Haematologic and Biochemical Changes in Bitches with Clinical and Subclinical Mastitis

Total Page:16

File Type:pdf, Size:1020Kb

Haematologic and Biochemical Changes in Bitches with Clinical and Subclinical Mastitis Haematologic and biochemical changes in bitches with clinical and subclinical mastitis 1* 1 1 1 Iosif VASIU , Orsolya SARPATAKI1 , Ioana BEDECEAN , Raul Alexandru POP , Florinel Gheorghe BRUDAŞCĂ 1 Faculty of Veterinary Medicine,[email protected] University of Agricultural Science and Veterinary Medicine Cluj- Napoca, 3-5 CaleaMănăştur, Cluj-Napoca, Romania * Corresponding author: Bulletin UASVM Veterinary Medicine 73(2)/2016 Print ISSN 1843-5270; Electronic ISSN 1843-5378 doi:10.15835/buasvmcn-vm:11995 Abstract Mastitis in bitch is in general superficially researched and evaluated. Data regarding blood tests Lactatioduring bitch sine graviditateglandular tissue inflammation is scarcely documented, therefore this paper aims to assess blood response in such cases. A total of 74 blood samples were obtained from lactating dams. These included females with , with or without overt signs of mammary gland illness and with or without other signs of disease. Routine complete blood count and serum total proteins were evaluated. Complete blood count and total serum protein levels showed great flexibility, thus making it very difficult to establish and describe a clear and common haematological and biochemical pathway during mastitis inflammatory response. Clincians shoulds not relay only on blood tests whenever dealing with such pathology. Complete blood count and total serum protein levels should only be usedKeywords as complementary: bitch, complete tests, alongsideblood count, other mastitis, assays such serum as milktotal microbiology protein or cytology. INTRODUCTION et al. important changes in total serum protein levels In curent veterinary practice, mammary (Ververidis , 2007). ( gland inflammationet al. diagnostic is based mainly on The aim of this research was antepartumto evaluate history, clinical and microbiological examination postpartumwhether completeLactatio blood count sine graviditateCBC) and serum (Trasch , 2008). There is scarce data regardinget al. total proteins in lactating bitches ( , blood changes during clinical or subclinical and ), with mastitis episodeset al. in this species (Hasegawa , or without overt signs of mastitis and other 1993). However, there is one experimental study concurrent signs of illness, follow the same (Ververidis , 2007). Where leukocytosis type of haematological or biochemical blood was observed immediately after mammary response.MATERIALS AND METHODS gland bacterial challenge. At 12 hours, shortly after inoculation, a drop in the leukocyte count was observed, then followed by an immediate In order to evaluate haematological and increase. On the sixt day, after challenge, biochemical changes during bitch mastitis cases, leukocytes were in normal range. Neutrophilia 100 lactating dams were included in a case- was also observedth shortly after challenge, but controlled study, but because of owners reluctance, after the 6 day, this parameter dropped in range we were only able to obtain 74 blood samples. as well. Severe thrombocytopenia was recorded Dams in this study were divided into two in the first hours afterth inoculation, followed by groups. Females with primary mastitis and an increase in the 4 day. However, there were no females with secondary mastitis. During consult, 249 Haematologic and biochemical changes in bitches with clinical and subclinical mastitis females with concurrent affections were included The CBC showed that Eosinopenia was present in the second category (i.e. secondary mastitis), in 21% (4/19, CI 95%: 6.05-45.57) of cases whilst whereas clinically healthy females or just with Eosinophilia was present in only 5% (1/19, CI 95%: clinical or subclinical mastitis, were included in 0.13-26.03) of the tested females. Monocytopenia the first category. with eosinophilia was encountered in 11% (2/19, Haematology and biochemstriy assays were CI 95%: 1.30-33.14) of the samples, followed by processed on venous blood after a thorough local Monocytosis with eosinophilia and by Lymphocytosis disinfection with betadine (Betadine 100 ml, Egis with eosinopenia in 5% (1/19, CI 95%: 0.13-26.03) Pharmaceuticals Ltd., Budapest, Hungary). After of the cases, each (Tab.1) (p>0.05). collection, blood samples were rushed as quickly In 16% (3/19, CI 95%: 3.38-39.58) of as possible to the laboratory at the University of samples, CBC encountered Neutrophilia with left Agricultural Science and Veterinary Medicine Cluj- shift along with eosinophilia, 11% (2/19, CI 95%: Napoca. 1.30-33.14) were with Neutrophilia with left shift Complete blood count was determined with along with monocytosis, showing chronic signs of Abacus Junior Vet analyzer (Diatron Messtechnik, disease (p>0.05). Budapest, Hungary) whilst differential blood Without correlation with clinical features, count was counted on blood film stained with 5% (1/19, CI 95%: 0.13-26.03) of the samples Dia-Quick Panoptic dye kit (Reag-Fix Panoptic, presented, Neutrophilia with a left shift with ReagensKft., Budapest Hungary). Biochemical eosinopenia, lymphocytosis and eosinopenia, results for total serum protein, were obtained with a lymphopenia, monocytopenia and eosinophilia Spectrophotometer analyzer UV-VIS Screen Master and also with Neutropenia with a right shift along Touch (Hospitex Diagnostix, Fiorentino, Italy). with monocytosis, lymphocytosis and eosinophilia, Complete blood count and serum proteinogram each (Tab.1) (p>0.05). changes prevalence andp its 95% confidence In 31% (5/16, CI 95%: 11.02-58.66) of tested intervals were assessed. The differences were samples Hyperproteinemia with hyperglo bulinemia considered significant if values were lower than was encountered, followed by 25% (4/16, CI 95%: 0.05. Data analysis was performed using EpiInfo 7 7.27-52.38) of dams with Hyperglobulinemia. In softwareRESULTS (CDC, ANDUSA). DISCUSSION 13% (2/16, CI 95%: 1.55-38.35) of cases presence of Hyperproteinemia with hyperalbuminemia and Hy per pro teinemia with hyperalbuminemia In bitches with primary mastitis, 40% and hyperglo bulinemia was noticed. In just 6% (4/10, CI 95%: 6.67-65.25) of cases were (1/16, CI 95%: 0.16-30.23) of cases Hyperalbumi- recorded with Normocytic hyperchromic nemia followed by Hyporproteinemia and followed by Normocytic normochromic and Hyperalbuminemia with hyperglobulinemia were Microcytic hypochromic mild anemia in 20% encountered (Tab.1) (p>0.05). (2/10, CI 95%: 2.52-55.61) of tested samples. Usually, elevated levels of total serum proteins, Normocytic normochromic moderate anemia and including, albumins and globulins could be caused Normocytic hypochromic mild anemia were also by dehydration, chronical inflammation or chronic present in 10% (1/10, CI 95%: 0.25-44.50) of the subacute bacterial infection (Kerr, 2002b). These tested cases, each (Tab.1) (p>0.05). Presence of hypothesis can explain the presenceMastitis of gangre high levels nosa mild anemia could have been caused by the loss of these parameters in primary mastitis bitches. of blood due to inflamed mammary glands and In one documented bitch infections (Kerr, 2002a). case report, where biochemical and haematological Thrombocytopenia was recorded in 60% changes were recorded, results showed presence (3/5, CI 95%: 14.66-94.73) of cases, whilst 40% of severe leukocytosis (36,300/µl) with marked (2/5, CI 95% 5.27-85.34) were recorded with elevated α, β and γ-globuline levels, moderate Thrombocytosis (p>0.05). anemia, a slightly increased level of alkaline Mild Lecukocytosis was encountered in 4 phosphatase and creatine phosphokinase with (4/4, CI 95%: 10.00) of the primary mastitis moderate hipernatremia and hypokalemia. On bitches (p>0.05). the day of admission, the amount of circulating leukocytes decreasedBulletin temporarilyUASVM Veterinary Medicineto 26,000/ml, 73 (2) / 2016 250 et al VASIU Tab. 1. Hemoleucogram and biochemical results in both types of bitch mastitis Percen- Diagnostic – Secondary mastitis Percen- No. Diagnostic – Primary mastitis No. tage tage WBC 1 WBC 2 Severe leukopenia 14% 1 3 Moderate leukocytosis 29% Mild leukocytosis 100% 4 Severe leukocytosis 29% RBC Mild leukocytosis RBC 29% 2 5 3 Normocytic normochromic moderate anemia 10% 6 Normocytic hypochromic moderate anemia 14% 4 Normocytic hypochromic mild anemia 10% 7 Normocytic hypochromic mild anemia 14% 5 Microcytic hypochromic mild anemia 20% 8 Normocytic normochromic mild anemia 14% 6 Normocytic normochromic mild anemia 20% Normocytic hyperchromic mild anemia 57% Normocytic hyperchromicPLT mild anemia 40% PLT 8 9 9 Thrombocytosis 40% 10 Thrombocytosis 33% Thrombocytopenia CBC 60% Thrombocytopenia CBC 67% 10 11 11 Eosinophilia 5% 12 Monocitopenia with eosinophilia 6% Neutrophilia with left shift with 12 Lymphocytosis with eosinopenia 5% 13 6% lymphocytosis and eosinopenia 13 Monocytosis with eosinophilia 5% 14 Neutrophilia with left shift with lymphopenia 6% Neutrophilia with left shift with lymphopenia, 14 Neutrophilia with left shift with eosinopenia 5% 15 6% monocytopenia and eosinopenia Neutrophilia with left shift with 15 5% 16 Neutrophilia with left shift with monocytosis 6% lymphocytosis and eosinopenia 16 Neutrophilia with left shift with lymphopenia 5% 17 Neutropenia with eosinophilia 6% Neutrophilia with left shift with 17 5% 18 Neutrophilia with left shift 12% monocytopenia and eosinophilia Neutropenia with right shift with monocytosis, 18 5% 19 Neutrophilia with left shift with eosinopenia 12% lymphocytosis and eosinophilia Neutrophilia with left shift with 19 Monocytopenia with eosinophilia 11% 20 12% monocytosis and eosinophilia Neutrophilia with
Recommended publications
  • • 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).
    [Show full text]
  • My Beloved Neutrophil Dr Boxer 2014 Neutropenia Family Conference
    The Beloved Neutrophil: Its Function in Health and Disease Stem Cell Multipotent Progenitor Myeloid Lymphoid CMP IL-3, SCF, GM-CSF CLP Committed Progenitor MEP GMP GM-CSF, IL-3, SCF EPO TPO G-CSF M-CSF IL-5 IL-3 SCF RBC Platelet Neutrophil Monocyte/ Basophil B-cells Macrophage Eosinophil T-Cells Mast cell NK cells Mature Cell Dendritic cells PRODUCTION AND KINETICS OF NEUTROPHILS CELLS % CELLS TIME Bone Marrow: Myeloblast 1 7 - 9 Mitotic Promyelocyte 4 Days Myelocyte 16 Maturation/ Metamyelocyte 22 3 – 7 Storage Band 30 Days Seg 21 Vascular: Peripheral Blood Seg 2 6 – 12 hours 3 Marginating Pool Apoptosis and ? Tissue clearance by 0 – 3 macrophages days PHAGOCYTOSIS 1. Mobilization 2. Chemotaxis 3. Recognition (Opsonization) 4. Ingestion 5. Degranulation 6. Peroxidation 7. Killing and Digestion 8. Net formation Adhesion: β 2 Integrins ▪ Heterodimer of a and b chain ▪ Tight adhesion, migration, ingestion, co- stimulation of other PMN responses LFA-1 Mac-1 (CR3) p150,95 a2b2 a CD11a CD11b CD11c CD11d b CD18 CD18 CD18 CD18 Cells All PMN, Dendritic Mac, mono, leukocytes mono/mac, PMN, T cell LGL Ligands ICAMs ICAM-1 C3bi, ICAM-3, C3bi other other Fibrinogen other GRANULOCYTE CHEMOATTRACTANTS Chemoattractants Source Activators Lipids PAF Neutrophils C5a, LPS, FMLP Endothelium LTB4 Neutrophils FMLP, C5a, LPS Chemokines (a) IL-8 Monocytes, endothelium LPS, IL-1, TNF, IL-3 other cells Gro a, b, g Monocytes, endothelium IL-1, TNF other cells NAP-2 Activated platelets Platelet activation Others FMLP Bacteria C5a Activation of complement Other Important Receptors on PMNs ñ Pattern recognition receptors – Detect microbes - Toll receptor family - Mannose receptor - bGlucan receptor – fungal cell walls ñ Cytokine receptors – enhance PMN function - G-CSF, GM-CSF - TNF Receptor ñ Opsonin receptors – trigger phagocytosis - FcgRI, II, III - Complement receptors – ñ Mac1/CR3 (CD11b/CD18) – C3bi ñ CR-1 – C3b, C4b, C3bi, C1q, Mannose binding protein From JG Hirsch, J Exp Med 116:827, 1962, with permission.
    [Show full text]
  • Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
    Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck.
    [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]
  • University of Birmingham the Primary Immunodeficiency Disorders
    University of Birmingham The primary immunodeficiency disorders Shields, Adrian; Patel, Smita Y DOI: 10.1016/j.mpmed.2017.07.011 License: Creative Commons: Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) Document Version Peer reviewed version Citation for published version (Harvard): Shields, A & Patel, SY 2017, 'The primary immunodeficiency disorders', Medicine, vol. 45, no. 10, pp. 597-604. https://doi.org/10.1016/j.mpmed.2017.07.011 Link to publication on Research at Birmingham portal Publisher Rights Statement: Shields, A. Patel, S. (2017) The primary immunodeficiency disorders, Medicine, volume 45, issue 10, pages 597-604, https://doi.org/10.1016/j.mpmed.2017.07.011 General rights Unless a licence is specified above, all rights (including copyright and moral rights) in this document are retained by the authors and/or the copyright holders. The express permission of the copyright holder must be obtained for any use of this material other than for purposes permitted by law. •Users may freely distribute the URL that is used to identify this publication. •Users may download and/or print one copy of the publication from the University of Birmingham research portal for the purpose of private study or non-commercial research. •User may use extracts from the document in line with the concept of ‘fair dealing’ under the Copyright, Designs and Patents Act 1988 (?) •Users may not further distribute the material nor use it for the purposes of commercial gain. Where a licence is displayed above, please note the terms and conditions of the licence govern your use of this document. When citing, please reference the published version.
    [Show full text]
  • Trapped Neutrophil Syndrome in a Border Collie Dog: Clinical, Clinico-Pathologic, and Molecular Findings
    NOTE Internal Medicine Trapped Neutrophil Syndrome in a Border Collie Dog: Clinical, Clinico-Pathologic, and Molecular Findings Keijiro MIZUKAMI1), Tomoaki SHOUBUDANI2), Seira NISHIMOTO2), Ryuta KAWAMURA2), Akira YABUKI1) and Osamu YAMATO1)* 1)Laboratory of Clinical Pathology, Department of Veterinary Medicine, Kagoshima University, 1–21–24 Kohrimoto, Kagoshima 890–0065, Japan 2)Athena Pet Care Clinic, 3 Tamaike-cho, Nishi-ku, Nagoya 452–0812, Japan (Received 21 October 2011/Accepted 27 December 2011/Published online in J-STAGE 12 January 2012) ABSTRACT. Trapped neutrophil syndrome (TNS) is an autosomal recessive inherited neutropenia known in Border Collies since the 1990’s. Recently, the causative mutation has been identified in the canine VPS13B gene and a DNA-based diagnosis has now become available. The present paper describes clinical and clinico-pathologic findings in a Border Collie with TNS that was molecularly diag- nosed for the first time in Japan. In a 10-week-old male Border Collie with microgenesis and symptoms related to recurrent infections, a hematological examination revealed severe leukopenia due to neutropenia, suggesting the dog to be affected by inherited neutro- penic immunodeficiency. Direct DNA sequencing demonstrated that the dog was homozygous for the causative mutation of TNS and both its parents were heterozygous carriers. In addition, a simple and rapid polymerase chain reaction-based length polymorphism analysis coupled with microchip electrophoresis was developed for the genotyping of TNS. This assay could discriminate clearly all genotypes, suggesting that it was suitable for both individual diagnosis and large-scale surveys for prevention. KEY WORDS: Border Collie dog, Cohen syndrome, neutropenia, trapped neutrophil syndrome.
    [Show full text]
  • The Importance of Eosinopenia for Predicting Treatment Response In
    ORIGINAL ARTICLE The Importance of Eosinopenia for Predicting Treatment Response in Patients with Cholangitis Cengiz Karacaer1, Ahmet Tarik Eminler2, Bilal Toka2, Mukaddes Tozlu2, Erkan Parlak2 and Aydin Seref Koksal2 1Department of Internal Medicine, Sakarya University Research and Education Hospital, Sakarya, Turkey 2Department of Gastroenterology, Sakarya University Research and Education Hospital, Sakarya, Turkey ABSTRACT Objective: To compare recovery of eosinopenia, C-reactive protein (CRP) and procalcitonin levels in predicting the response to treatment in patients with cholangitis. Study Design: Descriptive, analytical study. Place and Duration of Study: Department of Gastroenterology, Sakarya Training and Research Hospital, Turkey between September 2018 and February 2019. Methodology: Patients with cholangitis, who underwent endoscopic retrograde cholangiopancreatography (ERCP), were inducted. Those with choledocholic thiasis alone were considered controls. Eosinophil count above 100.5 cells/µL was the limit value accepted as improvement. ERCP repeat was decided according to eosinophil count below 100.5 and not clinically improving. Relationship between inflammatory markers such as CRP, procalcitonin and eosinopenia values in patients with stone-associated cholangitis was investigated. Results: The cholangitis group was comprised of 62 patients [mean age 67±14.57 years; 26 (41.9%) female], while control group was comprised of 57 patients [mean age 57.4±18.10 years; 39 (68.4%) females, p=0.004].At time of admission, median eosinophils was significantly lower in cholangitis group at17.50 [9.82-84] ×103/µL compared to control group at168 [100.11-270] ×103/µL (p=0.001). ERCP were repeated on two patients as their clinical conditions and unremitting eosinophil counts worsened. Eosinophil and CRP markers and clinical improvement were observed after second ERCP procedure.
    [Show full text]
  • ESID Registry – Working Definitions for Clinical Diagnosis of PID
    ESID Registry – Working Definitions for Clinical Diagnosis of PID These criteria are only for patients with no genetic diagnosis*. *Exceptions: Atypical SCID, DiGeorge syndrome – a known genetic defect and confirmation of criteria is mandatory Available entries (Please click on an entry to see the criteria.) Page Acquired angioedema .................................................................................................................................................................. 4 Agammaglobulinaemia ................................................................................................................................................................ 4 Asplenia syndrome (Ivemark syndrome) ................................................................................................................................... 4 Ataxia telangiectasia (ATM) ......................................................................................................................................................... 4 Atypical Severe Combined Immunodeficiency (Atypical SCID) ............................................................................................... 5 Autoimmune lymphoproliferative syndrome (ALPS) ................................................................................................................ 5 APECED / APS1 with CMC - Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) .................. 5 Barth syndrome ...........................................................................................................................................................................
    [Show full text]
  • Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency Francisco A
    Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD*; I. Leonard Bernstein, MD†; David A. Khan, MD‡; Zuhair K. Ballas, MD§; Javier Chinen, MD, PhD¶; Michael M. Frank, MDʈ; Lisa J. Kobrynski, MD**; Arnold I. Levinson, MD††; Bruce Mazer, MD‡‡; Robert P. Nelson, Jr, MD§§; Jordan S. Orange, MD, PhD¶¶; John M. Routes, MDʈʈ; William T. Shearer, MD, PhD***; and Ricardo U. Sorensen, MD††† TABLE OF CONTENTS I. Preface....................................................................................................................................................................................S1 II. Executive Summary...............................................................................................................................................................S2 III. Algorithms .............................................................................................................................................................................S7 IV. Summary Statements ...........................................................................................................................................................S14 V. General Considerations........................................................................................................................................................S20 VI. Humoral Immunodeficiencies .............................................................................................................................................S24
    [Show full text]
  • N-Formyl-Methionyl-Leucyl-Phenylalanine in Man Thorax: First Published As 10.1136/Thx.47.4.284 on 1 April 1992
    284 Thorax 1992;47:284-287 Haematological effects of inhalation of N-formyl-methionyl-leucyl-phenylalanine in man Thorax: first published as 10.1136/thx.47.4.284 on 1 April 1992. Downloaded from M J Peters, A B X Breslin, A S Kemp, J Chu, N Berend Abstract Background including chemotaxis, lysosomal enzyme N-Formyl-methionyl- release and oxygen free radical generation.4 leucyl-phenylalanine (FMLP) is a bac- It also contracts smooth muscle. There is a terial oligopeptide which stimulates close correlation between chemotactic and neutrophil chemotaxis, degranulation spasmogenic activity5 between the different and superoxide generation. Inhalation of related formyl peptides. Following the finding FMLP produces bronchoconstriction in that inhaled FMLP produces broncho- man; in the rabbit this is in part neutro- constriction in normal phil dependent. subjects,6 we suggested The effects of inhalation that it may cause bronchoconstriction during of FMLP on peripheral blood leucocytes bacterial bronchial infection, particularly in in normal subjects has been studied. patients with chronic airflow limitation. Methods This was an open study in Although FMLP contracts human bron- non-asthmatic subjects. Change in total chial smooth muscle directly in vitro,7 its peripheral white cell count were studied bronchoconstrictor activity in vivo in for 15 minutes after may inhalation of 04 part be neutrophil dependent as neutropenic umol FMLP in six subjects. Change rabbits show a reduced bronchoconstrictor in total and differential white cell count response to FMLP.8 Infusions of substances and spontaneous neutrophil chemi- known to activate neutrophils (FMLP, luminescence were then studied five and platelet activating factor (PAF), C5a, 30 minutes after inhalation of 0 4 pmol granulocyte-monocyte colony stimulating FMLP (n = 7) or diluent (n = 4).
    [Show full text]
  • Blueprint Genetics Primary Immunodeficiency Panel
    Primary Immunodeficiency Panel Test code: IM0301 Is a 298 gene panel that includes assessment of non-coding variants. Is ideal for patients with a clinical suspicion of any type of primary immunodeficiency (PID). About Primary Immunodeficiency Primary immunodeficiencies (PIDs) are a genetically heterogeneous group of diseases. The International Union of Immunological Societies Expert Committee categorizes PIDs into nine different categories: 1) combined immunodeficiencies, 2) combined immunodeficiencies with associated or syndromic features, 3) predominantly antibody deficiencies, 4) diseases of immune dysregulation, 5) congenital defects of phagocyte number, function, or both, 6) defects in intrinsic and innate immunity, 7) autoinflammatory disorders, 8) complement deficiencies and 9) phenocopies of PIDs. Despite a heterogeneous genetic basis, the core symptoms are often very similar complicating the diagnosis. In addition, many PIDs may be included in more than one category. Treatment choice without knowing the specific mutation in the causative gene may therefore be complicated. Also, type and site of and specific organisms causing the infections may help to classify the disease. In addition to immune-related symptoms, many PIDs have non-immune manifestations. The prevalence of individual PIDs have a wide range, but the combined prevalence of all primary immunodeficiencies is reported to be as high as 5-8:10,000. Some recently identified PIDs are extremely rare. Availability 4 weeks Gene Set Description Genes in the Primary Immunodeficiency
    [Show full text]
  • Haematological Abnormalities in Human Immunodeficiency Virus (HIV) Disease
    J Clin Pathol: first published as 10.1136/jcp.41.7.711 on 1 July 1988. Downloaded from J Clin Pathol 1988;41:711-715 Review article Haematological abnormalities in human immunodeficiency virus (HIV) disease CHRISTINE COSTELLO From the Department ofHaematology, St Stephen's Hospital, London Peripheral blood and bone marrow changes are com- patients with AIDS and opportunistic tumours.2 Care monly seen in disease associated with human immun- must be taken when interpreting the ratio of T helper odeficiency virus (HIV). This annotation aims to to T suppressor cells. Only when there is lymphopenia summarise these changes and to suggest possible does a decreased ratio indicate depletion of T helper factors entailed in their occurrence. cells. In patients with a normal lymphocyte count a decreased ratio might result either from T helper cell The wideranging clinical and pathological changes in depletion or from T suppressor cell increase. patients infected with HIV virus are both fascinating Mir found a 79% incidence of lymphopenia in 40 and challenging to physicians and pathologists alike. patients with AIDS and in our series of 925 HIV Haematological abnormalities are well recognised in antibody positive patients studied during 1987, 305 HIV disease and result from diverse influences on the (33%) were lymphopenic; most of these patients had haemopoietic tissue. Changes in the peripheral blood AIDS or ARC.3 and bone marrow may reflect disease elsewhere in the Granulocytopenia is a less well recognised feature of body, may result from treatment for that disease, may HIV disease but was seen in 185 (20%) of 925 HIV reflect an attempt to attack the HIV virus itself, or may antibody positive patients (Haematological features of seem to be isolated haematological disorders.
    [Show full text]