DOCSLIB.ORG

Bronchiolitis Obliterans Organizing Pneumonia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Bronchiolitis Obliterans Organizing Pneumonia REVIEW ARTICLE Bronchiolitis Obliterans Organizing Pneumonia Gary R. Epler, MD ronchiolar disorders can be divided into 2 general categories: (1) airway disorders (cel- lular bronchiolitis and obliterative bronchiolitis) and (2) parenchymal disorders (res- piratory bronchiolitis–interstitial lung disease, which occurs in smokers and is treat- able with smoking cessation or corticosteroid therapy, and bronchiolitis obliterans organizingB pneumonia, an inflammatory lung disease simultaneously involving the terminal bron- chioles and alveoli). This article reviews the clinical findings and therapeutic management of bron- chiolitis obliterans organizing pneumonia. Arch Intern Med. 2001;161:158-164 Bronchiolitis obliterans organizing pneu- The BOOP pattern might also occur as a monia (BOOP) was described in 19851 as secondary process in several clinical set- a distinct entity, with different clinical, ra- tings, such as the inflammatory-appearing diographic, and prognostic features than lesion of UIP/IPF, with Wegener granulo- the airway disorder obliterative bronchi- matosis, in the walls of lung abscesses, olitis2 and the interstitial fibrotic lung dis- around lymphoma or other neoplasms, and order usual interstitial pneumonia/ with bronchiectasis. In these patients, the idiopathic pulmonary fibrosis (UIP/IPF).3 underlying process is the primary cause of BOOP is characterized by polyploid en- symptoms and the subsequent clinical dobronchial connective tissue masses com- course. posed of myxoid fibroblastic tissue resem- The terms organizing pneumonia and bling granulation tissue filling the lumens cryptogenic organizing pneumonia are some- of terminal and respiratory bronchioles and times used for the broad category of pa- extending in a continuous fashion into al- tients with organizing pneumonia. There veolar ducts and alveoli, representing an are several reasons that the term BOOP organizing pneumonia (Figure 1).1-3 should continue to be used for the clini- Other histological features include cen- cal disorder and corresponding pathologi- tral clusters of mononuclear inflamma- cal lesion described in this review. First, tory cells possibly found in the intralumi- investigators and clinicians throughout the nal polyps (the polyps appear to float freely world recognize the clinical and patho- within a bronchiole or are focally attached logical features of this disorder, and they to the wall), chronic inflammation in the commonly use the term BOOP. Second, walls of the surrounding alveoli with re- BOOP is a histological process that in- active type II cells, increased foamy mac- volves distal airways and alveoli simulta- rophages in the alveoli, and preserved lung neously. Although various lung diseases architecture.2 represent a chronic inflammatory pro- BOOP continues to be reported cess, it is now apparent that the pro- throughout the world.4-7 Most patients have cesses differ markedly among various idiopathic BOOP, but there are several diseases, such as chronic obstructive known causes of BOOP, and several sys- pulmonary disease, asthma, and BOOP, temic disorders have BOOP as an associ- with different inflammatory cells, media- ated primary pulmonary lesion (Table). tors, inflammatory effects, and response to treatment.8 Therefore, an inflamma- From Harvard Medical School, Pulmonary and Critical Care Medicine, Brigham and tory lesion that involves only airways or Women’s Hospital, Boston, Mass. only alveoli may have different in- (REPRINTED) ARCH INTERN MED/ VOL 161, JAN 22, 2001 WWW.ARCHINTERNMED.COM 158 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 A Classification of BOOP* Idiopathic BOOP Rapidly progressive BOOP Focal nodular BOOP Postinfection BOOP Chlamydia, Legionella, and Mycoplasma Adenovirus, cytomegalovirus, and influenza virus Malaria and Pneumocystis Cryptococcus Drug-related BOOP Antibiotics: amphotericin B, cephalosporins, minocycline, nitrofurantoin, sulfasalazine, and sulfamethoxypyridazine Bleomycin sulfate and methotrexate Gold Amiodarone Illicit use of cocaine B L-tryptophan Phenytoin Carbamazepine Ticlopidine hydrochloride Rheumatologic or connective tissue BOOP Lupus erythematosus Rheumatoid arthritis Sjögren syndrome and Sweet syndrome Polymyositis-dermatomyositis Scleroderma–progressive systemic sclerosis Ankylosing spondylitis Polymylagia rheumatica Behçet syndrome Immunologic disorder BOOP Common variable immunodeficiency syndrome Essential mixed cryoglobulinemia Organ transplantation BOOP Bone marrow, lung, and renal Figure 1. A, Intraluminal organization and polypoid granulation tissue within a small bronchiole. Radiotherapy BOOP B, Organization and polypoid granulation tissue within small bronchioles, alveolar ducts, and alveoli. Environmental exposures The associated alveolar walls show type II cell metaplasia and mild inflammatory thickening. Courtesy Textile printing dye of Thomas V. Colby, MD, Department of Pathology, Mayo Clinic Scottsdale (Ariz) (both parts). Penicillium mold dust House fire Miscellaneous BOOP Inflammatory bowel disease flammatory components than the PATHOGENESIS OF BOOP Lymphoma and cancer BOOP lesion that involves airway T-cell chronic lymphocytic leukemia and alveoli simultaneously. Third, BOOP is an inflammatory lung dis- Human immunodeficiency virus investigations of specific treat- ease and thus is related to the inflam- infection ments for BOOP will be more matory pathway rather than the fi- Myelodysplastic syndrome Hunner interstitial cystitis strongly positive if the specific defi- brosing pathway that occurs with Chronic thydroiditis and alcoholic nition of BOOP is used for inclu- UIP/IPF. The inflammatory re- cirrhosis sion of patients rather than using the sponse associated with disorders such Seasonal syndrome with cholestasis broad definition of organizing pneu- as asthma, chronic obstructive pul- Primary biliary cirrhosis monia. This is similar to IPF, in monary disease, granulomatous dis- Coronary artery bypass graft surgery which many distinct histological dis- eases, and BOOP have common fea- *BOOP indicates bronchiolitis obliterans orders were included in this cat- tures of the sequential inflammatory organizing pneumonia. egory in the past, resulting in dilu- response, yet these disorders seem to tion of the actual mechanism and have differences that have not yet poor treatment results. Now that IPF been fully characterized. These dif- and UIP/IPF; in BOOP it can be com- is limited to UIP,3 the opportunity ferences are important because treat- pletely reversed by corticosteroid to fully characterize the fibrotic path- ment directed toward one type of in- therapy, but in UIP/IPF this tissue way is much greater, and antifi- flammatory response might not be participates in the remodeling and brotic treatment tailored to this fi- effective against another type.8 destruction of the interstitium.9,10 brotic pathway will be tested more There is newly formed fibro- Reasons for the response to cortico- efficiently and accurately. myxoid connective tissue in BOOP steroid in BOOP and the destruc- (REPRINTED) ARCH INTERN MED/ VOL 161, JAN 22, 2001 WWW.ARCHINTERNMED.COM 159 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 A B C Figure 2. A, Chest radiograph of a 54-year-old man with a flulike illness, bilateral crackles, decreased vital capacity, and a decreased diffusing capacity that shows bilateral patchy infiltrates in the lower lungs. B, High-resolution chest computed tomographic scan shows areas of patchy consolidation and ground glass opacities. Courtesy of Philip Costello, MD, and Andetta R. Hunsaker, MD, Department of Radiology, Brigham and Women’s Hospital, Boston, Mass. C, Chest computed tomographic scan shows a triangular area of consolidation posteriorly. tion in UIP/IPF remain unknown.11 opacities occurring at the bases are be recommend as first-line treat- There seems to be abundant capil- usually associated with a poorer ment for patients with symptomatic larization in the intra-airway fibro- prognosis; however, a study6 of and progressive disease. Patients with myxoid lesions in BOOP compared BOOP in 23 patients in Korea indi- asymptomatic mass lesions or non- with minimal vascularization in UIP/ cated recovery in all patients regard- progressive disease can be observed IPF.9 This might be because of vas- less of their radiographic findings. and treated at a later time if needed. cular growth factors in BOOP that Generally, the infiltrates gradually The dosage is generally 1 mg/kg (60 will result in normal apoptosis (natu- enlarge from their original site or mg/d) for 1 to 3 months, then 40 ral-occurring cell death) in BOOP new infiltrates appear as the clini- mg/d for 3 months, then 10 to 20 mg/d but not in UIP/IPF. Results of an ad- cal course progresses; however, mi- or every other day for a total of 1 year. ditional study10 showed that the gratory or “mobile” pulmonary in- Every-other-day scheduling can be apoptotic activity is higher in the fi- filtrates have been reported6,14,15 in successfully used for this disorder. A bromyxoid lesion of BOOP com- 10% to 25% of patients. Unilateral shorter 6-month course may be suf- pared with UIP/IPF, suggesting that BOOP also has been reported.16,17 ficient in certain situations. Total and apoptosis has an important role in The chest computed tomo- permanent recovery is seen in most the resolution process of the newly graphic scan shows findings similar patients and is
Load more

Recommended publications
  • 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).
    [Show full text]
  • Hepatic Hydrothorax: an Updated Review on a Challenging Disease
    Lung (2019) 197:399–405 https://doi.org/10.1007/s00408-019-00231-6 REVIEW Hepatic Hydrothorax: An Updated Review on a Challenging Disease Toufc Chaaban1 · Nadim Kanj2 · Imad Bou Akl2 Received: 18 February 2019 / Accepted: 27 April 2019 / Published online: 25 May 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Hepatic hydrothorax is a challenging complication of cirrhosis related to portal hypertension with an incidence of 5–11% and occurs most commonly in patients with decompensated disease. Diagnosis is made through thoracentesis after exclud- ing other causes of transudative efusions. It presents with dyspnea on exertion and it is most commonly right sided. Patho- physiology is mainly related to the direct passage of fuid from the peritoneal cavity through diaphragmatic defects. In this updated literature review, we summarize the diagnosis, clinical presentation, epidemiology and pathophysiology of hepatic hydrothorax, then we discuss a common complication of hepatic hydrothorax, spontaneous bacterial pleuritis, and how to diagnose and treat this condition. Finally, we elaborate all treatment options including chest tube drainage, pleurodesis, surgical intervention, Transjugular Intrahepatic Portosystemic Shunt and the most recent evidence on indwelling pleural catheters, discussing the available data and concluding with management recommendations. Keywords Hepatic hydrothorax · Cirrhosis · Pleural efusion · Thoracentesis Introduction Defnition and Epidemiology Hepatic hydrothorax (HH) is one of the pulmonary com- Hepatic hydrothorax is defned as the accumulation of more plications of cirrhosis along with hepatopulmonary syn- than 500 ml, an arbitrarily chosen number, of transudative drome and portopulmonary hypertension. It shares common pleural efusion in a patient with portal hypertension after pathophysiological pathways with ascites secondary to por- excluding pulmonary, cardiac, renal and other etiologies [4].
    [Show full text]
  • Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
    INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI).
    [Show full text]
  • 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]
  • Treatment of Acute Fibrinous Organizing Pneumonia Following Hematopoietic Cell Transplantation with Etanercept
    OPEN Bone Marrow Transplantation (2017) 52, 141–143 www.nature.com/bmt LETTER TO THE EDITOR Treatment of acute fibrinous organizing pneumonia following hematopoietic cell transplantation with etanercept Bone Marrow Transplantation (2017) 52, 141–143; doi:10.1038/ Computed tomography (CT) of the chest showed rapidly bmt.2016.197; published online 15 August 2016 progressive pulmonary infiltrates (Figure 1a). He was admitted to the inpatient bone marrow transplant floor, started on broad- spectrum antimicrobials, and subsequently underwent broncho- Infectious and non-infectious pulmonary complications are scopy that was non-diagnostic. Over the next 2 days he developed reported in 30–60% of all hematopoietic cell transplant (HCT) worsening hypoxemia requiring transfer to the medical intensive – recipients and result in a high morbidity and mortality.1 3 care unit for hypoxemic respiratory failure. High-dose methyl- Non-infectious pulmonary complications encompass a hetero- prednisolone 125 mg every 6 h was initiated. On day +328 he geneous group of conditions including chronic GvHD, frequently underwent video-assisted thoracoscopic surgery (VATS) and left manifested as bronchiolitis obliterans and cryptogenic organizing upper lobe/left lower lobe wedge resection. pneumonia (COP), pulmonary edema, diffuse alveolar hemorrhage He was extubated on day +329, but remained hypoxic, 1 fi and idiopathic pneumonia syndrome. Acute organizing brinous requiring non-invasive ventilation. On day +331 the pathology fi 3 pneumonia (AFOP) was rst described by Beasley et al. in 2002 as from the wedge resections showed Acute organizing fibrinous a unique histological pattern of acute lung injury that is histologically different from diffuse alveolar damage, eosinophilic pneumonia, bronchiolitis obliterans and COP.
    [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]
  • How to Differentiate COVID-19 Pneumonia from Heart Failure with Computed
    medRxiv preprint doi: https://doi.org/10.1101/2020.03.04.20031047; this version posted March 6, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . How to differentiate COVID-19 pneumonia from heart failure with computed tomography at initial medical contact during epidemic period Running title: CT imaging for COVID-19 and heart failure Zhaowei Zhu1, MD, Jianjun Tang1, MD, Xiangping Chai2, MD, Zhenfei Fang1, MD, Qiming Liu3, MD, Xinqun Hu1, MD, Danyan Xu1, MD, Jia He1, MD, Liang Tang1, MD, Shi Tai1, MD, Yuzhi Wu3#, MD, Shenghua Zhou1#, MD 1.Department of Cardiovascular Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China. 2. Department of Emergency, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China. 3. Department of Radiology, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China. # These authors share the correspondence authorship. Correspondence to: Shenghua Zhou, MD, PhD Department of Cardiovascular Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, PR China. NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.03.04.20031047; this version posted March 6, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
    [Show full text]