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.