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Chronic Obstructive Pulmonary Disease (COPD)—Clinical Aspects, Early Detection and Pathogenesis
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Chronic Obstructive Pulmonary Disease (COPD)—Clinical Aspects, Early Detection and Pathogenesis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Respiratory Medicine".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 2458

Special Issue Editors

Prof. Dr. Gabriel Izbicki

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Guest Editor
Department of Medicine, Pulmonary Institute, Shaare Zedek Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 9103102, Israel
Interests: obstructive lung diseases; pulmonary function tests; smoking cessation; firefighters lung diseases
Prof. Dr. Yochai Adir

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Guest Editor
Pulmonary Division, Lady Davis Carmel Medical Center, Faculty of Medicine Technion Institute of Technology, Haifa, Israel
Interests: pulmonary hypertension; COPD; asthma; lung physiology
Dr. Ariel Rokach

E-Mail Website
Guest Editor
Department of Medicine, Pulmonary Institute, Shaare Zedek Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 9103102, Israel
Interests: COPD; asthma; pulmonary function test; early detection; cfDNA

Special Issue Information

Dear Colleagues,

Chronic Obstructive Pulmonary Disease (COPD) is a major cause of morbidity and mortality all over the world. The main causes of the disease are well known: exposure to noxious gases and cigarette smoking. The precise pathogenesis is vague. We still do not know why some heavy smokers develop COPD and others do not. COPD is a heterogenous disease. The clinical course might be different and the treatment should be personalized according to the phenotype. COPD diagnosis is based on clinical symptoms and a pulmonary function test. Most patients are not diagnosed properly. Underdiagnosis and overdiagnosis are still significant issues and early detection is still under debate. The medical literature on COPD is extensive, but there are many unanswered questions. We intend to publish a Special Issue with the aim of answering some of these questions and raising new ones. We would be glad to accept manuscripts dealing with the clinical aspects of COPD, as well as the early detection of COPD and pathogenesis of the disease from a clinician’s point of view.

Prof. Dr. Gabriel Izbicki
Prof. Dr. Yochai Adir
Dr. Ariel Rokach
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • COPD
  • pathophysiology
  • pulmonary function test
  • acute exacerbation
  • neutrophils
  • eosinophils
  • early detection

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Published Papers (2 papers)

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Research

12 pages, 724 KiB  
Article
Demographic and Clinical Characteristics of Mild, Young and Early COPD: A Cross-Sectional Analysis of 5468 Patients
by Cristina Aljama, Cristina Esquinas, Eduardo Loeb, Galo Granados, Alexa Nuñez, Ane Lopez-Gonzalez, Marc Miravitlles and Miriam Barrecheguren
J. Clin. Med. 2024, 13(23), 7380; https://doi.org/10.3390/jcm13237380 - 4 Dec 2024
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Abstract
Early, mild and young COPD concepts are not clearly defined and are often used interchangeably to refer to the onset of the disease. Objective: To describe and compare the characteristics of mild, young and early COPD in a large sample of COPD [...] Read more.
Early, mild and young COPD concepts are not clearly defined and are often used interchangeably to refer to the onset of the disease. Objective: To describe and compare the characteristics of mild, young and early COPD in a large sample of COPD from primary and secondary care. Methods: Pooled analysis of individual data from four multicenter observational studies of patients with stable COPD (≥40 years, FEV1/FVC < 0.7, smoking ≥ 10 pack-years). Mild COPD was defined as FEV1% ≥ 65%; young COPD as <55 years; and early COPD as <55 years and smoking ≤ 20 pack-years. The relationship between FEV1(%), age and pack-years was analyzed with linear regression equations. Results: We included 5468 patients. Their mean age was 67 (SD: 9.6) years, and 85% were male. A total of 1158 (21.2%) patients had mild COPD; 636 (11.6%) had young COPD and 191 (3.5%) early COPD. The three groups shared common characteristics: they were more frequently female, younger and with less tobacco exposure compared with the remaining patients. Early COPD had fewer comorbidities and fewer COPD admissions, but no significant differences were found in ambulatory exacerbations. In linear regression analysis, the decline in FEV1(%) was more pronounced for the first 20 pack-years for all age groups and was even more important in younger patients. Conclusions: Mild, young and early COPD patients were more frequently women. The steepest decline in FEV1(%) was observed in individuals <55 years and smoking between 10 and 20 pack-years (early COPD), which highlights the importance of an early detection and implementation of preventive and therapeutic measures. Full article
(This article belongs to the Special Issue Chronic Obstructive Pulmonary Disease (COPD)—Clinical Aspects, Early Detection and Pathogenesis)
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9 pages, 1237 KiB  
Article
Interleukin 16 and 25 (IL-17E) and Clinical Outcomes in Exacerbation of COPD—A Pilot Study
by Tomasz Karauda, Joanna Miłkowska-Dymanowska, Anna Kumor-Kisielewska, Wojciech J. Piotrowski and Adam J. Białas
J. Clin. Med. 2024, 13(17), 5188; https://doi.org/10.3390/jcm13175188 - 1 Sep 2024
Viewed by 966
Abstract
Background: Exacerbation of chronic obstructive pulmonary disease (ECOPD) significantly impact health status, hospitalization rates, and disease progression, and are linked to increased mortality. Predictive factors for ECOPD are therefore of considerable interest. The limited understanding of interleukin 16 (IL-16) and IL-25 role in [...] Read more.
Background: Exacerbation of chronic obstructive pulmonary disease (ECOPD) significantly impact health status, hospitalization rates, and disease progression, and are linked to increased mortality. Predictive factors for ECOPD are therefore of considerable interest. The limited understanding of interleukin 16 (IL-16) and IL-25 role in ECOPD provided the rationale for this study. Methods: Fifty ex-smokers diagnosed with COPD (22 ECOPD and 28 patients in the stable phase of the disease) underwent prospective analysis to evaluate the role of I IL-25 as predictive markers of clinical outcomes in ECOPD. Results: We observed a significantly lower IL-16 and higher IL-25 concentrations among ECOPD patients (p = 0.002 and p = 0.01 respectively). We also detected a significant negative correlation between IL-16 and neutrophil-to-lymphocyte ratio (NLR) (p = 0.04) and a significant negative correlation between IL-25 concentration and absolute eosinophil count (p = 0.04). In the entire group, we observed a positive correlation between IL-16 and both FEV1 and FVC, both expressed as a percentage of reference value, (p = 0.002 and p = 0.0004 respectively). However, after stratification to ECOPD and stable COPD group, significance maintained for FVC (p = 0.045 for ECOPD and p = 0.02 for stable COPD). In survival analysis, we detected significantly lower all-cause mortality for 3rd tertile of IL-16 concentrations, with a hazard ratio of 0.33 (95%CI: 0.11–0.98; p = 0.04). Conclusions: Lower IL-16 levels among ECOPD patients may indicate a feedback mechanism linked to heightened Th1 response activation. Observed correlations with ventilatory parameters and survival also seems to reflect this mechanism. The higher IL-25 concentrations observed in ECOPD patients, along with the negative correlation with absolute eosinophil count and eosinopenia, suggest multifactorial regulation and independent functions of eosinophils and IL-25. Hypothetically, this paradox may be related to the Th1/Th2 imbalance favoring Th1 response. Obtained results should be reproduced in larger size samples. Full article
(This article belongs to the Special Issue Chronic Obstructive Pulmonary Disease (COPD)—Clinical Aspects, Early Detection and Pathogenesis)
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