DOCSLIB.ORG

A Study of the Neonatal Haematology of Children with Down Syndrome

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
A Study of the Neonatal Haematology of Children with Down Syndrome A study of the neonatal haematology of children with Down syndrome Rebecca James submitted in accordance with the requirements for the degree of Doctor of Philosophy Department of Health Sciences University of York, March 2011 Abstract This thesis describes the establishment and initial findings of the Children with Down Syndrome Study, a birth cohort of children with DS. The Children with Down Syndrome Study was set up in order to characterise the haematology of neonates with Down syndrome and specifically to test the hypothesis that that this differed in this population. The study was carried out with the support of the Down Syndrome Association and the Down Syndrome Medical Interest Group, and through consultation with clinicians and families. Following a pilot study in the Yorkshire region it was established in over 60 hospitals across the north of England. The Children with Down Syndrome Study is the largest birth cohort of children with Down syndrome established to date, and this is the largest reported analysis of the haematology of neonates with Down syndrome. The results confirm that neonates with Down syndrome have a distinct haematological profile. Means and ranges for haematological parameters throughout the neonatal period are provided. The effects of gestational age, birth weight, postnatal age and the venepuncture to processing interval on the neonatal full blood count were examined, and this is the first report of factors that influence the haematological parameters in neonates with Down syndrome. In order to analyse the blood cell morphology a new approach to morphology was developed and validated. Morphological review of samples from neonates with Down syndrome demonstrated that blasts were common. Comparison with automated findings showed that manual review of a film is indicated to look for evidence of transient myeloproliferative disorder. This is also the largest longitudinal study of haematological parameters of children with Down syndrome beyond the neonatal period. The results showed that parameters changed between birth and 1 year, with most being stable thereafter. However, it appears that children with Down syndrome continue to have a distinct morphological profile. 1 Contents Abstract ................................................................................................................................. 1 Contents ................................................................................................................................ 2 List of Figures ........................................................................................................................ 7 List of Tables ......................................................................................................................... 9 Acknowledgements .............................................................................................................. 11 Author’s declaration ............................................................................................................. 12 Chapter 1 Introduction ..................................................................................................... 13 1.1 Purpose ................................................................................................................. 13 1.2 Aims ...................................................................................................................... 14 Chapter 2 Critical assessment of the literature ................................................................ 15 2.1 Introduction ............................................................................................................ 15 2.2 The haematology of neonates with Down syndrome .............................................. 16 2.2.1 Benign haematological changes ..................................................................... 16 2.2.2 Malignant haematological disorders ................................................................ 23 2.2.3 Blood cell morphology .................................................................................... 27 2.3 Existing and historical cohort studies ..................................................................... 28 2.3.1 Summary ........................................................................................................ 28 2.4 Haematological reference ranges for neonates...................................................... 29 2.4.1 Introduction ..................................................................................................... 29 2.4.2 Measurement of haematological parameters .................................................. 30 2.5 Red blood cell parameters in neonates .................................................................. 32 2.5.1 Development of reference ranges for red blood cell parameters ..................... 32 2.5.2 Factors affecting the red blood cell indices ..................................................... 33 2.6 White blood cell parameters in neonates ............................................................... 41 2.6.1 Development of reference ranges ................................................................... 41 2.6.2 Factors affecting white blood cell indices ........................................................ 45 2.6.3 Specific considerations: eosinophils, monocytes, basophils and lymphocytes 49 2.7 Platelet parameters in neonates ............................................................................ 52 2.7.1 Factors affecting neonatal platelet indices ...................................................... 54 2.8 Blood cell morphology in neonates ........................................................................ 58 2.9 Summary ............................................................................................................... 60 Chapter 3 Children with Down Syndrome Study: methods .............................................. 61 3.1 Introduction ............................................................................................................ 61 3.2 Consultation phase ................................................................................................ 62 3.2.1 Consultations with professional stakeholders ................................................. 62 3.2.2 Consultation with clinicians ............................................................................. 62 3.2.3 Consultation with families ............................................................................... 64 3.3 Key points emerging from consultations ................................................................ 65 3.3.1 Consultation with stakeholders ....................................................................... 65 3.3.2 Consultation with clinicians ............................................................................. 66 3.3.3 Consultation with families ............................................................................... 70 3.3.4 Summary of changes to study design following consultation........................... 71 3.4 Study design .......................................................................................................... 72 3.4.1 Study type ...................................................................................................... 72 2 3.4.2 Pilot phase ...................................................................................................... 72 3.4.3 Ethical permission .......................................................................................... 72 3.4.4 UKCRN Portfolio status .................................................................................. 72 3.5 Study setting .......................................................................................................... 72 3.6 Participants ............................................................................................................ 74 3.6.1 Identification of participants: newborn stage ................................................... 74 3.6.2 Action taken after initial recruitment ................................................................ 76 3.6.3 Identification of participants: follow up ............................................................ 77 3.7 Sample collection .................................................................................................. 78 3.8 Data collection ....................................................................................................... 78 3.8.1 Hospital referral form ...................................................................................... 78 3.8.2 Initial questionnaire ......................................................................................... 79 3.8.3 Abstraction from medical records ................................................................... 79 3.9 Sample management ............................................................................................. 80 3.9.1 Processing of neonatal blood samples ........................................................... 80 3.9.2 Processing of follow up blood samples ........................................................... 80 3.10 Data management .............................................................................................. 80 3.10.1 Data management .......................................................................................... 80 3.10.2 Data entry ......................................................................................................
Load more

Recommended publications
  • Hemolytic Disease of the Newborn
    Intensive Care Nursery House Staff Manual Hemolytic Disease of the Newborn INTRODUCTION and DEFINITION: Hemolytic Disease of the Newborn (HDN), also known as erythroblastosis fetalis, isoimmunization, or blood group incompatibility, occurs when fetal red blood cells (RBCs), which possess an antigen that the mother lacks, cross the placenta into the maternal circulation, where they stimulate antibody production. The antibodies return to the fetal circulation and result in RBC destruction. DIFFERENTIAL DIAGNOSIS of hemolytic anemia in a newborn infant: -Isoimmunization -RBC enzyme disorders (e.g., G6PD, pyruvate kinase deficiency) -Hemoglobin synthesis disorders (e.g., alpha-thalassemias) -RBC membrane abnormalities (e.g., hereditary spherocytosis, elliptocytosis) -Hemangiomas (Kasabach Merritt syndrome) -Acquired conditions, such as sepsis, infections with TORCH or Parvovirus B19 (anemia due to RBC aplasia) and hemolysis secondary to drugs. ISOIMMUNIZATION A. Rh disease (Rh = Rhesus factor) (1) Genetics: Rh positive (+) denotes presence of D antigen. The number of antigenic sites on RBCs varies with genotype. Prevalence of genotype varies with the population. Rh negative (d/d) individuals comprise 15% of Caucasians, 5.5% of African Americans, and <1% of Asians. A sensitized Rh negative mother produces anti-Rh IgG antibodies that cross the placenta. Risk factors for antibody production include 2nd (or later) pregnancies*, maternal toxemia, paternal zygosity (D/D rather than D/d), feto-maternal compatibility in ABO system and antigen load. (2) Clinical presentation of HDN varies from mild jaundice and anemia to hydrops fetalis (with ascites, pleural and pericardial effusions). Because the placenta clears bilirubin, the chief risk to the fetus is anemia. Extramedullary hematopoiesis (due to anemia) results in hepatosplenomegaly.
    [Show full text]
  • Section 8: Hematology CHAPTER 47: ANEMIA
    Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited.
    [Show full text]
  • Clinical Pathology Interpretation Barbara Horney
    CLINICAL PATHOLOGY PATHOLOGIE CLINIQUE Clinical pathology interpretation Barbara Horney History, physical examination, and Table 1. Hematologic findings from a lethargic, laboratory findings 4-year-old schipperke 4-year-old, spayed female, schipperke was pre- Blood cell count Reference range A sented because of mild lethargy. Pale mucous mem- White blood cells branes were observed on physical examination. Table 1 (WBC) gives the results of the hematological examination of Total 6.0 X 109/L 6.0-17.1 X 109/L blood at Differential samples taken this time. No significant abnor- segmented 65% 3.85 X 109/L 3.6-11.5 X 109/L malities were identified on the serum biochemical neutrophils profile. eosinophils 2% 0.12 X 109/L 0.01-1.25 X 109/L lymphocytes 27% 1.59 X 109/L 1.0-4.8 X 109/L Interpretation and discussion monocytes 6% 0.35 X 109/L 0.15-1.35 X 109/L Red blood cells The hematology results can be summarized as severe, Total 1.2 X 1012/L 5.5-8.5 X 109/L microcytic, normochromic, nonregenerative anemia nucleated 1/100 WBC <1-2 per 100 WBC associated with marked spherocytosis. spherocytes 4+ microcytosis 2+ The presence of spherocytes is often associated with immune-mediated hemolytic disease [1,2], although Platelets estimated normal hereditary membrane defects [3] and zinc toxicosis [4] in number can also result in spherocyte formation. A direct antibody Reticulocytes 0 X 109/L up to 120 X 109/L test (Coomb's test) was weakly positive. This finding can Hemoglobin 22 g/L 120-180 g/L support the tentative diagnosis of anemia of immune- Hematocrit 0.068 L/L 0.37-0.55 L/L mediated etiology, although this test is subject to both Mean corpuscular false positive and false negative results [2,5].
    [Show full text]
  • Correlation of Red Blood Cell Distribution Width (RDW) and Haemoglobin A1C (Hba1c) Levels in Diabetic Individuals
    ISSN(Online) : 2319-8753 ISSN (Print) : 2347-6710 International Journal of Innovative Research in Science, Engineering and Technology (An ISO 3297: 2007 Certified Organization) Website: www.ijirset.com Vol. 6, Issue 5, May 2017 Correlation of Red Blood Cell Distribution Width (RDW) and Haemoglobin A1C (HbA1C) Levels in Diabetic Individuals Ahmed Hasan Salimon, Dr.Harshal Anil Patil M. Sc Students, Department of Chemistry (Bio-Chemistry), Fergusson College Pune, Savitribai Phule Pune University, Pune, India Associate Consultant, Laboratory Ruby Hall Clinic, Pune, India ABSTRACT: Diabetes Mellitus (DM) is a metabolic disease characterized with persistent hyperglycemia due to , inappropriate glucose use or insufficient insulin production of pancreas. There is a defect in insulin effect, secretion or both. Due to sedentary life style and obesity, incidence of type 2 diabetes mellitus is increasing. Oral hypoglycaemic drugs or insulin therapy along with diet control and exercise helps the diabetic individual to keep proper glycemic control. Glycemic control is must in DM. Glycemic control is the main target of treatment in protection against organ damage and other complications of DM. Glycatedhemoglobin (HbA1C) follow-up is made in order to measure the efficiency of the treatment in DM and observe the glycemic control. HbA1C is formed as the result of non-enzymatic reaction of glucose to hemoglobin. It provides information on the average blood glucose levels of past 8-12 weeks in DM treatment. HbA1C is the golden standard in glycemic control of patients. Hyperglycemia tend to have effect on RBC survival and glycation of haemoglobin Red blood cell distribution width (RDW) is the symbol of red blood cell volume distribution width coefficient of variation.
    [Show full text]
  • Complete Blood Count in Primary Care
    Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document.
    [Show full text]
  • Red Blood Cell Morphology in Patients with Β-Thalassemia Minor
    J Lab Med 2017; 41(1): 49–52 Short Communication Carolin Körber, Albert Wölfler, Manfred Neubauer and Christoph Robier* Red blood cell morphology in patients with β-thalassemia minor DOI 10.1515/labmed-2016-0052 Keywords: β-thalassemia minor; erythrocytes; red blood Received July 11, 2016; accepted October 20, 2016; previously published cells; red blood cell morphology. online December 10, 2016 Abstract In β-thalassemias, the examination of a peripheral blood (PB) smear may provide relevant clues to initial diagnosis. Background: A systematic analysis of the occurrence of Complete laboratory investigation consists of the determina- red blood cell (RBC) abnormalities in β-thalassemia minor tion of the complete blood count, assessment of red blood has not been performed to date. This study aimed to iden- cell (RBC) morphology, high performance liquid chroma- tify and quantify the frequency of RBC abnormalities in tography (HPLC), hemoglobin electrophoresis and, where patients with β-thalassemia minor. necessary, DNA analysis [1]. Especially in the clinically Methods: We examined blood smears of 33 patients with severe forms referred to as β-thalassemia major and interme- β-thalassemia minor by light microscopy for the occur- dia, RBC abnormalities are often markedly apparent [2]. In rence of 15 defined RBC abnormalities. In the case of posi- β-thalassemia minor, also called β-thalassemia trait, the car- tivity, the abnormal cells/20 high power fields (HPF) at riers are usually clinically asymptomatic, showing persistent 1000-fold magnification were counted. microcytosis and hypochromia or mild microcytic anemia [1, Results: Anisocytosis, poikilocytosis and target cells 3]. The PB smear may show microcytosis, hypochromia and, (median 42/20 HPF) were observed in all, and ovalocytes infrequently, poikilocytosis [2].
    [Show full text]
  • Hematological Issues in Critical Care
    HEMATOLOGICAL ISSUES IN ACUTE CARE: PART A- RBC DISORDERS Dheeraj Reddy, MD Objectives- Part A To understand how various blood cell types are produced from pluripotent hematopoietic stem cells and how hematopoiesis is regulated To appreciate the importance of a thorough history and physical exam in the diagnostic approach to hematologic abnormalities Basic interpretation of peripheral blood smear Approach to RBC disorders Anemia Polycythemia Hematopoesis Production of all types of blood cells including formation, development, and differentiation of all types of blood cells. 11 12 10 –10 new blood cells are produced daily in our body to maintain steady state levels in the peripheral circulation All types of new blood cells are derived from “pluripotent stem cells” 1 Sites of Hematopoesis in pre- and postnatal periods MUCH SIMPLER! 2 Key Elements in History Weight loss Fever, night sweats (B symptoms) Fatigue, malaise, and lassitude Weakness Drugs and Chemicals Exposure Family History Sexual History Lumps and Bumps Bone Pain Skin rash/pruritus Surgical History Key Elements in Physical Exam LYMPH NODES 3 Splenomegaly Increased function Abnormal blood flow Infiltration (Congestion) Immune hyperplasia - Liver Cirrhosis Malignant - Response to infection (viral, - hepatic vein obstruction - Leukemias (acute, chronic, bacterial, fungal, parasitic) - portal vein obstruction lymphoid, and myeloid) - Disordered immunoregulation - Budd-Chiari syndrome - Lymphomas (Hodgkins and (RA, SLE, autoimmune hemolytic (associated with classical
    [Show full text]
  • Vitamin D Insufficiency Is a Frequent Finding in Pediatric and Adult
    al Dis ion ord rit e t rs u N & f T o h l e a r n a Winters et al., J Nutr Disorders Ther 2014, 4:2 r p u y o Journal of Nutritional Disorders & Therapy J DOI: 10.4172/2161-0509.1000140 ISSN: 2161-0509 Research Article Open Access Vitamin D Insufficiency is a Frequent Finding in Pediatric and Adult Patients with Sickle Cell Disease and Correlates with Markers of Cell Turnover Winters AC1, Kethman W2, Kruse-Jarres R3 and Kanter J4* 1Cincinnati Children's Hospital, Burnet Ave, Cincinnati, OH 45229, USA 2Stanford University, Serra Mall, Stanford, CA 94305, USA 3Tulane University, St Charles Ave, New Orleans, LA 70118, USA 4Medical University of South Carolina, Charleston, SC, USA *Corresponding author: Julie Kanter, Director, Sickle Cell Disease Research, MUSC, 135 Rutledge Avenue, MSC 558, Charleston, SC, 29425, USA, Tel: (843) 876-8483; E-mail: [email protected] Rec Date: April 14, 2014, Acc Date: Jun 16, 2014, Pub Date: Jun 18, 2014 Copyright: © 2014 Winters AC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Vitamin D insufficiency affects 33%-78% of children and 60-100% of adults with sickle cell disease (SCD). There are no previous reports demonstrating a correlation between vitamin D insufficiency and cell turnover in patients with SCD. We hypothesized that vitamin D insufficiency was prevalent in our SCD population (ages 0-60 years) and would correlate with reticulocyte counts in these patients.
    [Show full text]
  • Blood Count Free Download
    BLOOD COUNT FREE DOWNLOAD Robert Goddard | 464 pages | 16 Apr 2012 | Transworld Publishers Ltd | 9780552161305 | English | London, United Kingdom Understanding Blood Counts Red cell distribution width RDW is a measurement of the variation in the size of your red blood cells. White Blood Cells White blood cells, also called leukocytes, are cells that exist in the blood, the lymphatic systemand tissues and are an important part of the body's natural defense immune system. Manual platelet counts are performed in a similar manner, although some methods leave the red blood cells intact. The device was Blood Count designed for counting red blood cells, but with later modifications it proved effective for counting white blood cells. See the child's lab report for reference ranges. Accordion Title. Infection Inflammation Severe physical or emotional stress such as fever, injury or surgery Blood Count Kidney failure Lupus Rheumatoid arthritis Malnutrition, thyroid problems Certain medicines. Automated methods for measuring hemoglobin were developed in the s, and Maxwell Wintrobe introduced the Wintrobe hematocrit method inwhich in turn allowed him to define the red blood cell indices. Some therapies, such as chemotherapycan affect bone marrow production of cells. Louis: Mosby Elsevier;Pp Bleeding Blood Count. Assuming that the characteristics of the patient population remain roughly the same over time, the average should remain constant; large shifts in the average value can indicate instrument problems. What are thrombocythemia and thrombocytosis? The cell images are displayed to a human operator, who can Blood Count re-classify the cells if necessary. An abnormally low hemoglobin, hematocrit, or red blood cell count indicates anemia.
    [Show full text]
  • Hematological and Immune Changes in Piaractus Mesopotamicus in the Sepsis Induced by Aeromonas Hydrophila T
    Fish and Shellfish Immunology 88 (2019) 259–265 Contents lists available at ScienceDirect Fish and Shellfish Immunology journal homepage: www.elsevier.com/locate/fsi Full length article Hematological and immune changes in Piaractus mesopotamicus in the sepsis induced by Aeromonas hydrophila T Gustavo S. Claudianoa,b,Jefferson Yunis-Aguinagac, Fausto A. Marinho-Netoa, Renata L. Mirandad, Isabela M. Martinsa, Fabrizia S. Otanib, Antonio V. Mundimd, ∗ Cleni M. Marzocchi-Machadoe, Julieta R.E. Moraesa,c, , Flávio Ruas de Moraesa,1 a Department of Veterinarian Pathology, Faculty of Agrarian and Veterinarian Sciences, São Paulo State University, Unesp, Brazil b Institute of Biodiversity and Forests, Federal University of Western Pará, UFOPA, Pará, Brazil c Aquaculture Center of UNESP, Jaboticabal, São Paulo, Brazil d Clinical Analysis Laboratory, Veterinary Hospital, Federal University of Uberlândia (UFU), Uberlândia, MG, Brazil e Department of Clinical, Toxicological and Bromatological Analyses, Ribeirão Preto School of Pharmaceutical Sciences, University of São Paulo (USP), Brazil ARTICLE INFO ABSTRACT Keywords: The pathogenesis of sepsis involves complex systems and multiple interrelationships between the host and pa- Leukocytes thogen producing high mortality rates in various animal species. In this study, hematological disturbances, Innate immunity innate immunity and survival during the septic process in Piaractus mesopotamicus inoculated with Aeromonas Blood hydrophila were studied. For this aim, fish blood samples were taken from control and infected groups 1, 3, 6, Pacu and 9 h post-inoculation (HPI). Leukogram showed reduction in the number of leukocytes and thrombocytes, Bacteria followed by cessation of leukocyte chemotaxis 6 HPI and severe morphological changes in leukocytes and er- ythrocytes. At 3 HPI production of reactive oxygen species increased and at 6 HPI decreased.
    [Show full text]
  • Chapter Preview
    A TEXT BOOK OF PHYSIOLOGY Dr. Pratiti Ghosh, FABMS Ex-Visiting Fellow, National Institutes of Health, USA. Associate Professor & Head Department of Physiology West Bengal State University Kolkata. MUMBAI NEW DELHI NAGPUR BENGALURU HYDERABAD CHENNAI PUNE LUCKNOW AHMEDABAD ERNAKULAM BHUBANESWAR INDORE KOLKATA GUWAHATI © Author No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording and/or otherwise without the prior written permission of the publisher. First Edition : 2015 Published by : Mrs. Meena Pandey for Himalaya Publishing House Pvt. Ltd., “Ramdoot”, Dr. Bhalerao Marg, Girgaon, Mumbai - 400 004. Phone: 022-23860170/23863863, Fax: 022-23877178 E-mail: [email protected]; Website: www.himpub.com Branch Offices : New Delhi : “Pooja Apartments”, 4-B, Murari Lal Street, Ansari Road, Darya Ganj, New Delhi - 110 002. Phone: 011-23270392, 23278631; Fax: 011-23256286 Nagpur : Kundanlal Chandak Industrial Estate, Ghat Road, Nagpur - 440 018. Phone: 0712-2738731, 3296733; Telefax: 0712-2721216 Bengaluru : No. 16/1 (Old 12/1), 1st Floor, Next to Hotel Highlands, Madhava Nagar, Race Course Road, Bengaluru - 560 001. Phone: 080-22286611, 22385461, 4113 8821, 22281541 Hyderabad : No. 3-4-184, Lingampally, Besides Raghavendra Swamy Matham, Kachiguda, Hyderabad - 500 027. Phone: 040-27560041, 27550139 Chennai : New-20, Old-59, Thirumalai Pillai Road, T. Nagar, Chennai - 600 017. Mobile: 9380460419 Pune : First Floor, "Laksha" Apartment, No. 527, Mehunpura, Shaniwarpeth (Near Prabhat Theatre), Pune - 411 030. Phone: 020-24496323/24496333; Mobile: 09370579333 Lucknow : House No 731, Shekhupura Colony, Near B.D. Convent School, Aliganj, Lucknow - 226 022. Phone: 0522-4012353; Mobile: 09307501549 Ahmedabad : 114, “SHAIL”, 1st Floor, Opp.
    [Show full text]
  • Bone Marrow Morphology Is a Strong Discriminator Between Chronic Eosinophilic Leukemia, Not Otherwise Specified and Reactive
    ARTICLE Myeloproliferative DIsorders Bone marrow morphology is a strong Ferrata Storti EUROPEAN discriminator between chronic eosinophilic HEMATOLOGY Foundation ASSOCIATION leukemia, not otherwise specified and reactive idiopathic hypereosinophilic syndrome Sa A. Wang,1 Robert P. Hasserjian,2 Wayne Tam,3 Albert G. Tsai,4 Haematologica 2017 Julia T. Geyer,3 Tracy I. George,5 Kathryn Foucar,5 Heesun J. Rogers,6 Volume 102(8):1352-1360 Eric D. Hsi,6 Bryan A. Rea,7 Adam Bagg,7 Carlos E. Bueso-Ramos,1 Daniel A. Arber,8 Srdan Verstovsek9 and Attilio Orazi3 1Department of Hematopathology, M.D. Anderson Cancer Center, Houston, TX; 2Department of Pathology, Massachusetts General Hospital, Boston, MA; 3Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY; 4Department of Pathology, Stanford University, CA; 5Department of Pathology, University of New Mexico, Albuquerque, NM; 6Department of Laboratory Medicine, Cleveland Clinic, OH; 7Department of Pathology and Laboratory Medicine, the University of Pennsylvania, Philadelphia, PA; 8Department of Pathology and Laboratory Medicine, University of Chicago, IL and 9Department of Leukemia, M.D. Anderson Cancer Center, Houston, TX, USA ABSTRACT hronic eosinophilic leukemia, not otherwise specified can be dif- ficult to distinguish from idiopathic hypereosinophilic syndrome Caccording to the current World Health Organization guideline. To examine whether the morphological features of bone marrow might aid in the differential diagnosis of these two entities, we studied a total of 139 patients with a diagnosis of chronic eosinophilic leukemia, not oth- Correspondence: erwise specified (n=17) or idiopathic hypereosinophilic syndrome [email protected] (n=122). As a group, abnormal bone marrow morphological features, resembling myelodysplastic syndromes, myeloproliferative neoplasm or myelodysplastic/myeloproliferative neoplasm, were identified in 40/139 Received: January 25, 2017.
    [Show full text]