Skip to main content

Main menu

  • Home
  • Current issue
  • Early View
  • Archive
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

User menu

  • Log in
  • Subscribe
  • Contact Us
  • My Cart

Search

  • Advanced search
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

Login

European Respiratory Society

Advanced Search

  • Home
  • Current issue
  • Early View
  • Archive
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions

Clinical characteristics of immunoglobulin G4-positive interstitial pneumonia

Masamichi Komatsu, Hiroshi Yamamoto, Shoko Matsui, Yasuhiro Terasaki, Akira Hebisawa, Tae Iwasawa, Takeshi Johkoh, Tomohisa Baba, Atsushi Miyamoto, Tomohiro Handa, Keisuke Tomii, Yuko Waseda, Masashi Bando, Haruyuki Ishii, Yasunari Miyazaki, Akihiko Yoshizawa, Tamiko Takemura, Yoshinori Kawabata, Takashi Ogura the Tokyo Diffuse Lung Disease Study Group
ERJ Open Research 2021 7: 00317-2021; DOI: 10.1183/23120541.00317-2021
Masamichi Komatsu
1First Dept of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Masamichi Komatsu
Hiroshi Yamamoto
1First Dept of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: yama5252@shinshu-u.ac.jp
Shoko Matsui
2Health Administration Center, University of Toyama, Toyama, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yasuhiro Terasaki
3Dept of Analytic Human Pathology, Nippon Medical School, Tokyo, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Akira Hebisawa
4Division of Clinical Pathology, Asahi Central Hospital, Asahi, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Tae Iwasawa
5Dept of Radiology, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Takeshi Johkoh
6Dept of Radiology, Kansai Rosai Hospital, Amagasaki, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Tomohisa Baba
7Division of Respiratory Medicine, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Atsushi Miyamoto
8Dept of Respiratory Medicine, Respiratory Center, Toranomon Hospital, Tokyo, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Atsushi Miyamoto
Tomohiro Handa
9Dept of Advanced Medicine for Respiratory Failure, Graduate School of Medicine, Kyoto University, Kyoto, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Keisuke Tomii
10Dept of Respiratory Medicine, Kobe City Medical Center General Hospital, Kobe, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Keisuke Tomii
Yuko Waseda
11Third Dept of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Masashi Bando
12Division of Pulmonary Medicine, Dept of Medicine, Jichi Medical University, Tochigi, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Masashi Bando
Haruyuki Ishii
13Dept of Respiratory Medicine, Kyorin University School of Medicine, Tokyo, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yasunari Miyazaki
14Dept of Respiratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Akihiko Yoshizawa
15Dept of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Tamiko Takemura
16Dept of Pathology, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yoshinori Kawabata
17Division of Diagnostic Pathology, Saitama Cardiovascular and Respiratory Center, Kumagaya, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Takashi Ogura
7Division of Respiratory Medicine, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

This study suggests that IgG4+ IP with abundant IgG4+ cells and elevated serum IgG4 levels could be treated differently from IgG4-related respiratory disease due to potential differences in disease behaviour and response to corticosteroid therapy https://bit.ly/3dUo2cu

To the Editor:

Immunoglobulin G4-related disease is a systemic disease characterised by tumefactive lesions with abundant IgG4-positive plasma cells and elevated serum IgG4 concentrations [1–4]. We previously assessed IgG4-related respiratory disease (IgG4-RRD) with extrathoracic manifestations [5]. IgG4-RRD develops through the lymphatic routes in the lungs and responds well to corticosteroid therapy with a benign prognosis [5–7]. However, whether interstitial pneumonia (IP) with IgG4-positive plasma cell infiltration in the lungs without the extrathoracic lesions of IgG4-related disease could be considered a type of IgG4-RRD is controversial.

Here, we aimed to elucidate the clinico–radio–pathological characteristics of IP with abundant IgG4-positive cells in the lungs and elevated serum IgG4 levels without extrathoracic lesions. We defined this IP as “IgG4-positive IP” in this study.

We recruited patients suspected of having IgG4-positive IP nationwide from March 2019 to May 2019. This study was conducted by the Tokyo Diffuse Lung Disease Study Group. All procedures involving human participants were approved by the Ethics Committee of the Shinshu University School of Medicine (approval number 4465) and the relevant participating institutions. This study was performed in accordance with the Declaration of Helsinki and its subsequent amendments. Additionally, the review board waived the need for patient approval or informed consent because the study involved a retrospective review of patient records.

We reviewed the cases of 28 patients with suspected IgG4-positive IP from 17 institutions throughout Japan. All participants were diagnosed with IP via chest high-resolution computed tomography (HRCT), elevated serum IgG4 concentrations (≥135 mg·dL−1), and infiltrations of abundant IgG4-positive plasma cells (IgG4-positive/IgG-positive cell ratio >40% and IgG4-positive cells >10 per high-power field from the specimens obtained by surgical lung biopsies). HRCT and histopathology patterns of IP were determined according to the 2018 guidelines regarding interstitial pulmonary fibrosis [8] and the 2013 statement regarding idiopathic interstitial pneumonias (IIPs) [9]. Lung specimens were immunostained for IgG and IgG4 in addition to staining with haematoxylin-eosin and Elastica-Masson or Elastica-van Gieson. Patients’ clinical records and radiological and histopathological data were reviewed, and the final diagnoses were established after multidisciplinary discussion (MDD).

Of the 28 patients, 16 were diagnosed with IgG4-positive IP by MDD. Extrathoracic lesions suggesting IgG4-related disease were not present in these 16 patients during the study period. Of the remaining 12 patients, seven patients were diagnosed with IgG4-RRD with extrathoracic lesions, three were diagnosed with multicentric Castleman disease, one had rheumatoid arthritis, and one had lung cancer.

The median age of the 16 patients with IgG4-positive IP at the time of diagnosis was 66 years (range: 49–74 years), and 12 were male. 13 of the 16 patients had a history of smoking. In addition, 13 of the 16 patients had respiratory symptoms, such as cough or dyspnoea, at diagnosis.

Almost all 16 patients had abnormally high serum concentrations of Krebs von Lungen-6 and surfactant protein-D. Contrarily, the white blood cell count and C-reactive protein concentrations were nearly normal. Bronchoalveolar lavage was performed in eight patients; there were no specific trends in the cell fractions of bronchoalveolar lavage fluid. In pulmonary function tests, four patients showed restrictive changes (percentage of predicted vital capacity <80%). The median percentage of the predicted diffusing capacity of the lungs for carbon monoxide was 57.9% (range: 29.9–81.4%).

The most common characteristic findings observed on chest HRCT imaging were ground-glass opacities (n=16), reticular opacities (n=11), traction bronchiectasis (n=10), thickening of the interlobular septal wall (n=9), and hilar mediastinal lymphadenopathy (n=6). Ground-glass and reticular opacities were predominant in the lower and peripheral lung zones. Representative HRCT images are shown in figure 1a. The HRCT patterns found in the 16 patients were as follows: indeterminate for usual interstitial pneumonia (UIP) (n=8), desquamative interstitial pneumonia (DIP) (n=3), unclassifiable IIPs (n=3; two patients had nonspecific interstitial pneumonia (NSIP) with organising pneumonia and one patient had pleuroparenchymal fibroelastosis (PPFE) with UIP), and NSIP (n=2).

FIGURE 1
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1

Radiographic and pathological findings of IgG4-positive interstitial pneumonia. a–d) Transverse section of high-resolution computed tomography (HRCT) images of two cases of IgG4-positive interstitial pneumonia. a) Before treatment and b) 2 years after initiation of corticosteroid treatment. The HRCT pattern was indeterminate for usual interstitial pneumonia (UIP). The perilobular ground-glass opacities (circle) improved with corticosteroid treatment; however, reticular opacities remained (asterisk). c) Before treatment and d) 6 years after initiation of corticosteroid treatment. Ground-glass opacities and thickening of the interlobular septal wall (circle) improved with corticosteroid treatment, but traction bronchiectasis and reticular opacities deteriorated. The patient was also treated with an antifibrotic agent, but he eventually died because of an acute exacerbation. e–h) Histopathological features of a representative IgG4-positive interstitial pneumonia case. e, f) Architectural distortion with marked lymphoplasmacytic cell infiltration is seen at a low-power magnification (e) haematoxylin and eosin staining; f) Elastica-Masson staining; magnification 1.25×). The case was of interstitial pneumonia with an unclassifiable pattern because of the combined presentation of usual interstitial pneumonia and nonspecific interstitial pneumonia pattern. g, h) Images showing an increase in the IgG-positive and IgG4-positive cells in the fibrous parenchyma (g) IgG; h) IgG4 immunohistochemistry, respectively; magnification 20×).

Marked numbers of lymphoplasmacytic cells in the fibrous parenchyma were observed in the histopathology of 14 patients. However, none of these patients had either obliterative vasculitis or storiform fibrosis, which are characteristic findings of IgG4-related disease [1–3]. The representative pathological findings are shown in figure 1e–h. IgG4-positive plasma cells were conspicuously present in the fibrous parenchyma. The histopathology patterns of the 16 patients were as follows: unclassifiable IIPs (n=9; four patients had coexisting UIP and NSIP), NSIP (n=3), UIP (n=1), probable UIP (n=1), DIP (n=1), and PPFE (n=1).

The median follow-up period was 59 months (range: 13–126 months). All but one of the 16 patients were treated with corticosteroid monotherapy as initial therapy. With treatment, ground-glass opacities on HRCT improved in all 15 patients (figure 1b). By contrast, the reticular opacities deteriorated after initiation of treatment in six of the 15 patients. The typical HRCT findings before and after treatment are shown in figure 1c–d. The patients who did not receive corticosteroid treatment had a stable clinical course during the follow-up period.

Immunosuppressant and antifibrotic agents were administered as additional therapies to two patients owing to disease progression. Acute exacerbation occurred in two patients. Three patients died during the follow-up period: two patients due to chronic respiratory failure and one patient due to an acute exacerbation.

In this study, we examined the clinico–radio–pathological characteristics of IgG4-positive IP in 16 cases. On HRCT, ground-glass opacities were predominant in peripheral and peribronchovascular areas, and traction bronchiectasis and reticular opacities were observed. Lymphoplasmacytic inflammation into peribronchiolar regions and interlobular septa was seen in many patients. In addition, various types of fibrosis, such as UIP, NSIP, and DIP, were present. We found a correlation between the distribution of ground-glass opacities in HRCT and the lymphoplasmacytic inflammation in the lung tissue. Additionally, a correlation existed between the patterns of traction bronchiectasis and the reticular opacities at HRCT and histopathological fibrosis.

15 of the 16 patients received corticosteroid therapy. Although the ground-glass opacities improved on HRCT for all patients after treatment, reticular opacities, which indicate fibrosis, deteriorated in six patients despite treatment. Furthermore, despite treatment, three patients died during the follow-up period due to disease progression.

Notably, the clinical courses in the study participants differed significantly from that of the previously reported conventional IgG4-RRD [5]. Corticosteroid therapy is fully effective in patients with IgG4-RRD [5–7]. We speculate that the improvement in ground-glass opacities on HRCT reflected the elimination of IgG4-positive lymphoplasmacytic cell infiltration from the perilymphatic stromal area in the surgical lung biopsy specimens. Residual fibrosis may have been the essence of IP, leading to progressive fibrosis, even though the ground-glass opacities improved with corticosteroid treatment.

Some limitations of this study were its retrospective nature and the small sample size, although we did recruit patients with IgG4-positive IP throughout Japan. Further prospective research is necessary to confirm the disease behaviour of IgG4-positive IP.

In summary, we revealed the clinical characteristics of IgG4-positive IP. We believe that IgG4-positive IP needs to be treated as a separate entity from conventional IgG4-RRD because of the relative differences in disease behaviour and responses to corticosteroid therapy.

Acknowledgements

The authors thank Shinichi Sasaki (Juntendo University Urayasu Hospital) and Shinyu Izumi (Central Hospital of the National Center for Global Health and Medicine), who supported the clinical and pathologic review conferences. We also thank Kiminobu Tanizawa (Kyoto University Hospital), Sho Yamada (Kitano Hospital), Machiko Arita, Shinya Yokoe (Kurashiki Central Hospital), Ryosuke Hirabayashi (Kobe City Medical Center General Hospital), Takafumi Yamaya, Masato Asaoka (Kanagawa Cardiovascular and Respiratory Center), Miwa Yamanaka (Shinshu University School of Medicine), Yuhei Ito (Ise Red Cross Hospital), Naoki Hamada (Kyushu University), Toshikazu Takasaki, Hiroyoshi Yamauchi (Jichi Medical University), Nobuhito Arakawa (International University of Health and Welfare Hospital), Hiromi Tomioka (Kobe City Medical Center West Hospital), Kosuke Okuma, Kojiro Honda (Kyorin University School of Medicine), Seiko Takasawa (Tokyo Medical and Dental University), Shun Shinomiya (Saitama Medical University) and Yutaro Nakamura (Hamamatsu University School of Medicine) for case registrations from their respective institutions.

Footnotes

  • Provenance: Submitted article, peer reviewed.

  • Author contributions: M. Komatsu, H. Yamamoto, S. Matsui, M. Bando, H. Ishii, Y. Miyazaki and T. Ogura conceptualised the study. M. Komatsu, H. Yamamoto, S. Matsui and T. Ogura designed the study. M. Komatsu, H. Yamamoto, S. Matsui, Y. Terasaki, A. Hebisawa, T. Iwasawa, T. Johkoh, T. Baba, A. Miyamoto, T. Handa, K. Tomii, Y. Waseda, M. Bando, H. Ishii, Y. Miyazaki, A. Yoshizawa, T. Takemura and Y. Kawabata acquired and analysed the data. M. Komatsu performed the statistical analysis and interpreted the data. M. Komatsu, H. Yamamoto, S. Matsui and T. Ogura wrote the manuscript. H. Yamamoto, S. Matsui, Y. Terasaki, A. Hebisawa, T. Iwasawa, T. Johkoh, T. Baba, A. Miyamoto, M. Bando, H. Ishii, Y. Miyazaki and T. Ogura provided administrative support.

  • Conflict of interest: M. Komatsu has nothing to disclose.

  • Conflict of interest: H. Yamamoto has nothing to disclose.

  • Conflict of interest: S. Matsui has nothing to disclose.

  • Conflict of interest: Y. Terasaki has nothing to disclose.

  • Conflict of interest: A. Hebisawa has nothing to disclose.

  • Conflict of interest: T. Iwasawa has nothing to disclose.

  • Conflict of interest: T. Johkoh has nothing to disclose.

  • Conflict of interest: T. Baba has nothing to disclose.

  • Conflict of interest: A. Miyamoto has nothing to disclose.

  • Conflict of interest: T. Handa has nothing to disclose.

  • Conflict of interest: K. Tomii has nothing to disclose.

  • Conflict of interest: Y. Waseda has nothing to disclose.

  • Conflict of interest: M. Bando has nothing to disclose.

  • Conflict of interest: H. Ishii has nothing to disclose.

  • Conflict of interest: Y. Miyazaki has nothing to disclose.

  • Conflict of interest: A. Yoshizawa has nothing to disclose.

  • Conflict of interest: T. Takemura has nothing to disclose.

  • Conflict of interest: Y. Kawabata has nothing to disclose.

  • Conflict of interest: T. Ogura has nothing to disclose.

  • Support statement: This study was supported by the Ministry of Health, Labour and Welfare Research Program on Rare and Intractable Diseases (No. JPMH20FC1040), the Japan Society for the Promotion of Science (No. 21K08175), the Tokyo Diffuse Lung Disease Study Group and Shionogi Pharmaceutical, Co., Ltd. Funding information for this article has been deposited with the Crossref Funder Registry.

  • Received February 13, 2021.
  • Accepted June 23, 2021.
  • Copyright ©The authors 2021
http://creativecommons.org/licenses/by-nc/4.0/

This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions{at}ersnet.org

References

  1. ↵
    1. Umehara H,
    2. Okazaki K,
    3. Masaki Y, et al.
    Comprehensive diagnostic criteria for IgG4–related disease (IgG4-RD), 2011. Mod Rheumatol 2012; 22: 21–30. doi:10.3109/s10165-011-0571-z
    OpenUrlCrossRefPubMed
    1. Umehara H,
    2. Okazaki K,
    3. Kawa S, et al.
    The 2020 revised comprehensive diagnostic (RCD) criteria for IgG4-RD. Mod Rheumatol 2021; 31: 529–533. doi:10.1080/14397595.2020.1859710
    OpenUrl
  2. ↵
    1. Wallace ZS,
    2. Naden RP,
    3. Chari S, et al.
    The 2019 American College of Rheumatology/European League Against Rheumatism classification criteria for IgG4-related disease. Ann Rheum Dis 2020; 79: 77–87. doi:10.1136/annrheumdis-2019-216561
    OpenUrlAbstract/FREE Full Text
  3. ↵
    1. Stone JH,
    2. Zen Y,
    3. Deshpande V
    . IgG4-related disease. N Engl J Med 2012; 366: 539–551. doi:10.1056/NEJMra1104650
    OpenUrlCrossRefPubMed
  4. ↵
    1. Matsui S,
    2. Hebisawa A,
    3. Sakai F, et al.
    Immunoglobulin G4-related lung disease: clinicoradiological and pathological features. Respirology 2013; 18: 480–487. doi:10.1111/resp.12016
    OpenUrlCrossRefPubMed
    1. Sun X,
    2. Liu H,
    3. Feng R, et al.
    Biopsy-proven IgG4-related lung disease. BMC Pulm Med 2016; 16: 20. doi:10.1186/s12890-016-0181-9
    OpenUrl
  5. ↵
    1. Kang J,
    2. Park S,
    3. Chae EJ, et al.
    Long-term clinical course and outcomes of immunoglobulin G4-related lung disease. Respir Res 2020; 21: 273. doi:10.1186/s12931-020-01542-6
    OpenUrl
  6. ↵
    1. Raghu G,
    2. Remy-Jardin M,
    3. Myers JL, et al.
    Diagnosis of idiopathic pulmonary fibrosis. An official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med 2018; 198: e44–e68. doi:10.1164/rccm.201807-1255ST
    OpenUrlCrossRefPubMed
  7. ↵
    1. Travis WD,
    2. Costabel U,
    3. Hansell DM, et al.
    An official American Thoracic Society/European Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med 2013; 188: 733–748. doi:10.1164/rccm.201308-1483ST
    OpenUrlCrossRefPubMed
PreviousNext
Back to top
Vol 7 Issue 3 Table of Contents
ERJ Open Research: 7 (3)
  • Table of Contents
  • Index by author
Email

Thank you for your interest in spreading the word on European Respiratory Society .

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Clinical characteristics of immunoglobulin G4-positive interstitial pneumonia
(Your Name) has sent you a message from European Respiratory Society
(Your Name) thought you would like to see the European Respiratory Society web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Citation Tools
Clinical characteristics of immunoglobulin G4-positive interstitial pneumonia
Masamichi Komatsu, Hiroshi Yamamoto, Shoko Matsui, Yasuhiro Terasaki, Akira Hebisawa, Tae Iwasawa, Takeshi Johkoh, Tomohisa Baba, Atsushi Miyamoto, Tomohiro Handa, Keisuke Tomii, Yuko Waseda, Masashi Bando, Haruyuki Ishii, Yasunari Miyazaki, Akihiko Yoshizawa, Tamiko Takemura, Yoshinori Kawabata, Takashi Ogura
ERJ Open Research Jul 2021, 7 (3) 00317-2021; DOI: 10.1183/23120541.00317-2021

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Clinical characteristics of immunoglobulin G4-positive interstitial pneumonia
Masamichi Komatsu, Hiroshi Yamamoto, Shoko Matsui, Yasuhiro Terasaki, Akira Hebisawa, Tae Iwasawa, Takeshi Johkoh, Tomohisa Baba, Atsushi Miyamoto, Tomohiro Handa, Keisuke Tomii, Yuko Waseda, Masashi Bando, Haruyuki Ishii, Yasunari Miyazaki, Akihiko Yoshizawa, Tamiko Takemura, Yoshinori Kawabata, Takashi Ogura
ERJ Open Research Jul 2021, 7 (3) 00317-2021; DOI: 10.1183/23120541.00317-2021
del.icio.us logo Digg logo Reddit logo Technorati logo Twitter logo CiteULike logo Connotea logo Facebook logo Google logo Mendeley logo
Full Text (PDF)

Jump To

  • Article
    • Abstract
    • Acknowledgements
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Subjects

  • Interstitial and orphan lung disease
  • Tweet Widget
  • Facebook Like
  • Google Plus One

More in this TOC Section

  • Expansion of ST2-expressing macrophages in BOS
  • S. pneumoniae re-emerges as a cause of CAP
  • Comparison of the ACQ and patient diaries
Show more Research letters

Related Articles

Navigate

  • Home
  • Current issue
  • Archive

About ERJ Open Research

  • Editorial board
  • Journal information
  • Press
  • Permissions and reprints
  • Advertising

The European Respiratory Society

  • Society home
  • myERS
  • Privacy policy
  • Accessibility

ERS publications

  • European Respiratory Journal
  • ERJ Open Research
  • European Respiratory Review
  • Breathe
  • ERS books online
  • ERS Bookshop

Help

  • Feedback

For authors

  • Instructions for authors
  • Publication ethics and malpractice
  • Submit a manuscript

For readers

  • Alerts
  • Subjects
  • RSS

Subscriptions

  • Accessing the ERS publications

Contact us

European Respiratory Society
442 Glossop Road
Sheffield S10 2PX
United Kingdom
Tel: +44 114 2672860
Email: journals@ersnet.org

ISSN

Online ISSN: 2312-0541

Copyright © 2023 by the European Respiratory Society