immunohistochemistry and flow cytometry. We further assessed rearrangements of IgG VHDJH transcripts and found that AML-IgG had restricted (AML cell lines) or biased (primary myeloblasts) V usage. Moreover, its gene rearrangements showed evidence of somatic hypermutation. Anti-human IgG reduced cell viability and induced apoptosis in AML cell lines, whereas anti-human IgK increased cell migration and chemotaxis. Our findings suggest that AML-Ig may play a role in leukemogenesis and AML progression and it may serve as a useful molecular marker for monitoring minimal residual disease or designing target therapy. Study on the correlation between level of AML-Ig expression and morphologic and molecular genetics features as well as clinical outcome of AML patients is in progress.

Biography:

Simon Durrants has completed his undergraduate studies at the University of London and Postgraduate studies at Royal Postgraduate School of Medicine/Hammersmith Hospital. He is the Director of Clinical Hematology & Bone Marrow Transplantation, Royal Brisbane Hospital. He has published more than 100 papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

Polycythemia vera (PV) is a myeloproliferative neoplasm characterized by erythrocytosis, burdensome symptoms and an increased risk of thrombosis. Hematocrit (Hct) control (i.e., <45%) is a key therapeutic goal and has been shown to decrease the risk of cardiovascular death and major thrombotic events. Hydroxyurea (HU) is currently the first-line therapy for cytoreduction in high-risk patients; however, substantial proportions (15%) become resistant to or intolerant of HU by stringent ELN criteria. Ruxolitinib, a potent Janus kinase JAK1/JAK2 inhibitor, was well tolerated and superior to best available therapy (BAT) in maintaining Hct control without phlebotomy, normalizing blood cell count, reducing spleen volume and improving symptoms in the phase 3 RESPONSE-1 trial. RESPONSE-2 is an open-label, phase 3b study comparing the efficacy and safety of Ruxolitinib with BAT in HU-resistant/intolerant patients with PV without splenomegaly. In PV patients with an inadequate response to or unacceptable side effects from HU both with and without splenomegaly, Ruxolitinib is well tolerated and superior to BAT in controlling Hct without phlebotomy, achieving CHR and improving PV-related symptoms. Most patients in RESPONSE-2 (70.5%) had been treated with only 1 prior line of therapy (HU). In RESPONSE-1 and RESPONSE-2, patients treated with Ruxolitinib had fewer thromboembolic events compared with BAT. Taken together, findings from RESPONSE-1 and RESPONSE-2 suggest that Ruxolitinib could be considered as a standard of care for second-line therapy in this post-HU patient population.

Biography:

Osaro Erhabor is currently a Professor of Hematology, Transfusion Medicine and Laboratory Total Quality Management. He is an Alumni of Rivers State University of Science and Technology, Nigeria, University of Greenwich in the United Kingdom and Francis Tuttle College of Technology in Oklahoma, USA. He is the author of 5 books and 5 book chapters. He has published more that 190 papers in the field of infectious diseases, hematology, blood transfusion science and total quality management. He is also a Member of the Editorial Board as well as an article Reviewer to several international scientific journals.

Abstract:

Hypertension is a global public health problem that adversely affects the health status of individuals, families and communities. L-arginine and nitric oxide levels of a total of 90 consecutively recruited hypertensive subjects and 50 age-matched non-hypertensive controls were studied. Plasma from subjects and control participants were analyzed for L-arginine and nitric oxide L-arginine and nitric oxide levels was significantly lower among the hypertensive subjects compared to those of the non-hypertensive controls (p=0.04 and 0.05) respectively. There was no statistically significant difference in the L-arginine and nitric oxide levels of the hypertensive subjects based on gender and age group (p=0.87 and 0.22) and (p=0.23 and 0.47) respectively. L-arginine level was significantly higher among married hypertensive subjects compared to single subjects (p=0.03). There was no statistically significant difference in the nitric oxide level of hypertensive subjects based on marital status (p=0.81). The difference in the L-arginine and nitric oxide level of hypertensive subjects based on ethnicity was not statistically significant (p=0.57 and 0.25) respectively. The mean nitric oxide level was significantly higher among hypertensive subjects with mildly raised blood pressure compared to those with high blood pressure (p=0.01). The findings in this study confirm that that the level of L-arginine and nitric oxide is lower among hypertensive subjects compared to non-hypertensive controls. It may be necessary to routine prescribe nitric oxide generating L-arginine supplement to hypertensive patient. It may be necessary to carry out public enlightenment of hypertensive patients in the area on the need to maintain a balanced diet containing sufficient level of L-arginine.

Biography:

Abstract:

The Polycythemia Vera Study Group (PVSG) and WHO classifications distinguished the Philadelphia (Ph1) chromosome positive chronic myeloid leukemia from the Ph1 negative myeloproliferative neoplasms (MPN) essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (MF) or primary megakaryocytic granulocytic myeloproliferation (PMGM). Half of PVSG/WHO defined ET patients show low serum erythropoietin levels and carry the JAK2 V617F mutation, indicating prodromal PV. The positive predictive value of a JAK2 V617F PCR test is 95% for the diagnosis of PV and about 50% for ET and MF. The WHO defined JAK2 V617F positive ET comprises three ET phenotypes at clinical and bone marrow level when the integrated WHO and European Clinical, Molecular and Pathological (ECMP) criteria are applied: Normocellular ET (WHO-ET), hypercellular ET due to increased erythropoiesis (prodromal PV) and hypercellular ET associated with megakaryocytic granulocytic myeloproliferation (EMGM). Four main molecular types of clonal MPN can be distinguished: JAK2 V617F positive ET and PV; JAK2 wild-type ET carrying the MPL 515; mutations in the calreticulin (CALR) gene in JAK2/MPL wild-type ET and MF and a small proportion of JAK2/MPL/CALR wild-type ET and MF patients. The JAK2 V617F mutation load is low in heterozygous normocellular WHO-ET. The JAK2 V617F mutation load in hetero/homozygous PV and EMGM is clearly related to MPN disease burden in terms of splenomegaly, constitutional symptoms and fibrosis. The JAK2 wild-type ET carrying the MPL 515 mutation is featured by clustered small and giant megakaryocytes with hyperlobulated stag-horn like nuclei, in a normocellular bone marrow (WHO-ET) and lacks features of PV. JAK2/MPL wild-type, CALR mutated hypercellular ET associated with PMGM is featured by dense clustered large immature dysmorphic megakaryocytes and bulky (cloud-like) hyperchromatic nuclei, which are never seen in WHO-ECMP defined JAK2 V617F mutated ET, EMGM and PV and neither in JAK2 wild-type ET carrying the MPL 515 mutation. Two thirds of JAK2/MPL wild-type ET and MF patients carry one of the CALR mutations as the cause of the third distinct MPN entity. WHO-ECMP criteria are recommended to diagnose, classify and stage the broad spectrum of MPN of various molecular etiologies.

Biography:

C Cameron Yin has received her MD from Beijing Medical University and her PhD from the University of Wisconsin-Madison. She is currently an Associate Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. In addition to clinical responsibilities on the leukemia, lymphoma and molecular diagnostic services, she has been actively participating in multiple research projects in the molecular genetic abnormalities in leukemia and lymphoma, which has led to over 100 research papers and over 20 book chapters.

Abstract:

CD5-posiitve B-cell lymphomas are heterogenous group of neoplasms. Classification of this group of lymphomas has important clinical and prognostic significance. CD5-positive B-cell lymphomas consist primarily of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and mantle cell lymphoma (MCL). However, CD5 expression has been reported in a number of other B-cell lymphomas. We report the clinical, morphologic, immunophenotypic and molecular genetics features of several series of CD5-positive B-cell lymphomas that lack the prototypic characters of CLL/SLL or MCL, including follicular lymphoma, MALT lymphoma, nodal marginal zone lymphoma and lymphoplasmacytic lymphoma. Our results show that CD5 expression is often associated with an increased tendency of disseminated disease in MALT lymphoma and nodal marginal zone lymphoma, but these patients usually have an indolent clinical course and excellent overall survival with appropriate management. However, in follicular lymphoma, CD5 expression is associated with a higher International Prognostic Index, higher rate of transformation to diffuse large B-cell lymphoma and shorter progression-free survival. We summarize that CD5 expression not only produces diagnostic challenges in the classification of CD5-positive B-cell lymphomas but also bears prognostic significance.

Biography:

Ken Mills is the Chair of Experimental Hematology in the Centre for Cancer Research and Cell Biology (CCRCB) in Queen’s University Belfast. He coordinates the activities of the Blood Cancer Research Group with a focus on the molecular aspects of MDS and AML to identify novel therapies. He has published over 135 papers, several book chapters and he is an Editorial Board Member and Reviewer for high impact journals.

Abstract:

There is an urgent and unmet need for new effective and less toxic therapies for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients. This is particularly important for the elderly patients who are often unfit for intensive therapies. The number of mutations that have now been reported as being associated with both AML and MDS mean the potential mutation combinations would mean a plethora of drugs may be required. The number of new therapies being developed through the drug pipeline of pre-clinical, phase 1, 2 and 4 before FDA approval is very low and can take up to 15-18 years and billions of dollars. However, there are a large range of approved therapies for all types of conditions such as diabetes, epilepsy, cardiac diseases, mental disorders etc., which are known to the safe and well tolerated in humans. The question is could any of these therapies be repurposed or repositioned to be a treatment for AML or MDS and if so how can the most effective be identified? We have employed alternative approaches to identify candidate drugs for repurposing and these approaches and the results will be discussed in context of AML and MDS.

Biography:

Rashmi Kanagal-Shamanna is an Assistant Professor in Hematopathology and Molecular Diagnostics Laboratory at The University of Texas at MD Anderson Cancer Center, USA. She is board certified by the American Board of Pathology in Anatomic and Clinical Pathology, Hematopathology and Molecular Genetic Pathology. She has received her MD from St. John’s Medical College, Bangalore, India. She has completed Residency in Anatomic and Clinical Pathology from Henry Ford Hospital, Detroit, Michigan. She has completed her Fellowships in Hematopathology, Advanced Hematopathology as well as Molecular Genetic Pathology at The University of Texas MD Anderson Cancer Center, USA. She is actively involved in bone marrow/lymph node pathology and clinical development and reporting of next generation sequencing-based assays for cancers. Her primary research interest includes application of novel molecular techniques to understand tumor pathogenesis and ultimately guide therapy. She has numerous highly cited peer-reviewed publications in her field and has given talks at many national meetings.

Abstract:

Isolated isochromosome 17q, i(17q), accounts for less than 1% of myeloid neoplasms that are commonly classified as myelodysplastic/myeloproliferative neoplasms, acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) or myeloproliferative neoplasms (MPN). These cases have distinctive clinicopathologic features with an aggressive clinical course and poor prognosis. However, their molecular mutation profile has not been studied. Here, we present the mutation profile of myeloid neoplasms with isolated i(17q) that included AML, MDS/MPN, MDS and MPN. In addition to the i(17q) as a common finding, these neoplasms had frequent mutations in SRSF2 (55%), SETBP1 (59%), ASXL1 (55%) and NRAS (31%); TET2 and TP53 mutations were rare. Eight of 28 patients (29%) showed concurrent mutations in ASXL1, SRSF2, SETBP1 and RAS. There was a significant association between mutations in SETBP1 and RAS (p=0.003). The mutation pattern was independent of the morphologic diagnosis. Sequential mutational analysis of a subset of cases showing evolution from a diploid karyotype to i(17q) showed that SRSF2 and ASXL1 mutations precede the detection of i(17q) whereas SETBP1 mutations are associated with i(17q).

Biography:

Abstract:

Biography:

Jackleen Raafat Awadallah has received her PhD in Biochemistry, Faculty of Pharmacy, Suez Canal University, Egypt in 2014. She has completed her Master’s degree in Biochemistry at Faculty of Pharmacy, Cairo University, Egypt in 2010. Currently, she is working as a Researcher at the Medical Biochemistry Department, Medical Research Division and she is also a Member of the General Secretary Group of the Supreme Council of the Medical Division, National Research Center of Egypt.

Abstract:

Acute lymphocytic leukemia (ALL) is a malignant disorder common among children. Apoptosis is a morphological process that leads to controlled cellular self-destruction and defective apoptotic pathways are greatly involved in tumor formation, progression and metastasis. Apoptosis is the primary mechanism through which most chemotherapeutic agents induce tumor cell death. The purpose of this study was to monitor the expression of pro and anti-apoptotic proteins CD95 and Bcl-2 as well as copper and zinc levels in the peripheral blood of children with acute lymphocytic leukemia prior to and six months after starting chemotherapy. The study was performed on twenty five children attending the outpatient clinic of the National Cancer Institute, Cairo University. Ten normal children were included in the study and considered as control group. Results showed that Total Leukocyte Count (TLC) and bone marrow blast count were significantly higher in ALL children than controls while after treatment TLC was normalized whereas bone marrow blast count was significantly decreased, hemoglobin and platelet count were significantly decreased when compared to controls while significantly increased after treatment. CD95 was significantly decreased before treatment relative to controls while it was significantly increased after treatment whereas Bcl-2 concentration showed significant increase before treatment compared to controls while it was significantly decreased after treatment. Serum Cu level showed significant increase in ALL cases at presentation compared to controls while it was not significantly changed after treatment. Serum Zn level was significantly decreased before treatment compared to controls while it was normalized after treatment. Cu/Zn was significantly higher in newly diagnosed ALL children than controls while it showed significant decrease after treatment. Negative significant correlation was found between CD95 and Bcl-2 on one hand and between serum Cu and Zn levels on the other hand. It could be concluded that CD95 and Bcl-2 might be useful diagnostic markers not only in the diagnosis but also in the follow up of ALL cases.

Biography:

Mousa Mohammad Thalath Alhaosawi has completed his MD from Saudi Commission for Health Specialties in Orthopedic Surgery (Pediatric and Hip Surgeon). He is the Director of Almadinah General Hospital of Almadinah city in Saudi Arabia. He has published more than 9 papers in reputed journals

Abstract:

Introduction & Objectives: The hallmark of hemophilia is hemarthrosis. All efforts must be made to early diagnose joint bleeding as soon as it occurs and treat it not later than within 2 hours of onset by infusing the appropriate clotting factor. This will prevent the accumulation of blood in the joint as well as inflammation and a potential hemophilic arthropathy. Recurrent bleeding prevents the joint from regaining its range of motion, muscle strength and normal appearance. These changes become permanent, leading eventually to osteoarthritis. A bleeds joint requires urgent and comprehensive management, especially in young patients, if permanent damage is to be prevented.

Methods: The author conducted a comprehensive review and synthesis of the relevant literature. The author reviewed all compiled reports from computerized searches. Searches were limited to English language sources and human subjects. Literature citations were generally restricted to published manuscripts appearing in journals listed in Index Medicus and reflected literature published up to July, 2013.

Results: The aim of this study was to introduce the new criteria (joint at risk) for early identification of “bleeds joint” for early diagnosis and effective management to prevent the joint to become chronic synovitis “target joint”.

Conclusion: The new concept of identifying “target joint” in this study is aiming to prevent the joint of hemophilic patient to progress to stage of chronic synovitis “target joint” by early identification of bleeds joint.

Biography:

Ayesha Junaid is a graduate of King Edward Medical University, Pakistan and is a Fellow of Clinical Hematology (2002) from CPSP Pakistan. She has received training in Cytogenetics & FISH technique from UCLA, USA in year 2008. She has qualified the evaluation examination of Medical Council of Canada in year 2012. She is a Consultant Hematologist and In-Charge Blood Transfusion Services & Hematology Department at a tertiary care hospital Islamabad. She also works as a Transplant Consultant mainly involved in hematological malignancies. She is a Teacher in medical school since 17 years and is presently working as a Professor of Pathology in Shifa College of Medicine, Pakistan. She is an elected syndicate Member of Shifa Tameer-e-Millat University, Pakistan. She is Patron In-Charge of student organization for blood donation. She is also a Program Director, Hematology Fellowship in Shifa International Hospitals, Islamabad and Chairperson, Hospital Transfusion Committee. She works as a National Hemovigilance Coordinator appointed by Ministry of Health, Pakistan.

Abstract:

Thalassemia & hemophilia are two inherited blood disorders in which children are born with lifelong cellular or component dependency as curative treatment is either not available or not affordable. In Pakistan the estimated burden of the children suffering from inherited blood disorders is above six million. Thalassemia major & hemophilia claim more than 90% of this disease load. Considering factors affecting prevalence of these disorders like cultural, socioeconomic, education and awareness level, an increase is expected in near future. These disorders show up since early childhood and affect quality of life not only of the patients but of the families having these special children. Role of hematologists providing care to these under privileged patients becomes crucial, demanding and lifelong. Here not only skill and knowledge but a lot of passion is required to make a difference in effective management of these lifelong disorders. In Pakistan, Jamila Sultana Thalassemia Foundation and Pakistan Hemophilia Welfare Societies are two model organizations, among many who save lives and improve productivity of these young patients. JS foundation is working since year 2004 with a registered load of 611 thalassemic children, providing complete physical & psychological support free of cost. Their oldest patient maintained conservatively is 38 year old. Pakistan Hemophilia Society, with 510 registered hemophiliac children is delivering as a centre of excellence with free factor replacement and rehabilitation facilities. Though the journey of management of hereditary blood disorders in underserved country is tough but there is light at the end of the tunnel.

Biography:

Michael Retsky has received his PhD in Physics from University of Chicago in 1974 and made a career change into cancer research 30 years ago. He was on Judah Folkman’s staff for 12 years. He is a long term survivor of Stage IIIc colon cancer and noted for opting not to use maximum tolerated chemotherapy was the first person to use what is now called metronomic chemotherapy. He is the Founder and on the Board of Directors of Colon Cancer Alliance. He has published more than 70 papers in physics and cancer and currently editing a book on the cancer project for Nature/Springer.

Abstract:

My colleagues and I have been studying a bimodal relapse pattern for breast cancer patients treated with mastectomy. Most relapses occur in the 3 years post surgery and after a lull in the 4^th year, a broad period of late relapses extends from 5 to 15 and more years. Similar patterns have been seen in over 21 databases from US, Europe and Asia. We suspect that the host response to surgical wounding produces systemic inflammation that lasts for a week or so (identified by IL-6 in serum). Breast cancer patients can have circulating tumor cells and cancer cells that are dormant perhaps in marrow. Among the many possible results of systemic inflammation, capillaries become permeable and platelets degranulate that have previously sequestered angiogenesis controlling factors. According to our findings, the combination of these situations results in the wave of relapses in the initial 3 years after surgery. The surgery that triggers these events can be primary tumor removal, breast reconstruction or perhaps other such interventions. Based on a retrospective study, perioperative NSAID Ketorolac may reduce relapses by 5-fold in the 9-18 month period after surgery. There is one small randomized trial underway in Belgium and we are anxiously promoting other trials in locations where triple-negative breast cancer (that lack markers for targeted therapy) is common. This population will respond best to this perioperative NSAID therapy that incidentally is inexpensive, non-toxic and administered once just prior to surgery and perhaps over the 4 postoperative days.

Biography:

C D Atreya is an Associate Director for Research at the Office of Blood Research and Review, Center for Biologics Research and Review at the U.S. Food and Drug Administration, USA. He has more than 70 scientific publications in peer-reviewed journals and also serves on the Editorial Board for scientific journals of repute.

Abstract:

Hemophilia A (HA) is a bleeding disorder caused by deficiency of functional plasma clotting factor VIII (FVIII). Over a thousand different mutations have been reported in the F8 gene. Nonetheless, a CDC database (CHAMP, sample size 677 genotyped HA patients) illustrates that over 4% of HA patients with normal F8 do manifest the disease, suggesting that other molecular mechanisms such as suppression of normal F8 expression may also be involved in HA pathobiology. In the past decades, non-coding RNAs (ncRNAs), i.e., RNA transcripts not translated into proteins such as microRNAs (miRs), have emerged as key players that mediate post-transcriptional regulation of gene expression. Here we evaluated the role of miRs in HA disease manifestation. Global small ncRNA expression profiling analysis of whole blood from HA patients and controls was performed using high-throughput ncRNA microarrays. Patients were further sub-divided into those that developed neutralizing-anti-FVIII antibodies (inhibitors) and those that did not. We identified several ncRNAs and among them miR-1246 was significantly up-regulated in HA patients. In addition, miR-1246 showed a six-fold higher expression in HA patients without inhibitors. We further identified a miR-1246 target site in the non coding region of F8 mRNA and were able to demonstrate the suppressor role of miR-1246 on F8 expression in a stable lymphoblastoid cell line expressing FVIII. This study with HA patient blood samples indicates that besides the coding sequence of F8, non coding regions and other regulatory elements should also be studied to fully understand the causes and consequences of dysregulation of F8 gene expression.

Biography:

Nathan Visweshwar has completed his Medical training in Madras Medical College and proceeded to UK and later to Canada for his training in Medicine and Hematology. He was in Middle East & Asia practicing Clinical and Laboratory Hematology. He is presently the Director of the Hemophilia/Hematology program in the University of South Florida, Tampa, FL. He has taken part in more than 50 clinical trials, both academic and drug sponsored clinical trials.

Abstract:

It is anticipated that the child born in year 2013 with hemophilia will have a normal lifespan. About 80% of patients with hemophilia live in developing countries. The world federation of hemophilia is aiming for “treatment for all” patients with hemophilia. The treatment paradigm has shifted from on demand basis to primary prevention. In developing countries, primary prophylaxis with factor VIII (costing about 300,000 US dollars for each person) is unlikely to happen in the near future. On demand therapy, mainstay of treatment in developing parts of the world is about 150,000 USD. The cost escalates as the product specificity, purity and longevity improves. World federation of hemophilia chapters assist in importing factor concentrates. Patients in the remote parts of the developing world still depend on cryoprecipitate/fresh frozen plasma for their bleeds. Infective complications from these products cause HIV (1.2%), hepatitis B (6%) and hepatitis C (23%) and obesity secondary to lack of physical activity, add to the cost. There is paucity of scientific data to guide treatment in patients who are on demand therapy, as what is perceived as a bleed by the patient, may be pain from other causes. Ultrasound of the joint has shown consistent sensitivity and specificity is valuable in assessing joints for other complications including synovitis, fibrosis/osteoarthritis. Optimal utilization of the factor concentrates can only be achieved by education, expedited physical therapy and evaluation of the joint for secondary complications, early intervention and prenatal diagnosis for expectant mothers (5Es). We have long way to achieve the goal of “treatment for all” in hemophilia.

Biography:

J J Michiels is the founder of the Goodheart Institute & Foundation. He served as Assistant Professor to Professor of Nature Medicine at A. Kr. von dem Borne Department of Hematology, as a Consultant Scientist at Academic Medical Center Amsterdam during 1997-2000, as Consultant professor Hematology at Medical Diagnostic Center, Rijnmond Rotterdam 1998-2000. He is the Co-founder of Central European Vascular Forum: CEVF 2003 at University Hospital Antwerp, Belgium, Co-founder of European Society of Vascular Medicine: ESVM. He is also a founder of European Working Group on Myeloproliferatieve Disorders: EWG. MPD during 1999-2008 and European Working Group on Myeloproliferative Neoplasms: EWG.MPN. His research interests reflect in his wide range of publications in various national and international journals. He serves as a member of various associations apart from being Editorial board member of many reputed journals.

Abstract:

The WHO classification of the Myeloprolferative Neoplasms (MPN) distinguishes Essential Thrombocythemia (ET), Polycythemia Vera (PV) and Primary Myelofibrosis (PMF). Myelofibrosis (MF) is not a disease because reticulin and collagen fibrosis are produced by polyclonal fibroblasts in response to cytokines released from the clonal granulocytic and megakaryocytic progenitor cells in myeloproliferative disorders (MPD) in patients with ET and PV. The Hannover and Cologne Bone Marrow classification defined chronic or primary megakaryocytic granulocytic myeloproliferation (PMGM) as the third distinct prefibrotic MPN without features of PV. Vainchenker (2005) discovered the JAK2 V617F somatic mutation as the driver cause of ET, trilinear PV of erythrocytic, megakaryocytic and granulocytic myeloproliferation (EMGM) and myeloid neoplasia of the spleen with secondary MF. Prefibrotic JAK2 V617F mutated ET comprise three phenotypes: normocellular ET, ET with PV features in blood and bone marrow (prodromal PV) and hypercellular ET with predominant megakaryocytic granulocytic myeloproliferation (EMGM or masked PV) and moderate splenomegaly. JAK2 V617F mutated ET and PV are featured by medium sized to large (pleomorphic) megakaryocytes with only a few giant forms. JAK2 exon 12 mutated MPN usually present with idiopathic erythrocythemia or early PV. Bone marrow histology in MPL515 positive ET and MF show clustered small and giant megakaryocytes with hyperlobulated stag-horn like nuclei in a normocellular bone marrow with no features of PV already described in 1988 (Thiele). Bone marrow histology in prefibrotic CALR mutated ET and MF is associated with PMGM and dominated by dense clusters of large immature megakaryocytes with hypolobulated bulky (cloude-like) hyperchromatic nuclei, which are never seen in JAK2V617F, JAK2 exon 12 and MPL515 mutated MPN. Disease burden in JAK2, MPL and CALR mutated MPN is best reflected by the degree of anemia, splenomegaly, mutation allele burden, bone marrow cellularity and myelofibrosis.

Biography:

Chiaki Hidai has received MD in 1986 from Hokkaido University, Japan. He has worked as a House Officer and a Specialist Trainee of Cardiology in Tokyo Women’s Medical University and worked as a Postdoctoral fellow in Vanderbilt University in USA. He has received his PhD from Tokyo Women’s Medical University in 1997. He was an Assistant Professor in Tokyo Women’s Medical University from 1994-2000 and currently working as an Associate Professor in Nihon University School of Medicine from 2000.

Abstract:

Coagulation factor IX is thought to circulate in the blood as an inactive zymogen before being activated in the coagulation process. The effect of coagulation factor IX on cells is poorly understood. This study aimed to evaluate the effects of intact coagulation factor IX and its cleavage fragments on cell behavior. A431 cells (derived from human squamous cell carcinoma), Pro5 cells (derived from mouse embryonic endothelial cells), Cos7 cells and human umbilical vein endothelial cells were utilized in this study. The effects of coagulation factor IX and its cleavage fragments on cell behavior were investigated in several types of experiments, including wound healing assays and modified Boyden chamber assays. The effect of coagulation factor IX depended on its processing; full length coagulation factor IX suppressed cell migration, increased adhesion to matrix and enhanced intercellular adhesion. In contrast, activated coagulation factor IX enhanced cell migration, suppressed adhesion to matrix and inhibited intercellular adhesion. An activation peptide that is removed during the coagulation process was found to be responsible for the activity of full length coagulation factor IX and the activity of activated coagulation factor IX was localized to an EGF domain of the coagulation factor IX light chain. Full length coagulation factor IX has a sedative effect on cells, which is counteracted by activated coagulation factor IX in vitro. Thus, coagulation factor IX may play roles before, during and after the coagulation process.

Biography:

Tripathi Rajavashisth is an internationally renowned Scientist with Professor of Medicine appointments at the Charles R. Drew University of Medicine and Science and at the UCLA David Geffen School of Medicine. He has served at UCLA for over 26 years and Harvard University for 2 years as Assistant, Associate to full Professor, where he earned a reputation as a talented and hard-working Molecular Biologist who discovered aspects of lineage commitment of stem cells to white blood cells and pathological processes leading to their migration, growth and survival inside the vessel wall. He has acquired extensive experience as Director of research laboratories and related administration by implementing research programs funded by several governmental and non-governmental agencies including National Institute of Health, American Heart Association, Eisner Foundation and DBT, Ministry of Science and Technology, Government of India.

Abstract:

Numerous studies indicate that persistent inflammation importantly contributes to the pathophysiology of many chronic human diseases, including cardiovascular diseases, diabetes, cancer, arthritis, neurodegerative and autoimmune disorders. Interacting cells (among them mononuclear phagocytes, T cells, B cells, natural killer cells and mast cells), all thought to originate from circulating hematopoietic and immune precursors and key resident cells of the tissues orchestrate aspects of the acute and chronic inflammation that underlie diseases of many organs. Inflammatory diseases are accompanied by a coordinated series of common mechanisms that is initiated by expression of cytokines, growth factors, mitogens and morphogens leading to a disturbance in homeostatic balance causing oxidative stress, tissue injury, extracellular matrix remodeling, angiogenesis and fibrosis in diverse target tissues. Arterial disease atherosclerosis features prominently among diseases that involve inflammatory mechanisms. Serum lipoproteins diffusing through extracellular space become entangled in the arterial space and begin to undergo oxidative and covalent modifications that render them proinflammatory in this disease. Local recruitment of blood leukocytes follows with progression that involves many inflammatory mediators that are modulated by interacting cells of the arterial wall and immune (both innate and adaptive) systems and the homeostatic balance between normal proteolytic remodeling and inhibition of extracellular proteolytic activity tips toward excessive tissue destruction. Structural deterioration can result in erosion or rupture of the plaque cap, which directly precipitates arterial thrombosis with frequently disastrous consequences, all these complications of the disease may intimately involve proteomic variability contributing to inflammatory mechanisms. A better understanding of the inflammatory, molecules and mechanisms should result in novel strategies to the detrimental effects of chronic inflammation, control of the inflammatory mechanisms in various diseases and may aid the development of potential molecular targets to favorably modify inflammatory diseases.

Biography:

Shahtaj Khan is an assistant professor hematology, head department of Pathology at Hayatabad Medical Complex, Peshawar, Pakistan. She is also working as Consultant Hematologist, Rehman Medical Institute. Her research interests reflect in her wide range of publications in various national and international journals.

Abstract:

Objective: The aim of this study was to evaluate the prevalence of G6PD deficiency by G6PD quantitative method in jaundice infants coming from different districts of Khyber Pakhtunkhwa (KPK).

Materials & Methods: In this descriptive cross sectional study total no of three hundred (Male n=200, Female n=100) hyperbilirubinemia infants of <01 year were randomly selected for the study. By aseptic technique 4 ml blood was collected, 2 ml for bilirubin profile and 2 ml for G6PD enzyme assay. Serum bilirubin was determined by Diazo reaction method using Architect plus ci8200 (Abbott, USA) and G6PD quantitative enzyme assay was measured by ultraviolet kinetic method (Trinity biotech kit, USA). The collected data was recorded and analyzed in SPSS-20.P value was less than 0.005, it was considered as statistically significant.

Results: With this study 33 (11%) jaundiced infants were G6PD deficient and 267 (89%) infants were normal G6PD level. In all male jaundice neonates 25 (12.5%) were G6PD deficient and 175 (87.5%) with normal G6PD quantity, while 08 (08%) female infants were G6PD deficient and 92 (92%) within normal G6PD range out of all jaundiced female infants. No significant differences in G6PD enzyme level were seen among male and female jaundiced infants. The mean serum total bilirubin in G6PD deficient neonates and normal infants was 13.8 mg/dl and 12.2 mg/dl respectively.

Conclusion: Our study concluded that 11% of infants presenting with jaundice were G6PD deficient, which is a higher percentage. As the study was conducted in our area, which is endemic for malaria and poverty leads to frequent episodes of infection, certain drugs can cause fatal hemolysis. So as per WHO protocol our population needs screening for G6PD deficiency. We suggest that quantitative G6PD levels should be done at least prior to anti-malarial therapy in every infant.

Biography:

Nishit Kumar Gupta is a practicing Pathologist by profession running his own private pathology diagnostic laboratory: Nishit Clinical Laboratory Pvt. Ltd. He has completed his graduation from Meerut University and Post-graduation from JNMC Belgaum. He has been to NIMHANS, Bangalore for short training in Neuropathology with special inclination for hematology disorders specially hematooncology and coagulation disorders and with sub specialization in dermatopathology. He has learning and research interest in hematology automated counters for interpretation of RPD, histograms and Scattergrams. He is continuously associated in various teaching programs for FMG and PG entrance coaching.

Abstract:

Circulating plasma cells are not a common finding in multiple myeloma. Being able to detect plasma cells in peripheral blood is important as they are a prognostic indicator that correlates with disease progression. The peripheral blood sampling (EDTA whole blood) in LH750 Beckman Coulter can help us isolating and assist us in identifying circulating immature plasma cells in the human body. These plasma cells are subject to variations in morphology on slides and can be easily missed. It is understood that plasmablasts and proplasmacytes are known to have aggressive course with poor prognosis. My retrospective study of two patients using LH750 Beckman Coulter demonstrated and identified isolated group of (event) circulating plasma cells on histograms. Using white blood cell differential scatter plot to study the cases identified a unique pattern and distinct cellular characteristics of plasma cells. This distinct pattern helped us in our laboratory to identify the circulating immature plasma cells in the blood. We have studied this finding retrospectively to use it as flagging for future index new patients. By using this review policy, the laboratory can review and screen the plasma cell leukemia patients in a better way.

Biography:

Osaro Erhabor is currently a Professor of Hematology, Transfusion Medicine and Laboratory Total Quality Management. He is an Alumni of Rivers State University of Science and Technology, Nigeria, University of Greenwich in the United Kingdom and Francis Tuttle College of Technology in Oklahoma, USA. He is the author of 5 books and 5 book chapters. He has published more that 190 papers in the field of infectious diseases, hematology, blood transfusion science and total quality management. He is also a Member of the Editorial Board as well as an article Reviewer to several international scientific journals.

Abstract:

Background: Menopause which is defined as cessation of menstrual bleeding is assumed to lead to an increase in iron stores over the menopausal transition.

Method: This study was carried out to determine the level of serum ferritin between pre and postmenopausal women attending Usmanu Danfodiyo University Teaching Hospital, Sokoto. The study was conducted among 150 women (75 premenopausal and 75 postmenopausal) with mean age 43.99±19.22.

Result: The serum ferritin was significantly higher among postmenopausal women 47.38±43.00 compared to premenopausal women 21.96±20.15 (p=0.01). The prevalence of anemia based on serum ferritin level was higher among premenopausal women (8.7%) compared to postmenopausal women (2.7%). Low ferritin level <3.5 ng/ml was higher among Hausa/Fulani (6.02%) compared to other ethnic groups. The difference however was not statistically significant (p=0.91). The age range for premenopausal and postmenopausal women was 18-49 and 50-87 years respectively. Low ferritin level was higher among premenopausal women in the 25-34 years age group compared to other age group. Ferritin level <3.5 ng/ml was higher among subjects with no formal education (p=0.69).

Conclusion: This study has shown that serum ferritin and anemia based on serum ferritin level of <3.5 ng per ml was significantly higher among premenopausal compared to postmenopausal women. Serum ferritin should be used for the diagnosis and monitoring of iron deficiency anemia in pre and postmenopausal women. Ferritin level of <3.5 ng/ml should be used as cutoff for the diagnosis of depleted iron store.

Biography:

Bozena Sokolowska is currently working as an Associate Professor in Department of Hemato oncology and Bone Marrow Transplantation at Medical University in Lublin, Poland. She has received the Medical Doctor degree in 1982 at Medical University in Lublin, PhD degree in 1991 and in 2014, she received the Habilitation degree. In 2001, she received the second degree specialization in Hematology. She is the author and co-author of original and review papers and chapters of medical books. Her interest concerns coagulation disorders, thrombophilia, myeloproliferative disorders and Gaucher disease.

Abstract:

Acquired hemophilia is a suddenly occurring severe blood diathesis both females and males, which may lead to death among 8-42% of patients. So far 9 patients with acquired hemophilia have been successfully treated in the Department of Hemato oncology in Lublin. The patients include 4 men and 5 women (aged from 24-74; average age 50). Two women suffered from the disease due to pregnancy and puerperium, for the remaining patients acquired hemophilia resulted from: Psoriasis, chronic hepatitis and pemphigus foliaceus. In men the cause of emergence of auto antibodies against coagulation factor VIII might have been: Amyloidosis and bone marrow transplantation (2 patients), chronic respiratory tract disease. The most common manifestations of the disease include extensive subcutaneous hemorrhages and intramuscular hematomas. One female patient was referred to a surgery due to hematomas in the abdomen cavity. As a result some persistent bleedings from the surgical wound occurred. In another patient the fist manifestation of the disease was an epileptic seizure caused by hemorrhagic focus in the corpus callosum of the brain. Three patients were treated only with rVIIa, one female patient with aPCC as a monotherapy and one with both drugs. In the treatment of the remaining patients DDAVP, Factor VIII concentrate, FFP were used. In case of eliminating inhibitor the combination of prednisone with cyclophosphamide was the most effective first line treatment. Summing up only prompt diagnosis and proper treatment implementation can save the life of patients with acquired hemophilia.

Biography:

Mehrdad Payandeh has completed his MD from Kermanshah University of Medical Science (KUMS). He is a Chair of Hemophilia Center and Chair of Bone Marrow Transplantation Center of Kermanshah city. He has 8 years of experience in diagnoses and treatment of hematology, oncology, coagulative, BMT patient's disorder in private and university hospital. He has published many papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

Chronic lymphocytic leukemia (CLL) is the most common leukemia in adults in Western countries but is relatively rare in Asia. Immune hemolytic anemia, Evan’s syndrome, lymphadenopathy, organomegaly and B symptoms are the main complaints of patients in CLL. The present retrospective analysis evaluated a group of 109 patients with CLL over a 9 years period, studying correlations between sex, age and overall survival. The patients were hospitalized in the Clinic of Hematology and Oncology, Kermanshah, Iran, between 2006 and 2014. Data analysis for sex and age was performed using IBM SPSS 19 and overall survival was plotted by Kaplan-Meier plot, Log-rank test in Graph Pad prism 5 Software for five years period. The mean age of diagnosis for CLL patients was 60.73 years, 59.6% male. Survival rate of patients’ was 64% and mean overall survival rate was 38.5 months. In the Rai system, fourteen patients (12.8%) had stage ΙΙΙ and twenty eight patients (25.7%) had stage IV. Most frequent clinical features in patients with CLL were lymphadenopathy (38.7%) and organomegaly (34%), respectively. There is no relationship between sex and age in patients but overall survival rate in females was higher than in males. In Asian countries, CLL is more in male and in age above 60 years. Complaints about lymphadenopathy and virus infection are prevalent.

Biography:

Naser Mobarra has obtained his PhD from Tehran University of Medical Sciences, Iran. He has published more than 17 papers/articles in reputed journals and has been serving as an Editorial Board Member of some ISI journals.

Abstract:

Hemophilia patients are constrained to undergo repeated injections of clotting factors. Transplanted stem cell-derived and gene therapy for hemophilia showed great promises and provided new hope for these patients in clinical trials. Cell therapy, involving stem cells-derived transplanted can provide de novo protein synthesis and if implanted successfully could induce a steady-state production of low quantities of factors which may keep the patient above the level required to prevent spontaneous bleeding. Hematopoietic stem cells are an attractive source of target cells for hemophilia because they can self-renew and differentiate into all blood lineages during hematopoiesis. Another advantage is their accessibility for genetic modification and ease of transplantation. Targeting hematopoietic cells by ex vivo transduction followed by their transplantation allows for direct access of the clotting factors to the circulation. The field of gene therapy for hemophilia is being thoroughly explored. Gene therapy for patients with hemophilia B is ideal and has been more successful, mostly because a small increase in protein production can lead to significantly decreased bleeding diathesis. In contrast to hemophilia B, gene therapy for hemophilia A has seen significantly less recent progress into the clinic, despite it being the more common of the two diseases. The recent clinical success implementing a novel adeno-associated virus vector demonstrated sufficient FIX expression in patients to convert a severe hemophilia phenotype to mild, an achievement which has the potential to profoundly alter the impact of this disease on human society.

Biography:

Zahra Mozaheb has completed her Hematology-Oncology sub specialty from Tehran University of Medicine Science, Iran. She is an Assistant Professor of Mashhad University of Medical Science. She has published more than 22 papers in English and Persian journals and has been serving as Reviewer and an Editorial Board Member of repute. She has also published one book and one chapter of English book (Epidemiology Insight).

Abstract:

Human T-Cell Lymphotrophic Virus-1 (HTLV1), the first human retrovirus to be discovered, is estimated to infect 10-20 million people worldwide. Infection with HTLV1 is strongly related to adult T-cell leukemia/Lymphoma and HTLV1 associated myelopathy. HTLV1 is primarily transmitted by breast feeding, blood transfusion, sharing of needles and sexual transmission. It is endemic in southern Japan, the Caribbean and the Melanesian island, Papua New Guinea, the Middle East, central and southern Africa and South America. In these endemic areas, seroprevalence range is different from about one percent in Mashhad in southeast Iran (1-3%) to 30 percent in rural Miyazaki in southern Japan. Adult T-cell lymphoma leukemia (ATL) is an aggressive lymphoproliferative malignancy with short survival in acute form and an incidence of less than 5% in HTLV-1-infected people. The cumulative incidence of ATL among Japanese HTLV1 carrier is about 2.5% (3-5% in male and 1-2% in female). Although women are more infected with HTLV1 but ATL is more common in men, it shows that other factors also should be responsible. At first ATL was described in Japan and later in the Caribbean region and South America. In the United States and Europe, ATL was diagnosed in immigrants from regions of endemicity. ATL occurs at least 20 to 30 years after the onset of HTLV-1 infection and is more common in adult males. The occurrence of ATL in the fourth decade predominates in Brazil and in Jamaica, but in Japan, the fifth decade of life is predominant for the occurrence of ATL Possibly, local factors play a role in disease pathogenesis.

Biography:

Onwurah Winifred has completed her Master’s degree from University of Nigeria and currently pursuing her Doctoral studies in the Department of Hematology, Nnamdi Azikiwe University, Nigeria.

Abstract:

The toxicity of embalmment chemicals especially formaldehyde to human system including carcinogenicity and other adverse health effects have been reported. This study was designed to ascertain the possibility of exposure to these chemicals in the disruption of hematopoietic functions. 100 apparently healthy individuals (all males) were recruited for this research. Out of this number, 20, who were not mortuary workers and thus not exposed to the embalmment chemicals served as the control. The test groups were categorized as follows: 48 workers exposed to the chemicals for 1 to 7 years; 13 workers of 8-14 years exposure and 19 workers exposed for 15 years and above. The results of this study showed that the alterations in the peripheral blood cell counts and Hemoglobin (HB) levels of the exposed mortuary workers when compared with the control were not statistically significant (P>0.05). However, there was strong and statistically significant negative correlation (r=0.263, P<0.05) between the total white blood cell (TWBC) count and the duration of exposure to the chemicals. There was also significant variation (P<0.05) in lymphocytes (LYM), neutrophils (NEUT) and mixed field differential (MXD) counts among the exposed groups. The blood film results showed no significant alteration in the number and morphology of the blood cells. This research has succeeded in demonstrating that exposure to embalmment chemicals is capable of disrupting hematopoietic functions.

Biography:

M Shahzad Sarwar is currently working as a Chief Resident at Clinical Hematology Sub-Department in Department of Oncology at Aga Khan University, Pakistan. Her research interests reflect in his wide range of publications in various national and international journals. Her international experience includes various programs, contributions and participation in different countries for diverse fields of study.

Abstract:

Introduction: Solid tumors are well associated with thromboembolic complications but the incidence of thrombosis is not widely studied in patients with acute leukemia and their management which is a great challenge. However this may be obscured by the significant morbidity and mortality due to other complications such as bleeding and infections. No established guidelines are present to treat these difficult patients. Case-controlled studies of patients with cancer revealed a fourfold increase in thromboembolic occurrence in acute leukemia with about the same rate in acute myelogenous leukemia (AML) and in acute lymphocytic leukemia (ALL). Among patients with acute leukemia, thrombosis has the highest incidence in acute promyelocytic leukemia (APL). Of interest, increased thromboembolic events take place even prior to the diagnosis of acute leukemia, similar to the situation seen in solid tumors, indicating that a prothrombotic state is present even at the earliest phase of leukemia. The use of central venous catheter and chemotherapeutic agents such as L-asparaginase and other medicine used in the treatment of hematological malignancies particularly steroids may play an important thrombogenic role.

Aims & Objectives: To determine the frequency of venous thrombosis and treatment strategy in patients with acute leukemia at a tertiary care Hospital of Pakistan.

Material & Methods: Retrospective, observational study of case charts of hospitalized patients with diagnosed case of acute leukemia at Department of Oncology, Aga Khan University Hospital Karachi during the 18 months period (January 2014 to June 2015). Data was retrieved by using ICD 9 coding for acute leukemia patients. Investigations were obtained from electronic medical record system. Finally data was analyzed for frequencies and percentages by using SPSS version 19.

Results: Total of 107 patients presented during the study period. Among them 76 were males and 31 were females with median age ranges from 18 to 60 years. These patients were stratified into 2 major groups according to type of leukemia. 63.5% patients were with Acute myeloid leukemia in which 4.7% patient developed venous thrombosis among them highest in APML 22.2% while 36.4% patients were with acute lymphocytic leukemia (ALL) in which 2.5% of patients developed venous thrombosis. Three patients were treated successfully with LMWH during their consolidation phase of chemotherapy.

Conclusion: Venous thrombosis in acute leukemia is not uncommon which can lead to fatal results if left untreated. Anticoagulation with intermittent use of LMWH for 3-6 months with close monitoring of platelet counts would be the appropriate option for treatment.