Bronchiolitis After Lung Transplantation Lymphoid Tissue In

Total Page:16

File Type:pdf, Size:1020Kb

Bronchiolitis After Lung Transplantation Lymphoid Tissue In The Role of Intrapulmonary De Novo Lymphoid Tissue in Obliterative Bronchiolitis after Lung Transplantation This information is current as Masaaki Sato, Shin Hirayama, David M. Hwang, Humberto of September 25, 2021. Lara-Guerra, Dirk Wagnetz, Thomas K. Waddell, Mingyao Liu and Shaf Keshavjee J Immunol 2009; 182:7307-7316; ; doi: 10.4049/jimmunol.0803606 http://www.jimmunol.org/content/182/11/7307 Downloaded from References This article cites 46 articles, 4 of which you can access for free at: http://www.jimmunol.org/content/182/11/7307.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 25, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology The Role of Intrapulmonary De Novo Lymphoid Tissue in Obliterative Bronchiolitis after Lung Transplantation1 Masaaki Sato,* Shin Hirayama,* David M. Hwang,*† Humberto Lara-Guerra,* Dirk Wagnetz,* Thomas K. Waddell,* Mingyao Liu,* and Shaf Keshavjee2* Chronic rejection after lung transplantation is manifested as obliterative bronchiolitis (OB). The development of de novo lymphoid tissue (lymphoid neogenesis) may contribute to local immune responses in small airways. Compared with normal lungs, the lung tissue of 13 lung transplant recipients who developed OB demonstrated a significantly larger number of small, airway-associated, peripheral node addressin-positive (PNAd؉) high endothelial venules (HEVs) unique to lymphoid tissue (p < 0.001). HEVs were most abundant in lesions of lymphocytic bronchiolitis and “active” OB infiltrated by lymphocytes compared with those of “in- active” OB. T cells in lymphocytic bronchiolitis and active OB were predominantly of the CD45RO؉CCR7؊ effector memory phenotype. Similar lymphoid tissue was also observed in the rat lung after intrapulmonary transplantation of allograft trachea Downloaded from (Brown Norway (BN) to Lewis), but not after isograft transplantation. Subsequent orthotopic transplantation of the recipient ؋ Lewis lung containing a BN trachea into an F1 (Lewis BN) rat demonstrated stable homing of Lewis-derived T cells in the lung and their Ag-specific effector function against the secondary intrapulmonary BN trachea. In conclusion, we found de novo lymphoid tissue in the lung composed of effector memory T cells and HEVs but lacking delineated T cell and B cell zones. This de novo lymphoid tissue may play a critical role in chronic local immune responses after lung transplantation. The Journal of Immunology, 2009, 182: 7307–7316. http://www.jimmunol.org/ e novo lymphoid tissue formation or lymphoid neogen- However, formation of TLO after lung transplantation has not esis has recently been recognized as a potentially im- been reported and is controversial. Chronic rejection after lung D portant mechanism that supports chronic inflammation transplantation is manifested by obliterative bronchiolitis (OB), a in peripheral tissue (1). The best characterized de novo lymphoid chronic inflammatory and fibroproliferative condition in small air- tissue is the tertiary lymphoid organ (TLO),3 a structure resem- ways, and its clinical correlate, bronchiolitis obliterans syndrome bling a lymph node that includes high endothelial venules (HEVs), (BOS) (10). In the lung, TLO is considered to be represented by an well-defined T cell and B cell zones, and a germinal center ac- inducible form of bronchus-associated lymphoid tissue (BALT), by guest on September 25, 2021 companying follicular dendritic cells (2). TLO has been reported in namely iBALT (1, 11). Formation of iBALT has been reported in various chronic inflammatory conditions such as autoimmune (3, various chronic inflammatory lung diseases such as emphysema 4) and chronic infectious diseases (5, 6). (12), pulmonary fibrosis (13), and chronic hypersensitive pneumo- Chronic rejection after organ transplantation is a condition in nitis (14). In contrast, Hasegawa et al. demonstrated a negative which alloantigen persists and chronic inflammation occurs. In- result regarding the relationship between OB/BOS and BALT, deed, development of TLO has been reported in various tissues and which should theoretically include iBALT (15). Although the organs after transplantation, including human cardiac and renal study using transbronchial biopsies was limited in its sensitivity to allografts (7) and animal models of cardiac (8), skin (9), and vas- detect OB lesions and (i)BALT, it is possible that de novo lym- cular (7) allografts. phoid tissue after lung transplantation does not form the conven- tional structure of TLO with HEVs, T and B cell zones, and ger- minal center formation. *Latner Thoracic Surgery Research Laboratories, Toronto General Research Institute Interestingly, an evolving concept proposed by van Panhuys † and Department of Pathology, University Health Network, University of Toronto, et al. indicates the existence of “effector lymphoid tissue” (ELT) Toronto, Ontario, Canada that exerts effector function by collecting effector and effector Received for publication October 27, 2008. Accepted for publication March 31, 2009. memory T cells but does not necessarily take the conventional The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance anatomical form of TLO or iBALT (16). Increasing evidence sug- with 18 U.S.C. Section 1734 solely to indicate this fact. gests that the lung might be an important reservoir of effector and 1 This work was supported by the Canadian Cystic Fibrosis Foundation. M.S. is a effector memory T cells (17, 18). In a s.c. tracheal transplant model recipient of Wyeth/Canadian Institutes of Health Research Rx&D Industrial Partner of OB, preferential localization of effector memory CD4ϩ and Program Fellowship (2005–2007) and Canadian Cystic Fibrosis Foundation Postdoc- ϩ toral Fellowship (2007–2009). CD8 T cells to the lung parenchyma and airways has been dem- 2 Address correspondence and reprint requests to Dr. Shaf Keshavjee, Toronto Lung onstrated (19). Transplant Program, Toronto General Hospital, 200 Elizabeth Street 9N947, Toronto, Thus, we hypothesized that lymphoid neogenesis plays an im- Ontario, Canada M5G 2C4. E-mail address: [email protected] portant role in chronic rejection after lung transplantation. To ad- 3 Abbreviations used in this paper: TLO, tertiary lymphoid organ; BALT, bronchus- dress the hypothesis, we conducted careful histological and immu- associated lymphoid tissue; BN, Brown Norway; BOS, bronchiolitis obliterans; ELT, effector lymphoid tissue; HEV, high endothelial venule; iBALT, inducible BALT; nohistochemical analyses of the lungs that were explanted at the MAdCAM, mucosal addressin cell adhesion molecule; OB, obliterative bronchiolitis; time of retransplantation due to OB/BOS after the initial lung PNAd, peripheral node addressin. transplantation. Furthermore, we have devised an animal model Copyright © 2009 by The American Association of Immunologists, Inc. 0022-1767/09/$2.00 that combines a rat intrapulmonary tracheal transplant model of www.jimmunol.org/cgi/doi/10.4049/jimmunol.0803606 7308 LYMPHOID NEOGENESIS AFTER LUNG TRANSPLANTATION Table I. Demographics of lung transplant recipients who were diagnosed with OB/BOSa Age at Time from 1st Primary Examined Lung No. of Lymphocytic No. of Active OB No. of Inactive OB Sex 2nd Tx Tx (mo) Diagnosis Area (cm2) Bronchiolitis (area in cm2) (area in cm2) (area in cm2) Male 20 10.4 CF 4.30 3 (2.6) 2 (0.5) 2 (0.5) Female 36 10.7 CF 5.91 3 (2.0) 6 (1.0) 0 (0) Female 20 21.5 CF 1.15 0 (0) 1 (0.9) 0 (0) Male 36 34.2 BE 1.93 2 (0.4) 3 (1.6) 7 (3.6) Female 26 35.0 IPF 8.62 7 (4.0) 7 (0.8) 12 (1.4) Male 57 40.6 COPD 12.82 5 (5.8) 4 (0.3) 10 (0.8) Female 60 52.2 IPF 12.08 0 (0) 0 (0) 23 (1.9) Male 23 69.3 OB 3.85 6 (3.3) 2 (0.5) 0 (0) Female 40 82.2 IPF 3.76 4 (2.1) 2 (0.5) 4 (1.1) Female 53 88.2 OB 17.67 0 (0) 1 (0.1) 0 (0) Female 48 92.2 BE 3.90 6 (2.1) 5 (1.3) 0 (0) Female 35 132.1 OB 6.37 7 (2.2) 9 (1.4) 11 (1.7) Female 39b 18.6b BE 3.32 0 (0) 1 (1.2) 7 (2.1) Average Ϯ SEM 38.0 Ϯ 3.8 52.9 Ϯ 10.4 6.59 Ϯ 1.4 3.31 Ϯ 0.8 (1.89 Ϯ 0.5) 3.31 Ϯ 0.8 (0.77 Ϯ 0.1) 5.85 Ϯ 1.9 (1.00 Ϯ 0.3) a Tx, Transplantation; BE, bronchiectasis; CF, cystic fibrosis; COPD, chronic obstructive pulmonary disorder; IPF, idiopathic pulmonary fibrosis; OB, obliterative bronchi- olitis (idiopathic or secondary to hematopoietic stem cell transplantation). b This patient underwent open lung biopsy. The age at 2nd Tx indicates the age at the time of open lung biopsy. The other 12 patients underwent retransplantation for diagnosed OB/BOS after the initial lung transplantation. Downloaded from OB (20) and orthotopic lung transplantation to examine the effec- Histology and immunofluorescence labeling tor function of intrapulmonary de novo lymphoid tissue after Formalin-fixed, paraffin-embedded tissues cut into 5-␮m-thick sections transplantation. were used for standard H&E stain, elastic trichrome stain, and all human immunofluorescence labeling studies.
Recommended publications
  • The Lung in Rheumatoid Arthritis
    ARTHRITIS & RHEUMATOLOGY Vol. 70, No. 10, October 2018, pp 1544–1554 DOI 10.1002/art.40574 © 2018, American College of Rheumatology REVIEW The Lung in Rheumatoid Arthritis Focus on Interstitial Lung Disease Paolo Spagnolo,1 Joyce S. Lee,2 Nicola Sverzellati,3 Giulio Rossi,4 and Vincent Cottin5 Interstitial lung disease (ILD) is an increasingly and histopathologic features with idiopathic pulmonary recognized complication of rheumatoid arthritis (RA) fibrosis, the most common and severe of the idiopathic and is associated with significant morbidity and mortal- interstitial pneumonias, suggesting the existence of com- ity. In addition, approximately one-third of patients have mon mechanistic pathways and possibly therapeutic tar- subclinical disease with varying degrees of functional gets. There remain substantial gaps in our knowledge of impairment. Although risk factors for RA-related ILD RA-related ILD. Concerted multinational efforts by are well established (e.g., older age, male sex, ever smok- expert centers has the potential to elucidate the basic ing, and seropositivity for rheumatoid factor and anti– mechanisms underlying RA-related UIP and other sub- cyclic citrullinated peptide), little is known about optimal types of RA-related ILD and facilitate the development of disease assessment, treatment, and monitoring, particu- more efficacious and safer drugs. larly in patients with progressive disease. Patients with RA-related ILD are also at high risk of infection and drug toxicity, which, along with comorbidities, compli- Introduction cates further treatment decision-making. There are dis- Pulmonary involvement is a common extraarticular tinct histopathologic patterns of RA-related ILD with manifestation of rheumatoid arthritis (RA) and occurs, to different clinical phenotypes, natural histories, and prog- some extent, in 60–80% of patients with RA (1,2).
    [Show full text]
  • Pneumothorax in Patients with Idiopathic Pulmonary Fibrosis
    Yamazaki et al. BMC Pulm Med (2021) 21:5 https://doi.org/10.1186/s12890-020-01370-w RESEARCH ARTICLE Open Access Pneumothorax in patients with idiopathic pulmonary fbrosis: a real-world experience Ryo Yamazaki, Osamu Nishiyama* , Kyuya Gose, Sho Saeki, Hiroyuki Sano, Takashi Iwanaga and Yuji Tohda Abstract Background: Some patients with idiopathic pulmonary fbrosis (IPF) develop pneumothorax. However, the charac- teristics of pneumothorax in patients with IPF have not been elucidated. The purpose of this study was to clarify the clinical course, actual management, and treatment outcomes of pneumothorax in patients with IPF. Methods: Consecutive patients with IPF who were admitted for pneumothorax between January 2008 and Decem- ber 2018 were included. The success rates of treatment for pneumothorax, hospital mortality, and recurrence rate after discharge were examined. Results: During the study period, 36 patients with IPF were admitted with pneumothorax a total of 58 times. During the frst admission, 15 patients (41.7%) did not receive chest tube drainage, but 21 (58.3%) did. Of the 21 patients, 8 (38.1%) received additional therapy after chest drainage. The respective treatment success rates were 86.6% and 66.7% in patients who underwent observation only vs chest tube drainage. The respective hospital mortality rates were 13.3% and 38.0%. The total pneumothorax recurrence rate after hospital discharge was 34.6% (n 9). = Conclusions: Pneumothorax in patients with IPF was difcult to treat successfully, had a relatively poor prognosis, and showed a high recurrence rate. Keywords: Idiopathic pulmonary fbrosis, Hospitalization, Pneumothorax, Recurrence, Treatment Background pneumothorax was signifcantly associated with poor Idiopathic pulmonary fbrosis (IPF) is a specifc form survival in patients with IPF [11].
    [Show full text]
  • Interstitial Lung Disease (ILD) Is a Broad Category of Lung Diseases That Includes More Than 130 Disorders Which Are Characterized by Scarring (I.E
    Interstitial Lung Disease Interstitial lung disease (ILD) is a broad category of lung diseases that includes more than 130 disorders which are characterized by scarring (i.e. “fibrosis”) and/or inflammation of the lungs. ILD accounts for 15 percent of the cases seen by pulmonologists (lung specialists). In ILD, the tissue in the lungs becomes inflamed and/or scarred. The interstitium of the lung refers to the area in and around the small blood vessels and alveoli (air sacs). This is where the exchange of oxygen and carbon dioxide take place. Inflammation and scarring of the interstitium disrupts this tissue. This leads to a decrease in the ability of the lungs to extract oxygen from the air. There are different types of interstitial lung disease that fall under the category of ILD. Some of the common ones are listed below: Idiopathic (unknown) Pulmonary Fibrosis Connective tissue or autoimmune disease-related ILD Hypersensitivity Pneumonitis Wegener’s Granulomatosis Churg Strauss (vasculitis) Chronic Eosinophilic Pneumonia Eosinophilic granuloma (Langerhan’s cell histoiocytosis) Drug Induced Lung Disease Sarcoidosis Bronchiolitis Obliterans Lymphangioleiomyomatosis The progression of ILD varies from disease to disease and from person to person. It is important to determine the specific form of ILD in each person because what happens over time and the treatment may differ depending on the cause.. Each person responds differently to treatment, so it is important for your doctor to monitor your treatment. What are Common Symptoms of ILD? The most common symptoms of ILD are shortness of breath with exercise and a non- productive cough. These symptoms are generally slowly progressive, although rapid worsening can also occur.
    [Show full text]
  • Pulmonary Fibrosis What It Is and How It Affects Your Breathing
    Pulmonary fibrosis What it is and how it affects your breathing What is pulmonary fibrosis? Pulmonary fibrosis is a term that covers many different conditions that cause scar tissue to build up in your lungs. This build-up of scar tissue, which makes your lungs stiff, is called fibrosis. Pulmonary fibrosis is a type of interstitial lung disease (ILD). ‘Interstitial’ means the disease affects the interstitium, the lace-like network of tissue that supports the air sacs in your lungs. There are more than 200 different ILDs. Some types of pulmonary fibrosis have an identifiable cause. But for many types, a definite cause cannot be found. In ILDs, there can be scarring in your lungs or inflammation in your lungs. Some ILDs mostly cause scarring, some mostly cause inflammation. But often there is a combination of these processes going on. Which of these processes is dominant can determine what kind of treatment you may have. The treatment and outlook for different types of pulmonary fibrosis vary considerably, so if you’re not sure about your diagnosis, check with your doctor or nurse for the exact name of your lung condition. All types of pulmonary fibrosis are rare. We have specific information about those seen most often in other PDFs: • idiopathic pulmonary fibrosis or IPF • hypersensitivity pneumonitis formerly called extrinsic allergic alveolitis • pneumoconiosis, also known as an occupational interstitial lung disease • pulmonary fibrosis associated with connective tissue and autoimmune diseases • drug-induced pulmonary fibrosis Although we do not always know what causes pulmonary fibrosis, we do know it is not a form of cancer or cystic fibrosis, and it is not contagious.
    [Show full text]
  • Silicosis and Silica Exposure: What Physicians Need to Know
    Silicosis and Silica Exposure: What Physicians Need to Know What is silicosis and why are workers at risk? Why should I be aware of my patient’s work history? Silicosis is an incurable interstitial fibronodular lung disease frequently characterized Should your patient present with signs and symptoms of respiratory disease, consider by pulmonary fibrosis as the result of exposure to respirable crystalline silica dust. occupational exposure sources. Determining whether your patient has any Workers in industries such as mining, manufacturing, demolition, agriculture, workplace silica exposure is the first step towards preventing silicosis. construction, stone cutting, and pottery are all at risk for developing silicosis. How can I help protect my patients from silica dust? What are the diagnostic criteria for silicosis? Discuss prevention methods with your patient, and/or refer your patient to the Evidence of crystalline silica exposure New York State Occupational Health Clinic Network. Chest radiography with disease features Encourage patients to use all safety and exposure controls at their worksite, as Elimination of competing differentials well as appropriately maintained, approved, and fitted respirators. Observe for early signs and symptoms of respiratory disease. Provide medical New York State Occupational Health Clinic Network monitoring and emphasize the importance of routine medical exams. If you suspect your patient may suffer from an occupational disease, the Recommend smoking cessation programs. 1-866-NY-QUITS New York State Occupational Health Clinic Network is a statewide Urge patients to not bring dust home. This can be accomplished by changing into clean clothes and shoes, and if possible, showering prior to leaving their network of clinics specially equipped to handle workplace illness/injury, worksite.
    [Show full text]
  • Cryptogenic Organizing Pneumonia
    462 Cryptogenic Organizing Pneumonia Vincent Cottin, M.D., Ph.D. 1 Jean-François Cordier, M.D. 1 1 Hospices Civils de Lyon, Louis Pradel Hospital, National Reference Address for correspondence and reprint requests Vincent Cottin, Centre for Rare Pulmonary Diseases, Competence Centre for M.D., Ph.D., Hôpital Louis Pradel, 28 avenue Doyen Lépine, F-69677 Pulmonary Hypertension, Department of Respiratory Medicine, Lyon Cedex, France (e-mail: [email protected]). University Claude Bernard Lyon I, University of Lyon, Lyon, France Semin Respir Crit Care Med 2012;33:462–475. Abstract Organizing pneumonia (OP) is a pathological pattern defined by the characteristic presence of buds of granulation tissue within the lumen of distal pulmonary airspaces consisting of fibroblasts and myofibroblasts intermixed with loose connective matrix. This pattern is the hallmark of a clinical pathological entity, namely cryptogenic organizing pneumonia (COP) when no cause or etiologic context is found. The process of intraalveolar organization results from a sequence of alveolar injury, alveolar deposition of fibrin, and colonization of fibrin with proliferating fibroblasts. A tremen- dous challenge for research is represented by the analysis of features that differentiate the reversible process of OP from that of fibroblastic foci driving irreversible fibrosis in usual interstitial pneumonia because they may determine the different outcomes of COP and idiopathic pulmonary fibrosis (IPF), respectively. Three main imaging patterns of COP have been described: (1) multiple patchy alveolar opacities (typical pattern), (2) solitary focal nodule or mass (focal pattern), and (3) diffuse infiltrative opacities, although several other uncommon patterns have been reported, especially the reversed halo sign (atoll sign).
    [Show full text]
  • PULMONARY HYPERTENSION in SCLERODERMA PULMONARY HYPERTENSION Pulmonary Hypertension (PH) Is High Blood Pressure in the Blood Vessels of the Lungs
    PULMONARY HYPERTENSION IN SCLERODERMA PULMONARY HYPERTENSION Pulmonary hypertension (PH) is high blood pressure in the blood vessels of the lungs. If the high blood pressure in the lungs is due to narrowing of the pulmonary arteries leading to increased pulmonary vascular resistance, it is known as pulmonary arterial hypertension (PAH). When the blood pressure inside the pulmonary vessels is high, the right side of the heart has to pump harder to move blood into the lungs to pick up oxygen. This can lead to failure of the right side of the heart. Patients with scleroderma are at increased risk for developing PH from several mechanisms. Frequently patients with scleroderma have multiple causes of their PH. Patients who have limited cutaneous scleroderma (formerly known as CREST syndrome) are more likely to have PAH than those patients who have diffuse cutaneous systemic sclerosis. PAH may be the result of the same processes that cause damage to small blood vessels in the systemic circulation of patients with scleroderma. The lining cells of the blood vessels (endothelial cells) are injured and excessive connective tissue is laid down inside the blood vessel walls. The muscle that constricts the blood vessel may overgrow and narrow the blood vessel. Other scleroderma patients may have PH because they have significant scarring (fibrosis) of their lungs. This reduces the blood oxygen level, which in turn, may cause a reflex increase in blood pressure in the pulmonary arteries. WHAT ARE THE SYMPTOMS OF PULMONARY HYPERTENSION? Patients with mild PH may have no symptoms. Patients with moderate or severe PH usually notice shortness of breath (dyspnea), especially with exercise.
    [Show full text]
  • Idiopathic Pulmonary Fibrosis
    IDIOPATHIC PULMONARY FIBROSIS Guidelines for Diagnosis UPDATE 2019 and Management An ATS Pocket Publication ATS Pocket Guide _v11_051319 copy.indd 1 5/13/19 10:51 AM GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF IDIOPATHIC PULMONARY FIBROSIS: UPDATE 2019 AN AMERICAN THORACIC SOCIETY POCKET PUBLICATION This pocket guide is a condensed version of the 2011, 2015 and 2018 American Thoracic Society (ATS), European Respiratory Society (ERS), Japanese Respiratory Society (JRS), and Latin American Thoracic Association (ALAT) Evidence-Based Guidelines for Diagnosis and Management of Idiopathic Pulmonary Fibrosis (IPF). This pocket guide was complied by Ganesh Raghu, MD and Bridget Collins, MD, University of Washington, Seattle from excerpts taken from the published official documents of the ATS. Readers are encouraged to consult the full versions as well as the online supplements, which are available at http://ajrccm.atsjournals.org/content/183/6/788.long. All information in this pocket guide is derived from the 2011, 2015 and 2018 IPF guidelines unless otherwise noted. Some tables and figures are reprinted with the permission from the journals referenced. Produced in Collaboration with Boehringer Ingelheim Pharmaceuticals, Inc. 2 Guidelines for the Diagnosis and Management of Idiopathic Pulmonary Fibrosis ATS Pocket Guide _v11_051319 copy.indd 2 5/13/19 10:51 AM CONTENTS List of Figures and Tables ..................................................................................................................4 List of Abbreviations and Acronyms
    [Show full text]
  • Difficulty in Management of Pneumothorax in an Octogenarian with Pulmonary Fibrosis
    doi • 10.5578/tt.66527 Tuberk Toraks 2018;66(1):76-77 Geliş Tarihi/Received:03.02.2018 • Kabul Ediliş Tarihi/Accepted: 19.02.2018 Difficulty in management of pneumothorax in an octogenarian with pulmonary fibrosis 1 Shinichiro OKAUCHI 1 1 Division of Respiratory Medicine, Mito Medical Center, Tsukuba University, Hajime OSAWA Mito, Japan 1 Hiroaki SATOH 1 Tsukuba Üniversitesi Mito Tıp Merkezi, Solunum Bölümü, Mito, Japonya EDİTÖRE MEKTUP EDİTÖRE LETTER TO THE LETTER TO EDITOR Dear Editor, 23rd day (Figure 1-C). Two months after the removal of the chest tube, the respiratory condition of the patient Treatment of pneumothorax in patients with idiopathic does not deteriorate. pulmonary fibrosis (IPF) is often problematic. Especially in elderly patients with IPF, treatment of pneumothorax Pneumothorax is a common complication in IPF may often be unsuccessful due to unexpected compli- patients, who can present increased morbidity caused cations. We would like to share our experience in by exacerbation of the respiratory manifestations of the pneumothorax treatment in a very elderly patient with disease, which can lead to respiratory failure and death IPF. (1). Pneumothorax in patients with IPF, air leaks from complicatedly modified lungs are sustained, and pul- An 84-year-old man was referred to our hospital with monary re-expansion is difficult to achieve due to an exacerbation of dyspnea. Ten years prior to this contraction tendency. If the lungs are re-expanded, presentation, the patient was diagnosed with idiopath- fortunately, pleurodesis is a conceivable effective treat- ic pulmonary fibrosis (IPF) (Figure 1-A). In addition to ment, but this is also problematic.
    [Show full text]
  • Idiopathic Pulmonary Fibrosis
    Idiopathic Pulmonary Fibrosis Produced in collaboration with Boehringer Ingelheim Pharmaceuticals, Inc. PC-US-110950 Idiopathic Pulmonary Fibrosis History Why Family Physicians Knowledge of a patient’s medical history and exposures is vital to diagnosing IPF and essential to excluding other ILDs. Questions Should Know About IPF should focus on the following: As front-line health care providers, family physicians play an ● Smoking history. Cigarette smoking is strongly associated essential role in the early detection of idiopathic pulmonary with IPF, especially individuals with a history of more than fibrosis (IPF) and the timely referral to a pulmonologist. The 20 pack-years.2,4 disease is rare and includes signs and symptoms that make ● Other medical conditions. Gastroesophageal reflux disease, it difficult to distinguish among other interstitial lung diseases hiatal hernia, pulmonary malignancy, coronary artery disease, (ILDs). By identifying suspected cases of IPF at primary care obstructive sleep apnea, obesity, emphysema, and pulmonary visits, family physicians have an opportunity to refer patients hypertension are comorbid conditions frequently associated earlier and enable diagnosis and treatment sooner. This makes 2,4 education about IPF a key factor in early detection, which can with IPF. potentially lead to better health outcomes. Diagnostic criteria ● Occupational and environmental exposures. Chronic, and treatment options presented in this brochure are based on repeated exposure to metal dusts (brass, lead, and steel), wood specialist guidelines that have not been reviewed or endorsed dust (pine), and aerosolized organic antigens (primarily, molds, by the AAFP. However given the limited guidance for IPF, the bacteria, and bird antigens) have been associated with IPF.
    [Show full text]
  • Idiopathic Pulmonary Fibrosis and Nonspecific Interstitial Pneumonia Should Stay Separate
    data collection and J. Fonseca (Biostatistics and Medical diagnosed mild asthma: the effect of 6 months of treatment Informatics, Faculty of Medicine, University of Porto and with budesonide or disodium cromoglycate. Allergy 2004; Immuno-allergology, Hospital of Sa˜o Joa˜o, Porto, Portugal) for 59: 839–844. manuscript revision. 6 American Thoracic Society, European Respiratory Society. ATS/ERS recommendations for standardized procedures for the online and offline measurement of exhaled lower REFERENCES respiratory nitric oxide and nasal nitric oxide, 2005. Am J 1 Helenius I, Haahtela T. Allergy and asthma in elite summer Respir Crit Care Med 2005; 171: 912–930. sport athletes. J Allergy Clin Immunol 2000; 106: 444–452. 7 Sterk PJ, Fabbri LM, Quanjer PhH, et al. Airway responsive- 2 Helenius IJ, Tikkanen HO, Sarna S, Haahtela T. Asthma and ness. Standardized challenge testing with pharmacological, increased bronchial responsiveness in elite athletes: atopy physical and sensitizing stimuli in adults. Report Working and sport event as risk factors. J Allergy Clin Immunol 1998; Party Standardization of Lung Function Tests, European 101: 646–652. Community for Steel and Coal. Official Statement of the 3 Helenius IJ, Rytila¨ P, Metso T, Haahtela T, Venge P, European Respiratory Society. Eur Respir J 1993; 6: Suppl. 16, Tikkanen HO. Respiratory symptoms, bronchial responsive- 53–83. ness, and cellular characteristics of induced sputum in elite 8 Bonetto G, Corradi M, Carraro S, et al. Longitudinal swimmers. Allergy 1998; 53: 346–352. monitoring of lung injury in children after acute chlorine 4 Piacentini GL, Rigotti E, Bodini A, Peroni D, Boner AL. exposure in a swimming pool.
    [Show full text]
  • Navigating Pulmonary Fibrosis
    CHEST Foundation American College of Chest Physicians 2595 Patriot Boulevard Glenview, IL 60026 chestfoundation.org/pf Other patient education guides available from the CHEST Foundation in print and on our website: chestfoundation.org/patienteducation Disclaimer: The American College of Chest Physicians (“CHEST”) and its officers, regents, executive committee members, members, related entities, employees, representatives, and other agents (collectively, “CHEST Parties”) are not responsible in any capacity for, do not warrant and expressly disclaim all liability for, any content whatsoever in any CHEST publication or other product (in any medium) and the use or reliance on any such content, all such responsibility being solely that of the authors or the advertisers, as the case may be. By way of example, without limiting the Navigating Pulmonary Fibrosis foregoing, this disclaimer of liability applies to the accuracy, completeness, effectiveness, quality, appearance, ideas, or products, as the case may be, of or resulting from any statements, references, articles, positions, claimed diagnosis, claimed possible treatments, services, or advertising, express or implied, contained in any CHEST publication or other product. Furthermore, the content should not be considered medical advice PATIENT EDUCATION GUIDE and is not intended to replace consultation with a qualified medical professional. Under no circumstances, including negligence, shall any CHEST Parties be liable for any DIRECT, INDIRECT, INCIDENTAL, SPECIAL or CONSEQUENTIAL DAMAGES, or LOST PROFITS that result from any of the foregoing, regardless of legal theory and whether or not claimant was advised of the possibility of such damages. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication.
    [Show full text]