Chronic Airway Research Articles

Microbiology sampling in non-cystic fibrosis bronchiectasis cases from northern Alberta.

Non-cystic fibrosis bronchiectasis (NCFB) is a chronic respiratory disease resulting in chronic cough, thick sputum, and lower airway microbial colonization, akin to patients with cystic fibrosis (CF). NCFB is a common, yet under recognized entity which inflicts significant morbidity and mortality particularly to older individuals, with a rising prevalence in the developed world. Given that sputum cultures are a non-invasive method to characterize the lower airway microbiota in NCFB patients, for which pathogenic organisms are associated with worsened outcomes, we sought to characterize the microbiological pattern and clinical outcomes associated with sputum culture in a cohort of NCFB patients from Western Canada. A total of 20 subjects were prospectively recruited from various bronchiectasis clinics across the Greater Edmonton area. A retrospective chart review and a symptoms questionnaire was performed, gathering information not limited to symptoms, comorbidities, exacerbations, hospitalizations, sputum production, and sputum culture results over the prior 5 years. Subjects reported frequent hospitalization alongside a significant burden of symptoms. A large majority of sputum cultures grew pathogenic organisms such as Haemophilus influenzae and Pseudomonas aeruginosa. We also note the considerable waste and inefficiency associated with sputum cultures, outlining areas for which this important diagnostic modality can be improved. Accurate characterization of the airway microbiota alongside efficient delivery of health services are key to ensuring the proper treatment of individuals with NCFB, given their high disease burden and frequent hospitalization.

Post-tuberculosis lung disease and chronic obstructive pulmonary disease.

The burden of chronic airway diseases, including chronic obstructive pulmonary disease (COPD), continues to increase, especially in low- and middle-income countries. Post-tuberculosis lung disease (PTLD) is characterized by chronic lung changes after the "cure" of pulmonary tuberculosis (TB), which may be associated with the pathogenesis of COPD. However, data on its prevalence, clinical manifestations, computed tomography features, patterns of lung function impairment, and influencing factors are limited. The pathogenic mechanisms underlying PTLD remain to be elucidated. This review summarizes the recent advances in PTLD and TB-associated COPD. Research is urgently needed both for the prevention and management of PTLD.

Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD.

The airway epithelium comprises of different cell types and acts as a physical barrier preventing pathogens, including inhaled particles and microbes, from entering the lungs. Goblet cells and submucosal glands produce mucus that traps pathogens, which are expelled from the respiratory tract by ciliated cells. Basal cells act as progenitor cells, differentiating into different epithelial cell types, to maintain homeostasis following injury. Adherens and tight junctions between cells maintain the epithelial barrier function and regulate the movement of molecules across it. In this review we discuss how abnormal epithelial structure and function, caused by chronic injury and abnormal repair, drives airway disease and specifically asthma and chronic obstructive pulmonary disease (COPD). In both diseases, inhaled allergens, pollutants and microbes disrupt junctional complexes and promote cell death, impairing the barrier function and leading to increased penetration of pathogens and a constant airway immune response. In asthma, the inflammatory response precipitates the epithelial injury and drives abnormal basal cell differentiation. This leads to reduced ciliated cells, goblet cell hyperplasia and increased epithelial mesenchymal transition, which contribute to impaired mucociliary clearance and airway remodelling. In COPD, chronic oxidative stress and inflammation trigger premature epithelial cell senescence, which contributes to loss of epithelial integrity and airway inflammation and remodelling. Increased numbers of basal cells showing deregulated differentiation, contributes to ciliary dysfunction and mucous hyperproduction in COPD airways. Defective antioxidant, antiviral and damage repair mechanisms, possibly due to genetic or epigenetic factors, may confer susceptibility to airway epithelial dysfunction in these diseases. The current evidence suggests that a constant cycle of injury and abnormal repair of the epithelium drives chronic airway inflammation and remodelling in asthma and COPD. Mechanistic understanding of injury susceptibility and damage response may lead to improved therapies for these diseases.

Oxidised IL-33 drives COPD epithelial pathogenesis via ST2-independent RAGE/EGFR signalling complex.

Epithelial damage, repair and remodelling are critical features of chronic airway diseases including chronic obstructive pulmonary disease (COPD). Interleukin (IL)-33 released from damaged airway epithelia causes inflammation via its receptor, serum stimulation-2 (ST2). Oxidation of IL-33 to a non-ST2-binding form (IL-33ox) is thought to limit its activity. We investigated whether IL-33ox has functional activities that are independent of ST2 in the airway epithelium. In vitro epithelial damage assays and three-dimensional, air-liquid interface (ALI) cell culture models of healthy and COPD epithelia were used to elucidate the functional role of IL-33ox. Transcriptomic changes occurring in healthy ALI cultures treated with IL-33ox and COPD ALI cultures treated with an IL-33-neutralising antibody were assessed with bulk and single-cell RNA sequencing analysis. We demonstrate that IL-33ox forms a complex with receptor for advanced glycation end products (RAGE) and epidermal growth factor receptor (EGFR) expressed on airway epithelium. Activation of this alternative, ST2-independent pathway impaired epithelial wound closure and induced airway epithelial remodelling in vitro. IL-33ox increased the proportion of mucus-producing cells and reduced epithelial defence functions, mimicking pathogenic traits of COPD. Neutralisation of the IL-33ox pathway reversed these deleterious traits in COPD epithelia. Gene signatures defining the pathogenic effects of IL-33ox were enriched in airway epithelia from patients with severe COPD. Our study reveals for the first time that IL-33, RAGE and EGFR act together in an ST2-independent pathway in the airway epithelium and govern abnormal epithelial remodelling and muco-obstructive features in COPD.

Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?

Asthma is a chronic inflammatory airway disorder whose pathophysiological and immunological mechanisms are not completely understood. Asthma exacerbations are mostly driven by respiratory viral infections and characterised by worsening of symptoms. Despite current therapies, asthma exacerbations can still be life-threatening. Natural killer (NK) cells are innate lymphoid cells well known for their antiviral activity and are present in the lung as circulating and resident cells. However, their functions in asthma and its exacerbations are still unclear. In this review, we will address NK cell activation and functions, which are particularly relevant for asthma and virus-induced asthma exacerbations. Then, the role of NK cells in the lungs at homeostasis in healthy individuals will be described, as well as their functions during pulmonary viral infections, with an emphasis on those associated with asthma exacerbations. Finally, we will discuss the involvement of NK cells in asthma and virus-induced exacerbations and examine the effect of asthma treatments on NK cells.

Omalizumab in Severe Asthma: Effect on Oral Corticosteroid Exposure and Remodeling. A Randomized Open-Label Parallel Study.

Data on the clinical efficacy and remodeling of omalizumab therapy in patients on oral corticosteroids (OC) are limited. The purpose of the study is to show that in patients with corticosteroid-dependent asthma, omalizumab is a corticosteroid-sparing therapy able to inhibit airway remodeling and to reduce disease burden (lung function impairment, exacerbations). This study is a randomised open-label study evaluating the addition of omalizumab to the standard of care in patients with severe asthma receiving oral corticosteroids. The primary endpoint was represented by the change in OC monthly dose by the end of treatment and secondary endpoints included spirometry changes, airway inflammation (FeNO), number of exacerbations and airways remodelling assessed by bronchial biopsies studied by transmission electron microscopy. As a safety variable, adverse effects were recorded. Efficacy was assessed for 16 patients in the omalizumab group and 13 in the control group. The final cumulative mean monthly OC doses were 34.7mg and 217mg for the omalizumab and control group, respectively; the mean difference between groups adjusted for baseline was -148.1 [95% confidence interval (CI) -243.6, -52.5; p=0.004]. OC withdrawal of 75% versus 7.7% (p=0.001) was observed in the omalizumab and control group, respectively. Omalizumab provided a slowing of forced expiratory volume in one second (FEV1) loss (70 mL versus 260 mL), a significant decrease in FeNO values and a reduction in the annual relative risk of clinically significant exacerbations of 54%. The treatment was well tolerated. The morphological study showed a significant decrease in basement membrane thickness in the omalizumab group (6.7µm versus 4.6µm) compared with controls (6.9µm versus 7µm) [mean difference between groups adjusted for baseline was -2.4 (95% CI -3.7, -1.2; p<0.001], as well as a decrease in intercellular spaces (1.18µm versus 0.62µm and 1.21µm versus 1.20µm, p=0.011, respectively). A qualitative improvement was also observed in the treated group. Omalizumab showed a marked OC-sparing capacity and was associated with an improvement in clinical management that correlated with bronchial epithelial repair. In OC-dependent asthma, reversibility of remodelling is possible; the concepts that basement membrane enlargement is detrimental and that chronic airway obstruction is systematically irreversible are outdated (EudraCT: 2009-010914-31).

Measuring skill-based health literacy in chronic airway disease patients: the development and psychometric evaluation of the Vancouver airways health literacy tool (VAHLT).

This article describes the development of the Vancouver airways health literacy tool (VAHLT), a novel measure of skill-based health literacy specific to chronic airway diseases (CADs). Across several phases, psychometric characteristics of the VAHLT were examined and used to guide its development. An initial pool of 46 items was developed using input from patients, clinicians, researchers, and policy-makers. An initial patient sample (N = 532) was evaluated and used to inform item revisions. A revised 44-item pool was then evaluated using a second sample, the results of which aided in the selection of a final set of 30 items. The finalized 30-item VAHLT was then psychometrically evaluated using the second sample (N = 318). An item response theory approach was utilized to evaluate the VAHLT by assessing model fit, item parameter estimates, test and item information curves, and item characteristic curves. Reliability was assessed using ordinal coefficient alpha. We additionally assessed differential item functioning between asthma and COPD diagnoses. The VAHLT demonstrated a unidimensional structure and reasonably discriminated patients in the lower range of health literacy estimates. The tool demonstrated strong reliability (α = .920). Two of the 30 items were found to exhibit non-negligible differential item functioning. This study presents compelling evidence of validity in several areas for the VAHLT, including content and structural validity. Further external validation studies are needed and forthcoming. Overall, this work represents a strong first step towards a novel, skill-based, and disease-specific measure of CAD-related health literacy.

Therapeutic properties of Helicobacter pylori-derived vacuolating cytotoxin A in an animal model of chronic allergic airway disease

BackgroundIt has previously been shown that the Helicobacter pylori (H. pylori)-derived molecule vacuolating cytotoxin A (VacA) could be suitable for the treatment of allergic airway disease. The therapeutic activity of the protein, which acts through modulation of dendritic cells (DC) and regulatory T cells (Tregs), was demonstrated in murine short-term acute models. The aim of this study is to further evaluate the therapeutic potential of VacA by determining the effectiveness of different application routes and the suitability of the protein for treating the chronic phase of allergic airway disease.MethodsVacA was administered by the intraperitoneal (i.p.), oral (p.o.) or intratracheal (i.t.) routes, and long-term therapeutic effectiveness, allergic airway disease hallmarks, and immune phenotype were analyzed in murine models of acute and chronic allergic airway disease.ResultsAdministration of VacA via the i.p., p.o or i.t. routes was associated with a reduction in airway inflammation. The i.p. route showed the most consistent effect in reducing airway inflammation and i.p. treatment with VacA was the only treatment that significantly reduced mucus cell hyperplasia. In a murine model of chronic allergic airway disease, both short- and long-term treatment with VacA showed a therapeutic effect, with a reduction in a variety of asthma hallmarks, including bronchoalveolar lavage eosinophilia, lung inflammation and goblet cell metaplasia. Short-term treatment was associated with induction of Tregs, while repetitive long-term administration of VacA influenced immunological memory in the lung.ConclusionsIn addition to showing therapeutic efficacy in short-term models, treatment with VacA also appeared to be effective in suppressing inflammation in a chronic airway disease model. The observation that treatment was effective after administration via several different routes highlights the potential of VacA as a therapeutic agent with different routes of administration in humans.

Longitudinal effects of elexacaftor/tezacaftor/ivacaftor on sputum viscoelastic properties, airway infection and inflammation in patients with cystic fibrosis.

Recent studies demonstrated that the triple combination cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapy elexacaftor/tezacaftor/ivacaftor (ETI) improves lung function and reduces pulmonary exacerbations in cystic fibrosis (CF) patients with at least one F508del allele. However, effects of ETI on downstream consequences of CFTR dysfunction, i.e. abnormal viscoelastic properties of airway mucus, chronic airway infection and inflammation have not been studied. The aim of this study was to determine the longitudinal effects of ETI on airway mucus rheology, microbiome and inflammation in CF patients with one or two F508del alleles aged ≥12 years throughout the first 12 months of therapy. In this prospective observational study, we assessed sputum rheology, the microbiome, inflammation markers and proteome before and 1, 3 and 12 months after initiation of ETI. In total, 79 patients with CF and at least one F508del allele and 10 healthy controls were enrolled in this study. ETI improved the elastic modulus and viscous modulus of CF sputum at 3 and 12 months after initiation (all p<0.01). Furthermore, ETI decreased the relative abundance of Pseudomonas aeruginosa in CF sputum at 3 months and increased the microbiome α-diversity at all time points. In addition, ETI reduced interleukin-8 at 3 months (p<0.05) and free neutrophil elastase activity at all time points (all p<0.001), and shifted the CF sputum proteome towards healthy. Our data demonstrate that restoration of CFTR function by ETI improves sputum viscoelastic properties, chronic airway infection and inflammation in CF patients with at least one F508del allele over the first 12 months of therapy; however, levels close to healthy were not reached.

Progress of three kinds of treatment for asthma

Asthma is chronic inflammatory airway disease and may be induced by both genetic factors and epigenetic factors. Asthma has no particularly typical symptoms，and these symptoms include cough, expectoration, suffocation, chest tightness and even breathing difficulties. Drugs for asthma treatment are divided into rescue treatment and maintenance treatment, rescue treatments are for people with mild symptoms of asthma which means the frequency of onset does not exceed two times a week while maintenance treatments with inhalable drugs that deal with inflammation are for all other patients that suffer severely and to increase control. As in recent years, the population with asthma has shown to be increasing worldwide over time, the importance and necessity of understanding the mechanism of asthma and its main treatment methods and principles are also increasing. This article mainly focused on three types of most commonly seen maintenance treatment for asthma, including glucocorticoid, theophylline and leukotriene receptor antagonist.

Dectin-1-Independent Macrophage Phagocytosis of Mycobacterium abscessus.

Mycobacterium abscessus, a species of nontuberculous mycobacteria (NTM), is an opportunistic pathogen that is readily cleared by healthy lungs but can cause pulmonary infections in people with chronic airway diseases. Although knowledge pertaining to molecular mechanisms of host defense against NTM is increasing, macrophage receptors that recognize M. abscessus remain poorly defined. Dectin-1, a C-type lectin receptor identified as a fungal receptor, has been shown to be a pathogen recognition receptor (PRR) for both M. tuberculosis and NTM. To better understand the role of Dectin-1 in host defense against M. abscessus, we tested whether blocking Dectin-1 impaired the uptake of M. abscessus by human macrophages, and we compared M. abscessus pulmonary infection in Dectin-1-deficient and wild-type mice. Blocking antibody for Dectin-1 did not reduce macrophage phagocytosis of M. abscessus, but did reduce the ingestion of the fungal antigen zymosan. Laminarin, a glucan that blocks Dectin-1 and other PRRs, caused decreased phagocytosis of both M. abscessus and zymosan. Dectin-1-/- mice exhibited no defects in the control of M. abscessus infection, and no differences were detected in immune cell populations between wild type and Dectin-1-/- mice. These data demonstrate that murine defense against M. abscessus pulmonary infection, as well as ingestion of M. abscessus by human macrophages, can occur independent of Dectin-1. Thus, additional PRR(s) recognized by laminarin participate in macrophage phagocytosis of M. abscessus.

Daridorexant, a Recently Approved Dual Orexin Receptor Antagonists (DORA) in the Treatment of Insomnia.

Insomnia is one of the major challenges in medical science nowadays as it leads to the great socio-economic burden by impairing daytime function as well as the development of exhaustion, depression and memory disturbance in affected individuals. Several important classes of drugs have been tried including the BZDs and Non-BZD hypnotics. Available drugs to combat this disease have the limitations of abuse potential, tolerance and cognitive impairments. In some instances, withdrawal symptoms have been observed on abrupt cessation of those drugs. The Orexin system has been very recently targeted as a therapeutic option to overcome those limitations. Daridorexant as a Dual Orexin Receptor Antagonists (DORA) in the treatment of insomnia has been evaluated in several preclinical and clinical studies. Available information obtained from those studies has shown promising future for this drug in the management of insomnia. Beyond its effectiveness in insomnia, it has been successfully used in patients suffering from Obstructive sleep apnoea, Chronic Obstructive Airway Disease (COAD), Alzheimer's Disease (AD), hypertension and cardiovascular disorders. Larger studies need to address the safety issues as well as obtain robust pharmacovigilance information to safeguard the risk-benefit aspect of this drug in insomniac adults.

Summary of Korean Asthma Guideline.

Asthma is a chronic inflammatory airway disease that is characterized by variable airflow obstruction. The Korean Asthma Study Group of the Korean Academy of Tuberculosis and Respiratory Diseases has recently updated the Korean Asthma Guideline. This review summarizes the updated Korean Asthma Guideline. Asthma prevalence is increasing worldwide, and in Korea. Variable airflow obstruction can be confirmed by bronchodilator response or other tests, and should be established prior to the controller medication. A low-dose inhaled corticosteroid-formoterol is used to alleviate symptoms in all treatment step, and it can be used as a controller as well as reliever in steps 3-5. This approach is preferred, because it reduces the risk of severe exacerbations, compared to the use of short-acting β2-agonist as reliever. In severe asthma, phenotype/endotype based on the underlying inflammation should be evaluated. For type 2 severe asthma, the biologics should be considered.

Exploration and Validation of Potential Biomarkers and Therapeutic Targets in Ferroptosis of Asthma.

Asthma is a chronic inflammatory airway disease involving multiple mechanisms, of which ferroptosis is a form of programmed cell death. Recent studies have shown that ferroptosis may play a crucial role in the pathogenesis of asthma, but no specific ferroptosis gene has been found in asthma, and the exact mechanism is still unclear. The present study aimed to screen ferroptosis genes associated with asthma and find therapeutic targets, in order to contribute a new clue for the diagnosis and therapy of asthma. Ferroptosis-related differentially expressed genes (FR-DEGs) in asthma were selected by the GSE41861, GSE43696 and ferroptosis datasets. Next, the FR-DEGs were subjected by GO and KEGG enrichment, and the mRNA-miRNA network was constructed. Then, GSEA and GSVA enrichment analysis and Immune infiltration analysis were performed, followed by targeted drug prediction. Finally, the expression of FR-DEGs was confirmed using GSE63142 dataset and RT-PCR assay. We found 13 FR-DEGs by the GSE41861, GSE43696 and ferroptosis database. Functional enrichment analysis revealed that the 13 FR-DEGs were enriched in oxidative stress, immune response, ferroptosis, lysosome, necrosis, apoptosis etc. Moreover, our results revealed the mRNA-miRNA network of the FR-DEGs and identified candidate drugs. Also, immune infiltration revealed that ELAVL1, CREB5, CBR1 and NR1D2 are associated with the immune cells and may be potential targets in asthma. Finally, 10 FR-DEGs were validated by the GSE63142 database. It was verified that 7 FR-DEGs were differentially expressed by collecting asthma patients and healthy controls. This study ultimately identified 7 FR-DEGs for the diagnosis and therapy of asthma. These 7 FR-DEGs contribute to oxidative stress and immune responses. This study provides potential therapeutic targets and biomarkers for asthma patients, shedding further light on the pathogenesis of asthma as well as providing new insights into the treatment of asthma.

CTRP3 regulates NF-κB and TGFβ1/Smad3 pathways to alleviate airway inflammation and remodeling in asthmatic mice induced by OVA.

Asthma is a common illness with chronic airway inflammation. C1q/tumor necrosis factor (TNF)-related protein 3 (CTRP3) plays a vital role ininflammatory response, but its effect on asthma is imprecise. Herein, we analyzed the functions of CTRP3 in asthma. The BALB/c mice were randomized into four groups: control, ovalbumin (OVA), OVA+vector, and OVA+CTRP3. The asthmatic mice model was established by OVA stimulation. Overexpression of CTRP3 was implemented by the transfection of corresponding adeno-associated virus 6 (AAV6). The contents of CTRP3, E-cadherin, N-cadherin, smooth muscle alpha-actin (α-SMA), phosphorylated (p)-p65/p65, transforming growth factor-beta 1 (TGFβ1), and p-Smad3/Smad3 were determined by Western blot analysis. The quantity of total cells, eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage fluid (BALF) was assessed by using a hemocytometer. The contents of tumor necrosis factor-α and interleukin-1β in BALF were examined by enzyme-linked immunesorbent serologic assay. The lung function indicators and airway resistance (AWR) were measured. The bronchial and alveolar structures were evaluated by hematoxylin and eosin staining and sirius red staining. The CTRP3 was downregulated in mice of OVA groups; however, AAV6-CTRP3 treatment markedly upregulated the expression of CTRP3. Upregulation of CTRP3 diminished asthmatic airway inflammation by decreasing the number of inflammatory cells and the contents of proinflammatory factors. CTRP3 markedly lessened AWR and improved lung function in OVA-stimulated mice. Histological analysis found that CTRP3 alleviated OVA-induced airway remodeling in mice. Moreover, CTRP3 modulated NF-κB and TGFβ1/Smad3 pathways in OVA-stimulated mice. CTRP3 alleviated airway inflammation and remodeling in OVA-induced asthmatic mice via regulating NF-κB and TGFβ1/Smad3 pathways.

COVID-19 infection in Libyan chronic hemodialysis patients: Prevalence, risk factors, severity and predictors of mortality

Background: Chronic kidney disease (CKD) is associated with the increased risk of both outpatient and inpatient pneumonia. This association is independent of comorbid diabetes, cardio-vascular disease (CVD), asthma, and chronic obstructive airway disease. Dialysis patients are considered at risk groups for SARS-CoV-2 infection; Short-term mortality in patients on chronic hemodialysis who were hospitalized with COVID-19 was high. Outcomes in those requiring intensive care unit (ICU) and mechanical ventilation management were poor. Aim: This study mainly aimed to identify the prevalence, risk factors, severity and predictors of mortality in Libyan hemodialysis patients infected with COVID- 19. Methods: In this retrospective cohort study, data of CKD patients on maintenance hemodialysis diagnosed with COVID-19 infection from two large dialysis centers in Libya were collected and analyzed using SPSS version 22 for .demographic, clinical and laboratory profiles. Results: The data of 810 patients from two hemodialysis centers in Libya showed infection rate was 10.2 %, and the overall mortality was 26.5% (39/83) 47% of patients needed admission to ICU for supportive mechanical ventilation (SPO2 ranged from 76-92%). The biochemical and laboratory data showed a decreased mean absolute lymphocyte counts. A high neutrophil-lymphocyte ratio (NLR), and a mild decrease in platelet counts. C-reactive protein (CRP), fibrinogen, ferritin, and D-dimer were also high at admission. (22/83, 26.5%) of total patients, and (17/39) 43.6% of ICU patients died in less than 28 days after COVID-19 diagnosis. Conclusions: In CKD patients on maintenance hemodialysis diagnosed with COVID-19 infection; severity of disease at presentation, need for invasive supportive mechanical ventilation, older age, raised serum glutamic oxaloacetic transaminase, and lower level of albumin may have been valuable predictors of mortality and poor outcomes.

A study on the prevalence of RLS in OSA and the consequences of co-occurrence.

Restless leg syndrome (RLS) is common among patients with obstructive sleep apnoea (OSA) but the prognostic importance of this is not studied. We have called OSA and RLS coexistence as ComOSAR. A prospective observational study was done on patients referred for polysomnography (PSG) with the aims to evaluate 1) the prevalence of RLS in OSA and comparing it with RLS in non-OSA, 2) the prevalence of insomnia, psychiatric, metabolic and cognitive disorders in ComOSAR versus OSA alone, 3) chronic obstructive airway disease (COAD) in ComOSAR versus OSA alone. OSA, RLS and insomnia were diagnosed as per respective guidelines. They were evaluated for psychiatric disorders, metabolic disorders, cognitive disorders and COAD. Of 326 patients enrolled, 249 were OSA and 77 were non-OSA. 61/249 OSA patients, i.e. 24.4% had comorbid RLS, i.e. ComOSAR. RLS in non-OSA patients was similar (22/77, i.e. 28.5%); P = 0.41. ComOSAR had a significantly higher prevalence of insomnia (26% versus 10.1%; P = 0.016), psychiatric disorders (73.7% versus 48.4%; P = 0.00026) and cognitive deficits (72.1% versus 54.7%, P = 0.016) compared to OSA alone. Metabolic disorders like metabolic syndrome, diabetes mellitus, hypertension and coronary artery disease were also observed in a significantly higher number of patients with ComOSAR versus OSA alone (57% versus 34%; P = 0.0015). COAD was also seen in a significantly higher number of patients with ComOSAR compared to OSA alone (49% versus 19% respectively; P = 0.00001). It is essential to look for RLS in patients with OSA as it leads to a significantly higher prevalence of insomnia, and cognitive, metabolic and psychiatric disorders. COAD is also more common in ComOSAR compared to OSA alone.

Evaluation of the frequency of attention deficit hyperactivity disorder in patients with asthma

BackgroundAsthma is the most prevalent respiratory disease caused by chronic airway inflammation. Attention Deficit Hyperactivity Disorder (ADHD) is children's most common psychological and neurodevelopmental disorder. Increased risk for ADHD in patients with inflammatory and autoimmune diseases supports the role of inflammatory mechanisms in the occurrence of ADHD. However, the association between asthma and ADHD remains unclear.ObjectiveThis study was designed to evaluate the prevalence of ADHD in patients with asthma who were referred to the clinic of allergy and clinical immunology.MethodsThis cross-sectional study was conducted on children aged 6 to 18 with asthma at Imam Ali hospital, Karaj, Iran. The patient's demographic data, history of childbirth delivery type, premature birth, hospital admission, family income, birth rate, and family history information related to the patient's asthma and medicines were recorded. ADHD diagnosis was made using the Persian version of Conners Parent Behavioral Problems Rating Scale (CPRS-26).ResultsIn this study, 677 asthmatic patients were enrolled; 46 patients (6.8%) had ADHD. The probability of ADHD in asthmatic patients inhabited in a rural area, males, and patients with a history of food allergy, allergic rhinitis, urticaria, and eczema was significantly higher (p < 0.05). In addition, our result demonstrated that the likelihood of ADHD in patients with asthma and a history of PICU admission was significantly higher (p < 0.05).ConclusionsThe present study showed that severe asthma, was the risk factor for ADHD in patients with asthma. Physicians should be aware of this co-morbidity to refer asthmatic patients who have the symptoms of ADHD to a psychologist.

Clinical Characteristics and Economic Burden of Asthma in China: A Multicenter Retrospective Study.

Asthma is a common chronic airway inflammation that produces a healthcare burden on the economy. We aim to obtain a better understanding of the clinical status and disease burden of patients with asthma in China. A retrospective study was carried out based on the computerized medical records in the Jinan Health Medical Big Data Platform between 2011 and 2019 (available data from 38 hospitals). The asthma severity of each patient was assessed retrospectively and categorized as mild, moderate, or severe according to Global Initiative for Asthma 2020 (GINA 2020). The results revealed that the majority (75.0%) of patients suffered from mild asthma. Patients treated with inhaled corticosteroids (ICS)/long-acting beta-agonists (LABA) at emergency department visits had lower frequencies of exacerbations compared with non-ICS/LABA-treated patients. The incidence rates for 1, 2, 3, and 4 exacerbation of the patients treated with ICS/LABA are lower than those treated without ICS/LABA (14.49 vs. 15.01%, 11.94% vs. 19.12%, 6.51% vs.12.92% and 4.10% vs. 9.35%). The difference got a statistical significance Chronic obstructive pulmonary disease (COPD) and gastroesophageal reflux disease (GERD), two comorbidities related to asthma, were risk factors for asthma exacerbation. Finally, patients who suffered from exacerbations produced a heavier economic burden compared to the patients who never suffered exacerbations (mean costs are ￥3,339.67 vs. ￥968.45 separately). These results provide a reference for clinicians and patients to obtain a better treatment and therapy strategy management for people living with asthma.

Prevalence of anemia and its associated factors among adult asthmatic patients in Northwest Ethiopia

BackgroundAsthma is a heterogeneous disease characterized by chronic airway inflammation. The pathophysiologic processes of asthma can disrupt iron homeostasis, resulting in anemia. However, the association between asthma and anemia among adult asthma patients remains limited. Therefore, the main aim of this study was to determine the prevalence and factors associated with anemia among adult asthmatic patients from May to August 2021.MethodsAn institution-based, cross-sectional study was conducted among 291 asthmatic patients in Northwest Ethiopia. A pre-tested structured questionnaire and checklist were used to collect sociodemographic and clinical data. A blood specimen was collected from asthmatic patients for a complete blood count analysis and morphology assessment. The data were entered into the Epi data software and exported to the statistical package for social science version 20 software for analysis. Non-parametric Mann-Whitney U test was used to compare red blood cell parameters among groups with acute and chronic exacerbations. Binary logistic regression models were used to determine the factors associated with anemia. A p-value less than 0.05 was considered statistically significant.ResultThe overall prevalence of anemia in this study was 11% (95% CI: 7.2–14.8%). Acutely exacerbated asthmatic patients had significantly lower median values of red blood cell parameters such as red blood cell count, hemoglobin, and mean cell hemoglobin when compared to chronic exacerbations. In addition, using systemic corticosteroids (AOR = 4.07, 95% CI: 1.126–14.71, p = 0.032) and being hospitalized in the emergency department (AOR = 3.74, 95% CI: 1.26–11.07, p = 0.017) were found to be significantly associated with anemia.ConclusionThis study demonstrated that anemia was predominant in adult asthma patients. Red blood cell number, hemoglobin level, and mean corpuscular hemoglobin were significantly lower in acute asthma exacerbations. Therefore, appropriate intervention strategies should be undertaken to reduce the prevalence of anemia among adult asthma patients to reduce further complications and provide better monitoring of asthma patients.