Chronic Myeloid Leukemia
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Digitalcommons@UNMC Agranulocytosis
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Agranulocytosis Gordon A. Gunn University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Gunn, Gordon A., "Agranulocytosis" (1935). MD Theses. 386. https://digitalcommons.unmc.edu/mdtheses/386 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. AGRANULOOYTOSIS ,- Senior Thesis by GOrdon .M.. Gunn INTRODUCTION Fifteen years ago the medioal profession new nothing of the disease spoken of in this paper as agranulocytosis. Since Schultz, in 1922, gave an accurate description of a fulminat ing case, agranulocytosis has oomettoClOCo.'UPy more and more prominence in the medical field. Today, the literature is fairly teeming with accounts of isolated cases of all descriptions. Added to this a confus ing nomenclature, varied classifications, and heterogeneous forms of treatment; and the large question of whether it is a disease entity, a group of diseases, or only a symptom complex, and some idea may be garnered as to the progress made. Time is a most important factor in diagnosis of this disease, and the prognosis at best is grave. The treatment has gone through the maze of trials as that of any other new disease; there must be a cause and so there must be some specific treatment. -
Leukocyte Adhesion Deficiency-I
Clinical Communications Leukocyte adhesion deficiency-I: A this article’s Online Repository at www.jaci-inpractice.org for a comprehensive review of all published comprehensive listing of publications and patient numbers by cases country and Table E2 for a comprehensive listing of references). Elena Almarza Novoa, PhDa,b,*, Per investigator assessment, 113 patients were considered to have severe LAD-I, 63 moderate, and 147 not classified. Sanchali Kasbekar, PharmDc,*, d e Neutrophil CD18 expression was reported for 265 cases and was Adrian J. Thrasher, MD, PhD , Donald B. Kohn, MD , less than 2% in 135 patients (51%) and 2% or more in 130 Julian Sevilla, MD, PhDf, Tony Nguyen, MBAg, patients (49%). Four patients with CD18 greater than or equal Jonathan D. Schwartz, MDc,z, and to 2% were considered to have severe LAD-I (CD18% range, Juan A. Bueren, PhDa,b,z 2.4-17.3). Sex information was available for 282 patients, of which 148 (52%) were males. Clinical Implications Age at presentation was reported for 146 cases. For 63 patients with CD18 less than 2%, median presentation was at age 1 Leukocyte adhesion deficiency-I (LAD-I) is a rare, serious month (range, 0.03-18 months); for 62 patients with CD18 of disorder with severity determined by defective CD18 2% or more, median presentation was at age 6 months (range, expression. LAD-I is characterized by umbilical 0.03-192 months). HSCT was performed for 125 patients; 198 complications, granulocytosis, and diverse infections. patients did not undergo HSCT. Severe LAD-I is frequently fatal before the age of 2 years Infections were described for 248 (77%) of the 323 cases; fi without allogeneic transplant. -
• Cytosis: O Neutrophilia: Defined As an Increase in the Neutrophilic Count in the Peripheral Blood Above Reference Range for Age
HENATOLYMPHOID SYSTEM THIRD YEAR MEDICAL STUDENTS-UNIVERSITY OF JORDAN AHMAD T. MANSOUR, MD NONNEOPLASTIC DISEASES OF THE WHITE BLOOD CELLS • There are five major types of WBCs in the blood: neutrophils, lymphocytes, eosinophils, basophils and monocytes. • The normal function of the white blood cells depends on a tight regulation of their count and their function. Therefore, disease develops if there is a derangement of the cells count or function, it takes one of the following forms: o Cytosis: increase in the number of circulating cells above reference range. (Note: leukocytosis means an increase in the WBC count, neutrophilia means increase in the neutrophilic count, lymphocytosis means increase in the lymphocytic count, monocytosis means increase in the monocytic count, basophilia means increase in the basophilic count and eosinophilia means in crease in the eosinophilic count). o Cytopenia: decrease in the number of circulating cells below reference range. (Note: neutropenia means decreased neutrophils, lymphocytopenia, or simply lymphopenia, means decrease in lymphocytes, monocytopenia means decrease in monocytes, eosinopenia means decrease in eosinophils, and basopenia means decrease in basophils). o Abnormal or absent function • Cytosis: o Neutrophilia: defined as an increase in the neutrophilic count in the peripheral blood above reference range for age. o Causes: bacterial infection is the most common and most important etiology. Tissue necrosis in cases of burns or trauma and medications such as epinephrine and corticosteroids are also additional causes for neutrophilia. § Some physiologic conditions can lead to neutrophilia such as stress, smoking and pregnancy. o Pathophysiology: neutrophils are present in the blood in two populations: circulating and marginal (meaning neutrophils stuck to the vessel wall). -
Digitalcommons@UNMC Granulocytopenia
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1936 Granulocytopenia Howard E. Mitchell University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Mitchell, Howard E., "Granulocytopenia" (1936). MD Theses. 457. https://digitalcommons.unmc.edu/mdtheses/457 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. G PA~lULOCYTOPENI A SENIOR THESIS By Howard E. Mitchell April 17, 1936 TABLE OF CONT'ENTS Introduction Definition • · 1 History . • • • 1 Nomenclature • • • • • 4 ClassificBtion • • • • 6 Physiology • • • • .10 Etiology • • 22 Geographic Distribution • 23 Age, Sex, and R9ce • • ·• 23 Occupation • .. • • • • .. • 23 Ba.cteria • • • • .. 24 Glandu18.r Dysfunction • • • 27 Radiation • • • • 28 Allergy • • • 28 Chemotactic and Maturation Factors • • 28 Chemicals • • • • • 30 Pathology • • • • • 36 Symptoms • • • • • • • 43 DiEtgnosis • • • • • .. • • • • • .. • 4'7 Prognosis 48 '" • • • • • • • • • • • • Treatment • • • • • • • • 49 Non"'specific Therapy • • • • .. 50 Transfusion • • • • .. 51 X-Ray • • • • • • • • • 52 Liver ·Extract • • • • • • • 53 Nucleotides • • • • • • • • • • • 53 General Ca.re • • • • • • • • 57 Conclusion • • • • • • • • • 58 480805 INTHODUCTION Although t~ere is reference in literature of the Nineteenth Century to syndromes similating the disease (granulocytopenia) 9.8 W(~ know it todes, it "vas not un til the year 1922 that Schultz 8ctually described his C8se as a disease entity and by so doing, stimulated the interest of tne medical profession to further in vestigation. -
Integrins, Selectins and Cams
SAMJ ARTICLES I REVIEW ARTICLE recently we have found similarly impaired neutrophil endothelial cell interactions in patients with chronic liver I disease.' Other workers have shown low levels of essential Integrins, selectins and CAMs on p-cells in patients with Burkitt's lymphoma.' I Because adhesion between leucocytes is central to the CAMs - the 'glue of life' regulation of Iymphocyte proliferation, abnormal adhesiveness caused by dysfunctional CAMs is thought to I Steven Froese, Enid Shephard, Susan Adams, result in poor immune surveillance and an increased risk of Simon Robson, Ralph Kirsch cancer, Certain inflammatory processes are associated with I acquired leucocyte adhesion defects and impaired neutrophil adhesion to endothelium. Patients with sepsis, The ability of cells to adhere to one another and to adult respiratory distress syndrome and myocardial surrounding structural tissue proteins is essential to the life infarction are among those affected,6 process of all multicellular organisms. Specific receptors, their Iigands and their counter-receptors, collectively referred to in Time' as the 'glue of life', play a major role in maintaining organ and tissue integrity. Progress in molecular The nature and function of and cell biology has advanced knowledge of these cellular CAMs adhesion molecules (CAMs) to a point where they will soon be part of the everyday vocabulary of practising doctors. The search for the processes which mediate cell-cell CAMs, first recognised for their role in the organisation of recognition and interaction was based on the assumption developing embryological neural tissue, respond to neural, that, in order to establish and maintain specialised tissues endocrine and paracrine stimuli and in turn influence and organs, multicellular organisms must have a mechanism immune and inflammatory cell function, cell repair processes by which cells interact with each other and with constituents and the integrity of specialised organs and tissues. -
Neutropenia : an Analysis of the Risk Factors for Infection Steven Ira Rosenfeld Yale University
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1980 Neutropenia : an analysis of the risk factors for infection Steven Ira Rosenfeld Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Rosenfeld, Steven Ira, "Neutropenia : an analysis of the risk factors for infection" (1980). Yale Medicine Thesis Digital Library. 3087. http://elischolar.library.yale.edu/ymtdl/3087 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. NEUTROPENIA: AN ANALYSIS OF THE RISK FACTORS FOR INFECTION by Steven Ira Rosenfeld B.A. Johns Hopkins University 1976 A Thesis Submitted to The Yale University School of Medicine In Partial Fulfillment of the Requirements for the Degree of Doctor of Medicine 1980 Med Li^> Ya ABSTRACT The risk factors for infection were evaluated retrospectively in 107 neutropenic patients without underlying malignancy or cyto¬ toxic drug therapy. Neutrophil count was an independent risk factor for infection, with the incidence of infection increasing as the neutrophil count decreased. The critical neutrophil count, below which the incidence of infection was significantly increased was 250/mnr*, (p<.001). Eighty five percent of the <250 group entered with, or developed infection. Additional risk factors for infection included increased duration of neutropenia, age less than 1 year old, male sex, hypogammaglobulinemia, and recent antibiotic therapy. -
Lazy Leucocyte Syndrome-Disorder of the Granulocyte Membrane?
J Clin Pathol: first published as 10.1136/jcp.31.4.300 on 1 April 1978. Downloaded from Journal of Clinical Pathology, 1978, 31, 300-308 Lazy leucocyte syndrome-disorder of the granulocyte membrane? P. H. PINKERTON, JEAN B. ROBINSON, AND J. S. SENN From the Departments ofLaboratory Haematology and Medicine, Sunnybrook Medical Centre and Departments ofPathology and Medicine, University of Toronto, Toronto, Ontario, Canada SUMMARY An adult with long-standing neutropenia had the functional granulocyte abnormalities typical of the lazy leucocyte syndrome. Scanning electron microscopy of the patient's neutrophils showed alteration in the surface configuration of the cell with coarsening of the normal fine ruffles and the appearance of knob-like projections. Similar functional and anatomical changes were induced in normal neutrophils by treatment with vinblastine. The lazy leucocyte syndrome may be a consequence of altered membrane microfilamentous protein structure or function, and undue rigidity of the affected neutrophils may explain the clinicopathological features of the disease. Neutrophil microbicidal activity consists of a com- Rebuck and Crowley (1955), using a 12-mm diameter plex series of functions including migration, phago- round coverslip, replaced at two- or four-hourly cytosis of organisms, production of bactericidal intervals for a period of 20 hours, over an abraded substances and their release into the phagosome, and area on the volar aspect of the forearm. The cells digestion of the ingested material. A variety of adhering to the coverslips were stained with congenital and acquired disorders of these functions Romanowsky stain, examined by light microscopy, has been described (Baehner, 1974; Gallin and Wolff, and counted. -
A Case of Acute Eosinophilic Granulocytic Leukemia with PML
Leukemia (1997) 11, 609–618 1997 Stockton Press All rights reserved 0887-6924/97 $12.00 CORRESPONDENCE CASE REPORT A case of acute eosinophilic granulocytic leukemia with PML-RAR alpha fusion gene expression and response to all-trans retinoic acid R-Q Yu1, W Huang2, S-J Chen2, S-D Jiang1 and Z Chen2 1Division of Hematology, Department of Internal Medicine, Shanghai Chang-Zheng Hospital; and 2Laboratory of Molecular Biology, Shanghai Institute of Hematology, China A typical case of eosinophilic granulocytic leukemia with PML- RAR alpha fusion gene expression is reported. The patient achieved complete remission after oral administration of all- trans retinoic acid without any exposure to cytotoxic agents. The facts strongly suggest that the genetic event occurred at the level of pluripotent stem cells. Keywords: leukemia; eosinophilic; PML-RAR alpha; retinoic acid Introduction It has been well demonstrated that the presence of a fusion gene, PML-RAR alpha, resulting from the reciprocal translo- cation of human chromosome 15 and 17, t(15;17)(q22:q21) is a specific molecular marker of acute promyelocytic leuke- mia, and plays an important role in the pathogenesis of that disease.1–4 Until now PML-RAR alpha fusion gene has not been found in other malignant cells. Recently, we saw a typi- Figure 1 Bone marrow smear showing coarse refractile eosino- cal case of acute eosinophilic granulocytic leukemia with philic granules in leukemic cells. PML-RAR alpha fusion gene expression that achieved com- plete remission after differentiation therapy with all-trans larity with a G/E ratio of 14.1:1. The differential count showed retinoic acid (ATRA). -
Counts Homeostatic Regulation of Blood Neutrophil
Homeostatic Regulation of Blood Neutrophil Counts Sibylle von Vietinghoff and Klaus Ley Blood neutrophil counts are determined by the differenti- regulated sequential gene expression that leads to the formation ation and proliferation of precursor cells, the release of ma- of a granule with specific protein contents (9). Hematopoietic ture neutrophils from the bone marrow, margination, traf- cytokines promote neutrophil progenitor proliferation and dif- ficking and transmigration through the endothelial lining, ferentiation, acting in a complex network (10). The major cy- neutrophil apoptosis, and uptake by phagocytes. This brief tokine for neutrophil proliferation and survival is G-CSF. Mice review summarizes the regulation of blood neutrophil and humans deficient in either G-CSF or its receptor suffer counts, which is in part controlled by G-CSF, IL-17, and from profound neutropenia (11–13). G-CSF currently is the IL-23. Neutrophils are retained in the bone marrow major therapeutic agent for neutropenia of iatrogenic as well as through interaction of CXCL12 with its receptor CXCR4. genetic and various other origins (14–16). Extensive preclinical The relevance of this mechanism is illustrated by rare dis- and clinical data exist on the role of other granulopoietic cyto- eases in which disrupting the desensitization of CXCR4 re- kines such as M-CSF, GM-CSF, IL-6, IL-3, IL-17, and, most recently, IL-22 (11, 17–23), which have been reviewed else- sults in failure to release mature neutrophils from bone where in detail (24). Genetic modification of intracellular mes- marrow. Although blood neutrophil numbers in inbred sengers downstream of G-CSF (25) showed for example that mouse strains and individual human subjects are tightly both STAT3 and SOCS3 (suppressor of cytokine signaling 3) controlled, their large variation among outbred popula- deficiency resulted in neutrophilia and an increased pool of late tions suggests genetic factors. -
Blood and Immunity
Chapter Ten BLOOD AND IMMUNITY Chapter Contents 10 Pretest Clinical Aspects of Immunity Blood Chapter Review Immunity Case Studies Word Parts Pertaining to Blood and Immunity Crossword Puzzle Clinical Aspects of Blood Objectives After study of this chapter you should be able to: 1. Describe the composition of the blood plasma. 7. Identify and use roots pertaining to blood 2. Describe and give the functions of the three types of chemistry. blood cells. 8. List and describe the major disorders of the blood. 3. Label pictures of the blood cells. 9. List and describe the major disorders of the 4. Explain the basis of blood types. immune system. 5. Define immunity and list the possible sources of 10. Describe the major tests used to study blood. immunity. 11. Interpret abbreviations used in blood studies. 6. Identify and use roots and suffixes pertaining to the 12. Analyse several case studies involving the blood. blood and immunity. Pretest 1. The scientific name for red blood cells 5. Substances produced by immune cells that is . counteract microorganisms and other foreign 2. The scientific name for white blood cells materials are called . is . 6. A deficiency of hemoglobin results in the disorder 3. Platelets, or thrombocytes, are involved in called . 7. A neoplasm involving overgrowth of white blood 4. The white blood cells active in adaptive immunity cells is called . are the . 225 226 ♦ PART THREE / Body Systems Other 1% Proteins 8% Plasma 55% Water 91% Whole blood Leukocytes and platelets Formed 0.9% elements 45% Erythrocytes 10 99.1% Figure 10-1 Composition of whole blood. -
Late Effects of Therapy in Childhood Acute Lymphoblastic Leukemia Survivors REVIEW
REVIEW DOI: 10.4274/tjh.galenos.2018.2018.0150 Turk J Hematol 2019;36:1-11 Late Effects of Therapy in Childhood Acute Lymphoblastic Leukemia Survivors Çocukluk Çağı Akut Lenfoblastik Lösemi Tedavisi Sonrası Geç Yan Etkiler Hande Kızılocak1, Fatih Okcu2 1Istanbul University-Cerrahpaşa Faculty of Medicine, Department of Pediatric Hematology and Oncology, İstanbul, Turkey 2Texas Children’s Hematology and Oncology Centers, Baylor College of Medicine, Department of Pediatrics, Division of Hematology and Oncology, Houston, TX, USA Abstract Öz Over the last 50 years, the survival rates in children with acute Son 50 yıldaki gelişmeler ile akut lenfoblastik lösemili (ALL) lymphoblastic leukemia (ALL) have increased remarkably. The optimal çocuklardaki tedavi sonrası sağkalım oranında belirgin derecede artış use of antileukemic agents in cooperative group protocols, central saptandı. Antilösemik ilaçların akılcı kullanımı, santral sinir sistemini nervous system-directed treatment, improvements in supportive hedefleyen lokal tedaviler ve destek tedavisindeki gelişmeler ile 5 care, and recognition of biological, clinical, and treatment response yıllık olaysız sağkalım %85’e ve 5 yıllık genel sağkalım %90’a ulaştı. characteristics that predict patients with a higher or a lower risk of Uzamış sağkalım süreleri, tedavinin uzun dönem yan etkilerine olan treatment failure have improved 5-year event-free survival rates, farkındalığı da arttırdı. Geç dönem mortalite, ikincil maligniteler, reaching more than 85%, and 5-year overall survival rates, reaching -
Late Effects of Treatment
Late Effects of Treatment A Guide for Patients Introduction Your cancer treatment can cause side effects. Some of these will occur at the time of treatment and will normally stop when treatment ends. Some of these side effects may last for a long time after treatment; these are long- term effects. Some side effects do not occur for months or even years after treatment ends; these side effects are called late effects. These late effects can be physical or emotional. Not everyone gets late effects, the risk depends on the type of treatment, the dose of treatment and the patient’s age at the time of treatment. This booklet is designed to and peer reviewed by Dr Panos provide you with information Kottaridis, Royal Free Hospital. about the late effects you may The rewrite was put together by experience, what to expect and Lisa Lovelidge and reviewed by how they may be managed. If Dr Victoria Grandage. We are also you need specific advice or are grateful to our patient reviewers, concerned about a particular Simon Walker, John Watson and late effect, please contact your Steve Colbourne and the Brighton medical team or Clinical Nurse support group. The booklet has Specialist. since been updated by our Patient Information Writer, Isabelle Leach. This booklet has been compiled by Dr Victoria Grandage (UCLH) If you would like any information on the sources used for this booklet, please email [email protected] for a list of references. Version 3 Printed: 10/2020 2 www.leukaemiacare.org.uk Review date: 10/2022 In this booklet Introduction