Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 11th International Conference on Hematology & Hematological Oncology Las Vegas, Nevada, USA.

Day 1 :

Keynote Forum

Knox Van Dyke

West Virginia University Medical School, USA

Keynote: Luminescence reveals the cause of diabetes 1, 2 and 3 (Alzheimer’s disease)

Time : 10:00-10:40

Conference Series Hematology 2017 International Conference Keynote Speaker Knox Van Dyke photo
Biography:

Dr. Van Dyke is a Professor of Biochemistry and Molecular Pharmacology at West Virginia University Medical School with 50 years of research experience. He developed the first effective screening system for antimalarial drugs by measuring the effects of drugs on synthesis of malarial parasite DNA and RNA. He screened more than 10,000 drugs and found mefloquine and halofantrine which were developed commercially. Prof. Knox Van Dyke began to study diabetes 1 and 2 and found the actual cause of these diseases originates from a toxic peroxide called peroxynitrite. The first observation of him was that all the drugs developed to treat diabetes essentially only control blood glucose (sugar). Excessive sugar is not the cause of diabetes nor is it lack of weight control. These problems increase peroxynitrite, but they do not destroy excessive peroxynitrite per se, so the disease and its 6 major pathological consequences continue. He has developed a combination of non-toxic substances which will control these diseases effectively and prevent its many devastating pathologies. He has over 300 publications and 150 patents.

Abstract:

The fundamental basis of diabetes continues unrecognized and mostly untreated. Depending on the type of diabetes 1 or 2-treatment generally consists of insulin injections or anti-diabetic drugs that lower excessive blood glucose and/or hemoglobin A1C. Often patients are asked to lose weight and exercise more frequently. Blood glucose can be tightly controlled and still diabetic pathologies continue. Using a diabetic Streptozotocin (STZ) rat model, we demonstrated that diabetes and cataracts could be completely prevented with carboxy-PTIO which oxidizes nitric oxide and a nitration target Acetaminophen (Tylenol). This indicated that the action of STZ could be destroyed without harm to the animals. How does STZ cause diabetes in the first place? STZ is a molecule of 2-deoxyglucose (2-DG) linked to methyl nitrosourea (MNU). STZ enters the blood stream and to the pancreatic-Beta cells where it enters Glut-2 receptors. Once inside the cell, the molecule splits into its two pieces i.e., 2DG and MNU. MNU begins generating a peroxide known as peroxynitrite (OON=O-). The peroxynitrite attacks DNA, protein and lipids of the cell and damages mitochondria which kill the cell via apoptosis or necrosis. When beta cells die, alpha cells replaced them, producing excessive glucagon and increasing blood glucose thereby creating a diabetic state. When STZ is injected intra-articularly in the brain of normal mice, they develop decreased brain glucose metabolism and insulin resistance in a few days and in a few months Alzheimer’s disease with plaques and tangles. We have developed a reaction with peroxynitrite and L-012 to produce blue luminescence via oxidation. Now we demonstrate that STZ generates peroxynitrite based luminescence which is inhibited by the same substances that inhibit peroxynitrite-based luminescence itself. We show that STZ nicks plasmid DNA similarly to peroxynitrite, which we believe initiates both Alzheimer’s disease and diabetes.

  • Hematology | Hematological Oncology| Hematology: Case Report
Speaker

Chair

Prof. Tomas Kozak

Charles University, Czech Republic

Session Introduction

Shimin Hu

The University of Texas MD Anderson Cancer Center, USA

Title: Cytogenetic landscape and impact in blast phase of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy

Time : 10:40-11:10

Speaker
Biography:

Shimin Hu is currently a faculty member at The University of Texas MD Anderson Cancer Center. He received his MD from Peking University and PhD from University of Michigan. He did his pathology residency training at Hartford Hospital, CT and hematopathology fellowship training at The University of Texas MD Anderson Cancer Center. He has published about 60 papers during past three years in highly-regarded journals, including many in Blood and Leukemia.

Abstract:

The high fatality of patients with blast phase (BP) chronic myeloid leukemia (CML) urges identification of high-risk patients to prevent onset of BP. Here we investigated the risk of BP based on additional chromosomal abnormality (ACA) profiles in a cohort of 2,326 CML patients treated with tyrosine kinase inhibitors (TKIs). We examined the time intervals from initial diagnosis to ACA emergence (Interval 1), from ACA emergence to BP (Interval 2) and survival after onset of BP (Interval 3). Based on the BP risk associated with each ACA, patients were stratified into intermediate-1, intermediate-2 and high-risk groups, with a median Interval 2 of unreached, 19.2 months and 1.9 months respectively. There was no difference in Interval 1 or Interval 3 among three risk groups. Including patients without ACAs who formed the standard-risk group, the overall 5-year cumulative probability of BP was 9.8%, 28.0%, 41.7% and 67.4% for these four risk groups, respectively. The pre-BP disease course in those who developed BP was similar regardless of cytogenetic alterations, and 79.7% of BP patients developed BP within first 4 years of diagnosis. In summary, Interval 2 is the predominant determinant of BP risk and patient outcome.  By prolonging the duration of Interval 2, TKI therapy mitigates the BP risk associated with low-risk ACAs but did not alter the natural course of CML with high-risk ACAs. Thus, we have identified a group of patients who have a high risk of rapid BP and may benefit from timely alternative treatment to prevent onset of BP.

Jianrong Wang

Soochow University School of Medicine, China

Title: Autophagy in hematopoiesis and leukemogenesis

Time : 11:25-11:55

Speaker
Biography:

Jianrong Wang earned his PhD degree in The Shanghai Institute of Biochemistry, Chinese Academy of Sciences in July of 1997. In October of that year, he was appointed as a research professor in a municipal institute in Shanghai China. After moving to the US in January of 1999, he conducted research primarily at Cornell University. In March of 2010, he was offered a professorial position at the Hematology Center of Cyrus Tang Medical Institute Soochow University. His laboratory focuses on the understanding of the biology of autophagy in hematopoiesis and leukemogenesis, with an ultimate goal of preventing hematological oncogenic germination by protecting normal stem cells from malignant transformation. 

Abstract:

Autophagy, a unique protective cytoplasmic machinery involving lysosomal degradation, is required for hematopoietic stem cell multilineage differentiation that protects against leukemogenesis, but the underlying mechanism is unknown. We uncovered a mechanistic link between autophagy and hematopoietic stem cell differentiation. Physiological autophagy activity was found to be inversely correlated with Notch signaling during hematopoietic stem cell differentiation whilst pathologically low autophagy activity was associated with upregulated Notch signaling in dysfunctional hematopoietic stem cells of leukemia patients. Furthermore, we show that autophagy directly degrades intracellular Notch whereas conditional autophagy defects lead to elevated intracellular Notch and its downstream targets as well as failed hematopoietic stem cell differentiation. Hematopoietic stem cell differentiation potential, however, was restored in an autophagy defective system when Notch signaling was pharmacologically or genetically abrogated. Finally, we identified mitochondrial reactive oxygen species (ROS) as an upstream trigger for autophagy to physiologically downregulate Notch signaling and drive hematopoietic stem cell differentiation. Hence, in the cause of development when mitochondrial ROS are progressively produced, autophagy is triggered by the ROS to target Notch signaling to sustain hematopoietic stem cell differentiation. Autophagy dysfunction is attributed to the differentiation blockades which are often the cause of hematological malignancies. Therefore, our present findings provide a critical insight into the current mechanistic understanding of physiological and pathological connections between autophagy and hematopoietic stem cell differentiation, thereby proposing a novel mechanism by which autophagy maintains hematopoiesis and protects against leukemogenesis. 

Speaker
Biography:

Jongkol Akahat has completed her M.Sc. (Clinical Pathology) , B.Sc.(Med.Tech) from Mahidol and Khon Kaen university, respectively. She is a medical technician specialist in all blood transfusion science; HLA, genotyping, serology, etc. At present, her position is the head of blood components preparation in Blood Transfusion Centre, Faculty of Medicine, Khon Kaen University, Thailand.

Abstract:

Background and objective: Platelet additive solutions (PAS) are crystalloid nutrient media used in place of plasma for platelet storage. They replace 60-70% of plasma in platelet components. So the amount of storage plasma can be decreased. Platelet stored in PAS have been demonstrated to have a lower risk for allergic transfusion reactions and appeared to have equivalent clinical efficacy for controlling bleeding, compared to platelets stored in 100% plasma. We try to bring PAS to replace plasma in making leukocyte poor platelet concentrates (LPPC) compared with conventional methods that use plasma, 1 bag of total buffy coat 4 units.

Objective: The objective of this study was to prepare LPPC in PAS in our routine work, instead of the traditional LPPC.

Methods: PAS and plasma using a ratio of 65:35 in accordance with the standard reference. Then LPPC in PAS  were measured for the volume, content of platelet concentrates, white blood cell contamination and the titer of anti-A and anti-B compared to traditional methods.

Results: LPPC in PAS had volumes 304±20 ml, content of platelet concentrates 2.8±0.5X1011 cells/unit and had 0.1X109 white blood cells contamination. LPPC from traditional methods had volumes 324±16 ml, contents of platelet concentrates 3.9±0.3X1011 cells/unit and had 0.1X109 white blood cells contamination. The titer of anti-A and anti-B in LPPC in PAS is less than or equal to 64, all of which are classified as low titer, but LPPC from the traditional way with a titer of anti-A and anti-B over 64 about 20 %.

Speaker
Biography:

Bethlehem Solomon has completed her MPH, concentrating in both epidemiology and global health from Boston University School of Public Health. She is an associate epidemiologist, with a focus on oncology, at Decision Resources Group. Previous to her current position, Bethlehem was a visiting scientist at the University of Cambridge/Wellcome Trust Sanger Institute, where she participated in the design and implementation of various studies focusing on non-communicable diseases, particularly in low- and middle-income countries.

Abstract:

Acute Lymphoblastic Leukemia (ALL) incidence is increasing globally and the case burden is expected to rise among adults in whom the disease is particularly fatal. The aim was to estimate changes in ALL risk and disease burden globally over the next decade. Using data from country-specific cancer registries, incidence was estimated for 45 countries, representing approximately 90% of the world population. Increasing age and male sex were the non-modifiable risk factors with the largest effects. To account for additional risk factors such as the increasing adoption of ‘Western’ lifestyles characterized by dietary changes and more sedentary lifestyles, the proxy measure of forecast gross domestic product (GDP) were used.

Prevalence was also estimated as a cumulative incidence over the preceding 12-month period with adjustments for disease-specific and competing-cause mortality. In 2020, we estimate ALL incidence to range from 0.4 to 2 per 100,000 in Asia-Pacific and South American countries, respectively; while prevalence will range from 0.37 to 1.6 per 100,000 in these regions.

In terms of case burden, when accounting for the approximate 10% of the world’s population not covered by the 45 countries in whom we forecast incident and prevalent cases, there were a total of 53,000 cases in 2016 worldwide. Incorporating the aforementioned risk factors into a forecast model using demographic and GDP data published by the United Nations and World Bank, respectively, this number should increase to 56,000 cases by 2020. Most of these cases are in the Asia Pacific region, representing 55% of the worldwide total. 

Speaker
Biography:

Olutayo Ifedayo Ajayi holds a Diploma in Hematology and Blood Transfusion Science and a Fellowship Diploma in Clinical Chemistry from the Medical Laboratory Council of Nigeria. He later proceeded to University of Benin to study Human Physiology where he bagged his MSc and PhD degrees. He has many publications in both local and international journals. He is currently an Associate Professor and Head of Department of Physiology at University of Benin in Nigeria.

Abstract:

Erythrocyte sickling and adhesion are favored by cellular dehydration, which increases the rate of hemoglobin polymerization and cell sickling. Potassium chloride co-transport and calcium-activated potassium channel (Gardos channel) mediate erythrocyte dehydration in sickle cell disease and β-thalassemia. We investigated the in vitro and in vivo effects of various concentrations of K+ ions in physiological solutions (PSS) as well as in Cocos nucifera water (CNw) which is known for its natural high potassium content and isotonicity. This study was aimed at ascertain the efficacy of high potassium isotonic solutions in rehydrating sickle cell and possibly reversing the sickling phenomenon at in vivo and in vitro situations. Erythrocytes from 20 sickle cell anemia (SCA) as well as 46 healthy subjects were studied. One part was treated with sodium metabisulfite (Na2S5O7) solution to induce maximum sickling as controls while the other was subjected to different high concentrations of K+ in PSS as well as Cocos nucifera water (40 mM, 80 mM and CNw – 65 mmol/L) respectively. The procedure was repeated for the normal HB AA subjects. Also, both groups of subjects were given 10 ml/kg body weight of coconut water to drink as a single dose for the in vivo experiment. Blood samples were collected longitudinally before and after the oral ingestion at 1 hour and at 24 hours for analysis of red cell indices as well as stained blood films used to ascertain the percentage sickled erythrocytes count before and after the treatment in both cases. Maximum percentage counts of sickled cells after the addition of Na2S5O7 (45%) were observed which decreased significantly (P<0.05, respectively) to about 2% with Cocos nucifera and 10% with 80 mM K+ PSS. The count in 40 mM K+-PSS was not statistically significant. In both Hb AA and SS subjects, MCH and MCV remained relatively stable when compared with the pre-ingestion sample (P>0.05, respectively) while MCHC increased significantly in both groups as early as 1 hour and sustained till the 24th hour. MCHC was equally raised in the in vitro samples (P<0.05, respectively). The morphology of red cells also indicated a lesser count of sickled red cells after the oral ingestion. Cocos nucifera water and other high potassium ion solutions can activate the rehydration of sickled erythrocytes by probably de-activating the Gardos channel to increase the mean corpuscular hemoglobin concentration (MCHC) and thereby restoring the normal red cell shape. We suggest a probable pharmacological value of the Cocos nucifera water as well as other formulated high potassium but isotonic fluids in SCA management.

Speaker
Biography:

Chinedu Kingsley Dike holds a Bachelor’s degree in Medical Laboratory Science with a bias in Clinical Chemistry. He is currently pursuing Postgraduate degree in Medical Laboratory Science. His main research interest is immunological studies of hemoparasites.

Abstract:

Plasmodium falciparum infected erythrocytes have been reported to display several dramatic morphological changes that affect membrane integrity such as rigidity, antigenic character and permeability. These modifications occur both at the erythrocyte cytoskeleton and extracellular surface of the membrane resulting in sub-cellular modifications of adhesive properties exhibited by the affected cells. It is plausible therefore to hypothesize possible alterations of blood group antigenic reactivity during the infection process that could cause danger in serological procedures. Our objective therefore was to ascertain the possible changes in the reactivity of α and β antigens to their corresponding antibodies in parasitized erythrocytes. A total of 200 blood samples comprising of 50 each from parasitemic subjects of blood groups A and B respectively. They were compared with 50 samples each from control subjects from corresponding blood groups respectively who tested negative for plasmodiasis. Confirmatory tests for malaria parasites were done by two algorithms of microscopy and rapid diagnostic tests. Standard tile and tube methods were used for direct and reverse blood grouping techniques with washed and unwashed red cells while time taken for agglutination reactions to take place was recorded as a score of avidity of the antibodies used on the red cell antigens. We recorded a significantly reduced reaction times in malaria parasitized red cells compared with non-parasitized controls in both blood groups A and B (P<0.05, respectively). Also, there were statistically reduced reaction times in unwashed cells compared with washed cells in both test and control erythrocytes (P<0.05, respectively). The reaction times using sera from subjects and controls on standard cells during reverse grouping were equally affected. We hereby conclude that, irrespective of density of parasitemia, reaction times of α and β antigens with their corresponding antibodies are reduced significantly. This could lead to errors in serological interpretations with malaria infected red cells especially during emergency cross match and with less avid sera. The continuous use of washed red cells for serological procedures is equally re-emphasized.

Speaker
Biography:

Nova Thomas John has completed her MBBS degree from Kasturba Medical College, Manipal University, Karnataka, India and Internal Medicine Residency from University of Illinois Urbana-Champaign, Illinois, USA. She is currently practicing as a Hospitalist Medicine Physician with Starling Physicians Group at Hartford Hospital, Connecticut, USA since August 2015.

Abstract:

Catastrophic antiphospholipid syndrome (CAPS) is a systemic autoimmune disease which occurs in <1% of patients with Antiphospholipid syndrome (APS). It is the most severe variant of the classic APS, characterized by histopathologic and clinical evidence of widespread small vessel microthrombi. The resulting inflammatory cytokine storm causes multi-organ failure over a short period and laboratory confirmation of high antiphospholipid antibody titers. Sarcoidosis is a systemic inflammatory disorder characterized by granulomatous inflammation of various organs. Although the association of APS and sarcoidosis may be explained by shared immune dysregulation, cases with concurrent sarcoidosis and APS are extremely rare. Here, we present the 12th reported case, presenting with digital gangrene and review the literature on CAPS. A 66 year-old gentleman presented with rapidly progressive ischemic changes of extremities with skin ulcerations and gangrene of peripheral digits. Autoantibodies testing revealed elevated levels of anti-beta2 glycoprotein IgM and anti-cardiolipin IgM antibodies. Skin ulceration biopsy showed vasculitis with intravascular microthrombi deposition. First-line treatment was initiated for “Probable CAPS” with anticoagulation, glucocorticoids and therapeutic plasma exchange. Subsequent, bone marrow biopsy workup for acute leucopenia with lymphopenia, revealed non-necrotizing granuloma, suggestive of sarcoidosis. This was further substantiated with high serum Angiotensin converting enzyme level. CAPS is a challenging systemic disease requiring a high index of clinical awareness, as outcomes are poor without prompt recognition and early initiation of targeted multimodal therapy. This case highlights the need for a collaborative team approach. It is also the first case reported of probable CAPS associated with sarcoidosis of bone marrow.

James Granfortuna

University of North Carolina Medical Center at Chapel Hill, USA

Title: Integrating new treatment options into the management of adult ITP

Time : 15:30-16:00

Speaker
Biography:

James Granfortuna MD FACP graduated from Mount Sinai School of Medicine in 1980 and completed a Hematology Oncology Fellowship at the State University of NY. Health Sciences Center in Syracuse NY in 1987. He is board certified in both specialties. He is currently an Associate Professor of Clinical Medicine at the Cone Health Internal Medicine Teaching Program in Greensboro, NC.

Abstract:

Treatment of Steroid resistant ITP in adults can be challenging in patients who are actively bleeding. The majority of novel therapies that have been developed in the last few years including anti CD 20 monoclonal antibody therapy (Rituximab) and thrombopoietic growth factors, romiplostim and eltombopag, take time to work. Combinations of active agents may accelerate the response rate. Splenectomy and the use of immunosuppressive agents may still have an important role in the acute management. A case of resistant ITP will be discussed in the context of currently available treatment modalities.

Biography:

Erhabor Osaro is a Professor of Hematology, Blood Transfusion Medicine and Laboratory Total Quality Management. He has received his PhD in Immuno-Hematology from the Rivers State University of Science and Technology in Port Harcourt, Nigeria. He is also an Alumni of University of Greenwich in the United Kingdom and Francis Tuttle College of Technology in Oklahoma, USA. Currently, he is a Professor in Usmanu Danfodiyo University, Sokoto, Nigeria, where he teaches best practices in hematology, blood transfusion science and laboratory total quality management. He has more than 200 published articles in both local and international journals, 5 scientific books and 5 chapters of scientific books. He is on the Editorial Board of several reputable local and international journals and Editor-in-Chief of the renowned Sokoto Journal of Medical Laboratory Science. He is an expert reviewer to several international scientific journals. He has recently bagged the Specialist Certificate in Blood Transfusion Science Practice (SCTSP) from the British Blood Transfusion Society in the United Kingdom. He is a recipient of several awards and honors including the Margaret Kenwright Award from the British Blood Transfusion Society (BBTS). He is the President of Board of Directors of Nelon Medical Limited, UK.

Abstract:

Protein energy malnutrition is the most widespread nutritional deficiency disorder of mankind and continues to be a major public health burden in developing countries. The aim of this case-control study was to determine the changes in some hematological parameters, ascorbic acid and pantothenic acid levels among children with Protein Energy Malnutrition (PEM) in Sokoto, North Western Nigeria. The study included a total of 90 children (47 subjects with PEM and 43 apparently healthy controls) aged 6 months to 5 years, admitted to the Pediatric Unit of Usmanu Danfodiyo University Teaching Hospital and Specialist Hospital, Sokoto. Some hematological parameters (packed cell volume, total white blood cell count and platelet count) were analyzed using the auto-hematology analyzer (Genesis, HA6000). Ascorbic acid levels were assayed by a standard chemical method. Nutritional status was determined using the Welcome Trust Classification. Data were analyzed using SPSS 22.0 statistical package. A p-value ≤0.05 was considered significant in all statistical comparisons. The result indicated that subjects with protein energy malnutrition had a lower mean packed cell volume (25.50±6.83%) compared to controls (32.73±6.85 %) (p=0.0001). The mean total white cell count was significantly higher among subjects with protein energy malnutrition (12.16±4.94×109/l) compared to controls (7.59±3.20×109/l) (p=0.0001). There were no statistically significant differences in the mean value of platelet counts of subjects (260.40±148.8×109/l) and controls (1237.61±99.20×109/l) (p=0.400). The mean value of ascorbic acid was significantly lower among subjects (0.82±0.27 mg/dl) compared to controls (1.06±0.15 mg/dl) (p=0.0001). Children with Kwashiorkor had higher value of packed cell volume compared to those with marasmic-kwashiorkor (p=0.0001). Children with marasmic-kwashiorkor had a higher total white cell count when compared with other types of protein energy malnutrition (p= 0.0001). Underweight subjects had lower ascorbic acid levels when compared with other types of protein energy malnutrition (p=0.0001). Platelet count and pantothenic acid levels showed no significant difference within the various types of protein energy malnutrition (p=0.331 and 0.391, respectively). This study has shown that children with protein energy malnutrition have lower packed cell volume and ascorbic acid levels compared to controls. The total white cell count was higher among children with protein energy malnutrition compared to controls. Protein energy malnutrition was more prevalent among children from low socioeconomic class whose mothers have no formal education. Marasmus was the most common type of protein energy malnutrition. Children with kwashiorkor have a higher packed cell volume compared to other types of protein energy malnutrition. Total white blood cell count of children with marasmic-kwashiorkor was significantly higher compared with other types. Immune boosters (vitamins and other micronutrient) should be provided for school children particularly children with protein energy malnutrition. There is need for infant feeding practice to be strengthened by promoting exclusive breast feeding. There is need for increased enrollment of women in schools, enlightenment on nutritional education and empowerment so as to improve their socioeconomic status.

Rosemary Omomo Ekpeh

University of Benin, Nigeria

Title: Altered leucocyte functions in HIV infected subjects

Time : 16:45-17:15

Biography:

Rosemary Omomo Ekpeh is a graduate of Medical Laboratory Science with a bias in Hematology and Blood Transfusion Science. She is currently pursuing MSc in Hematology at the University of Benin, Nigeria. She works as a Medical Scientist with the APIN/PEPFAR Laboratory of Edo State Health Management Board.

Abstract:

Polymorphonuclear neutrophils play an important role in host defense and they have the ability to recognize and phagocytose bacteria and other microorganisms. Previous studies have shown that, leucocyte functions are impaired in human immunodeficiency virus infection. This study was undertaken to investigate changes of phagocytic function and oxidative burst activity occurring in HIV infected subjects. A total of 191 patients were recruited for this study, comprising 58 HIV negative individuals (control), 72 HIV infected subjects that are not on antiretroviral therapy and 61 HIV infected subjects on antiretroviral therapy. Trypan blue was used to determine viability test, Nitroblue Tetrazolium test was used to measure the oxidative burst, and phagocytosis was assessed by incubating leucocyte suspension with Escherichia coli and measuring the ability of leucocytes to ingest bacteria. The CD4 cell count and CD8 cell count was analyzed using BD FACSCount auto analyzer. Our results showed significantly decreased phagocytic function and oxidative burst activity (p<0.05, respectively) in the HIV group both on ART and not on ART (untreated group) as compared with the controls group. Similarly, a significant (p<0.05, respectively) decrease in leucocytes viability was observed in both HIV groups compared with controls. Furthermore, leucocyte viability of HIV infected subjects who were not on ART were significantly reduced (P<0.05) when compared with HIV infected subjects on ART. This finding may suggest that leucocytes from HIV infected individuals have impaired ability to phagocytose and undergo oxidative burst activity, however may contribute to the increased risk of bacterial infections in HIV-infected subjects. It was observed that oxidative activity and phagocytic function was inversely correlated to the change in CD4 count value, that is, the greater the CD4 value the better the oxidative activity and phagocytic function. It is recommended that further studies on mechanisms of failure of phagocytosis and oxidative burst potentials of HIV infected subjects.

Biography:

Augustine Okwesili has completed his MSc from the Usmanu Danfodiyo University Sokoto, Nigeria. He is a Lecturer in the Department of Hematology in the same university and has published more than 27 papers in different journals of medicine both internationally and locally.

Abstract:

Background & Aim: Malaria is a global public health problem affecting people particularly in tropical and sub-tropic regions of the world. Immune mediated hemolysis is thought to occur in malaria infection. The aim of this study was to investigate the incidence of direct antiglobulin positivity among 100 patients with P. falciparum malaria in Sokoto, North Western, Nigeria.

Method: Evidence of immune mediated hemolysis with characteristic positive direct Coombs test was investigated among a cohort of 100 Plasmodium falciparum parasitized subjects aged 6 to 45 years and mean age 26.9±8.25 years, made of 56 males (56%) and 44 females (44%) resident in Sokoto, North Western, Nigeria.

Result: Amongst the 100 subjects with uncomplicated malaria infection, 3 (3%) had a positive Direct Antiglobulin Test (DAT). The incidence of positive DAT was concentrated among subjects in the 6-15 years age groups (p=0.001). There are no gender-related differences in the incidence of positive DAT among the subjects.

Conclusion: These findings indicate that a positive DAT is common in Plasmodium falciparum parasitized Nigerians. Malaria-related positive DAT may be responsible for the anemia seen in patients with malaria. There is the need for the routine monitoring of malaria parasitized subjects, particularly those with anemia in the area.