Chronic Inflammatory Lung Diseases Research Articles

Illness Perceptions, Cognitions, and Beliefs on COPD Patients' Adherence to Treatment - A Systematic Review.

Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory lung disease characterized by persistent respiratory symptoms and airflow limitation. Besides its irreversibility, COPD is a treatable condition, and patients would strongly benefit from being adherent to their treatments. However, almost half of them are non-adherent, and, according to several recent studies, the way the patient perceives the disease might influence this variable. This systematic review provided a synthesis of studies about the relationships between illness perceptions (IP), cognitions, beliefs, and adherence in COPD. English language publications were searched in PubMed, Medline, Scopus, ResearchGate, PsycINFO, and Cochrane Library databases from November 2022 to February 2023, following PRISMA guidelines. The reference lists of eligible studies were also searched. Data extraction and critical appraisal were undertaken by two reviewers working independently. A total of 14 studies were included. Adherence to treatment in COPD is confirmed to be low, using both self-report questionnaires and objective assessment systems. Most studies concluded that COPD is perceived as a moderate threat destined to last forever, even if many participants referred to little disease knowledge. This perception did not change between adherent and non-adherent groups. Those who considered more necessary to take their medicines and had a caregiver were more adherent and less concerned about their future. On the other side, forgetfulness, lack of trust in medications, and difficulties in understanding how to take them were perceived as the main causes of non-adherence. Other predictors of non-adherence, like depression, low self-efficacy, and severity of disease were confirmed. The systematic review highlights the variability of the relationship between IP, cognitions and beliefs, and COPD treatment adherence. A new level of awareness of the relationship between patients' subjective point of view and treatment adherence may inform future treatment options and promote a more personalized intervention.

PEAK EXPIRATORY FLOW RATE DURING VARIOUS PHASES OF MENSTRUAL CYCLE IN ASTHMATICS PRESENTING TO A TERTIARY CARE CENTRE

Introduction: Asthma is a chronic inflammatory lung disease characterized by airway hyper responsiveness and reversible airway obstruction. Worsening of asthma symptoms and pulmonary functions in relation to menstruation has been documented by some authors. Objectives: To determine peak expiratory flow rate during various phases of menstrual cycle among adult asthmatic women. Methods: A Prospective studyof1 year duration (July 2020 to June2021) A consecutive series of 100 patients with asthma, attending the outpatient clinic of department of chest diseases, satisfying inclusion criteria were included in the study. The socio demographic details and the relevant clinical details was collected using the socio demographic Performa prepared specifically for the study, Patients asked to record asthma symptom scores, morning Peak Expiratory Flow Rate (m-PEFR) (best out of 3 readings taken) daily during the one month screening period to identify women with and without pre-menstrual asthma Results And Discussion: From our study we found highest mean PEFR value is during post ovulatory phase. Lowest during perimenstrual phase. Fall in PEFR seen mostly during perimenstrual phase (43%). Then during preovulatory phase (34%). No such fall seen during periovulatory and postovulatory phase. Severe symptoms were present during perimenstrual phase (19%) and preovulatory phase (14%) only. Similarly, moderate symptoms also during perimenstrual (22%) and preovulatory phase (21%). Both severe and moderate symptoms were not seen during periovulatory and postovulatory phase. Conclusion: Premenstrual exacerbation of asthma occurs in a significant proportion of female adult asthmatics. Thus proper history including menstrual variation of asthma of all these patients should be taken for effective management.

Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.

Asthma is a heterogenous chronic inflammatory lung disease with endotypes that manifest different immune system profiles, severity, and responses to current therapies. Regardless of endotype, asthma features increased immune cell infiltration, inflammatory cytokine release, and airway remodeling. Lung macrophages are also heterogenous in that there are separate subsets and, depending on the environment, different effector functions. Lung macrophages are important in recruitment of immune cells such as eosinophils, neutrophils, and monocytes that enhance allergic inflammation and initiate T helper cell responses. Persistent lung remodeling including mucus hypersecretion, increased airway smooth muscle mass, and airway fibrosis contributes to progressive lung function decline that is insensitive to current asthma treatments. Macrophages secrete inflammatory mediators that induce airway inflammation and remodeling. Additionally, lung macrophages are instrumental in protecting against pathogens and play a critical role in resolution of inflammation and return to homeostasis. This review summarizes current literature detailing the roles and existing knowledge gaps for macrophages as key inflammatory orchestrators in asthma pathogenesis. We also raise the idea that modulating inflammatory responses in lung macrophages is important for alleviating asthma.

The Role of Leukemia Inhibitory Factor in Counteracting the Immunopathology of Acute and Chronic Lung Inflammatory Diseases

Leukemia inhibitory factor (LIF), a member of the IL-6 cytokine family, is highly expressed throughout the body in multiple tissues and cell types. LIF is primarily known to induce the differentiation of myeloid leukemia cells, but recent studies show that LIF has many other functions, including playing multiple roles in cancer and normal physiology. LIF expression is linked to cellular proliferation, metastasis, inflammation, and chemoresistance. LIF expression and secretion are triggered by many means and its downstream signaling can vary based on tissue types. Recent publications suggest that LIF may play a role in pulmonary diseases and its regulation is altered through external factors, such as cigarette smoke, inflammation stimuli, or infections. This review outlines the current knowledge of the function of LIF protein, mediators of LIF expression, receptors it interacts with, downstream LIF signaling, and possible pulmonary outcomes mediated by LIF.

Rev-erbα agonists suppresses TGFβ1-induced fibroblast-to-myofibroblast transition and pro-fibrotic phenotype in human lung fibroblasts

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by excessive scarring of the lungs that can lead to respiratory failure and death. Lungs of patients with IPF demonstrate excessive deposition of extracellular matrix (ECM) and an increased presence of pro-fibrotic mediators such as transforming growth factor-beta 1 (TGFβ1), which is a major driver of fibroblast-to-myofibroblast transition (FMT). Current literature supports that circadian clock dysfunction plays an essential role in the pathophysiology of various chronic inflammatory lung diseases such as asthma, chronic obstructive pulmonary disease, and IPF. The circadian clock transcription factor Rev-erbα is encoded by Nr1d1 that regulates daily rhythms of gene expression linked to immunity, inflammation, and metabolism. However, investigations into the potential roles of Rev-erbα in TGFβ-induced FMT and ECM accumulation are limited. In this study, we utilized several novel small molecule Rev-erbα agonists (GSK41122, SR9009, and SR9011) and a Rev-erbα antagonist (SR8278) to determine the roles of Rev-erbα in regulating TGFβ1-induced FMT and pro-fibrotic phenotypes in human lung fibroblasts. WI-38 cells were either pre-treated/co-treated with or without Rev-erbα agonist/antagonist along with TGFβ1. After 48 h, the following parameters were evaluated: secretion of COL1A1 (Slot-Blot analysis) and IL-6 (ELISA) into condition media, expressions of α-smooth muscle actin (αSMA: immunostaining and confocal microscopy), and pro-fibrotic proteins (αSMA and COL1A1 by immunoblotting), as well as gene expression of pro-fibrotic targets (qRT-PCR: Acta2, Fn1, and Col1a1). Results revealed that Rev-erbα agonists inhibited TGFβ1-induced FMT (αSMA and COL1A1), and ECM production (reduced gene expression of Acta2, Fn1, and Col1a1), and decreased pro-inflammatory cytokine IL-6 release. The Rev-erbα antagonist promoted TGFβ1-induced pro-fibrotic phenotypes. These findings support the potential of novel circadian clock-based therapeutics, such as Rev-erbα agonist, for the treatment and management of fibrotic lung diseases and disorders.

Evaluation of human neutrophil gelatinase-associated lipocalin level in asthma-COPD overlap syndrome of elderly patients

Aims: Human neutrophil gelatinase-associated lipocalin (NGAL) is a protein considered as a noninvasive prognostic biomarker in Asthma-COPD overlap syndrome (ACO). In this study we aimed to show the usability of NGAL as a biomarker in ACO characterized with airway inflammation in over 65 years old. Methods: Three patient groups (Group I: COPD, n: 50, Group II: Asthma, n:50, Group III: ACO, n:50) and a healhty non smoker group (Group IV, n:50) are taken into study. The serum NGAL levels of groups are compared. In Group I, II, III the level of serum NGAL is compared with the age, duration of smoking (pocket/year), number of attack per year, respiratory function values, serum C reaktive protein (CRP, mg/dL), serum IgE (IU/mL) and blood neutrophil-to-lymphocyte rate and atopy. Results: In patients having ACO when the maximum level of serum exist, it is observed that serum NGAL level is increased as the number of attacks is increased (p<0.002). On the other hand in the patients having ACO there was also positive correlation between NLR and serum NGAL level (p<0.05). Conclusion: The increase in serum NGAL levels in chronic inflammatory lung diseases suggests that serum NGAL levels can be used as a biomarker to assess inflammation severity

Dipeptidyl peptidase-1 inhibition with brensocatib reduces the activity of all major neutrophil serine proteases in patients with bronchiectasis: results from the WILLOW trial

BackgroundBrensocatib is an oral, selective, reversible inhibitor of dipeptidyl peptidase-1 (DPP-1), responsible for activating neutrophil serine proteases (NSPs) including neutrophil elastase (NE), proteinase 3 (PR3), and cathepsin G (CatG). In chronic inflammatory lung diseases such as non-cystic fibrosis bronchiectasis (NCFBE), neutrophils accumulate in the airways resulting in excess active NSPs that cause damaging inflammation and lung destruction.MethodsThe 24-week WILLOW trial (NCT03218917) was a randomized, double-blind, placebo-controlled, parallel-group trial in patients with NCFBE conducted at 116 sites across 14 countries. In this trial, treatment with brensocatib was associated with improvements in clinical outcomes including time to first exacerbation, reduction in exacerbation frequency and a reduction in NE activity in sputum. An exploratory analysis of NE activity in white blood cell (WBC) extracts and NE, PR3 and CatG activity in sputum was conducted to further characterize brensocatib’s effect and identify potential correlated effects.ResultsNE, PR3 and CatG activities were reduced in sputum and NE activity was reduced in WBC extracts in a dose-dependent manner after four weeks of brensocatib treatment, with a return to baseline four weeks after the end of treatment. Brensocatib produced the greatest reduction in the sputum activity of CatG, followed by NE and then PR3. Positive correlations among the sputum NSPs were observed both at baseline and in response to treatment, with the strongest correlation among the sputum NSPs for NE and CatG.ConclusionsThese results suggest a broad anti-inflammatory effect of brensocatib underlying its clinical efficacy observed in NCFBE patients.Trial registration: The study was approved by the corresponding ethical review boards of all participating centers. The trial was approved by the Food and Drug Administration and registered at clinicaltrials.gov (NCT03218917) on July 17, 2017 and approved by the European Medicines Agency and registered at the European Union Clinical trials Register (EudraCT No. 2017-002533-32). An independent, external data and safety monitoring committee (comprising physicians with pulmonary expertise, a statistician experienced in the evaluation of clinical safety, and experts in periodontal disease and dermatology) reviewed all adverse events.

Verproside, the Most Active Ingredient in YPL-001 Isolated from Pseudolysimachion rotundum var. subintegrum, Decreases Inflammatory Response by Inhibiting PKCδ Activation in Human Lung Epithelial Cells.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease which causes breathing problems. YPL-001, consisting of six iridoids, has potent inhibitory efficacy against COPD. Although YPL-001 has completed clinical trial phase 2a as a natural drug for COPD treatment, the most effective iridoid in YPL-001 and its mechanism for reducing airway inflammation remain unclear. To find an iridoid most effectively reducing airway inflammation, we examined the inhibitory effects of the six iridoids in YPL-001 on TNF or PMA-stimulated inflammation (IL-6, IL-8, or MUC5AC) in NCI-H292 cells. Here, we show that verproside among the six iridoids most strongly suppresses inflammation. Both TNF/NF-κB-induced MUC5AC expression and PMA/PKCδ/EGR-1-induced IL-6/-8 expression are successfully reduced by verproside. Verproside also shows anti-inflammatory effects on a broad range of airway stimulants in NCI-H292 cells. The inhibitory effect of verproside on the phosphorylation of PKC enzymes is specific to PKCδ. Finally, in vivo assay using the COPD-mouse model shows that verproside effectively reduces lung inflammation by suppressing PKCδ activation and mucus overproduction. Altogether, we propose YPL-001 and verproside as candidate drugs for treating inflammatory lung diseases that act by inhibiting PKCδ activation and its downstream pathways.

Development of severe colitis is associated with lung inflammation and pathology.

Inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis are chronic relapsing diseases that affect the gastrointestinal tract, most commonly the colon. A link between the gut and the lung is suggested since patients with IBD have an increased susceptibility for chronic inflammatory lung disease. Furthermore, in the absence of overt lung disease, IBD patients have worsened lung function and more leukocytes in sputum than healthy individuals, highlighting a conduit between the gut and lung in disease. To study the gut-lung axis in the context of IBD, we used TCRδ-/- mice, which are highly susceptible to dextran sulfate sodium (DSS) due to the importance of γδ T cells in maintenance of barrier integrity. After induction of experimental colitis using DSS, the lungs of TCRδ-/- mice exhibited signs of inflammation and mild emphysema, which was not observed in DSS-treated C57BL/6 mice. Damage to the lung tissue was accompanied by a large expansion of neutrophils in the lung parenchyma and an increase in alveolar macrophages in the lung wash. Gene expression analyses showed a significant increase in Csf3, Cxcl2, Tnfa, and Il17a in lung tissue in keeping with neutrophil infiltration. Expression of genes encoding reactive oxygen species enzymes and elastolytic enzymes were enhanced in the lungs of both C57BL/6 and TCRδ-/- mice with colitis. Similarly, surfactant gene expression was also enhanced, which may represent a protective mechanism. These data demonstrate that severe colitis in a susceptible genetic background is sufficient to induce lung inflammation and tissue damage, providing the research community with an important tool for the development of novel therapeutics aimed at reducing co-morbidities in IBD patients.

Discovery and Optimization of a Novel Macrocyclic Amidinourea Series Active as Acidic Mammalian Chitinase Inhibitors.

Our research group has been involved for a long time in the development of macrocyclic amidinoureas (MCAs) as antifungal agents. The mechanistic investigation drove us to perform an in silico target fishing study, which allowed the identification of chitinases as one of their putative targets, with 1a showing a submicromolar inhibition of Trichoderma viride chitinase. In this work, we investigated the possibility to further inhibit the corresponding human enzymes, acidic mammalian chitinase (AMCase) and chitotriosidase (CHIT1), involved in several chronic inflammatory lung diseases. Thus, we first validated the inhibitory activity of 1a against AMCase and CHIT1 and then designed and synthesized new derivatives aimed at improving the potency and selectivity against AMCase. Among them, compound 3f emerged for its activity profile along with its promising in vitro ADME properties. We also gained a good understanding of the key interactions with the target enzyme through in silico studies.

Key Role of Mesenchymal Stromal Cell Interaction with Macrophages in Promoting Repair of Lung Injury.

Lung macrophages (Mφs) are essential for pulmonary innate immunity and host defense due to their dynamic polarization and phenotype shifts. Mesenchymal stromal cells (MSCs) have secretory, immunomodulatory, and tissue-reparative properties and have shown promise in acute and chronic inflammatory lung diseases and in COVID-19. Many beneficial effects of MSCs are mediated through their interaction with resident alveolar and pulmonary interstitial Mφs. Bidirectional MSC-Mφ communication is achieved through direct contact, soluble factor secretion/activation, and organelle transfer. The lung microenvironment facilitates MSC secretion of factors that result in Mφ polarization towards an immunosuppressive M2-like phenotype for the restoration of tissue homeostasis. M2-like Mφ in turn can affect the MSC immune regulatory function in MSC engraftment and tissue reparatory effects. This review article highlights the mechanisms of crosstalk between MSCs and Mφs and the potential role of their interaction in lung repair in inflammatory lung diseases.

Current Perspective on the Role of the Circadian Clock and Extracellular Matrix in Chronic Lung Diseases.

The circadian clock is a biochemical oscillator that rhythmically regulates physiological and behavioral processes such as inflammation, immunity, and metabolism in mammals. Circadian clock disruption is a key driver for chronic inflammatory as well as fibrotic lung diseases. While the mechanism of circadian clock regulation in the lung has been minimally explored, some evidence suggests that the transforming growth factor β (TGFβ) signaling pathway and subsequent extracellular matrix (ECM) accumulation in the lung may be controlled via a clock-dependent mechanism. Recent advancements in this area led us to believe that pharmacologically targeting the circadian clock molecules may be a novel therapeutic approach for treating chronic inflammatory lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Here, we update the current perspective on the circadian clock role in TGFβ1 signaling and extracellular matrix production during chronic lung diseases.

Long-term exposure to house dust mites accelerates lung cancer development in mice

BackgroundIndividuals with certain chronic inflammatory lung diseases have a higher risk of developing lung cancer (LC). However, the underlying mechanisms remain largely unknown. Here, we hypothesized that chronic exposure to house dust mites (HDM), a common indoor aeroallergen associated with the development of asthma, accelerates LC development through the induction of chronic lung inflammation (CLI). MethodsThe effects of HDM and heat-inactivated HDM (HI-HDM) extracts were evaluated in two preclinical mouse models of LC (a chemically-induced model using the carcinogen urethane and a genetically-driven model with oncogenic KrasG12D activation in lung epithelial cells) and on murine macrophages in vitro. Pharmacological blockade or genetic deletion of the Nod-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome, caspase-1, interleukin-1β (IL-1β), and C–C motif chemokine ligand 2 (CCL2) or treatment with an inhaled corticosteroid (ICS) was used to uncover the pro-tumorigenic effect of HDM. ResultsChronic intranasal (i.n) instillation of HDM accelerated LC development in the two mouse models. Mechanistically, HDM caused a particular subtype of CLI, in which the NLRP3/IL-1β signaling pathway is chronically activated in macrophages, and made the lung microenvironment conducive to tumor development. The tumor-promoting effect of HDM was significantly decreased by heat treatment of the HDM extract and was inhibited by NLRP3, IL-1β, and CCL2 neutralization, or ICS treatment.ConclusionsCollectively, these data indicate that long-term exposure to HDM can accelerate lung tumorigenesis in susceptible hosts (e.g., mice and potentially humans exposed to lung carcinogens or genetically predisposed to develop LC).

Identification of Potential Differentially-Methylated/Expressed Genes in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. DNA methylation can regulate gene expression. Understanding the potential molecular mechanism of COPD is of great importance. The aim of this study was to find differentially methylated/expressed genes in COPD. DNA methylation and gene expression profiles in COPD were downloaded from the dataset, followed by functional analysis of differentially-methylated/expressed genes. The potential diagnostic value of these differentially-methylated/expressed genes was determined by receiver operating characteristic (ROC) analysis. Expression validation of differentially-methylated/expressed genes was performed by in vitro experiment and extra online datasets. Totally, 81 hypermethylated-low expression genes and 121 hypomethylated-high expression genes were found in COPD. Among which, 9 core hypermethylated-low expression genes (CD247, CCR7, CD5, IKZF1, SLAMF1, IL2RB, CD3E, CD7 and IL7R) and 8 core hypomethylated-high expression genes (TREM1, AQP9, CD300LF, CLEC12A, NOD2, IRAK3, NLRP3 and LYZ) were identified in the protein-protein interaction (PPI) network. Moreover, these genes had a potential diagnostic utility for COPD. Some signaling pathways were identified in COPD, including T cell receptor signaling pathway, cytokine-cytokine receptor interaction, hematopoietic cell lineage, HTLV-I infection, endocytosis and Jak-STAT signaling pathway. In conclusion, differentially-methylated/expressed genes and involved signaling pathways are likely to be associated with the process of COPD.

NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

Silica-induced lung epithelial injury and fibrosis are vital pathogeneses of silicosis. Although the NOD-like receptor protein 3 (NLRP3) inflammasome contributes to silica-induced chronic lung inflammation, its role in epithelial injury and regeneration remains unclear. Here, using mouse lung stem/progenitor cell-derived organotypic systems, including 2D air-liquid interface and 3D organoid cultures, we investigated the effects of the NLRP3 inflammasome on airway epithelial phenotype and function, cellular injury and regeneration, and the potential mechanisms. Our data showed that silica-induced NLRP3 inflammasome activation disrupted the epithelial architecture, impaired mucociliary clearance, induced cellular hyperplasia and the epithelial-mesenchymal transition in 2D culture, and inhibited organoid development in 3D system. Moreover, abnormal expression of the stem/progenitor cell markers SOX2 and SOX9 was observed in the 2D and 3D organotypic models after sustained silica stimulation. Notably, these silica-induced structural and functional abnormalities were ameliorated by MCC950, a selective NLRP3 inflammasome inhibitor. Further studies indicated that the NF-κB, Shh-Gli and Wnt/β-catenin pathways were involved in NLRP3 inflammasome-mediated abnormal differentiation and dysfunction of the airway epithelium. Thus, prolonged NLRP3 inflammasome activation caused injury and aberrant lung epithelial regeneration, suggesting that the NLRP3 inflammasome is a pivotal target for regulating tissue repair in chronic inflammatory lung diseases.

Study on the theory and prescription of pulmonary interstitial fibrosis in Traditional Chinese Medicine

Pulmonary interstitial fibrosis (PIF) is a chronic progressive fibrotic interstitial inflammatory lung disease. The pathogenesis and pathogenesis of PIF are still unclear and there is a lack of effective treatment. As the incidence of PIF increases year by year, the mortality of PIF is not optimistic This paper will summarize the TCM theories related to pulmonary interstitial fibrosis excavated from HowNet database and draw the following conclusions: the theoretical understanding of pulmonary interstitial fibrosis includes the following: lung collaterals, toxic damage to lung collaterals, fire subduing yin collaterals, triple energizer gasification, yin deficiency and blood stasis, Xuanfu theory, yang transforming qi and yin forming, lung being blood viscera; Study on single medicine of traditional Chinese medicine, such as Hongqi, earthworm, Astragalus, Polygonum cuspidatum and other ancient prescriptions, such as Maimendong Decoction, Xiefei Decoction and Yang, and Tang physician prescriptions, such as Qidong Huoxue Yin Feixian Prescription, can effectively delay pulmonary interstitial fibrosis.

Diagnosis of asthma: new developments in general internal medicine

Asthma, a chronic inflammatory lung disease affecting about 10 % of the population, involves both the general internist and the pulmonologist. The risk of over and underdiagnosis generates significant health costs and evitable clinical consequences. Improved screening through dedicated anamneses and questionnaires, as well as use of fractional exhaled nitric oxide (FeNO) may improve the diagnosis of asthma in general internal medicine.

Obesity, Charlson comorbidity index, and neutrophil-to-lymphocyte ratio in chronic obstructive pulmonary disease: relationship to disease severity.

Chronic obstructive pulmonary disease (COPD) is a common chronic inflammatory lung disease with high mortality and morbidity rates. Obesity, various comorbid diseases, and inflammation often coexist in chronic obstructive pulmonary disease (COPD), exhibiting a complex interaction with disease severity. The aim of the study was to examine the relationship between COPD markers and obesity, the Charlson Comorbidity Index (CCI), and neutrophil/lymphocyte ratio (NLR). Eighty male patients with stable COPD admitted to the pulmonology unit were included in the study. The presence of comorbidities was investigated in obese and non-obese individuals with COPD. Pulmonary function tests and the mMRC dyspnea scale were examined, and CCI scores were calculated. 60.9 % with mild/moderate COPD, and 64.7 % with severe COPD had a comorbid disease. The incidence of hypertension and diabetes was significantly higher in obese patients. The obesity rate was 41.3 % in patients with mild/moderate COPD (FEV1 ≥ 50) and 26.5 % in those with severe COPD (FEV1 < 50). There was a positive and significant correlation between CCI value and BMI and mMRC dyspnea scale. NLR was significantly higher in patients with FEV1 < 50 and mMRC ≥ 2. As a result, it is essential to screen obese patients with COPD, who are among the groups with the highest incidence of comorbidities, in terms of such diseases that exacerbate the symptoms of their disease. Findings may support the potential applicability of simple blood count indices (such as NLR) in the clinical assessment of disease in stable COPD patients (Tab. 4, Fig. 1, Ref. 46).

Added value of a chest multidetector computed tomography scoring system in the assessment of chronic lung disease among pediatric patients

BackgroundPediatric chronic lung disease (CLD) represents a heterogeneous group of several distinct clinical entities, with its prevalence increasing over the last decade. The current study aimed to identify the role of chest multidetector computed tomography (MDCT) using modified Bhalla scoring for the early diagnosis of CLD in pediatric patients and determine the most common chest MDCT findings. This prospective study involved 45 pediatric patients with chronic respiratory symptoms, all of whom underwent MDCT. Thereafter, data were analyzed using the modified Bhalla score.ResultsChronic lung diseases were classified according to their radiological and clinical criteria. The total CT score, which was the most significant factor for chronic inhalation and chronic recurrent inflammatory lung diseases, varied between 2 and 21 points, with those having autoimmune diseases exhibiting the largest value for the mean CT score. The clinical severity of symptoms was not correlated with CT score.ConclusionOur findings showed that MDCT was a useful tool for diagnosing pediatric CLD and assessing disease extent, severity, and superimposed complications. The modified Bhalla CT scoring system allowed for systematic primary and follow-up assessments of various lung lesions in cases with varying CLD etiologies.

Evaluation of anthropometric methods for fat mass measurement in chronic obstructive pulmonary disease patients.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. The obesity is a global problem, which is set to increase over time. Chronic obstructive lung disease is the third-leading cause of death globally, and both obesity and diet appear to play roles in its pathophysiology (e.g., role in the development of obstructive sleep apnoea and obesity hypoventilation syndrome). However, the effects of obesity on the respiratory system are often underappreciated. The objective of this study was to compare three anthropometric methods to evaluate of fat mass in COPD patients. Three anthropometric methods of evaluation fat mass in a group of 60 patients with COPD were compared. To the measurement of fat mass were used: (1) Dual Energy X-ray Absorptiometry method (DEXA), specifically by DEXA densitometer QDR Discovery Wi (S/N 80227) with additional software (Body Composition Analysis); (2) four-frequency bioelectrical impedance analysis (BIA) device Bodystat Quadscan 4000 (Bodystat Ltd, British Isles); (3) skin folds measurement (SFM) with caliper (Harpenden Lange Skinfold Caliper, Cambridge Scientific Industries, Inc. Cambridge, Maryland). The measured values were statistically processed and evaluated in a statistical program Statistica Cz. version 7.1 and Microsoft Office Excel 2010 (Los Angeles, CA, USA). Differences among anthropometric methods of measurement fat mass were tested with one-way analysis of variance (ANOVA). The data were presented as mean ± standard deviation (SD). DEXA method, generally accepted for assessing body composition, showed an average value of 22.48 ±11.32 kg of fat mass, which corresponds in percentage terms to the value of 29.62±9.28. BIA method for the parameter fat mass in the monitored group of COPD patients was found the mean value 25.08±10.14 kg (in percentages 30.85±8.15). An average value 28.50±8.08% of fat mass, was determined from the skinfolds measurements (SFM) and subsequent calculations. When comparing these methods (DEXA, BIA and SFM) used to determine body composition, a statistically insignificant difference was found (P >0.05). In this study a good correlation between three anthropometric methods (DEXA, BIA, SFM) for measuringfat mass in patients with COPD and statistically insignificant differences between them were observed. To better definechanges in the nutritional status of patients with COPD using anthropometric methods over time, further studies areneeded that also monitor the consequences of clinical status, rehabilitation, and nutritional treatment.