Fixed Airflow Limitation Research Articles

The relationship of airway structural changes to blood and bronchoalveolar lavage biomarkers, and lung function abnormalities in asthma.

Airway structural changes are important in asthma pathology and require further investigations. We sought to evaluate which computed tomography (CT) indices, bronchial histological traits, or blood and bronchoalveolar lavage (BAL) biomarkers correlate best with lung function abnormalities in asthma. In 105 white adult asthmatics (53 with a component of fixed airflow obstruction), we determined airway cross-sectional geometry of two proximal (the right upper lobe apical segmental and the left apicoposterior) and two distal (the right and the left basal posterior) bronchi, quantified the low-attenuation lung area (LAA%), and analysed clusters based on airway CT-metrics. We also performed bronchofiberoscopy with BAL and endobronchial biopsy, assessed blood and BAL biomarkers, including interleukin (IL)-4, IL-5, IL-6, IL-10, IL-12p70, IL-17A, IL-23, interferon (INF)γ and periostin, together with circulating a disintegrin and metalloproteinase domain-containing protein (ADAM)33, and investigated interplays between analysed variables. Patients with fixed airflow limitation were characterized by lower lumen area and increased wall area and wall thickness ratios in distal airways, accompanied by raised LAA%. They had also higher blood neutrophilia, blood and BAL eosinophilia, increased circulating fibrinogen, periostin, and ADAM33. Blood neutrophilia, serum high density lipoproteins, thyroid-stimulating hormone, and shortened activated partial thromboplastin time were determinants of thicker reticular basement membrane (RBM). BAL eosinophilia was the only positive predictor of collagen I accumulation. Surprisingly, we observed a negative correlation between RBM thickening and collagen I deposit. Cluster analysis based on CT-metrics of the right lower lobe basal posterior bronchus revealed three well-separated clusters similar in age, asthma duration, and BMI, but different in RBM thickness, collagen I accumulation, and inflammatory markers. Airway remodelling traits are mainly related to the Th2 profile, higher circulating ADAM33, and blood neutrophilia. Lung function abnormalities and RBM thickening correlate better with CT-metrics of distal than proximal airways.

Physiological and morphological differences of airways between COPD and asthma\u2013COPD overlap

Overlap of asthma and COPD has attracted attention recently. We aimed to clarify physiological and morphological differences of the airways between COPD and asthma–COPD overlap (ACO). Respiratory resistance and reactance and three-dimensional computed tomography data were evaluated in 167 patients with COPD. Among them, 43 patients who fulfilled the diagnosis of asthma were defined as having ACO. Among 124 patients with COPD without ACO, 86 with a comparable smoking history and airflow limitation as those with ACO were selected using propensity score matching (matched COPD). The intraluminal area (Ai) and wall thickness (WT) of third- to sixth-generation bronchi were measured and adjusted by body surface area (BSA; Ai/BSA and WT/√BSA, respectively). Patients with ACO had higher respiratory resistance and reactance during tidal breathing, but a smaller gap between the inspiratory and expiratory phases, compared with matched patients with COPD. Patients with ACO had a greater WT/√BSA in third- to fourth-generation bronchi, smaller Ai/BSA in fifth- to sixth-generation bronchi, and less emphysematous changes than did matched patients with COPD. Even when patients with ACO and those with COPD have a comparable smoking history and fixed airflow limitation, they have different physiological and morphological features of the airways.

A scoring system to detect fixed airflow limitation in smokers from simple easy-to-use parameters

No validated screening method currently exists for Chronic Obstructive Pulmonary Disease (COPD) in smokers. Therefore, we constructed a predictive model with simple parameters that can be applied for COPD screening to detect fixed airflow limitation. This observational cross-sectional study included a random sample of 222 smokers with no previous diagnosis of COPD undertaken in a Spanish region in 2014–2016. The main variable was fixed airflow limitation by spirometry. The secondary variables (COPD factors) were: age, gender, smoking (pack-years and Fagerström test), body mass index, educational level, respiratory symptoms and exacerbations. A points system was developed to predict fixed airflow limitation based on secondary variables. The model was validated internally through bootstrapping, determining discrimination and calibration. The system was then integrated into a mobile application for Android. Fifty-seven patients (25.7%) presented fixed airflow limitation. The points system included as predictors: age, pack-years, Fagerström test and presence of respiratory symptoms. Internal validation of the system was very satisfactory, both in discrimination and calibration. In conclusion, a points system has been constructed to predict fixed airflow limitation in smokers with no previous COPD. This system can be integrated as a screening tool, though it should be externally validated in other geographical regions.

Focus on Innuvair® Inhaler for Asthma

No abstract available.

Serum periostin levels serve as a biomarker for both eosinophilic airway inflammation and fixed airflow limitation in well-controlled asthmatics

ABSTRACTObjective: Periostin, a matricellular protein, is produced from airway epithelial cells and lung fibroblasts by IL-13. It has been suggested that periostin is involved in allergic inflammation and fibrosis. However, the usefulness of serum periostin measurement in the assessment of airway inflammation and remodeling and management of asthmatic patients is still debated. We aimed to determine whether serum periostin levels reflect eosinophilic airway inflammation and airway remodeling in asthma. Methods: We examined the relationship of serum periostin levels with clinical features, biomarkers for eosinophilic airway inflammation, fraction of exhaled nitric oxide (FeNO) levels and blood eosinophil counts, and pulmonary functions in 235 well-controlled asthmatic patients on inhaled corticosteroids (ICS) treatment. Results: Serum periostin levels were positively correlated with blood eosinophil counts (%) and age (r = 0.36 and 0.23, respectively), and were negatively correlated with body weight and FEV1/FVC (%) (r = −0.24 and − 0.23, respectively) in well-controlled asthmatic patients on ICS treatment (daily dose of 453 µg equivalent to fluticasone propionate). Blood eosinophil counts and serum periostin levels were similarly associated with increased FeNO levels (≥40 ppb) in the asthmatics. Serum periostin levels were better associated with fixed airflow limitation (FEV1/FVC ratio <70%) than FeNO levels, blood eosinophil counts or total IgE levels in the asthmatics. Multivariate analysis showed that fixed airflow limitation was significantly associated with high serum periostin levels (≥97 ng/ml) (Odds ratio 3.2). Conclusions: Serum periostin levels serve as a biomarker for both eosinophilic airway inflammation and fixed airflow limitation in well-controlled asthmatics on ICS treatment.

Distinct Phenotypes of Smokers with Fixed Airflow Limitation Identified by Cluster Analysis of Severe Asthma.

Smoking may have multifactorial effects on asthma phenotypes, particularly in severe asthma. Cluster analysis has been applied to explore novel phenotypes, which are not based on any a priori hypotheses. To explore novel severe asthma phenotypes by cluster analysis when including smoking patients with asthma. We recruited a total of 127 subjects with severe asthma, including 59 current or ex-smokers, from our university hospital and its 29 affiliated hospitals/pulmonary clinics. Clinical variables obtained during a 2-day hospital stay were used for cluster analysis. After clustering using clinical variables, the sputum levels of 14 molecules were measured to biologically characterize the clinical clusters. Five clinical clusters, including two characterized by low forced expiratory volume in 1 second/forced vital capacity, were identified. When characteristics of smoking subjects in these two clusters were compared, there were marked differences between the two groups: one had high levels of circulating eosinophils, high immunoglobulin E levels, and a high sinus score, and the other was characterized by low levels of the same parameters. Sputum analysis revealed intriguing differences of cytokine/chemokine pattern in these two groups. The other three clusters were similar to those previously reported: young onset/atopic, nonsmoker/less eosinophilic, and female/obese. Key clinical variables were confirmed to be stable and consistent 3 years later. This study reveals two distinct phenotypes with potentially different biological pathways contributing to fixed airflow limitation in cigarette smokers with severe asthma.

Biologinio vaisto Mepolizumabo poveikis gyvenimo kokybei ir plaučių funkcijai sergant sunkia eozinofiline astma: MUSCA tyrimo duomenys

Ilgalaikio astmos gydymo tikslas – pasiekti simptomų kontrolę, sumažinti paūmėjimų riziką, bronchų obstrukciją ir su vartojamais vaistais susijusius nepageidaujamas reakcijas. Ne mažiau svarbu gerinti su sveikata susijusią gyvenimo kokybę. Sergančiųjų sunkia eozinofiline astma gyvenimo kokybės gerinimas prilygsta iššūkiui, nes eozinofilinei astmai būdingi pasikartojantys paūmėjimai, bloga ligos kontrolė, sparčiai blogėjanti plaučių funkcija, blogėjanti su sveikata susijusi gyvenimo kokybė. Pastebėta, kad, gydant mepolizumabu – anti-IL-5 monokloniniu antikūnu, – gyvenimo kokybė reikšmingai pagerėja, o pats gydymas saugus. Todėl šie rezultatai rodo, kad mepolizumabo pridėjimas prie standartinio astmos gydymo gali turėti reikšmingą teigiamą poveikį.

Identification and validation of asthma phenotypes in Chinese population using cluster analysis

BackgroundAsthma is a heterogeneous airway disease, so it is crucial to clearly identify clinical phenotypes to achieve better asthma management. ObjectiveTo identify and prospectively validate asthma clusters in a Chinese population. MethodsTwo hundred eighty-four patients were consecutively recruited and 18 sociodemographic and clinical variables were collected. Hierarchical cluster analysis was performed by the Ward method followed by k-means cluster analysis. Then, a prospective 12-month cohort study was used to validate the identified clusters. ResultsFive clusters were successfully identified. Clusters 1 (n = 71) and 3 (n = 81) were mild asthma phenotypes with slight airway obstruction and low exacerbation risk, but with a sex differential. Cluster 2 (n = 65) described an “allergic” phenotype, cluster 4 (n = 33) featured a “fixed airflow limitation” phenotype with smoking, and cluster 5 (n = 34) was a “low socioeconomic status” phenotype. Patients in clusters 2, 4, and 5 had distinctly lower socioeconomic status and more psychological symptoms. Cluster 2 had a significantly increased risk of exacerbations (risk ratio [RR] 1.13, 95% confidence interval [CI] 1.03–1.25), unplanned visits for asthma (RR 1.98, 95% CI 1.07–3.66), and emergency visits for asthma (RR 7.17, 95% CI 1.26–40.80). Cluster 4 had an increased risk of unplanned visits (RR 2.22, 95% CI 1.02–4.81), and cluster 5 had increased emergency visits (RR 12.72, 95% CI 1.95–69.78). Kaplan-Meier analysis confirmed that cluster grouping was predictive of time to the first asthma exacerbation, unplanned visit, emergency visit, and hospital admission (P < .0001 for all comparisons). ConclusionWe identified 3 clinical clusters as “allergic asthma,” “fixed airflow limitation,” and “low socioeconomic status” phenotypes that are at high risk of severe asthma exacerbations and that have management implications for clinical practice in developing countries.

Coexisting COPD in elderly asthma with fixed airflow limitation: Assessment by DLco %predicted and HRCT

ABSTRACTBackground: Asthma patients with fixed airflow limitation (FL) are theoretically classified into two phenotypes, that is, coexisting chronic obstructive pulmonary disease (COPD) and asthmatic airway remodeling. However, the precise percentages of such patients are not known. Objective: To assess the prevalence of patients with both FL and COPD components in elderly asthma. Methods: We evaluated patients by lung diffusion impairment and emphysematous findings in high-resolution computed tomography (HRCT) as candidates for COPD components, as a multicenter, cross-sectional survey. Asthma outpatients ≥ 50 years of age were enrolled from Tohoku University Hospital, Sendai, Japan, and four hospitals (Tohoku Medical and Pharmaceutical University Wakabayashi Hospital, Sendai, JAPAN; Wakayama Medical University Hospital, Kimiidera, Japan; Hiraka General Hospital, Yokote, Japan; Iwate Prefectural Isawa Hospital, Oshu, Japan) with pulmonary physicians from March 1, 2013 to November 30, 2014. Results: The prevalence of patients with FEV1/FVC <70% was 31.0% of those in their 50s, 40.2% of those in their 60s and 61.9% of those in their 70s or older. The prevalence of those patients with lung diffusion impairment (i.e. the percent predicted values of diffusing capacity of the lung for carbon monoxide (DLco %predicted) <80%) or emphysematous findings in HRCT (i.e. the appearance of low attenuation area (LAA)) was 18.3% of those in their 50s, 13.8% of those in their 60s and 35.7% of those in their 70s or older. Conclusions: Nearly half of the patients with FL in elderly asthma show coexisting COPD components when assessed by DLco %predicted and LAA in HRCT.

Clinical profile of patients with adult-onset eosinophilic asthma.

Adult-onset eosinophilic asthma is increasingly recognised as a severe and difficult-to-treat subtype of asthma. In clinical practice, early recognition of patients with this asthma subtype is important because it may have treatment implications. Therefore, physicians need to know the distinct characteristics of this asthma phenotype. The objective of the present study was to determine the characteristic profile of patients with adult-onset eosinophilic asthma.130 patients with adult-onset (>18 years of age) asthma and high blood eosinophil counts (≥0.3×109 L−1) were compared with 361 adult-onset asthma patients with low (<0.3×109 L−1) blood eosinophils. Measurements included a series of clinical, functional and imaging parameters.Patients with high blood eosinophils were more often male, had less well controlled asthma and higher exacerbation rates, despite the use of higher doses of inhaled corticosteroids. They had higher levels of total IgE without more sensitisation to common inhaled allergens. In addition, these patients had worse lung function, and more often showed fixed airflow limitation, air trapping, nasal polyposis and abnormalities on sinus computed tomography scanning. Chronic rhinosinusitis, air trapping and male sex were three independent factors associated with blood eosinophilia (adjusted OR 3.8 (95% CI 1.7–8.1), 3.0 (95% CI 1.1–8.1) and 2.4 (95% CI 1.3–4.4), respectively).Patients with adult-onset asthma with elevated blood eosinophils exhibit a distinct profile, which can readily be recognised in clinical practice.

Assessment of Consistency of Fixed Airflow Obstruction Status during Budesonide/Formoterol Treatment and Its Effects on Treatment Outcomes in Patients with Asthma

The consistency of fixed airflow limitation status during treatment in patients with asthma is unknown. The objective of this study was to determine the consistency of fixed airflow obstruction (FAO) status during treatment and effects on treatment response. This post hoc analysis from a 12-week study (NCT00652002) assessed patients aged 12 years or more with moderate-to-severe asthma randomized to twice-daily budesonide/formoterol (BUD/FM) via pressurized metered-dose inhaler (pMDI) 320/9 μg, BUD pMDI 320 μg, FM 9 μg via dry-powder inhaler, or placebo. FAO status was assessed postbronchodilator at screening and after study drug administration at weeks 2, 6, and 12 via the forced expiratory volume in 1 second to forced vital capacity (FEV1/FVC) ratio < lower limit of normal (LLN) (FAO+) or ≥ LLN (FAO-). Patients with persistent FAO- and FAO+ retained their screening FAO status at all visits. Patients with inconsistent FAO changed categories at least once during the study. Assessments included early withdrawal due to predefined worsening asthma events (PAEs), lung function, and symptoms. Of 386 patients, 29% had persistent FAO+, 31% inconsistent FAO, and 40% persistent FAO-. PAEs were lowest in the FAO- group overall and with BUD/FM treatment in patients with FAO+ and inconsistent FAO. Baseline demographics and treatment responses of the inconsistent FAO group were most similar to the FAO+ group. The greatest improvements in asthma control days and use of rescue medications were seen with BUD/FM treatment, regardless of FAO status. Approximately one third of patients with moderate-to-severe asthma in this study had inconsistent FAO, and their treatment responses were most similar to patients with FAO+. Regardless of FAO status, patients treated with BUD/FM experienced the most improved treatment responses and fewest withdrawals due to PAEs.

Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD.

Chronic obstructive pulmonary disease (COPD) is characterized by fixed airflow limitation and progressive decline of lung function and punctuated by occasional exacerbations. The disease pathogenesis may involve activation of the bone marrow stimulating mobilization and lung-homing of progenitor cells. We investigated the hypothesis that lower circulating numbers of vascular endothelial progenitor cells (VEPCs) are a consequence of increased lung-sequestration in COPD. Nonatopic, current or ex-smokers with diagnosed COPD and nonatopic, nonsmoking normal controls were enrolled. Blood and induced sputum extracted primitive hemopoietic progenitors (HPCs) and VEPC were enumerated by flow cytometry. Migration and adhesive responses to fibronectin were assessed. In sputum, VEPC numbers were significantly greater in COPD compared to normal controls. In blood, VEPCs were significantly lower in COPD versus normal controls. There were no differences in HPC levels between the two groups in either compartment. Functionally, there was a greater migrational responsiveness of progenitors from COPD subjects to stromal cell-derived factor-1alpha (SDF-1α) compared to normal controls. This was associated with greater numbers of CXCR4+ progenitors in sputum from COPD. Increased migrational responsiveness of progenitor cells may promote lung-homing of VEPC in COPD which may disrupt maintenance and repair of the airways and contribute to COPD disease pathogenesis.

The Wnt/β-catenin signaling pathway regulates the development of airway remodeling in patients with asthma

Airway remodeling is a key characteristic of chronic asthma, particularly in patients with a fixed airflow limitation. The mechanisms underlying airway remodeling are poorly understood, and no therapeutic option is available. The Wnt/β-catenin signaling pathway is involved in various physiological and pathological processes, including fibrosis and smooth muscle hypertrophy. In this study, we investigated the roles of Wnt/β-catenin signaling in airway remodeling in patients with asthma. Wnt7a mRNA expression was prominent in induced sputum from patients with asthma compared with that from healthy controls. Next, we induced a chronic asthma mouse model with airway remodeling features, including subepithelial fibrosis and airway smooth muscle hyperplasia. Higher expression of Wnt family proteins and β-catenin was detected in the lung tissue of mice with chronic asthma compared to control mice. Blocking β-catenin expression with a specific siRNA attenuated airway inflammation and airway remodeling. Decreased subepithelial fibrosis and collagen accumulation in the β-catenin siRNA-treated mice was accompanied by reduced expression of transforming growth factor-β. We further showed that suppressing β-catenin in the chronic asthma model inhibited smooth muscle hyperplasia by downregulating the tenascin C/platelet-derived growth factor receptor pathway. Taken together, these findings demonstrate that the Wnt/β-catenin signaling pathway is highly expressed and regulates the development of airway remodeling in chronic asthma.

Distinct Phenotypes of Cigarette Smokers Identified by Cluster Analysis of Patients with Severe Asthma.

Smoking may have multifactorial effects on asthma phenotypes, particularly in severe asthma. Cluster analysis has been applied to explore novel phenotypes, which are not based on any a priori hypotheses. To explore novel severe asthma phenotypes by cluster analysis when including cigarette smokers. We recruited a total of 127 subjects with severe asthma, including 59 current or ex-smokers, from our university hospital and its 29 affiliated hospitals/pulmonary clinics. Twelve clinical variables obtained during a 2-day hospital stay were used for cluster analysis. After clustering using clinical variables, the sputum levels of 14 molecules were measured to biologically characterize the clinical clusters. Five clinical clusters were identified, including two characterized by high pack-year exposure to cigarette smoking and low FEV1/FVC. There were marked differences between the two clusters of cigarette smokers. One had high levels of circulating eosinophils, high IgE levels, and a high sinus disease score. The other was characterized by low levels of the same parameters. Sputum analysis revealed increased levels of IL-5 in the former cluster and increased levels of IL-6 and osteopontin in the latter. The other three clusters were similar to those previously reported: young onset/atopic, nonsmoker/less eosinophilic, and female/obese. Key clinical variables were confirmed to be stable and consistent 1 year later. This study reveals two distinct phenotypes of severe asthma in current and former cigarette smokers with potentially different biological pathways contributing to fixed airflow limitation. Clinical trial registered with www.umin.ac.jp (000003254).

Asthma and chronic obstructive pulmonary disease overlap: asthmatic chronic obstructive pulmonary disease or chronic obstructive asthma?

Asthma and chronic obstructive pulmonary disease (COPD) are different disease entities. They are both clinical diagnoses, with diagnostic tools to discriminate between one another. However, especially in older patients (>55 years) it seems more difficult to differentiate between asthma and COPD. This has led to the definition of a new phenotype called asthma COPD overlap syndrome (ACOS). However, our understanding of ACOS is at a very preliminary stage, as most research has involved subjects with existing diagnoses of asthma or COPD from studies with different definitions for ACOS. This has led to different and sometimes opposing results between studies on several features of ACOS, also depending on the comparison with COPD alone, asthma alone or both, which are summarized in this review.We suggest not using the term ACOS for a patient with features of both asthma and COPD, but to describe a patient with chronic obstructive airway disease as completely as possible, with regard to characteristics that determine treatment response (e.g. eosinophilic inflammation) and prognosis (such as smoking status, exacerbation rate, fixed airflow limitation, hyperresponsiveness, comorbidities). This will provide a far more clinically relevant diagnosis, and would aid in research on treatment in more homogenous groups of patients with chronic airways obstruction. More research is certainly needed to develop more evidence-based definitions for this patient group and to evaluate biomarkers, which will help to further classify these patients, treat them more adequately and unravel the underlying pathophysiological mechanism.

Clinical asthma phenotypes in the real world: opportunities and challenges.

Key PointsAsthma is a heterogeneous syndrome ranging from mild disease with barely noticeable symptoms to very severe disease with constant symptoms that may greatly hinder patients’ quality of life.The aim of asthma treatment is control of asthma and the prevention of risk of exacerbations and fixed airflow limitation.Asthma management must be individualised; tailored not only to the severity of the disease but importantly, to the phenotypic characteristics of the patient and modified according to response to treatment.Educational AimsTo inform readers about the current understanding on the treatment of asthma.To highlight the usefulness of phenotypes in treating asthmatic patients, especially those with severe disease.To introduce the issues of severe asthma management and future planning.Asthma is a common, chronic and heterogeneous syndrome, affecting people of all ages, all races and both sexes. It may range from mild disease with barely noticeable symptoms, to very severe disease with constant symptoms that greatly hinder the life of the patient. Guidelines issued by various medical societies provide guidance on how to diagnose and manage asthmatic patients. It is now increasingly recognised that asthma management must be individualised, tailored not only to the severity of the disease but to the phenotypic characteristics of each patient. The aim of asthma treatment is control of asthma and the prevention of risk of exacerbations and fixed airflow limitation. Asthma control can be easily assessed clinically through simple screening tools such as the use of validated questionnaires and spirometry. The use of inflammatory biomarkers can be an alternative approach that, however, requires more time and resources. Asthma treatment involves the use of controllers, mainly inhaled corticosteroids and long-acting β2-agonists, and relievers, mainly rapid-acting β2-agonists. Controller medications reduce airway inflammation, lead to better symptom control and reduce the risk of future exacerbations. Reliever (rescue) medications alleviate symptoms and prevent exercise-induced bronchoconstriction. Treatment must be based on a “stepwise approach” in order to achieve good control of symptoms and to minimise future risks of exacerbations. That is, less treatment for mild disease, more treatment for severe, uncontrolled disease. Once good asthma control has been achieved and maintained, treatment should be stepped down. In severe asthmatics, phenotypic characterisation becomes more clinically useful and add-on treatment such as anti-immunoglobulin E monoclonal antibodies may be required. Despite our better understanding of asthma, there are still patients who will not respond to treatment and remain symptomatic. Dissemination of guidelines and national plans allowing early diagnosis of asthma as well as access to specialised primary and secondary care for asthmatic patients, personalised treatment and continuity of care may lead to excellence in care and controlled asthma for the majority of patients. Education of the patient in asthma is also very important, as in every chronic disease, as the patients live with the disease every day while they visit a healthcare professional a few times a year. Future planning for new treatments should focus on the needs of such severe asthma patients.

The revised 2014 GINA strategy report: opportunities for change.

This document reviews a major revision of the Global Initiative for Asthma (GINA) Strategy for Asthma Management and Prevention that was published in 2014. The report aimed not only to update evidence-based recommendations for asthma diagnosis and management but also to innovate through a new format and layout to make its recommendations more clinically relevant and easier to implement. The GINA 2014 report includes a new definition of asthma that recognizes the heterogeneity of the disease and its phenotypes, and a new chapter about the asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome. Among key messages, the report stresses that therapeutic decisions should be based not only on assessment of symptoms but also on risk factors for exacerbations, side effects of therapy and development of fixed airflow limitation. Asthma management includes not only medications but also nonpharmacological therapies and strategies, in a coordinated and personalized approach to individual patient care. On the basis of evidence about how to achieve behaviour change by health professionals, the recommendations are presented in a user-friendly format, with numerous tables, algorithms and flow-charts facilitating implementation. Background supporting material has been gathered online. The GINA 2014 report provides updated and more easily implementable recommendations on optimal asthma management.

Implementing clinical guidelines for chronic obstructive pulmonary disease: barriers and solutions.

Chronic obstructive pulmonary disease (COPD) is a complex chronic lung disease characterised by progressive fixed airflow limitation and acute exacerbations that frequently require hospitalisation. Evidence-based clinical guidelines for the diagnosis and management of COPD are now widely available. However, the uptake of these COPD guidelines in clinical practice is highly variable, as is the case for many other chronic disease guidelines. Studies have identified many barriers to implementation of COPD and other guidelines, including factors such as lack of familiarity with guidelines amongst clinicians and inadequate implementation programs. Several methods for enhancing adherence to clinical practice guidelines have been evaluated, including distribution methods, professional education sessions, electronic health records (EHR), point of care reminders and computer decision support systems (CDSS). Results of these studies are mixed to date, and the most effective ways to implement clinical practice guidelines remain unclear. Given the significant resources dedicated to evidence-based medicine, effective dissemination and implementation of best practice at the patient level is an important final step in the process of guideline development. Future efforts should focus on identifying optimal methods for translating the evidence into everyday clinical practice to ensure that patients receive the best care.

Risk factors associated with irreversible airway obstruction in nonsmoking adult patients with severe asthma.

Persistent airways obstruction (PAO) may affect some patients with severe asthma and may significantly worsen the prognosis. This study was designed to detect risk factors associated with persistent airflow limitation in nonsmoking adult patients with severe asthma. A total of 68 adults with severe asthma were recruited and followed prospectively for four to six weeks during the stable phase of disease. For all patients, at every visit spirometry with reversibility test was performed. Based on the results, patients were stratified into group 1 (reversible obstruction) or group 2 (PAO). In both cohorts, associations of postbronchodilatator forced expiratory volume in one second/forced vital capacity ratio (FEV1/FVC) with patients' age, gender, asthma duration, history of atopy and allergy, family history, medications, frequency of previous exacerbations, infections, hospitalizations, and artificial ventilation due to the asthma attack-related respiratory failure were investigated. Using a univariate logistic regression analysis, we have shown that older age, more than six exacerbations per year, artificial ventilation in the past, at least one hospitalization per year, the presence of atopic dermatitis, and exposure to domestic visible mold were all independent risk factors of PAO. Furthermore, multivariate regression analysis demonstrated that especially those with domestic exposure to visible molds, with very frequent exacerbations and with at least one hospitalization throughout the last year, were at risk for developing PAO. Domestic exposure to molds, hospitalization during the last year, and very frequent exacerbations were associated with PAO in patients with severe asthma. These factors may help in predicting fixed airflow limitation in nonsmoking patients with severe asthma.

English

Total of 104 patients were studied with an average age of 47.952 + 16.9112, with 77% of the patients being male. The maximum no of patient were of the middle aged adult males age group 31 - 40.The study comprised of 104 individuals of which 79 patients were males and 25 were females. The average weight of the 104 patients was 68.615 kg . The body mass index of our patients had a mean of 26.146 with a minimum BMI of 14.382 a maximum BMI of 48.828. Forced expiratory volume in 1 st second in our OBESE asthmatics was 1.78 ± 0.8150.& Forced vital capacity in the obese group was 2.102 ± 0.8638 .FEV1% was > 70 % in all the patients of the study population demonstrating no fixed airflow limitation in patients of our study population . ERV in the obese groups was .441 ± 0.2190 liters. The inspiratory capacity in the obese group was 1.771 ± 0.6628 liters . No significant statistical correlation was demonstrated in between the obese and no obese group . Significant correlation was demonstrated between BMI & Waist Circumference. BMI correlated with FEV1, FVC, FEV1% in the study population and a negative correlation was demonstrable. A statistically significant co relation could not be established between BMI & the dynamic spirometric variables. BMI correlated with ERV & VC in the study population and a negative correlation was demonstrable. A statistically significant co relation could not be established between BMI & the static spirometric variables. Waist circumference correlated with the FEV1, FVC, FEV1% in the study population and a negative correlation was demonstrable. A statistically significant co relation could not be established between waist circumference & the dynamic spirometric variables. Waist circumference correlated with ERV & VC in the study population and a negative correlation was demonstrable. A statistically significant co relation could not be established between waist circumference & the static spirometric variables.