Common Lung Disease Research Articles

Quality of life in idiopathic pulmonary fibrosis in Latin American countries

BackgroundIdiopathic pulmonary fibrosis (IPF) is the most common Interstitial Lung Disease (ILD). It is characterized by dyspnoea and a progressive decline in lung function, which negatively affects life. This study aimed to evaluate Health-Related Quality of Life (HRQoL) in IPF patients in Latin American countries.MethodsSix countries (Argentina, Bolivia, Colombia, Chile, Mexico, and the Dominican Republic) enrolled patients with IPF. They answered the Saint George’s Respiratory Questionnaire for Idiopathic Pulmonary Fibrosis (SGRQ-I) and the Hospital Anxiety and Depression Scale (HADS). Demographic characteristics, the Torvan index, and a lung function test were also assessed. IPF was diagnosed according to the ATS/ERS/JRS/ALAT 2018 criteria.ResultsWe enlisted 75 patients diagnosed with IPF; 81% were male, with an average age of 74 ± 7. The total SGRQ-I score was 49 ± 23, with a higher score in the activity domain of 70 ± 23. Torvan index average was 17 ± 6. We found that 28% presented anxiety and 35% depression. Besides, we observed that patients requiring oxygen had a worse quality of life (total SGRQ-I 62 ± 22 vs. 45 ± 22, p = 0.003) without finding differences in antifibrotic therapy. We did not find differences in HRQoL when dividing groups according to their altitude above sea level, except for a higher frequency of anxiety in patients living at sea level.ConclusionsWe found similar data compared to those reported in real-life European populations. We also found that anxiety and depression are prevalent. However, they are often underdiagnosed and, therefore, left untreated.

Cyclin G1 Regulates the Alveolarization in Models of Bronchopulmonary Dysplasia by Inhibiting AT2 Cell Proliferation.

Disrupted neonatal lung alveologenesis often leads to bronchopulmonary dysplasia (BPD), the most common chronic lung disease in children. The inhibition of type 2 alveolar (AT2) cell proliferation plays an important role in the arrest of alveologenesis. However, the mechanism of AT2 cell proliferation retardation in BPD is still not fully elucidated. The purpose of the present study was to explore the effects of cyclin G1 (CCNG1) on AT2 cell proliferation in hyperoxia-induced lung injury in neonatal mice. Our findings revealed that hyperoxia significantly reduced the proportion of AT2 cells in the lungs of neonatal mice and coincided with an upregulation of CCNG1 expression. Notably, this upregulation of CCNG1 was accompanied by an increase in Wnt signaling. We observed colocalization of CCNG1 and Wnt3a within AT2 cells in the hyperoxia group. Further analysis showed that inhibiting CCNG1 expression regressed the expression of Wnt signaling and enhanced cell proliferation. These results suggest that CCNG1 plays a pivotal role in suppressing AT2 cell proliferation, at least partly by counteracting the effects of Wnt signaling to modulate AT2 cell growth in the BPD model. Our findings contribute to a better understanding of the mechanisms underlying BPD.

Retraction Note: Distance and similarity measures for (p, q)-fuzzy sets and their application in assessing common lung diseases

Retraction Note: Distance and similarity measures for (p, q)-fuzzy sets and their application in assessing common lung diseases

Stage-Dependent Fibrotic Gene Profiling of WISP1-Mediated Fibrogenesis in Human Fibroblasts.

Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease with unknown etiology, characterized by chronic inflammation and tissue scarring. Although, Pirfenidone and Nintedanib slow the disease progression, no currently available drugs or therapeutic interventions address the underlying cause, highlighting the unmet medical need. A matricellular protein, Wnt-1-induced secreted protein 1 (WISP1), also referred to as CCN4 (cellular communication network factor 4), is a secreted multi-modular protein implicated in multi-organ fibrosis. Although the precise mechanism of WISP1-mediated fibrosis remains unclear, emerging evidence indicates that WISP1 is profibrotic in nature. While WISP1-targeting therapy is applied in the clinic for fibrosis, detailed interrogation of WISP1-mediated fibrogenic molecular and biological pathways is lacking. Here, for the first time, using NanoString® technology, we identified a novel WISP1-associated profibrotic gene signature and molecular pathways potentially involved in the initiation and progression of fibrosis in primary human dermal and lung fibroblasts from both healthy individuals and IPF patients. Our data demonstrate that WISP1 is upregulated in IPF-lung fibroblasts as compared to healthy control. Furthermore, our results confirm that WISP1 is downstream of the transforming growth factor-β (TGFβ), and it induces fibroblast cell proliferation. Additionally, WISP1 induced IL6 and CCL2 in fibroblasts. We also developed a novel, combined TGFβ and WISP1 in vitro system to demonstrate a role for WISP1 in the progression of fibrosis. Overall, our findings uncover not only similarities but also striking differences in the molecular profile of WISP1 in human fibroblasts, both during the initiation and progression phases, as well as in disease-specific context.

Leukemia inhibitory factor (LIF) receptor amplifies pathogenic activation of fibroblasts in lung fibrosis

Fibrosis drives end-organ damage in many diseases. However, clinical trials targeting individual upstream activators of fibroblasts, such as TGFβ, have largely failed. Here, we target the leukemia inhibitory factor receptor (LIFR) as an "autocrine master amplifier" of multiple upstream activators of lung fibroblasts. In idiopathic pulmonary fibrosis (IPF), the most common fibrotic lung disease, we found that lung myofibroblasts had high LIF expression, and the fibroblasts in fibroblastic foci coexpressed LIF and LIFR. In IPF, fibroblastic foci are the "leading edge" of fibrosis and a key site of disease pathogenesis. TGFβ1, one of the principal drivers of fibrosis, up-regulated LIF expression in IPF fibroblasts. We found that TGFβ1, IL-4, and IL-13 stimulations of fibroblasts require the LIF-LIFR axis to evoke a strong fibrogenic effector response in fibroblasts. In vitro antibody blockade of LIFR on IPF lung fibroblasts reduced the induction of profibrotic genes after TGFβ1 stimulation. Silencing LIF and LIFR reduced profibrotic fibroblast activation following TGFβ1, IL-4, and IL-13 stimulations. We also demonstrated that LIFR amplified profibrotic stimuli in precision-cut lung slices from IPF patients. These LIFR signals were transduced via JAK2, and STAT1 in IPF lung fibroblasts. Together, we find that LIFR drives an autocrine circuit that amplifies and sustains pathogenic activation of IPF fibroblasts. Targeting a single, downstream master amplifier on fibroblasts, like LIFR, is an alternative therapeutic strategy that simultaneously attenuates the profibrotic effects of multiple upstream stimuli.

Regulated Cell Death of Alveolar Macrophages in Acute Lung Inflammation: Current Knowledge and Perspectives.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a common and serious clinical lung disease characterized by extensive alveolar damage and inflammation leading to impaired gas exchange. Alveolar macrophages (AMs) maintain homeostatic properties and immune defenses in lung tissues. Several studies have reported that AMs are involved in and regulate ALI/ARDS onset and progression via different regulated cell death (RCD) programs, such as pyroptosis, apoptosis, autophagic cell death, and necroptosis. Notably, the effects of RCD in AMs in disease are complex and variable depending on the environment and stimuli. In this review, we provide a comprehensive perspective on how regulated AMs death impacts on ALI/ARDS and assess its potential in new therapeutic development. Additionally, we describe the crosstalk between different RCD types in ALI, and provide new perspectives for the treatment of ALI/ARDS and other severe lung diseases.

The Relationship Between PM2.5 and Eight Common Lung Diseases: A Two-Sample Mendelian Randomization Analysis.

Air pollutants have both acute and chronic impacts on human health, affecting multiple systems and organs. While PM2.5 exposure is commonly assumed to be strongly associated with all respiratory diseases, this relationship has not been systematically analyzed. This study employed a two-sample Mendelian randomization approach to investigate the effects of PM2.5 on eight common lung diseases, using data from GWAS. Additionally, multivariable Mendelian randomization was applied to assess the direct effects of various air pollutants and the mediating roles of common factors such as BMI and smoking. At a significance threshold of 5×10-8, PM2.5 showed a significant causal relationship with both asthma and COPD. When the screening threshold was relaxed to 5× 10-6, this exposure continued to demonstrate significant associations not only with asthma and COPD, but also with other respiratory diseases, including pneumonia, emphysema/chronic bronchitis, and lung cancer. In the multivariable Mendelian randomization analysis, which controlled for smoking and bacterial infections, the association with pneumonia became non-significant, while the relationships with the other four diseases persisted. This study provides a systematic exploration of the relationship between PM2.5 and eight pulmonary diseases from a new perspective, deepening our understanding of the impact of air pollution on health and laying the foundation for future efforts to mitigate these effects.

The value of lung ultrasound in the differential diagnosis of common lung diseases in newborns.

To investigate the value of lung ultrasound in the differential diagnosis of common neonatal lung diseases. A total of 160 newborns with suspected lung diseases admitted to the Department of Neonatology of Linping Branch of the Second Affiliated Hospital of Zhejiang University from January 2020 to June 2023, were selected for examination. Perform lung ultrasound within 24 hours of admission for above newborns, using the final clinical diagnosis as standard. Calculate the accuracy, sensitivity, and specificity of lung ultrasound technology in the diagnosing neonatal lung diseases, and assess its value in the differential diagnosis of common neonatal lung diseases. A total of 160 newborns suspected of having lung disease were finally diagnosed with lung disease in 142 cases. The accuracy of lung ultrasound in differentiating neonatal pneumonia, respiratory distress syndrome of the newborn, meconium aspiration syndrome, transient tachypnea of the newborn, pneumothorax, atelectasis, and pulmonary hemorrhage was 96.8%, 98.1%, 98.8%, 100%, 100%, 100%, and 100%, respectively. The detection rate of lung ultrasound examination for lung disease in newborns was 85.00%, with a sensitivity of 95.77%, specificity of 77.77%, positive predictive value of 97.14% and negative predictive value of 70.0%. The consistency test kappa value between lung ultrasound findings and the final clinical diagnosis of neonatal lung diseases is 0.846. Lung ultrasound holds significant value in the differential diagnosis of common lung diseases in newborns.

Downstream Effects of Market Changes on Inhalers: Impacts on Individuals With Chronic Lung Disease.

COPD and asthma are two of the most common chronic lung diseases, affecting over 545 million people globally and 34 million in the United States. Annual health care costs related to chronic lung disease are estimated at €380 billion in the European Union, and $24-$50 billion in the United States averaging to $4,000 in out-of-pocket costs per person in the U.S. A full-text literature search was conducted for English publications between January 1, 2005-March 18, 2024. It returned over 5,000 publications that were further narrowed using key search words, resulting in 172 peer-reviewed articles. Using their experience and subject expertise, the authors further narrowed the peer-reviewed articles to 55 that were in their opinion relevant. Also, 38 recently published industry reports and news articles specific to downstream effects of inhaler market changes and the future impact were included. The literature suggests that individuals with chronic lung disease face increased challenges with access to inhaled medication due to rising medication costs, discontinuation of branded medications, introduction of generic medications not covered by insurance, exclusionary preferred drug list tactics that force health care providers into non-medical switching of medication or devices, and ongoing medication shortages. Providers experience ongoing hurdles in prescribing appropriate inhaled medications for individuals with chronic lung disease, including increased time and costs spent on administrative tasks due to inhaler denials, a loss of patient trust, and limits on their ability to prescribe appropriate inhaled medication for individuals with chronic lung disease.

Principles of resuscitation for infants with severe bronchopulmonary dysplasia

Severe bronchopulmonary dysplasia (sBPD) requiring invasive mechanical ventilation is a heterogeneous disease process that contributes to morbidity and mortality in infants. As the most common lung disease of prematurity, sBPD has a multitude of overlapping cardiac, airway, pulmonary vascular, and infectious phenotypic presentations that progress through four different phases of care. Premature infants with sBPD are at a high risk of acute decompensation and subsequent cardiopulmonary arrest. A comprehensive determination of the complex phenotypes that contribute to the clinical presentation will help clinicians decipher the phase of care, identify cardiopulmonary compromise earlier and guide targeted therapeutic intervention during acute episodes of deterioration. The approach to resuscitation of premature infants with sBPD undergoing an acute decompensation differs from general neonatal and pediatric resuscitation practices. This review summarizes the phenotypes of sBPD, the phases of care, the common triggers of acute exacerbations, and the principles of resuscitation of a deteriorating infant with sBPD. We offer a framework for sBPD resuscitation with a focus on prevention, assessment, and post-resuscitative care.

Characterization of Pseudomonas aeruginosa from subjects with diffuse panbronchiolitis.

Diffuse panbronchiolitis (DPB), a chronic lung disease characterized by persistent P. aeruginosa infection, serves as an informative comparator to more common chronic lung diseases, such as cystic fibrosis (CF). This study aimed to better address the interplay between P. aeruginosa and chronically compromised airway environments through the examination of DPB P. aeruginosa strains, as existing literature regarding DPB is limited to case reports, case series, and clinical treatment guidelines. The evaluation of these features in the context of DPB, in tandem with prevailing knowledge of P. aeruginosa strains collected from more common chronic lung diseases (e.g., CF), can aid in the development of more effective strategies to combat respiratory P. aeruginosa infections in patients with chronic lung diseases.

Automated 3D-Body Composition Analysis as a Predictor of Survival in Patients With Idiopathic Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease, with a median survival time of 2 to 5 years. The focus of this study is to establish a novel imaging biomarker. In this study, 79 patients (19% female) with a median age of 70 years were studied retrospectively. Fully automated body composition analysis (BCA) features (bone, muscle, total adipose tissue, intermuscular, and intramuscular adipose tissue) were combined into Sarcopenia, Fat, and Myosteatosis indices and compared between patients with a survival of more or less than 2 years. In addition, we divided the cohort at the median (high=≥ median, low=<median) of the respective BCA index and tested the impact on the overall survival using the Kaplan-Meier methodology, a log-rank test, and adjusted multivariate Cox-regression analysis. A high Sarcopenia and Fat index and low Myosteatosis index were associated with longer median survival (35 vs. 16mo for high vs. low Sarcopenia index, P=0.066; 44 vs. 14mo for high vs. low Fat index, P<0.001; and 33 vs. 14mo for low vs. high Myosteatosis index, P=0.0056) and better 5-year survival rates (34.0% vs. 23.6% for high vs. low Sarcopenia index; 47.3% vs. 9.2% for high vs. low Fat index; and 11.2% vs. 42.7% for high vs. low Myosteatosis index). Adjusted multivariate Cox regression showed a significant impact of the Fat (HR=0.71, P=0.01) and Myosteatosis (HR=1.12, P=0.005) on overall survival. The fully automated BCA provides biomarkers with a predictive value for the overall survival in patients with IPF.

Relationship between functional status and fatigue after COVID-19 infection: a multicenter study from Türkiye.

Symptoms of COVID-19 may persist for months. One of the persistent symptoms of COVID-19 is fatigue, which reduces functional status. The relationship between fatigue, functional status, and various other factors has received little attention, which this study aims to address.. Patients with COVID-19 infection were included in this multicenter cross-sectional study. Age, sex, body mass index (BMI), marital status, smoking status, presence and duration of chronic disease, comorbidity index, regular exercise habits, time since COVID-19 diagnosis, hospitalization status, length of hospital stay, intubation status, home oxygen therapy after discharge, participation in a pulmonary rehabilitation program, presence of dyspnea, presence of cough, presence of sputum, and modified Medical Research Council, Post-COVID Functional Status (PCFS), Fatigue Severity Scale (FSS), and EQ-5D-5L Questionnaire scores were recorded. We enrolled 1095 patients, including 603 (55%) men and 492 (45%) women with a mean age of 50 ± 14 years. The most common chronic lung disease was COPD (11%) and 266 (29%) patients had nonpulmonary disease. The median time elapsed since COVID-19 diagnosis was 5 months; the hospitalization rate was 47%. The median PCFS grade was 1 (0-4) and the median FSS score was 4.4 (1-7). The PCFS and FSS were positively correlated (r = 0.49, p < 0.01; OR: 1.88, 95% CI: 1.68-2.10). Both functional status and fatigue were associated with quality of life, which was lower in older patients, those with higher BMI, those with systemic disease, those not exercising regularly, and those with more severe COVID-19 infection (defined by dyspnea, pneumonia as indicated by computed tomography, hospitalization, length of stay, ICU admission, intubation, and the need for home oxygen after discharge). Fatigue may cause poorer functional status regardless of the time since COVID-19 diagnosis. In this study, patients with FSS scores of >4.78 showed moderate to severe functional limitations. It is important to address modifiable patient risk factors and reduce the severity of COVID-19 infection.

EQ-5D Based Utility Values for Adults with Chronic Obstructive Pulmonary Disease: A Systematic Review, Meta-Analysis, and Meta-Regression

Chronic obstructive pulmonary disease (COPD) is a common lung disease that negatively affects health-related quality of life (QoL). Utility values, which measure QoL by weighting health states with societal preferences, are required for the cost-utility models that drive economic evaluations and policy decisions. Moayeri et al. published a systematic review and meta-analysis of utilities (EQ-5D) in COPD in June 2016. The current study investigated changes in mean utilities in more recent studies thereafter, exploring heterogeneity in utilities across diverse clinical and study characteristics. Systematic searches of databases, such as MEDLINE and Embase were undertaken from 1 July 2015 until 20 May 2024. A random-effects meta-analysis of utilities (EQ-5D) was performed which addressed inter-study heterogeneity and subgroup analyses. The pooled general mean (95% CI) utility value was 0.761 (0.726–0.795) from 43 studies, whereas Moayeri et al. reported 0.673 (0.653–0.693) from 32 studies. This improvement in mean utilities could be due to increased awareness, early detection, and better medical interventions over the past decade, but demonstrates that a general utility value should be approached with caution given significant heterogeneity. Four meta-regressions were performed on each subgroup: region, method of elicitation, reported comorbidities, and disease stage; of which, method of elicitation, disease stage, and region were found to be significant moderators of utilities. It is, therefore, important to use meta-analysed utilities for cost-utility analyses that reflect the context and patient population of the model. Moreover, these results provide additional evidence for the precision and sensitivity of EQ-5D-5L over EQ-5D-3L.

‘Destroyed Lung’: A Marker of Sequel of ‘Far Advanced’ Radiological Type of Pulmonary Tuberculosis’

Pulmonary Tuberculosis is caused by bacilli mycobacterium tuberculosis and known to infect human race since the dawn of history and archaeological evidence has traced its association in neolithic times. Tuberculosis is the most common infectious lung disease in India with significant mortality and morbidity. Tuberculosis can cause diverse thoracic presentations ranging from nodules, consolidations&amp; cavitation, mediastinal adenopathy, pleural effusion to diffuse endobronchial disease presenting like bronchial asthma. Due to diverse presentations, diagnosis is many times delayed due to lack of suspicion by treating general physicians and rational treatment not offered in time. In spite of awareness by government organizations and considered as a ‘global health issue of concern’ by the World Health organization, tuberculosis is still considered as a social stigma. Destroyed lung is described in literature and known as a complication of pulmonary tuberculosis. Destroyed lung is defined as combination of pleural and parenchymal lung destruction with cavitation, bronchiectasis, loss of lung volume and mediastinal herniation to diseased side. In this case series, we have reported two cases with history of pulmonary tuberculosis in the past and received adequate anti-tuberculosis treatment. Both were having residual chronic lung disease and symptoms causing significant impact on quality of life with recurrent hospitalization, hospital visits and cost of care. One patient has a history of delayed diagnosis and ATT was started after maximum lung destruction due to a tuberculous process that has already occurred. In this patient tuberculosis was cured but residual lung damage or sequel presenting as destroyed lung. In the second case, tuberculosis was diagnosed in adequate time but the patient has defaulted due to adverse events of ATT and he has taken medications as per his own tolerance. Neither adherence nor compliance was acceptable in the second case and resulted in a partially treated case of pulmonary tuberculosis. Ongoing lung destruction in the second case would be the cause for destroyed lungs in absence of irrational medicines in today’s era of good quality ATT. Destroyed lung is preventable with early diagnosis, prompt evaluation with microscopy and nucleic acid amplification tests and treatment with universally available, acceptable and affordable free ATT as National guidelines. 'Destroyed lung' are having a significant impact on quality of life and health expenditure and are considered as ‘radiological stigma’ of Tuberculosis. Radiological classifications of tuberculosis are less used now, and, it can be justified in grading of disease severity and aggressive treatment planning. Radiological classifications also help in predicting complications such as ‘destroyed lung’ during evolution of advanced pulmonary tuberculosis disease which can be prevented with timely diagnosis and use of rational treatment with good clinical and radiological outcome.

The Role of Serum IgG Precipitins against Six Typical Organic Antigens Involved in Hypersensitivity Pneumonitis: A 10-Year Retrospective Study of a Referral Interstitial Lung Disease Centre

Hypersensitivity pneumonitis (HP) represents the third common interstitial lung disease caused by an exaggerated immune response following the inhalation of organic and/or chemical environmental antigens. The aim of this study was to determine the cut-off values of specific IgG antibodies (named precipitins) and their association with clinical data in the diagnosis of HP. In this 10-year retrospective study, the IgG concentrations against six antigens, Penicillium chrysogenum/notatum, Aspergillus fumigatus, Alternaria alternata, Aspergillus niger, Micropolyspora faeni, and pigeon droppings, were retrieved. The controlled group was made of 1516 healthy subjects without diagnosis of lung pathologies, while the case group consisted of 54 individuals affected by HP. Considering all six IgG antibodies together and the 97.5% percentiles determined in the control group, 30 of 54 subjects (56%) had one or more positive precipitins. In these patients, the major frequencies found were IgG antibodies against pigeon droppings, followed by Penicillium chrysogenum/notatum and Aspergillus niger. Although the sensitivity of serum precipitins depends on the population enrolled and the method used, the cut-off values determined in this study can be a valuable tool for clinicians in the diagnosis of HP, in eliminating the antigens responsible from the environment, and in establishing more specific IgG panels.

Single-cell combined with transcriptome sequencing to explore the molecular mechanism of cell communication in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a common, chronic, and progressive lung disease that severely impacts human health and survival. However, the intricate molecular underpinnings of IPF remains elusive. This study aims to delve into the nuanced molecular interplay of cellular interactions in IPF, thereby laying the groundwork for innovative therapeutic approaches in the clinical field of IPF. Sophisticated bioinformatics methods were employed to identify crucial biomarkers essential for the progression of IPF. The GSE122960 single-cell dataset was obtained from the Gene Expression Omnibus (GEO) compendium, and intercellular communication potentialities were scrutinized via CellChat. The random survival forest paradigm was established using the GSE70866 dataset. Quintessential genes were selected through Kaplan-Meier (KM) curves, while immune infiltration examinations, functional enrichment critiques and nomogram paradigms were inaugurated. Analysis of intercellular communication revealed an intimate potential connections between macrophages and various cell types, pinpointing five cardinal genes influencing the trajectory and prognosis of IPF. The nomogram paradigm, sculpted from these seminal genes, exhibits superior predictive prowess. Our research meticulously identified five critical genes, confirming their intimate association with the prognosis, immune infiltration and transcriptional governance of IPF. Interestingly, we discerned these genes' engagement with the EPITHELIAL_MESENCHYMAL_TRANSITION signalling pathway, which may enhance our understanding of the molecular complexity of IPF.

Use of Antibiotics in Infancy and Asthma in Childhood: Confounded or Causal Relationship? A Critical Review of the Literature

Childhood asthma is among the most common chronic lung diseases in the pediatric population, having substantial consequences on the everyday life of children and their caregivers. There remains a lack of a singular, efficacious strategy for averting the inception of childhood asthma. The rate of pediatric antibiotic usage continues to be high, which makes it crucial to understand whether there exists a causal link between the use of antibiotics in infancy and the development of asthma in childhood. In this rostrum, we conduct a critical review of the literature concerning the association of infant antibiotic use and the onset of childhood asthma. Drawing upon the results of 5 meta-analyses addressing this topic and of a recent randomized controlled trial, a notable association emerges between antibiotic exposure in the first year of life and the occurrence of childhood asthma that appears to be beyond potential study limitations (such as reverse causation, confounding by indication, and recall bias). Furthermore, we highlight the need for additional research in this field that could improve our understanding of important aspects of this association and lead to the design of an intervention aimed to deliver antibiotics safely during early life and reduce the burden of childhood asthma.

Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable lung disease. It is characterized by chronic respiratory symptoms and airflow limitation due to abnormalities of the airways caused by continuous exposure to noxious particles or gases. COPD occupies the third position for the cause of death worldwide. The major risk factor for the development of COPD is tobacco smoking. The inhalation of toxic particles, biomass exposure and outdoor air pollution along with other host factors including abnormal lung development and accelerated lung aging can also contribute. Spirometry characterized by non-fully reversible airflow limitation i.e., FEV1/FVC &lt; 0.7 post bronchodilation, confirms the diagnosis of COPD. The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage associated illnesses. The conservative management comprising of antibiotics, inhaled corticosteroids, mucolytics etc. offer promising results in this condition. But tachycardia, glossitis, glaucoma, nausea are some of the common adverse reactions noticed on chronic use of these group of drugs. The contemporary health scenario demands more contribution in this regard from the indigenous system of medicine. In Āyurvedic view, COPD can be considered under the spectrum of Prāṇavaha srotodushti vikaras. The clinical features and etiology mentioned for diseases mentioned in Ayurveda such as Kāsa, Tamaka śvāsa, Rajayakshma etc has similarity with that of COPD. Though COPD cannot be correlated to any single condition of Prāṇavaha sroto duṣti, Tamaka śvāsa can be considered as includes most of the clinical features including cough. When the etiological factors favour, the vitiated and aggravated Kapha dosha blocks the channels of Prāna and Udāna vāta causing the onset and symptoms of the disease.

Incidence and Predictors of Bronchopulmonary Dysplasia Development and Severity Among Preterm Infants Born at 32 Weeks of Gestation or Less.

Background As the most common chronic lung disease (CLD) related to premature birth, bronchopulmonary dysplasia (BPD) is associated with long-term lung disease along with cardiovascular and neurodevelopmental disorders. However, data on the incidence and predictors of BPD in Qatar are lacking. Objectives In this study, we aimed to determine the incidence of BPD among infants born at ≤ 32 weeks gestational age (GA) at our neonatal unit, and identify risk factors for the development of BPD and moderate-severe BPD. Methods This was a retrospective observational cohort study conducted at a single site: a level-III neonatal intensive care unit (NICU) in Qatar. We included 1539 neonates born at ≤ 32 weeks of gestation with birth weights of ≤ 1500 grams who were admitted to the NICU between 2017 and 2020. Univariate and multivariate logistic regression analyses were performed to identify potential factors and predictors and their possible associations with the development of BPD and moderate-severe BPD. We also applied BPD classifications to determine the variability in the incidence of BPD in our cohort according to various definitions (2001 National Institute of Child Health and Human Development (NICHD) Diagnostic Criteria, 2016 Revisions of NICHD Criteria, and 2019 Neonatal Research Network Jensen Grading). Results A total of 451 infants (29.3%) had BPD (BPD group) while 1088 (70.7%) did not (non-BPD group), and the overall incidence of BPD was 29.3%. The most relevant risk factors associated with a higher risk of developing BPD identified in the multivariate logistic regression analysis were appropriate weight for gestational age (adjusted OR (aOR) 3.67, 95%CI 2.02-6.67, P < 0.001), presence of patent ductus arteriosus (PDA) (aOR 2.61, 95%CI 1.86-3.66, P < 0.001), late-onset sepsis (aOR 2.16; 95%CI 1.29-3.62; P = 0.003), and use of invasive ventilation (aOR 1.90; 95%CI 1.35-2.69; P < 0.001). The most relevant independent risk factors associated with a higher risk for developing moderate-severe BDP were postnatal steroids (aOR 7.12, 95%CI 3.77-13.44, P < 0.001), use of inhaled nitric oxide (aOR 3.65, 95%CI 1.48-9.01, P = 0.005), use of invasive ventilation (aOR 2.13, 95%CI 1.13-4.00, P = 0.019), late-onset sepsis (aOR 2.07, 95%CI 1.10-3.91, P = 0.025), and male sex (aOR 2.04, 95%CI 1.24-3.36, P = 0.005). The difference in the distribution of BPD severity across the three different definitions of NICHD was significant (P < 0.001). Conclusion The results of this study showed that the incidence of BPD remained high in infants born at ≤ 32 weeks of gestational age and birth weight <1500 g with appropriate weight for gestational age. The presence of PDA at birth or first echocardiography, late-onset sepsis, and use of invasive ventilation were significant risk factors for the incidence of BPD. The identification of risk factors will contribute to the implementation of lung-protective strategies for at-risk infants who may benefit from potential preventive therapy.