Rbcs) in Both the Sinus and Cord, Histiocytes Werc Swollen by a Granu}Ar Substance in the Cytoplasm and Also Many Secondary Lysosomes

Total Page:16

File Type:pdf, Size:1020Kb

Rbcs) in Both the Sinus and Cord, Histiocytes Werc Swollen by a Granu}Ar Substance in the Cytoplasm and Also Many Secondary Lysosomes The UOEHAssociationUOEH Association ofofHealth Health Sciences JUOEH20(1)!11-19 (1998) 11 [Original) Pathological Study Splenomegaly Associated with Cadmium-inducedof Anemia in Rats Tetsuo HAMADA', Akihide TANIMOT02, Nobuyuki ARIMA!, Yoshihiro IDEL, Takakazu SASAGURI2, Shohei SHIMiVIRI2, Yoshitaka MURATA', Ke-Yong WANG2 and Yasuyuki SASAGURIL' 'Dopartment of'Surgical Pathotogy, University llosPital ?Dopartment qf Palhology and Cell Biotogy, Scheol of' Adlrdicine, (1itib'ersity of Occapational and Environmental Health., .lapan. }'dhatanishi-ku, Kiialp,ztshu 807-8imr, .1apan Ahstract : Splenomegaly was observcd both in male and R)malc Spraguc-Dawley rats after 1 week of exposure to CdC12 (O,6 mg (:d/kg/day), Sp]een weight reached about double that in controls by 8 weeks of Cd exposure. Histopathologica] cxamination of the enlargcd spleen rcvcaled that iron- and lipid-laden histiocytes were clustered in tha periarterial lymphatic sheath, and the red pulp appeared to be expanded. It is noteworthy that electron microscopy rcvealed markcd poikilocytosis and Hcinz body formation in red blood cells (RBCs) in both the sinus and cord, Histiocytes werc swollen by a granu}ar substance in the cytoplasm and also many secondary lysosomes. Thesc morphological findings indicatc that degradation of damagcd RBCs induced by exposure to Cd might bc promoted in the splccn and possibly cause splenomcgaly, This RBC damage-hcmolysis-splcnomegaly sequence is also considered to be associated with the etioiogy of Cd-induced anemia, In addition to the abnormal RBC degradation, nuclel of ]ymphocytes in thc Cd-cxposcd spleen exhibited high elcctron density, consistent with a preapoptotic statc suggesting the immunosupprcssive effhct ofCd. Kay woralf :spienomegaly, poiki]ocytosis, Heinz body, cadmiurn, anemia, (Received 18 November 1997, accepted I9January 1998) Introduction Cd was reported to cause anemia in dogs as early as 1896 [1], and subsequently, anemia was found in humans after Cd exposure [2]. A later study indicated that anemia appearcd to be onc of the carliest signs of Cd poisoning in higher vertebrates [3]. The main characteristic of Cd-induced ancmia is the presence of microcytic, hypochromic red blood cells (RBCs), possibly resulting from iron deficicncy [4] . However, other investigators havc NII-Electronic Library Service The UOEHAssociationUOEH Association ofofHealth Health Sciences 12 THApt・IADA et al suggested that hemolysis or bone marrow suppression may be the cause of the anemia [5, 6] ; thus, the pathogenesis of Cd-induccd anemia is still a subject of debate. NVe noticcd that in rats given subcutancous (sc) irijections ofCd, splenomegaly developed during thc early stages of administration in association with anemia onsct. Aithough exposure to Cd has been reportcd to induce splenomegaly in mice [7, 8] and rats [9, 10], to our knowlcdgc there have bcen no reports describing the histopathological as well as ultrastructural features ofsplenomegaly in relation to Cd-induced anemia. In this study, we focused on patholc)gic changes in the spleen of rats with subchronic Cd intoxication and assessed the significance ol' splenomegaly in relation to thc ctiology of Cd-induced ancmia. Materials and Methods Animats Ninety-six Sprague-Dawlcy rats (Kyudo,Japan), IO or 1 1 weeks ofage, were given a conventional tbod Oapan CLEA, CE2) and tap water ad libitum. Rats in the exposure group were administered O.6 mg Cd/kg/day as CdC12 solution rlihc (about 1/100 LD50) subcutaneously lbr 5 days a week fbr up to 8 wecks, same volume ofphysiological saline was injected into control rats, Body weights of the rats were measured ()nce a week. HistqPathotogical examination Six rats including 4 in the exposure group and 2 in the control group were sacrificed every week from 1 to 8 weeks during the experimental period under general anesthesia by inhalation of cthyl ether, and the spleens were removed immcdiately. The rcsected spleens were weighed, photographed, hemisected sagittally across the splenic hilus, and fixed in 15% fbrmalin solution, Then, paraflin sections (3 ptm thick) were stained with hematoxylin and eosin (H&E), Berlin blue, Turnbull blue and periodic acid-Shiff (PAS). Oii red O staining was using frozen sections of tissue after immersion pcrfbrmcd 5 ,um formalin-fixed in gum-sucrose solution overnight, Electron microscopic examination Small tissuc blocks cut from the resected spleen, about 1 × 1 × 1 mm in sizc, were fixed with cacodylate-buffered (O.l M, pH 7.4-) glutaraldehyde solution (2.5%) for 2 h and postfixecl with cacodylate-buflered osmium tetroxide (1.0%) for 1 h. After embedding in Epon 812 (TAAB, I.ondon, UK), ultrathin sections wcre cut, stained with uranyl acetate and lcad citratc, and examined using an electron microscope (1200CX, JEOL, Tokyo, Japan), NII-Electronic Library Service The UOEHAssociationUOEH Association ofofHealthSciences Health Sciences Splenomegaly Induccd by Cadmiurn 13 Results Animals There was no s{gnificant difference in body weight change between Cd- exposed and control rats during the administration period (not shown). Splenomegaly developed and was significant (P<O,Ol) at 1 week both in males and in females aftcr Cd administration (Fig, 1). Transient and high increase of spleen weight occurred only in female rats exposed to Cd in l w. Macroscopic examination The spleens excised from these rats exposed to Cd fbr more than 1 week were enlarged with an incrcased consistency and rough surface. The capsules ofthese "sugar-icing" splcens were distended, and showed a appearance (Fig. 2), Histopathological examination H&E sections of the enlarged spleen exposed to Ccl revealed an expansion of the red pulp and clustered histiocytes with brown granules in their cytoplasm in the periarterial lymphatic sheath (Fig. 3nl). These brown granules showcd positive staining with Berlin blue, indicating iron deposition in the cytoplasm (Fig. 3-2). Oil red O staining also demonstrated lipid deposits corresponding to the Berlin blue-positive granules (data not shown). 2.2 o---N;ngBcoo)・.--N-oec 2.0 1.8 1.4 1.0 O 2 4 6 8 Administration period(VVeeks) Fig. 1. Relative spleen to body w'eight (SW/BW) ratio of' cadmium exposed rats, Relative SivVIBI'V ratio meaiis (cadniium exposed spleenlbody'wcight)f<control spleen/ bod>, weight). Increase ofSNNFIBN-i ratio is signiticant in 1 w in ma]e (open circ]e) and in fernalc Copcn square) rats af'ter exposure. Splenemegal>, is remarkable as twicc that of control spleen in 8 w Cd expnsure. NII-Electronic Library Service The UOEHAssociationUOEH Association ofofHealthSclences Health Sciences 14 T H"ADA et a( Fig 2llepresentahNe rriac rosLopic dcatures ot control dnd Ccl cxposcd spleens The spLeen exposed Lo O 6 mg CdClplKg {sL) foi 8" showcd marked cnlargerncnt, thc capgulc havmg a rough surfacc and suqar icing appearance (× 2O, Bar = 1O crn) es Fig 3 Histopatholoqical changes in Cd cxpesecl splecn rhere aie gome ciustcred histiocNtes (arroM) scattercd in thc pemartctial lymphatic sheath in caclmium exposed spleLn (1, H&h hectien) l"hLsc hisnoqtes arc posiuve foi iron staming == = {2, Beilin blue stdining) CBdr 1 100,rim, Bar 2 5UIim) NII-Electronic Library Service The UOEHAssociationUOEH Association ofofHealth Health Sciences SpLcnomegaly Induced b}, Cadmiutn I5 Electron mieroscopic examination Ultrastructural examination of the enlarged spleen revealed the diffuse presence of RBCs with a defbrmed and irregular contour in the splcnic tissue, particularly in thc dilated cords, Some of the dcformcd RBCs were fbund to be reticulocytes, recognizable by their small number of organelles (Fig. 4-1), These damaged RBCs contained granular or angular inclusions with high electron density in both the cord and sinus. The electron-densc inclusions were compatible with Heinz bodies [11, 12] . Some electron-dcnse globules in thc histiocytes were fbund to be consistent with phagocytosed RBC fragmcnts (Fig. 4-2), Thcre were many secondary lysosomes and membranous or g'ranular substances in the cytoplasm ofswollen histiocytes. A noteworthy feature was the presence o{' glycogenosomes engulfing a largc amount of glycogcn in the autophagic vacuolcs [13] . I.ymphocytes showed mild morphoEogical alterations, fbr example, a split fbrmation between the inner and outer nuclear membranes, and higher nuclear electron density in comparison with control specimens (Fig. 4m3). wwww ` ee , ,/X,ma ,/ ,,ee.k bu.,x Fig. 4. Poikilocytosis in caclmium-exposcd gplccn. (l) Elcctron micrograph demonstrates that /Kacanthocyte tear drop or bizarrc RBCs are in sinii$ or clilated cords of as(A), Cl') CB) present Ladmium-exposecl spleen (Bar = 5 ,am). Hcinz bodics in ad-exposed splecn. (2) Granular to anbuular Heinz bedies (arrow) arc noticcd in RBCs in cadmium-exposed splcen. Somc HcinL bodics arc attachcd to RBC mcmbrane and c)thers are floatlng in RBC cytoplasm Onseit). (Bar = 5,ttm) Ultrastructural alterdtions in the histiocytes and 1>・rriphocyLes in Cd-exposed splecn. (3) In Cd-cxposcd splccn, a large gl>,cogenosemc (G), various heLeiophasFosomes and incmbranous substances are found m the histiocytes, High eLectron density in nucleoso]ne and == cli]atat{on of nuc/lcar rnembrane (ariow) are noted m the Iyrnphocytcs (Bar 2ptmm). Discussion Therc havc reports of studics dcscri the splenomegaly inbccnducedseveral by Cd. Earlyexperimentalstudies showed that Cdbinghad an NII-Electronic Library Service The UOEHAssociationUOEH Association ofofHealth Health Sciences 'l' 16 I'EAMADA et at immunosuppressive efi'ect on mice and induccd splcnome.ffaly
Recommended publications
  • Erythrocytes: Overview, Morphology, Quantity by AH Rebar Et
    In: A Guide to Hematology in Dogs and Cats, Rebar A.H., MacWilliams P.S., Feldman B.F., Metzger F.L., Pollock R.V.H. and Roche J. (Eds.). Publisher: Teton NewMedia, Jackson WY (www.veterinarywire.com). Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org), 8-Feb-2005; A3304.0205 Erythrocytes: Overview, Morphology, Quantity A.H. Rebar1, P.S. MacWilliams2, B.F. Feldman 3, F.L. Metzger 4, R.V.H. Pollock 5 and J. Roche 6 1Dept of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, IN,USA. 2Dept of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, WI, USA. 3Dept of Biomedical Sciences & Pathobiology, VA-MD - Regional College of Veterinary Medicine, Virginia Tech, VA, USA. 4Metzger Animal Hospital,State College,PA, USA. 5Fort Hill Company, Montchanin, DE, USA. 6 Hematology Systems, IDEXX Laboratories, Westbrook, ME, USA. Overview Production Red blood cells (RBC) are produced in the bone marrow. Numbers of circulating RBCs are affected by changes in plasma volume, rate of RBC destruction or loss, splenic contraction, erythropoietin (EPO) secretion, and the rate of bone marrow production. A normal PCV is maintained by an endocrine loop that involves generation and release of erythropoietin (EPO) from the kidney in response to renal hypoxia. Erythropoietin stimulates platelet production as well as red cell production. However, erythropoietin does not stimulate white blood cell (WBC) production. Erythropoiesis and RBC numbers are also affected by hormones from the adrenal cortex, thyroid, ovary, testis, and anterior pituitary. Destruction Red cells have a finite circulating lifespan. In dogs, the average normal red cell circulates approximately 100 days.
    [Show full text]
  • Congenital Heinz-Body Haemolytic Anaemia Due to Haemoglobin Hammersmith
    Postgrad Med J: first published as 10.1136/pgmj.45.527.629 on 1 September 1969. Downloaded from Case reports 629 TABLE 1 After transfusion Before transfusion 24 hr 72 hr 6 days Haemoglobin (g) ND 7-5 7-6 7-6 PCV 20 29 23 29 Plasma free Hb (mg/100 ml) 241 141 5 6 Bleeding time 14 6 4 1 Clotting time No clot 8 5-5 2 Haemolysins 3±+ - - Serum bilirubin (mg/100 ml) 4-0 4-8 1-3 0-6 Urine volume/24 hr (ml) 970 1750 1500 1300 Haemoglobinuria 4+ 1 + - - Urobilin 2+ 3+ 3 + 1+ Blood urea (mg/100 ml) 30 148 75 32 Serum Na (mEq/l) 128 132 136 140 Serum K (mEq/l) 3-8 4-2 4-6 4-6 Serum HCO3 (mEq/l) 21-2 27-6 28-4 30 0 SGOT Frankel Units ND 110 84 36 SGPT Frankel Units 94 96 68 Acknowledgment Reference We are greatly indebted to Dr P. E. Gunawardena, REID, H.A. (1968) Snake bite in the tropics. Brit. med. J. 3, Superintendent of the National Blood Transfusion Service 359. for his help in this case. Protected by copyright. Congenital Heinz-body haemolytic anaemia due to Haemoglobin Hammersmith N. K. SHINTON D. C. THURSBY-PELHAM M.D., M.R.C.P., M.C.Path. M.D., M.R.C.P., D.C.H. H. PARRY WILLIAMS M.R.C.S., F.R.C.P. Coventry and Warwickshire Hospital and City General Hospital, Stoke-on-Trent http://pmj.bmj.com/ THE ASSOCIATION of haemolytic anaemia with red shown by Zinkham & Lenhard (1959) to be associ- cell inclusion bodies was well recognized at the end ated with an hereditary deficiency of the red cell ofthe Nineteenth Century in workers exposed to coal enzyme glucose-6-phosphate dehydrogenase.
    [Show full text]
  • TOPIC 5 Lab – B: Diagnostic Tools & Therapies – Blood & Lymphatic
    TOPIC 5 Lab – B: Diagnostic Tools & Therapies – Blood & Lymphatic Disorders Refer to chapter 17 and selected online sources. Refer to the front cover of Gould & Dyer for normal blood test values. Complete and internet search for videos from reliable sources on blood donations and blood tests. Topic 5 Lab - A: Blood and Lymphatic Disorders You’ll need to refer to an anatomy & physiology textbook or lab manual to complete many of these objectives. Blood Lab Materials Prepared slides of normal blood Prepared slides of specific blood pathologies Models of formed elements Plaque models of formed elements Blood typing model kits Blood Lab Objectives – by the end of this lab, students should be able to: 1. Describe the physical characteristics of blood. 2. Differentiate between the plasma and serum. 3. Identify the formed elements on prepared slides, diagrams and models and state their main functions. You may wish to draw what you see in the space provided. Formed Element Description / Function Drawing Erythrocyte Neutrophil s e t y c Eosinophils o l u n a r Basophils Leukocytes G e Monocytes t y c o l u n Lymphocytes a r g A Thrombocytes 4. Define differential white blood cell count. State the major function and expected range (percentage) of each type of white blood cell in normal blood. WBC Type Function Expected % Neutrophils Eosinophils Basophils Monocytes Lymphocytes 5. Calculation of the differential count? 6. Define and use in proper context: 1. achlorhydria 5. amyloidosis 2. acute leukemia 6. anemia 3. agnogenic myeloid metaplasia 7. autosplenectomy 4. aleukemic leukemia 8. basophilic stippling 9.
    [Show full text]
  • A New Familial Disorder with Abnormal Ervthrocvte Morphology and Increased Permeability of the Erythrocytes to Sodium and Potassium
    Pediat. Res. 5:159-166 (1971) cation permeability ion transport cell lysis osmosis erythrocyte potassium g1ucose sodium hemolysis A New Familial Disorder with Abnormal Ervthrocvte Morphology and Increased Permeability of the Erythrocytes to Sodium and Potassium GEORGE R. HONIG1351, PERPETUA s. LACSON, AND HELEN s. MAURER The Department of Pediatrics, The Abraham Lincoln School of Medicine, University of Illinois, Chicago, Illinois, and The Departments of Pediatrics and of Laboratories, University of the East, Ramon Magsaysay Memorial Medical Center, Quezon City, Philippines Extract A newborn infant of Philippine parents was found to have a morphological abnor- mality of his erythrocytes consisting of an elliptical shape of the cells and one or more transverse slitlike areas of decreased density. These changes were also present in eryth- rocytes of the patient's father, a half-sister of the father, and four of the patient's six siblings. None of the affected family members had anemia or evidence of abnormal hemolysis, and erythrocyte survival by the radiochromium method was normal in three of the individuals studied. Erythrocytes from the affected family members had an increased degree of autohemolysis after incubation for 48 hr, but this was pre- vented almost entirely by addition of glucose. Glucose consumption in vitro by erythro- cytes of the propositus occurred at a rate approximately 60% greater than that of normal controls. The intracellular sodium concentration of the erythrocytes was not different from that of erythrocytes from normal individuals, but a moderate decrease in intracellular potassium was found. When washed cells were incubated in a glucose- free medium, sodium gain and potassium loss were significantly greater than from cells of normal controls.
    [Show full text]
  • Morphologic Evaluation of Anemia – I Adewoyin S
    nd M y a ed g ic lo i o n i e B Adewoyin and Ogbenna, Biol Med (Aligarh) 2016, 8:6 DOI: 10.4172/0974-8369.1000322 ISSN: 0974-8369 Biology and Medicine Review Article Open Access Morphologic Evaluation of Anemia – I Adewoyin S. Ademola1* and Ogbenna A. Abiola2 1Department of Haematology and Blood Transfusion, University of Benin Teaching Hospital, PMB 1111, Ugbowo, Benin City, Nigeria 2Department of Haematology and Blood Transfusion, Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria *Corresponding author: Adewoyin S. Ademola, Department of Haematology and Blood Transfusion, University of Benin Teaching Hospital, PMB 1111, Ugbowo, Benin City, Nigeria, Tel: +2347033966347; E-mail: [email protected] Received date: June 20, 2016; Accepted date: July 15, 2016; Published date: July 22, 2016 Copyright: © 2016 Adewoyin AS, 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 Anaemia is a feature of many tropical diseases. Anaemia diagnosis therefore remains a crucial intervention among physicians in developing countries. A barrage of laboratory test (anaemic work-up) is usually deployed in differentiating its underlying cause. However, central to anaemia evaluation is the morphology of the red cells and other cell lines. Conventionally, initial laboratory tests include full blood count, reticulocyte count and peripheral blood film (PBF). PBF is often a clinical request, performed by skilled technologist and reported by haematologist/ haematomorphologist. Findings from PBF are reviewed and reported in the light of patient’s clinical history and examination findings.
    [Show full text]
  • E-Learn LAB — RCD 1708
    e-Learn LAB — Hemoglobinopathy Based on IQMH Centre for Proficiency Testing Survey RCD-1708-WB Confidence. Elevated. © Institute for Quality Management in Healthcare 1 Disclaimer and Copyright Disclaimer This document contains content developed by IQMH. IQMH’s work is guided by the current best available evidence at the time of publication. The application and use of this document is the responsibility of the user, and IQMH assumes no liability resulting from any such application or use. This document may be reproduced without permission for non-commercial purposes only and provided that appropriate credit is given to IQMH. Copyright The reader is cautioned not to take any single item, or part thereof, of this document out of context. Information presented in this document is the sole property and copyright of the Institute for Quality Management in Healthcare (IQMH). The logos and/or symbols used are the property of IQMH or other third parties. © Institute for Quality Management in Healthcare. All rights reserved. Confidence. Elevated. © Institute for Quality Management in Healthcare 2 Focus of this Presentation • This is a case study of a hemoglobinopathy investigation to familiarize participants with the laboratory features of the unstable hemoglobins, as well as the pathophysiology of common red cell inclusions. • You will be presented with clinical information, images, and laboratory results and will be prompted with self- learning questions. Confidence. Elevated. © Institute for Quality Management in Healthcare 3 Credits Case and discussion provided by members of the 2017 IQMH Hematology Scientific Committee, and the IQMH Consultant Technologist. Confidence. Elevated. © Institute for Quality Management in Healthcare 4 Clinical Information A 14-year-old female is being assessed for gall stones.
    [Show full text]
  • Hemoglobin Abraham Lincoln, Β32 (B14) Leucine → Proline an UNSTABLE VARIANT PRODUCING SEVERE HEMOLYTIC DISEASE
    Hemoglobin Abraham Lincoln, β32 (B14) Leucine → Proline AN UNSTABLE VARIANT PRODUCING SEVERE HEMOLYTIC DISEASE George R. Honig, … , David J. Gnarra, Helen S. Maurer J Clin Invest. 1973;52(7):1746-1755. https://doi.org/10.1172/JCI107356. Research Article An unstable hemoglobin variant was identified in a Negro woman with hemolytic anemia since infancy. A splenectomy had been performed when the patient was a child. The anemia was accompanied by erythrocyte inclusion bodies and excretion of darkly pigmented urine. Neither parent of the proposita demonstrated any hematologic abnormality, and it appeared that this hemoglobin variant arose as a new mutation. Erythrocyte survival in the patient was greatly reduced: the erythrocyte t½ using radiochromium as a tag was 2.4 days, and a reticulocyte survival study performed after labeling the cells with L-[14C]leucine indicated a t½ of 7.2 days. When stroma-free hemolysates were heated at 50°C, 16-20% of the hemoglobin precipitated. The thermolability was prevented by the addition of hemin, carbon monoxide, or dithionite, suggesting an abnormality of heme binding. An increased rate of methemoglobin formation was also observed after incubation of erythrocytes at 37°C. The abnormal hemoglobin could not be separated from hemoglobin A by electrophoresis or chromatography, but it was possible to isolate the variant β-chain by precipitation with p- hydroxymercuribenzoate. Purification of the β-chain by column chromatography followed by peptide mapping and amino acid analysis demonstrated a substitution of proline for β32 leucine. It appears likely that a major effect of this substitution is a disruption of the normal orientation of the adjacent leucine residue at β31 to impair […] Find the latest version: https://jci.me/107356/pdf Hemoglobin Abraham Lincoln, i32 (B14) Leucine Proline AN UNSTABLE VARIANT PRODUCING SEVERE HEMOLYTIC DISEASE GEORGE R.
    [Show full text]
  • Pathology Heme/Onc Outline
    Pathology Heme/Onc Outline Anemia General Considerations for Anemia, regardless of causation. ‐ Is defined as a decreased oxygen carrying capacity for any reason. ‐ To diagnose, a panel will show you o CBC = Hemoglobin/Hematocrit Hemoglobin is a little higher in males (~45, instead of ~35) rd Reticulocytes are blue on Hematocrit is about 1/3 of hemoglobin H&E peripheral smear 5:15:45 = Millions of RBCs: mg/dL Hgb: %Hgb = 5x3=15, 15x3=45, normal males A hematocrit less than 13 is anemia o MCV = mean cell volume Tells you what the volume of RBCs are; are they large or are they small? This allows categorization into microcyctic (small), macrocytic (large), and normocytic (normal sized) anemia, useful for you to keep them straight o Reticulocyte = Can the marrow respond to anemia? Reticulocytes are immature cells that contain nuclear content (RNA) Bone marrow revs up the production of RBCs and kicks out premature cells into circulation to accommodate the decreased oxygen carrying supply Is the blood loss begin accounted for by the bone marrow? ‐ 3 categories of anemia o Blood isn’t made = nutritional deficiencies o Blood is destroyed = hemolysis o Blood is lost = bleeding, trauma, menstruation ‐ Erythropoietin o Hormone released by the kidneys that induces proliferation of myeloblasts to RBCs o Increased erythropoietin = increased RBCs = oxygen carrying capacity. + ‐ Differentiation o If you turn yellow, get dark urine, and your bone marrow is fine, but your CBC is screwy, you likely have a hemolytic anemia o If you are pale, poor pallor, with small RBCs without a lot of color, you probably have a genetic abnormality or Iron deificiency: either Iron Deficiency, Alpha‐Thal, or Beta‐Thal o If your cells are huge, or there are 5+ lobes on a neutrophil, you have a megaloblastic anemia usually a result of folate or B12 deficiency o If there is no accommodation by the bone marrow, or there is an inappropriate overexpression of any one cell type, you probably have a myeloproliferative disorder resulting in anemia.
    [Show full text]
  • Leek Diet May Cause Hemolytic Anemia: a Case Report in a Cat
    LEEK DIET MAY CAUSE HEMOLYTIC ANEMIA: A CASE REPORT IN A CAT. F. Granat, A. Geffré, N. Bourgès Abella, C. Trumel. Laboratoire Central de Biologie Médicale, Institut National Polytechnique-Ecole Nationale Vétérinaire de Toulouse (INP-ENVT), France. Signalement A 7 year-old neutered female domestic shorthair cat. Clinical History The cat was presented because of the ingestion of a bone. No abnormalities were noted at clinical examination, and an abdominal radiography showed the presence of a bone in the stomach. A medical treatment composed of a leek-based high fiber diet and steroidal anti-inflammatory drugs was decided to try naturally eliminating the bone. At the following presentation, eight days later, no abnormality in the behavior of the cat was reported by the owners. Clinical findings At the second clinical presentation, the cat was bright, alert and did not present abdominal pain. The only significant clinical findings were pale mucous membranes and a slight hepatomegaly was suspected. Diagnostic procedures Abdominal radiography and ultrasound suggested that the bone had been eliminated. However, a diffuse hepatopathy was suspected. A complete blood cell count, blood film, biochemical and urine analyses were also performed. Results are in tables 1, 2 and 3. Hematology results obtained with the analyzer Sysmex XT-2000iV® showed a macrocytic normochromic and highly regenerative anemia, and a moderate leukocytosis due to a neutrophilia according to a manual differential count (no differential count was given by the analyzer).A discrepancy between the platelet count obtained by impedance (PLT-I = 105.109/L) and optical technology (PLT-O = 285.109/L) was observed.
    [Show full text]
  • Direct Antiglobulin (“Coombs”) Test-Negative Autoimmune Hemolytic Anemia: a Review
    YBCMD-01786; No. of pages: 9; 4C: Blood Cells, Molecules and Diseases xxx (2013) xxx–xxx Contents lists available at ScienceDirect Blood Cells, Molecules and Diseases journal homepage: www.elsevier.com/locate/bcmd Direct antiglobulin (“Coombs”) test-negative autoimmune hemolytic anemia: A review George B. Segel a,b, Marshall A. Lichtman b,⁎ a Department of Pediatrics, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642-0001, USA b Department of Medicine, 601 Elmwood Avenue, Rochester, NY 14642-0001, USA article info abstract Article history: We have reviewed the literature to identify and characterize reports of warm-antibody type, autoimmune hemo- Submitted 5 December 2013 lytic anemia in which the standard direct antiglobulin reaction was negative but a confirmatory test indicated Available online xxxx that the red cells were opsonized with antibody. Three principal reasons account for the absence of a positive direct antiglobulin test in these cases: a) IgG sensitization below the threshold of detection by the commercial (Communicated by M. Lichtman, M.D., antiglobulin reagent, b) low affinity IgG, removed by preparatory washes not conducted at 4 °C or at low ionic 5December2013) strength, and c) red cell sensitization by IgA alone, or rarely (monomeric) IgM alone, but not accompanied by fi Keywords: complement xation, and thus not detectable by a commercial antiglobulin reagent that contains anti-IgG and Autoimmune hemolytic anemia anti-C3. In cases in which the phenotype is compatible with warm-antibody type,
    [Show full text]
  • A Laboratory Guide to Clinical Hematology
    A Laboratory Guide to Clinical Hematology A Laboratory Guide to Clinical Hematology A Laboratory Guide to Clinical Hematology VALENTIN VILLATORO AND MICHELLE TO EDMONTON A Laboratory Guide to Clinical Hematology by Michelle To is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted. Please be aware that the content for the entirety of this eBook is subject to a creative common license: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) You are free to: Share — copy and redistribute the material in any medium or format Adapt — remix, transform, and build upon the material The licensor cannot revoke these freedoms as long as you follow the license terms. Under the following terms: Attribution — You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use. NonCommercial — You may not use the material for commercial purposes. No additional restrictions — You may not apply legal terms or technological measures that legally restrict others from doing anything the license permits. Contents Authors & Editors ................................................................................................................................... xii Creative Commons License and Citation ............................................................................................... xiii Contact Information and Feedback ........................................................................................................
    [Show full text]
  • Dyspnea After Treatment of Recurrent Urinary Tract Infection
    THE CLINICAL PICTURE KRISHNA B. GHIMIRE, MD BARSHA NEPAL, MBBS Assistant Professor, Des Moines Mason City, IA University, College of Osteopathic Medicine, Mercy Medical Center–North Iowa, Mason City The Clinical Picture Dyspnea after treatment of recurrent urinary tract infection phenazopyridine for dysuria, and she noticed that her urine was dark-colored. She was of northern European descent. She was un- aware of any family history of blood-related disorders. She had been admitted to the hospital 6 weeks earlier for symptomatic anemia after taking nitrofurantoin for a urinary tract infection. At that time, she received 2 units of packed red blood cells and then was discharged. Follow-up blood work done 2 weeks later—including a glucose-6 phosphate dehydrogenase (G6PD) assay— was normal. On physical examination, she was pale and weak. Her hemoglobin level was 5.5 g/dL (reference range 14.0–17.5), with normal white blood cell and plate- let counts and an elevated reticulocyte count. A com- FIGURE 1. A peripheral blood smear in our patient prehensive metabolic panel showed elevated indirect shows several “bite cells” with one or two bites (ar- bilirubin and lactate dehydrogenase levels. A direct rows). These are indicators of a Heinz body hemo- Coombs test for autoimmune hemolytic anemia was lytic anemia and suggest the possibility of glucose-6 negative, as was a haptoglobin assay to look for intra- phosphate dehydrogenase deficiency or an unstable vascular hemolytic anemia. G6PD levels were normal, hemoglobin. Heinz bodies, visible only after su- yet a peripheral blood smear (FIGURE 1) showed features pravital staining (and not in this smear with con- of G6PD deficiency.
    [Show full text]