scholarly journals Exhalative Breath Markers Do Not Offer for Diagnosis of Interstitial Lung Diseases: Data from the European IPF Registry (eurIPFreg) and Biobank

2019 ◽  
Vol 8 (5) ◽  
pp. 643 ◽  
Author(s):  
Ekaterina Krauss ◽  
Maike Froehler ◽  
Maria Degen ◽  
Poornima Mahavadi ◽  
Ruth C. Dartsch ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Enzyme Linked Immunosorbent Assay ◽  
Chronic Obstructive ◽  
Exhaled Breath ◽  
Obstructive Pulmonary Disease ◽  
Significant Difference ◽  
New Biomarkers ◽  
Diagnostic Benefit

Background: New biomarkers are urgently needed to facilitate diagnosis in Interstitial Lung Diseases (ILD), thus reducing the need for invasive procedures, and to enable tailoring and monitoring of medical treatment. Methods: In this study we investigated if patients with idiopathic pulmonary fibrosis (IPF; n = 21), non-IPF ILDs (n = 57) and other lung diseases (chronic obstructive pulmonary disease (COPD) n = 24, lung cancer (LC) n = 16) as well as healthy subjects (n = 20) show relevant differences in exhaled NO (FeNO; Niox MINO), or in eicosanoid (PGE2, 8-isoprostane; enzyme-linked immunosorbent assay (ELISA)) levels as measured in exhaled breath condensates (EBC) and bronchoalveolar lavage fluids (BALF). Results: There was no significant difference in FeNO values between IPF, non-IPF ILDs and healthy subjects, although some individual patients showed highly elevated FeNO. On the basis of the FeNO signal, it was neither possible to differentiate between the kind of disease nor to detect exacerbations. In addition, there was no correlation between FeNO values and lung function. The investigation of the eicosanoids in EBCs was challenging (PGE2) or unreliable (8-isoprostane), but worked out well in BALF. A significant increase of free 8-isoprostane was observed in BALF, but not in EBCs, of patients with IPF, hypersensitivity pneumonitis (HP) and sarcoidosis, possibly indicating severity of oxidative stress. Conclusions: FeNO-measurements are not of diagnostic benefit in different ILDs including IPF. The same holds true for PGE2 and 8-isoprostane in EBC by ELISA.

scholarly journals Smoking and interstitial lung diseases

2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Langerhans Cell Histiocytosis ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Langerhans Cell Histiocytosis

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.

scholarly journals Deregulated angiogenesis in chronic lung diseases: a possible role for lung mesenchymal progenitor cells (2017 Grover Conference Series)

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321773980 ◽  
Author(s):  
Jonathan A. Kropski ◽  
Bradley W. Richmond ◽  
Christa F. Gaskill ◽  
Robert F. Foronjy ◽  
Susan M. Majka
Keyword(s):  
Progenitor Cells ◽  
Lung Diseases ◽  
Normal Function ◽  
Interstitial Lung Diseases ◽  
Chronic Obstructive ◽  
Mesenchymal Progenitor Cells ◽  
Obstructive Pulmonary Disease ◽  
Chronic Lung Diseases ◽  
Co Morbidity ◽  
Progression Of Disease

Chronic lung disease (CLD), including pulmonary fibrosis (PF) and chronic obstructive pulmonary disease (COPD), is the fourth leading cause of mortality worldwide. Both are debilitating pathologies that impede overall tissue function. A common co-morbidity in CLD is vasculopathy, characterized by deregulated angiogenesis, remodeling, and loss of microvessels. This substantially worsens prognosis and limits survival, with most current therapeutic strategies being largely palliative. The relevance of angiogenesis, both capillary and lymph, to the pathophysiology of CLD has not been resolved as conflicting evidence depicts angiogenesis as both reparative or pathologic. Therefore, we must begin to understand and model the underlying pathobiology of pulmonary vascular deregulation, alone and in response to injury induced disease, to define cell interactions necessary to maintain normal function and promote repair. Capillary and lymphangiogenesis are deregulated in both PF and COPD, although the mechanisms by which they co-regulate and underlie early pathogenesis of disease are unknown. The cell-specific mechanisms that regulate lung vascular homeostasis, repair, and remodeling represent a significant gap in knowledge, which presents an opportunity to develop targeted therapies. We have shown that that ABCG2pos multipotent adult mesenchymal stem or progenitor cells (MPC) influence the function of the capillary microvasculature as well as lymphangiogenesis. A balance of both is required for normal tissue homeostasis and repair. Our current models suggest that when lymph and capillary angiogenesis are out of balance, the non-equivalence appears to support the progression of disease and tissue remodeling. The angiogenic regulatory mechanisms underlying CLD likely impact other interstitial lung diseases, tuberous sclerosis, and lymphangioleiomyomatosis.

scholarly journals Venous Thromboembolic Disease in Chronic Inflammatory Lung Diseases: Knowns and Unknowns

2021 ◽  
Vol 10 (10) ◽  
pp. 2061
Author(s):  
George Keramidas ◽  
Konstantinos I. Gourgoulianis ◽  
Ourania S. Kotsiou
Keyword(s):  
Lung Diseases ◽  
Thrombotic Event ◽  
Interstitial Lung Diseases ◽  
Chronic Obstructive ◽  
Predisposing Factor ◽  
Obstructive Pulmonary Disease ◽  
Chronic Lung Diseases ◽  
Increased Risk ◽  
Chronic Pulmonary Diseases ◽  
The Relationship

Persistent inflammation within the respiratory tract underlies the pathogenesis of numerous chronic pulmonary diseases. There is evidence supporting that chronic lung diseases are associated with a higher risk of venous thromboembolism (VTE). However, the relationship between lung diseases and/or lung function with VTE is unclear. Understanding the role of chronic lung inflammation as a predisposing factor for VTE may help determine the optimal management and aid in the development of future preventative strategies. We aimed to provide an overview of the relationship between the most common chronic inflammatory lung diseases and VTE. Asthma, chronic obstructive pulmonary disease, interstitial lung diseases, or tuberculosis increase the VTE risk, especially pulmonary embolism (PE), compared to the general population. However, high suspicion is needed to diagnose a thrombotic event early as the clinical presentation inevitably overlaps with respiratory disorders. PE risk increases with disease severity and exacerbations. Hence, hospitalized patients should be considered for thromboprophylaxis administration. Conversely, all VTE patients should be asked for lung comorbidities before determining anticoagulant therapy duration, as those patients are at increased risk of recurrent PE episodes rather than DVT. Further research is needed to understand the underlying pathophysiology of in-situ thrombosis in those patients.

scholarly journals Pulmonary Hypertension in Parenchymal Lung Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Iraklis Tsangaris ◽  
Georgios Tsaknis ◽  
Anastasia Anthi ◽  
Stylianos E. Orfanos
Keyword(s):  
Pulmonary Hypertension ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Diffuse Parenchymal Lung Diseases ◽  
Pulmonary Arterial ◽  
Parenchymal Lung Disease ◽  
Parenchymal Lung

Idiopathic pulmonary arterial hypertension (IPAH) has been extensively investigated, although it represents a less common form of the pulmonary hypertension (PH) family, as shown by international registries. Interestingly, in types of PH that are encountered in parenchymal lung diseases such as interstitial lung diseases (ILDs), chronic obstructive pulmonary disease (COPD), and many other diffuse parenchymal lung diseases, some of which are very common, the available data is limited. In this paper, we try to browse in the latest available data regarding the occurrence, pathogenesis, and treatment of PH in chronic parenchymal lung diseases.

scholarly journals Impact of Pulmonary Rehabilitation Services in Patients with Different Lung Diseases

2022 ◽  
Vol 11 (2) ◽  
pp. 407
Author(s):  
Diana C. Sanchez-Ramirez
Keyword(s):  
Lung Cancer ◽  
Exercise Capacity ◽  
Self Efficacy ◽  
Pulmonary Rehabilitation ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Chronic Obstructive ◽  
Publicly Funded ◽  
Obstructive Pulmonary Disease ◽  
The Impact

Background: the effect of pulmonary rehabilitation (PR) services, beyond research contexts, on patients with lung diseases other than COPD requires further study. Objectives: to (i) assess the impact of a publicly funded PR on patients’ exercise capacity, self-efficacy, and health-related quality of life (HRQoL), and (ii) explore whether the effects vary across lung diseases. Methods: this retrospective pre–post study analyzed data from the Winnipeg Regional Health Authority PR program between 2016 and 2019. Results: 682 patients completed the full PR program. Pooled analyses found significant improvements in the patients’ exercise capacity (six-minute walk test (6MWT) (13.6%), fatigue (10.3%), and dyspnea (6.4%)), Self-Efficacy for Managing Chronic Disease 6-Item Scale (SEMCD6) (11.6%), and HRQoL (Clinical COPD Questionnaire (CCQ) (18.5%) and St George’s Respiratory Questionnaire (SGRQ) (10.9%)). The analyses conducted on sub-groups of patients with chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis, interstitial lung diseases (ILDs), other restrictive lung diseases (e.g., obesity, pleural effusion, etc.), lung cancer, and pulmonary hypertension (PH) indicated that, except for patients with PH, all the patients improved in the 6MWT. Fatigue decreased in patients with COPD, ILDs, and other restrictive lung diseases. Dyspnea decreased in patients with COPD, asthma, and lung cancer. SEMCD6 scores increased in COPD, ILDs and PH patients. CCQ scores decreased in all lung diseases, except lung cancer and PH. SGRQ scores only decreased in patients with COPD. Conclusion: PR services had a significant impact on patients with different lung diseases. Therefore, publicly funded PR should be available as a critical component in the management of patients with these diseases.

scholarly journals Association of serum deiodinase type 2 level with chronic obstructive pulmonary disease in the Polish population

2019 ◽  
Author(s):  
Elżbieta Gałecka ◽  
Anna Kumor-Kisielewska ◽  
Paweł Górski
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Healthy Subjects ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Protein Levels

Backgrounds: Deiodinase type 2 (DIO2) is a selenoenzyme involved in the synthesis of thyroid hormones. Chemerin is a newly investigated adipokine known also as novel chemokine. Both molecules have been recently expected and found to play an important role in inflammation and immunity. DIO2, for example, is upregulated during acute and chronic inflammation. In addition, inflammation-induced expression of DIO2 in macrophages has been confirmed, while chemerin modulates the activation and chemotaxis of immune cells. It is widely known that chronic obstructive pulmonary disease (COPD) – the most common lung disease in the world – is accompanied by an inflammatory process and immune activation. There are no studies demonstrating an association between DIO2, chemerin and COPD. The aim of this study was to estimate DIO2 and chemerin concentration in serum collected from patients suffering from COPD and to compare it with healthy subjects, as well as to correlate with basic and clinical characteristics. Methods: The study group included 50 patients with COPD and 30 healthy subjects. DIO2 and chemerin serum levels as well as c-reactive protein levels were determined in all the subjects using commercial enzyme-linked immunosorbent assay kits. The association between serum DIO2 and chemerin with sociodemographic and clinical variables was assessed. Results: DIO2 serum levels were significantly higher in the patients with COPD as compared to the control group (50.3±23.2 U/L vs. 13.3±13.1; p<0.00001). No differences were observed in serum chemerin levels between the patients and controls (107.559±86.695.6 vs. 100.701±53.805; p=0.54). Furthermore, there was no association between DIO2 and chemerin levels and other variables, and no correlation between both molecules. Conclusions: This study demonstrated that DIO2 levels were higher in the patients with COPD than in the control subjects. The examined molecules should be further investigated if they are intended to be considered markers of processes involved in COPD mechanisms.

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