DOCSLIB.ORG

Comparison of Serum Markers for Allergic Bronchopulmonary Aspergillosis in Cystic Fibrosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Comparison of Serum Markers for Allergic Bronchopulmonary Aspergillosis in Cystic Fibrosis Eur Respir J 2008; 31: 36–42 DOI: 10.1183/09031936.00078107 CopyrightßERS Journals Ltd 2008 Comparison of serum markers for allergic bronchopulmonary aspergillosis in cystic fibrosis P. Latzin*,#,", D. Hartl#,", N. Regamey*, U. Frey*, M.H. Schoeni* and C. Casaulta* ABSTRACT: The diagnosis of allergic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis AFFILIATIONS (CF) is a challenge. Thymus- and activation-regulated chemokine (TARC) has recently been *Division of Respiratory Medicine, Children’s University Hospital of reported to play a role in ABPA. The aim of this study was to compare the diagnostic value of Bern, Bern, Switzerland, TARC with that of known serological markers for diagnosis of ABPA in CF patients. #Children’s Hospital of the Ludwig The present study longitudinally followed 48 CF patients, of whom 12 had a diagnosis of ABPA Maximilian University of Munich, according to Nelson’s criteria, for 1–8 yrs with repeated measurements of serum total Munich, Germany. "Both authors contributed equally to immunoglobulin (Ig)E, specific Aspergillus fumigatus IgE and IgG, specific IgE against this article. recombinant A. fumigatus allergens (rAsp f) 1, 3, 4 and 6, and TARC. Median (interquartile range) TARC levels were 589 (465–673) pg?mL-1 in ABPA patients and 232 CORRESPONDENCE (189–289) pg?mL-1 in non-ABPA patients. Receiver operating characteristic curves revealed that P. Latzin Division of Respiratory Medicine TARC was superior to the other markers for diagnosis of ABPA. Diagnostic accuracy was greater Dept of Paediatrics for TARC (93%) than for total IgE (74%), or rAsp f 4 (75%) or f 6 (79%). University Children’s Hospital of Bern The present study indicates that thymus- and activation-regulated chemokine may be useful in Inselspital the diagnosis of allergic bronchopulmonary aspergillosis in cystic fibrosis patients. However, 3010 Bern Switzerland larger studies are needed before thymus- and activation-regulated chemokine can routinely be Fax: 41 316324807 used in diagnostic algorithms. E-mail: [email protected] KEYWORDS: Allergic bronchopulmonary aspergillosis, cystic fibrosis, diagnostic value, Received: June 26 2007 immunoglobulin E, serum marker, thymus- and activation-regulated chemokine Accepted after revision: September 11 2007 llergic bronchopulmonary aspergillosis lung colonisation with A. fumigatus occurs in SUPPORT STATEMENT (ABPA) is a pulmonary hypersensitivity 20–25% of CF patients [9–11]. Therefore, as This study was supported by a Swiss A disease mediated by an allergic response stated in the most recent consensus document National Foundation (Berne, to Aspergillus fumigatus [1]. ABPA occurs in ,10% on diagnosis and therapy of ABPA in CF Switzerland) grant 3200-B0-112099 to U. Frey, a grant from the German of cystic fibrosis (CF) patients and may lead to patients, serological findings should contribute Society for Paediatric Pneumology acute worsening of respiratory status and strongly to the confirmation or exclusion of (Hanover, Germany) to D. Hartl and a ongoing decline in lung function [2], ultimately clinically suspected ABPA [5]. grant from the Mu¨nchener progressing to a chronic state and lung fibrosis Medizinische Wochenschrift (Munich, Animal studies suggest a pathophysiological role without adequate treatment [3]. Despite the Germany) to P. Latzin. existence of the gold-standard Nelson criteria of the chemokine thymus- and activation-regu- [4], diagnosis of ABPA in CF patients remains lated chemokine (TARC) in ABPA by linking an STATEMENT OF INTEREST difficult [5]. The wide variation in diagnostic antifungal immune response with the promotion None declared. practices between clinics [6], different estimates of T-helper cell (Th) type 2-mediated hypersen- of prevalence and a delay in recognition lead to sitivity to A. fumigatus [12]. It has recently been undertreatment [7]. shown, in a cross-sectional study, that serum levels of TARC are elevated in CF patients with The main reason for the difficulties in diagnosis of ABPA [13]. However, longitudinal clinical data ABPA and ABPA exacerbations in CF patients is on the usefulness of this marker are lacking and the overlap of diagnostic criteria for ABPA with no further study has been performed validating common manifestations of CF. Pulmonary infil- TARC in comparison to other putative ABPA trates, obstructive lung disease and bronchiec- serum markers. The present study aimed to tasis occur regularly in CF patients, due to the answer the following questions. 1) Can the results European Respiratory Journal underlying disease with bacterial colonisation, and of the previously published cross-sectional study Print ISSN 0903-1936 thus are not specific to ABPA [8]. Furthermore, [13] be confirmed in another CF population? Online ISSN 1399-3003 36 VOLUME 31 NUMBER 1 EUROPEAN RESPIRATORY JOURNAL P. LATZIN ET AL. TARC AS SERUM MARKER FOR ABPA 2) What is the diagnostic value (sensitivity and specificity) of skin-prick testing, elevated total immunoglobulin (Ig)E levels TARC compared to other serological markers of ABPA? 3) Is (cut-off 500 IU?mL-1), increased levels of specific serum IgE TARC useful for the early detection of ABPA development? (cut-off 17.5 IU?mL-1) and IgG (cut-off 20 kU?L-1) directed against A. fumigatus [4]. METHODS Study design Serum markers From 1998 onwards, a group of 48 patients (23 females and 25 In the collected serum samples, the following parameters were males; median (interquartile range (IQR)) age 9 (7–14) yrs) measured: total IgE, specific IgE (radioallergosorbent test) to A. with CF were systematically followed longitudinally [14]. All fumigatus, specific IgG to A. fumigatus extract (ELISA) and patients underwent careful clinical assessment, lung function specific IgE against the recombinant A. fumigatus allergens testing and microbiological diagnosis at all visits during the (rAsp f) 1, 3, 4 and 6 [14, 15] and TARC. study period. Skin testing against A. fumigatus was routinely TARC levels were analysed in triplicate by sandwich ELISA performed using Bencard skin test antigens (SmithKline (R&D Systems, Minneapolis, MN, USA) according to the Beecham, Mu¨ nchenbuchsee, Switzerland). Chest radiography manufacturer’s instructions, and concentrations calculated from was performed on study entry and thereafter at least annually. standard curves with detection limits of 7–3,000 pg?mL-1. Intra- In addition, serum samples were collected at the study visits, assay variability was determined by evaluating five serum resulting in an average of six serum samples per patient for samples 10 times within the same assay run and showed a analysis (table 1). The Ethics Committee of Berne (Berne, coefficient of variation of 6–9%. Interassay variability was Switzerland) approved the study and written consent was determined by measuring five serum samples in five consecu- obtained on enrolment. tive assay runs and showed a coefficient of variation of 8–17%. Clinical diagnosis of ABPA Statistical analysis According to Nelson’s criteria, patients were diagnosed as Data are presented as median (IQR) unless otherwise having clinical ABPA when at least six out of the seven indicated. The diagnostic value of the serological markers following criteria were fulfilled: wheezing, positive A. fumiga- and receiver operator characteristic (ROC) curves were tus sputum culture, presence of defined infiltrates on chest calculated. Cut-off levels were set at the level that resulted in radiography, positive acute reaction to A. fumigatus on the optimal diagnostic accuracy, defined as correctly positively classified plus correctly negatively classified as a percentage of the total. TABLE 1 Patient data and results of serum measurements in cystic fibrosis patients with and without allergic Nested matched case–control analysis bronchopulmonary aspergillosis (ABPA) In order to assess whether TARC level elevation was specific to ABPA Non-ABPA ABPA or an epiphenomenon of the hypersensitivity against A. fumigatus in ABPA patients, a nested matched case–control analysis was performed and TARC levels compared between Patients 12 36 cases (ABPA patients) and controls (non-ABPA patients), Age at study entry yrs 10 (8–12) 9 (7–14) matched for total IgE and rAsp f 6 levels, respectively. Males/females 7/5 19/17 Study duration months 40 (35–80) 40 (27–55) RESULTS + + Serum samples 7 (4–12); 87 5 (1–8); 178 Of the 48 CF patients, 12 were diagnosed with clinical ABPA FEV1 on study entry % pred 73 (77–81) 89 (72–99) based on Nelson’s criteria. Nine patients were diagnosed with A. fumigatus in sputum# 12 20 # ABPA before study entry and three developed their first P. aeruginosa in sputum 12 34 episode of clinical ABPA during the study period; all were Serum measurements assigned to the ABPA group. The other 36 CF patients did not Total IgE IU?mL-1 965 (324–1961) 59 (21–433) -1 fulfil six out of seven of Nelson’s criteria for diagnosis at any Specific IgG to A. fumigatus kU?L 145 (66–244) 51 (17–105) time before or during the study period and were assigned to Specific IgE to A. fumigatus RAST class" 4 (3–5) 1 (0–3) -1 the non-ABPA group. Details of the patients’ characteristics are rAsp f 1 EU?mL 128 (60–364) 21 (6–59) given in table 1. rAsp f 3 EU?mL-1 253 (99–739) 37 (14–94) -1 rAsp f 4 EU?mL 23 (11–53) 4 (1–12) TARC compared to other serological markers for the -1 rAsp f 6 EU?mL 25 (8–67) 3 (2–8) diagnosis of ABPA -1 TARC pg?mL 589 (465–673) 232 (189–289) Median (IQR) TARC levels were 589 (465–673) pg?mL-1 in ABPA patients compared to 232 (189–289) pg?mL-1 in non- Data are presented as n or median (interquartile range) unless otherwise stated. ABPA patients (table 1). In the 16 non-ABPA patients with FEV1:forcedexpiratoryvolumeinonesecond;%pred:%predicted; neither sensitisation to A. fumigatus nor elevation of total IgE A. fumigatus: Aspergillus fumigatus; P. aeruginosa: Pseudomonas aeruginosa; levels, TARC levels were 207 (178–282) pg?mL-1.
Load more

Recommended publications
  • Trends in COPD (Chronic Bronchitis and Emphysema): Morbidity and Mortality
    Trends in COPD (Chronic Bronchitis and Emphysema): Morbidity and Mortality Please note, this report is designed for double-sided printing American Lung Association Epidemiology and Statistics Unit Research and Health Education Division March 2013 Page intentionally left blank Table of Contents COPD Mortality, 1999-2009 COPD Prevalence, 1999-2011 COPD Hospital Discharges, 1999-2010 Glossary and References List of Tables Table 1: COPD – Number of Deaths by Ethnic Origin and Sex, 1999-2009 Figure 1: COPD – Number of Deaths by Sex, 1999-2009 Figure 2: COPD – Age-Adjusted Death Rates by Ethnic Origin and Sex, 2009 Table 2: COPD – Age-Adjusted Death Rate per 100,000 Population by Ethnic Origin and Sex, 1999- 2009 Figure 3: COPD – Deaths and Age-Adjusted Death Rate by Sex, 2009 Figure 4: COPD – Diagnosed Cases and Evidence of Impaired Lung Function Figure 5: Chronic Bronchitis – Prevalence Rates per 1,000, 2011 Table 3: Chronic Bronchitis – Number of Conditions and Prevalence Rate per 1,000 Population by Ethnic Origin, Sex and Age, 1999-2011 Figure 6: Emphysema – Prevalence Rates per 1,000, 2011 Table 4: Emphysema – Number of Conditions and Prevalence Rate per 1,000 Population by Ethnic Origin, Sex and Age, 1997-2011 Table 5: COPD – Adult Prevalence by Sex and State, 2011 Figure 8: COPD – Age-Adjusted Prevalence in Adults by State, 2011 Table 6: Characteristics Among Those Reporting a Diagnosis of COPD by State (%), 2011 Figure 9: COPD – First-Listed Hospital Discharge Rates per 10,000, 2010 Table 7: COPD – Number of First-Listed Hospital Discharges and Rate per 10,000 Population by Race, Sex and Age, 1999-2010 Figure 9: National Projected Annual Cost of COPD, 2010 Introduction Chronic obstructive pulmonary disease (COPD) is a term which refers to a large group of lung diseases characterized by obstruction of air flow that interferes with normal breathing.
    [Show full text]
  • Chronic Obstructive Lung Disease &​Bronchiectasis
    PLEASE CHECK Editing file BEFORE! ​ ​ ​ ​ Chronic Obstructive lung Disease & Bronchiectasis ​ ★ Objectives: ​ 1. Definition of the two conditions 2. Clinical and radiological diagnosis 3. Differential diagnosis 4. General outline of management 5. Create a link to 341 clinical teaching ★ Resources Used in This lecture: Davidson, Guyton and Becker step 1 lecture notes ​ Done by: Mohammad Alkharraz Contact us at: [email protected] Chronic Obstructive Pulmonary Diseases (COPD) COPD contains two diseases which are chronic bronchitis and emphysema ​ ​ ​ ■ COPD is classified under obstructive pulmonary diseases along with other ​(no kidding!)​ diseases such as asthma and bronchiectasis ■ Chronic bronchitis and emphysema are grouped together under COPD because they are both mainly caused by smoking and they usually present together. ​ ■ Brainless pathology textbooks (Robbins) try to confuse us students with “Pink Puffers” and “Blue Bloaters”. Forget about that as it is not clinically relevant1. Let us quickly point out some points (pathology) that are relevant to each disease (chronic bronchitis and emphysema) and then we will discuss the clinical presentation, management, etc. of COPD Chronic bronchitis It is mainly a clinical diagnosis patients cough up lots of sputum for a long period of time ​ ​ “3 months per year for at least 2 consecutive years2” ● Pathogenesis: Cigarette smoke causes hyperplasia of mucus glands which increase the ​ secretion of mucus → mucus plugs cause obstruction of bronchioles→ COPD Emphysema It is mainly a pathological diagnosis. ​ ​ ● Pathogenesis: 1. Pollutants (smoking)→ increased inflammatory mediators in the lung that destroy the lung parenchyma (trypsin and elastase) 2. We have defense mechanisms to fight these inflammatory mediators (alpha1 antitrypsin) ○ However, the amount of inflammatory mediators exceeds our ability to counteract them 3.
    [Show full text]
  • Allergic Bronchopulmonary Aspergillosis As a Cause of Bronchial Asthma in Children
    Egypt J Pediatr Allergy Immunol 2012;10(2):95-100. Original article Allergic bronchopulmonary aspergillosis as a cause of bronchial asthma in children Background: Allergic bronchopulmonary aspergillosis (ABPA) occurs in Dina Shokry, patients with asthma and cystic fibrosis. When aspergillus fumigatus spores Ashgan A. are inhaled they grow in bronchial mucous as hyphae. It occurs in non Alghobashy, immunocompromised patients and belongs to the hypersensitivity disorders Heba H. Gawish*, induced by Aspergillus. Objective: To diagnose cases of allergic bronchopulmonary aspergillosis among asthmatic children and define the Manal M. El-Gerby* association between the clinical and laboratory findings of aspergillus fumigatus (AF) and bronchial asthma. Methods: Eighty asthmatic children were recruited in this study and divided into 50 atopic and 30 non-atopic Departments of children. The following were done: skin prick test for aspergillus fumigatus Pediatrics and and other allergens, measurement of serum total IgE, specific serum Clinical Pathology*, aspergillus fumigatus antibody titer IgG and IgE (AF specific IgG and IgE) Faculty of Medicine, and absolute eosinophilic count. Results: ABPA occurred only in atopic Zagazig University, asthmatics, it was more prevalent with decreased forced expiratory volume Egypt. at the first second (FEV1). Prolonged duration of asthma and steroid dependency were associated with ABPA. AF specific IgE and IgG were higher in the atopic group, they were higher in Aspergillus fumigatus skin Correspondence: prick test positive children than negative ones .Wheal diameter of skin prick Dina Shokry, test had a significant relation to the level of AF IgE titer. Skin prick test Department of positive cases for aspergillus fumigatus was observed in 32% of atopic Pediatrics, Faculty of asthmatic children.
    [Show full text]
  • Cryptogenic Organizing Pneumonia—Results of Treatment with Clarithromycin Versus Corticosteroids—Observational Study
    RESEARCH ARTICLE Cryptogenic organizing pneumoniaÐResults of treatment with clarithromycin versus corticosteroidsÐObservational study Elżbieta Radzikowska1*, Elżbieta Wiatr1☯, Renata Langfort2³, Iwona Bestry3³, Agnieszka Skoczylas4, Ewa Szczepulska-Wo jcik2³, Dariusz Gawryluk1☯, Piotr Rudziński5³, Joanna Chorostowska-Wynimko6³, Kazimierz Roszkowski-Śliż1³ 1 III Department of Lung Disease National Tuberculosis and Lung Diseases Research Institute, Warsaw, Poland, 2 Pathology Department National Tuberculosis and Lung Diseases Research Institute, Warsaw, Poland, 3 Radiology Department National Tuberculosis and Lung Diseases Research Institute, Warsaw, a1111111111 Poland, 4 Geriatrics Department National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, a1111111111 Poland, 5 Thoracic Surgery Department National Tuberculosis and Lung Diseases Research Institute, a1111111111 Warsaw, Poland, 6 Laboratory of Molecular Diagnostics and Immunology National Tuberculosis and Lung Diseases Research Institute, Warsaw, Poland a1111111111 a1111111111 ☯ These authors contributed equally to this work. ³ These authors also contributed equally to this work. * [email protected] OPEN ACCESS Abstract Citation: Radzikowska E, Wiatr E, Langfort R, Bestry I, Skoczylas A, Szczepulska-WoÂjcik E, et al. (2017) Cryptogenic organizing pneumoniaÐ Background Results of treatment with clarithromycin versus Cryptogenic organizing pneumonia (COP) is a clinicopathological syndrome of unknown ori- corticosteroidsÐObservational study. PLoS ONE 12(9): e0184739.
    [Show full text]
  • Chronic Obstructive Pulmonary Disease (Copd) in the Americas
    CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) IN THE AMERICAS KEY STATISTICS FOR THE AMERICAS An estimated 13.2 million people live with COPD (1). COPD caused over 235,000 deaths in 2010, ranking as the sixth leading cause of death (2). 7 in 10 COPD deaths are attributable to tobacco (3). In 2012, COPD was responsible for the loss of 8.3 million disability-adjusted life years (DALYs) (3). KEY MESSAGES CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) IS A LEADING CAUSE OF MORBIDITY AND MORTALITY IN THE 1 AMERICAS, REPRESENTING AN IMPORTANT PUBLIC HEALTH CHALLENGE THAT IS BOTH PREVENTABLE AND TREATABLE. COPD is an incurable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response to noxious particles or gases in the airways and the lungs. Common symptoms include breathlessness, abnormal sputum and a chronic cough. Exacerbations and comorbidities – such as cardiovascular diseases, skeletal muscle dysfunction, metabolic syndrome, osteoporosis, depression and lung cancer – contribute to the overall severity of individual patients (4,5). In 2010, COPD accounted for over 235,000 deaths in the Americas, ranking as the sixth leading cause of mortality regionally. About 23% of these deaths occurred prematurely, in people aged 30-69 years (2). An estimated 13.2 million people live with COPD in the region (1). Many people suffer from this disease for years, experiencing disa- bility and major adverse effects on their quality of life (5,6). In 2012, COPD was responsible for the loss of 8.3 million DALYs, representing the seventh leading cause of disability-adjusted life years lost (DALYs) in the Americas, with one DALY representing the loss of the equivalent of one year of full health (3,6).
    [Show full text]
  • Interstitial Lung Disease—Raising the Index of Suspicion in Primary Care
    www.nature.com/npjpcrm All rights reserved 2055-1010/14 PERSPECTIVE OPEN Interstitial lung disease: raising the index of suspicion in primary care Joseph D Zibrak1 and David Price2 Interstitial lung disease (ILD) describes a group of diseases that cause progressive scarring of the lung tissue through inflammation and fibrosis. The most common form of ILD is idiopathic pulmonary fibrosis, which has a poor prognosis. ILD is rare and mainly a disease of the middle-aged and elderly. The symptoms of ILD—chronic dyspnoea and cough—are easily confused with the symptoms of more common diseases, particularly chronic obstructive pulmonary disease and heart failure. ILD is infrequently seen in primary care and a precise diagnosis of these disorders can be challenging for physicians who rarely encounter them. Confirming a diagnosis of ILD requires specialist expertise and review of a high-resolution computed tomography scan (HRCT). Primary care physicians (PCPs) play a key role in facilitating the diagnosis of ILD by referring patients with concerning symptoms to a pulmonologist and, in some cases, by ordering HRCTs. In our article, we highlight the importance of prompt diagnosis of ILD and describe the circumstances in which a PCP’s suspicion for ILD should be raised in a patient presenting with chronic dyspnoea on exertion, once more common causes of dyspnoea have been investigated and excluded. npj Primary Care Respiratory Medicine (2014) 24, 14054; doi:10.1038/npjpcrm.2014.54; published online 11 September 2014 INTRODUCTION emphysema, in which the airways of the lungs become narrowed Interstitial lung disease (ILD) is an umbrella term, synonymous or blocked so the patient cannot exhale completely.
    [Show full text]
  • Radioaerosol Lung Scanning in Chronic Obstructive Pulmonary Disease (COPD) and Related Disorders
    88 XAOIOOIOO Radioaerosol Lung Scanning in Chronic Obstructive Pulmonary Disease (COPD) and Related Disorders Yong Whee Bahk, M.D. and Soo Kyo Chung, M.D. Introduction As a coordinated research project of the International Atomic Energy Agency (IAEA) a multicentre joint study on radioaerosol lung scan using the BARC nebulizer [1] has prospectively been carried out during 1988-1992 with the participation of 10 member countries in Asia [Bangladesh, China, India, Indonesia, Japan, Korea, Pakistan, Philippines, Singapore and Thailand]. The study was designed so that it would primarily cover chronic obstructive pulmonary disease (COPD) and the other related and common pulmonary diseases. The study also included normal controls and asymptomatic smokers. The purposes of this presentation are three fold: firstly, to document the useful- ness of the nebulizer and the validity of user's protocol in imaging COPD and other lung diseases; secondly, to discuss scan features of the individual COPD and other disorders studied and thirdly, to correlate scan alterations with radiographie find- ings. Before proceeding with a systematic analysis of aerosol scan patterns in the disease groups, we documented normal pattern. The next step was the assessment of scan features in those who had been smoking for more than several years but had no symptoms or signs referable to airways. The lung diseases we analyzed included COPD [emphysema, chronic bronchitis, asthma and bronchiectasis], bron- chial obstruction, compensatory overinflation and other common lung diseases such as lobar pneumonia, tuberculosis, interstitial fibrosis, diffuse panbronchiolitis, lung edema and primary and metastatic lung cancers. Lung embolism, inhalation burns and glue-sniffer's lung are seperately discussed by Dr.
    [Show full text]
  • Global Initiative for Chronic Obstructive Lung Disease (2006)
    Global Initiative for Chronic Obstructive Lung Disease GLOBAL STRATEGY FOR THE DIAGNOSIS, MANAGEMENT, AND PREVENTION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE 2006 Copyright © 2006 MCR VISION, Inc. All Rights Reserved GLOBAL INITIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE GLOBAL STRATEGY FOR THE DIAGNOSIS, MANAGEMENT, AND PREVENTION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (2006) © 2006 Global Initative for Chronic Obstructive Lung Disease i Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2006) GOLD EXECUTIVE COMMITTEE* Roberto Rodriguez Roisin, MD Hospital Clinic A. Sonia Buist, MD, Chair Barcelona, Spain Oregon Health & Science University Portland, Oregon, USA Thys van der Molen, MD University of Groningen Antonio Anzueto, MD Groningen, The Netherlands (Representing the American Thoracic Society) University of Texas Health Science Center Chris van Weel, MD San Antonio, Texas, USA (Representing the World Organization of Family Doctors (WONCA)) Peter Calverley, MD University of Nijmegen University Hospital Aintree Nijmegen, The Netherlands Liverpool, UK GOLD SCIENCE COMMITTEE* Teresita S. deGuia, MD Philippine Heart Center Klaus F. Rabe, MD, PhD, Chair Quezon City, Philippines Leiden University Medical Center Leiden, The Netherlands Yoshinosuke Fukuchi, MD (Representing the Asian Pacific Society for Respirology) A. G. Agusti, MD (Effective June 2006) Tokyo, Japan Hospital Universitari Son Dureta Palma de Mallorca, Spain Christine Jenkins, MD Woolcock Institute of Medical Research Antonio Anzueto, MD Sydney, NSW, Australia University of Texas Health Science Center San Antonio, Texas, USA Nikolai Khaltaev, MD (Representing the World Health Organization) Peter J. Barnes, MD Geneva, Switzerland National Heart and Lung Institute London, UK James Kiley, PhD (Representing the National Heart, Lung, and Blood Institute, A.
    [Show full text]
  • 2020 GOLD Pocket Guide
    DISTRIBUTE OR COPY NOT DO - MATERIAL COPYRIGHT POCKET GUIDE TO COPD DIAGNOSIS, MANAGEMENT, AND PREVENTION A Guide for Health Care Professionals 2020 REPORT GLOBAL INITIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE POCKET GUIDE TO COPD DIAGNOSIS, MANAGEMENT, AND PREVENTION A Guide for Health Care Professionals 2020 EDITION DISTRIBUTE OR COPY NOT DO - MATERIAL COPYRIGHT © 2020 Global Initiative for Chronic Obstructive Lung Disease, Inc. i GOLD BOARD OF DIRECTORS GOLD SCIENCE COMMITTEE* (2019) (2019) Alvar Agusti, MD, Chair Claus Vogelmeier, MD, Chair Maria Montes de Oca, MD Respiratory Institute, University of Marburg Hospital Universitario de Caracas Hospital Clinic, IDIBAPS Marburg, Germany Universidad Central de Venezuela Univ. Barcelona and Ciberes Caracas, Venezuela Barcelona, Spain Alvar Agusti, MD Respiratory Institute, Hospital Alberto Papi, MD Richard Beasley, MD Clinic, IDIBAPS University of Ferrara Medical Research Institute of NZ, Univ. Barcelona and Ciberes Ferrara, Italy Wellington, New Zealand Barcelona, Spain Ian Pavord, MA DM Bartolome R. Celli, MD Antonio Anzueto, MD Respiratory Medicine Unit and Oxford Brigham and Women’s Hospital South Texas Veterans Health Care System, Respiratory NIHR Biomedical Research Boston, Massachusetts, USA University of Texas, Health Centre San Antonio, Texas, USA Nuffield Department of Medicine Rongchang Chen, MD University of Oxford Guangzhou Institute of Respiratory Peter Barnes, DM, FRS Oxford, UK Disease National Heart & Lung Institute, Guangzhou, PRC Imperial College Nicolas Roche, MD London,
    [Show full text]
  • Copd: Myths & Misconceptions
    COPD: MYTHS & MISCONCEPTIONS Chronic obstructive pulmonary disease or COPD is a chronic disease of the lungs. Although COPD is a common lung disease there are still misconceptions that surround it. Read on to find out some of the more common COPD myths and the facts that dispel them. 1 MYTH: SHORTNESS OF BREATH IS THE ONLY SYMPTOM OF COPD FACT: Breathlessness is one of the symptoms of COPD but other common signs to look out for include tiredness, a persistent cough which produces phlegm, chest infections and wheezing.1 MYTH: COPD ONLY HAPPENS TO OLDER PEOPLE 2 FACT: COPD can begin in your 40s, or even earlier, although many people are often not diagnosed until their 50s and 60s.2 3 MYTH: COPD IS THE SAME AS ASTHMA FACT: Although symptoms appear similar, asthma and COPD are not the same.3 It is important to get the correct diagnosis from your doctor. MYTH: EXERCISE WILL MAKE COPD WORSE 4 FACT: Exercise has been shown to be safe and beneficial for most people with COPD.4,5 Speak to your doctor or nurse about gentle exercises that are suitable for you. 5 MYTH: SMOKING IS THE ONLY CAUSE OF COPD FACT: Although smoking is a leading cause, exposure to fumes, chemicals, dust or harmful pollutants can also result in COPD developing.6,7 MYTH: A HEALTHY DIET WILL NOT HELP WITH COPD 6 FACT: Maintaining a well-balanced diet, including eating fresh fruit and vegetables, can help you to increase your energy levels and improve your health.8,9,10 7 MYTH: WEIGHT DOES NOT AFFECT COPD FACT: Extra weight can make you more breathless and your symptoms worse.
    [Show full text]
  • Surgical Pathology of Non-Neoplastic Lung Disease Thomas V
    SHORT COURSE Surgical Pathology of Non-Neoplastic Lung Disease Thomas V. Colby, M.D. Department of Laboratory Medicine and Pathology, Mayo Clinic Scottsdale, Scottsdale, Arizona At inception, this course included some neoplastic Case 1: Acute Exacerbation of Idiopathic lesions, but each year, the case mix was changed in Pulmonary Fibrosis response to the comments (and criticism) of the A 51-year-old man had experienced 3 to 4 years attendees. As cases were added and deleted, in the of progressive dyspnea and interstitial infiltrates as end only examples of non-neoplastic lung disease observed on chest radiographs. One week before were discussed. Of the 19 cases used during the death, there was acute worsening of his dyspnea, course of 5 years, the following 8 were selected for with some associated chills and a sore throat. At this presentation. admission, he was hypoxemic, tachypneic, and afe- brile. The clinical impression was an acute (possibly CASES 1, 2, AND 3: IDIOPATHIC INTERSTITIAL infectious) process superimposed on idiopathic PNEUMONIAS AND RELATED LESIONS pulmonary fibrosis (IPF). An open-lung biopsy was performed. The patient died 1 week later. Cultures To the clinician, there are well over 100 causes of and special stains were negative. interstitial pneumonia, but among these, there is a select subgroup that has been called the idiopathic Histologic findings interstitial pneumonias. This group has evolved The open biopsy shows subpleural scarring and from Liebow and Carrington’s (1) classic classifica- microscopic honeycombing, with associated tion of chronic interstitial pneumonias: smooth muscle metaplasia and fibroblastic foci Usual interstitial pneumonia (UIP) (Figs. 1 and 2).
    [Show full text]
  • Aspergillus Fumigatus During Stable State and Exacerbations of Chronic
    ERJ Express. Published on April 18, 2013 as doi: 10.1183/09031936.00162912 Aspergillus fumigatus during stable state and exacerbations of chronic obstructive pulmonary disease Mona Bafadhel1 PhD, [email protected] Susan Mckenna1 RGN, [email protected] Joshua Agbetile1 MBChB, [email protected] Abbie Fairs1 BSc,[email protected] Dhananjay Desai1 MBBS, [email protected] Vijay Mistry1 BSc, [email protected] Joseph P Morley1 BSc, [email protected] Mitesh Pancholi1 BSc, [email protected] Ian D Pavord1 MD, [email protected] Andrew J Wardlaw1 PhD, [email protected] *Catherine H Pashley1 PhD, [email protected] *Christopher E Brightling1 PhD, [email protected] * Joint senior authors Running title: Aspergillus fumigatus in COPD Manuscript word count: 2500 Keywords Aspergillus; Atopy; COPD; exacerbation; FEV1; fungi; neutrophil; 1 Copyright 2013 by the European Respiratory Society. 1Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, The University of Leicester, Leicester. United Kingdom Address for correspondence: Dr Mona Bafadhel, Institute for Lung Health, Glenfield Hospital, Leicester, LE3 9QP, UK; Tel: +44 116 256 3789; Email: [email protected] Source of funding The study was funded by the Medical Research Council (UK), a senior Wellcome Fellowship (CEB) and the Midlands Asthma Allergy Research Association (MAARA); and the research was performed in laboratories part funded by the European Regional Development Fund (ERDF 05567). This article presents independent research funded by the National Institute for Health Research (NIHR). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.
    [Show full text]