Increased Asthma Severity Research Articles

Reductions in eosinophil biomarkers by benralizumab in patients with asthma

BackgroundEosinophilic inflammation is frequently associated with increased asthma severity. Benralizumab is a humanized, afucosylated, anti–interleukin-5Rα monoclonal antibody that selectively depletes eosinophils and basophils through enhanced antibody-dependent cell-mediated cytotoxicity. ObjectiveTo study effects of benralizumab on eosinophil counts and activity following administration to asthma patients. MethodsSera were collected from asthma patients enrolled in two clinical studies. Placebo or benralizumab was subcutaneously administered to patients in Phase I (100 or 200 mg, multiple doses; N = 14; NCT00659659) and Phase IIa (25, 100, or 200 mg every 4 weeks; N = 24; NCT00783289) studies. Sera were also collected from healthy volunteers (N = 20) for comparison. Blood eosinophils, IL-5, eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), eotaxin/chemokine (C–C motif) 11 (CCL11), eotaxin-2/CCL24, tumor necrosis factor (TNF), and interferon-γ (IFN-γ) were measured at baseline and post-treatment. ResultsIncreased EDN concentrations were observed in sera of patients from both studies relative to healthy volunteers (p < 0.05). At baseline, sera EDN concentrations correlated with blood eosinophil counts (rs = 0.5; p < 0.05). Benralizumab reduced blood eosinophil numbers and sera EDN and ECP relative to baseline (p < 0.05). No changes in TNF or IFN-γ were observed, while serum IL-5, eotaxin/CCL11, and eotaxin-2/CCL24 increased after benralizumab administration vs. placebo (p < 0.05). ConclusionsIn two independent studies, serum IL-5, EDN, and ECP were modulated following benralizumab. Eosinophil depletion after benralizumab also resulted in significant reductions in EDN and ECP concentrations, suggesting that cytotoxic granule proteins were not released after eosinophil reduction.

Serum Magnesium and Vitamin D Levels as Indicators of Asthma Severity.

Background. Serum magnesium levels affect the concentration of circulating vitamin D in blood and subsequently it affects the immunity; thus it plays significant role in the pathogenesis of asthma. Asthma, in adults, is less studied and hypomagnesemia along with vitamin D deficiency and insufficiency is common in asthmatic individuals, which causes frequent asthma attacks, respiratory infections, severe exacerbations, and poor response to bronchodilators. Objective. To detect the magnitude of vitamin D insufficiency and deficiency and serum magnesium levels among asthmatic patients and to correlate them with the severity of asthma. Materials and Methods. This is a cross-sectional case-control study which includes 60 patients of chronic stable asthma and 60 healthy controls. After taking clinical history and systemic examination, pulmonary function test was done. Serum levels of magnesium, 25-hydroxycholecalciferol [25(OH)D], and calcium were measured in all the subjects. Results. Significant correlation was found between vitamin D deficiency, hypomagnesemia, and asthma severity. Serum calcium levels were unaffected by that. Conclusion. Vitamin D and serum magnesium deficiency are highly prevalent in patients with asthma. Increased asthma severity, frequency of attacks, and exacerbation are associated with lower levels of one or both. Serum 25(OH)D and magnesium levels may serve as important markers of asthma severity.

Prothrombotic state in patients with severe and prednisolone-dependent asthma

Epidemiologic studies have shown that asthmatic patients, in particular those with severe disease, have increased risk of pulmonary embolism. It is unknown whether these patients have a prothrombotic state under stable conditions. We sought to compare coagulation and fibrinolysis parameters between healthy subjects and patients with mild, severe, and prednisolone-dependent asthma under stable conditions and to investigate whether hemostatic markers correlate with airway inflammation. In 126 adults (33 healthy control subjects, 31 patients with mild asthma, 32 patients with severe asthma, and 30 patients with prednisolone-dependent asthma) parameters of inflammation (peripheral blood eosinophils and neutrophils) and markers of hemostasis (endogenous thrombin potential [ETP], thrombin-antithrombin complex, plasmin-α2-antiplasmin complex, plasminogen activator inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were measured in plasma. One-way ANOVA with the post hoc Bonferroni test was used for group comparison, and linear regression analysis was used for correlations. We observed increased ETP (121% vs 99%, overall P<.01), plasmin-α2-antiplasmin complex (520 vs 409μg/L, overall P=.04), PAI-1 (10 vs 7ng/mL, overall P=.02), and vWF (142% vs 87%, overall P<.01) levels in asthmatic patients compared with healthy control subjects. ETP, PAI-1, and vWF levels increased with increasing asthma severity. In addition, we found a correlation between ETP and vWF with neutrophil but not eosinophil counts. Asthmatic patients have a prothrombotic state that increases with asthma severity. This might explain why patients with asthma, in particular those with severe disease, have an increased risk of venous thromboembolism.

Correlation between oxidative stress and the NF-κB signaling pathway in the pulmonary tissues of obese asthmatic mice.

The obesity-asthma phenotype is characterized by increased asthma severity and decreased glucocorticoid responsiveness. To date, the mechanism underlying the association between obesity and asthma remain to be fully elucidated. The present study investigated the correlation between oxidative stress and the nuclear factor (NF)-κB pathway in obese asthmatic mice. The animals were divided into the following groups: Control (n=8), comprising C57BL/6J mice without exposure to a high-fat diet; non-obese asthma group (n=8), comprising mice of a normal weight subjected to the induction of asthma; obese control group (n=8), comprising C57BL/6J mice subjected to a high-fat diet; and obese asthmatic group (n=8), comprising obese mice subject to the induction of asthma. The levels of the malondialdehyde (MDA) oxidant and glutathione (GSH) antioxidant in the lungs and bronchoalveolar lavage fluid (BALF) were measured using ELISA. The expression levels of inhibitory κB kinase-β (IKK-β) and the inhibitor of κBα (IκB-α) in the pulmonary tissues was determined using western blot analysis. An electrophoretic mobility shift assay was performed to determine the transcription activity of NF-κB. The levels of MDA in the BALF and lung tissues increased significantly in the two asthmatic groups, compared with the control groups (P<0.01). The asthmatic mice showed significantly lower concentrations of GSH in the BALF and lung tissues, compared with the control groups (P<0.01). In the asthmatic animals, the expression of IκB kinase (IKK)-β and activation of NF-κB were upregulated in the pulmonary tissues, compared with those in the control groups (P<0.01). The expression of IKK-β and transcriptional activity of NF-κB were significantly higher the in obese asthmatic mice, compared with the non-obese asthmatic mice (P<0.01). On examining the expression levels of IκB-α in the pulmonary tissues, a significant reduction was found in the asthmatic animals, compared with the controls (P<0.01). In addition, the level of IκB-α was significantly lower in the obese asthmatics, compared with the non-obese asthmatics (P<0.01). MDA was positively correlated with NF-κB in the obese asthmatic group (R=0.83; P<0.05) and non-obese asthmatic group (R=0.82; P<0.05). Oxidative stress was upregulated in the pulmonary tissues of the asthmatic mice. This upregulation was more marked in the obese asthmatic mice, and was positively correlated with activation of the NF-κB signaling pathway in the pulmonary tissues. The results in the present study indicated that higher oxidative stress and activation of the NF-κB signaling pathway were observed in the lung tissues of the obese asthmatics. Furthermore, a positive correlation was identified between oxidative stress and NF-κB.

Obesity shifts house dust mite-induced airway cellular infiltration from eosinophils to macrophages: effects of glucocorticoid treatment.

Although classically characterized by chronic airway inflammation with eosinophil infiltration, asthma is a complex and multifactorial condition with numerous clinical phenotypes. Epidemiological studies strongly support the link between obesity and asthma and suggest that obesity precedes and promotes asthma development, increases asthma severity, and reduces steroid responsivity. Using a house dust mite (HDM) model of airway hyperresponsiveness in C57BL/6 mice, we examined the effects of diet-induced obesity on allergic airway inflammation and its treatment with dexamethasone. When compared to lean mice treated with HDM, obese-HDM mice had reduced plasma adiponectin, an anti-inflammatory adipokine, lower eosinophil and higher macrophage infiltration into the lungs and bronchoalveolar lavage (BAL) fluid, increased expression of total, M1, and M2 macrophage markers in the lungs, and enhanced Th2 and non-Th2 cytokine expression in the lungs. While Th2-associated responses in obese-HDM mice were suppressed by systemic dexamethasone, several Th2-independent responses, including total and M1 macrophage markers in the lungs, and lung CXC-motif ligand 1 (CXCL1) levels, were not improved following dexamethasone treatment. Thus, HDM combined with obesity promotes mixed localized inflammatory responses (e.g., M1, M2, Th1, and Th2) and shifts the cellular infiltration from eosinophils to macrophages, which are less sensitive to dexamethasone regulation. Because obese asthmatics exhibit more severe symptoms, lack a predominance of Th2 biomarkers, and are predicted to experience more steroid resistance when compared to lean asthmatics, this model could be used to study blunted steroid responses in obese-HDM mice and to define the macrophages found in the lungs.

Correlation Between Helicobacter Pylori Infection and Severity of Asthma

Background: Microbial exposures have been suggested to confer protection from allergic disorders, and reduced exposures to gastrointestinal microbes have been proposed as an explanation for the increase in asthma severity and prevalence. Since the general prevalence of Helicobacter pylori has been decreasing, we hypothesized that H. pylori serostatus may be inversely related to the severity of asthma. Objective: The aim of this study is to find whether infection with H. pylori reduces the probability of development of severe asthma in patients with persistent asthma. Methodology: In this study fifty patients with persistent asthma includes 19 males and 31 females their ages range between (17 – 66) years For all those patients, full history and complete physical examination have been done, then after, the patients subjected to pulmonary function test. After that, two milliliters sample of venous blood have been drawn, then, the sample centrifuged and sent to assess for H. pylori infection serology. Data was analyzed by using SPSS. Results: There is significant association between severity of asthma and result of H. pylori so with increase severity of asthma there is decrease in percentage of positive H. pylori serology. And there is no statistical significant are noted between patients sex or age and results of H. pylori infection test. Conclusion: There is significant inverse association between severity of asthma and result of H. pylori infection serology. This association not affected by ages and sex of patients. Recommendations: Since the exact mechanism by which H. pylori affect asthma is not clear, there is need for further studies to explore it.

Non-eosinophilic Asthma Endotypes

Several recent studies spanning from induced sputum to gene signature identified non-eosinophilic asthma (NEA) as a distinct asthma phenotype with several relevant clinical features such as increased asthma severity, increased remodelling and lower response to bronchodilator and anti-inflammatory treatment. Two major mechanisms leading to neutrophilic inflammation are postulated: the dysregulated innate immune response, including neutrophil intrinsic abnormalities, and the activation of the IL-17-dependent pathway. Several factors such as age, metabolic or epigenetic factors or the activation of the epithelial-mesenchimal trophic unit have been identified as modulators. The endotyping of NEA is far behind the eosinophilic asthma, and until now, no endotype-driven interventions have been proved to be effective.

Blood lead levels and childhood asthma.

To measure blood lead levels in children (5-14 y) with bronchial asthma, and correlate with asthma severity. Cross-sectional analytical. Pediatric Allergy and Immunology Clinic of a Childrens hospital in Cairo, Egypt. 200 children (127 males) with bronchial asthma and 125 age- and sex-matched healthy controls (80 males). Blood lead levels were measured by atomic absorption spectrophotometer technique, and were subsequently correlated with asthma severity. No significant difference in mean (SD) blood lead levels was observed between children with asthma [13.3 (4.8) ug/dL] and control group [11.4 (3.9) ug/dL]. 190 children (58.5%) had elevated blood lead levels (>10 ug/dL), with no significant difference between patients (60%) and controls (56%). Patients with elevated blood lead levels had significantly higher frequency of eosinophilia (66.7%) and increased total immunoglobulin E (83.3%) compared to other patients with blood lead levels <10ug/dL (10% and 43.8%, respectively). Patients of asthma with elevated blood lead levels had higher grades of severity of asthma compared to those with blood lead levels <10 ug/dL. Blood lead levels are not significantly associated with diagnosis of asthma but elevated blood lead levels seem to be associated with increased asthma severity and higher frequency of eosinophilia and elevated immunoglobulin E levels.

Cost-Effectiveness of Bronchial Thermoplasty in Patients with Poorly Controlled, Severe, Persistent Asthma

Despite many pharmacological and immunological treatments for asthma, some patients remain not well-controlled and continue to experience asthma exacerbations. Existing FDA-approved treatments for asthma do not address excessive airway smooth muscle mass (ASM), an anatomical feature associated with increased asthma severity and morbidity in some patients. We sought to examine the cost-effectiveness of Bronchial Thermoplasty (BT) to treat poorly controlled, severe, persistent asthma patients. This novel technology uses thermal energy to target and reduce ASM, resulting in a durable reduction in asthma exacerbations.

The prevalence of sleep-disordered breathing in children with asthma and its behavioral effects.

To determine the prevalence of sleep-disordered breathing (SDB) in children with asthma compared to non-asthmatic children and to determine if behavior problems are associated with asthma and SDB. Cross-Sectional. Parents of 263 children with asthma and 266 controls ages 2 to 15 years attending routine pediatric office visits completed the Pediatric Sleep Questionnaire (PSQ) and the Child Behavior Checklist. Asthma severity was classified based on NIH guidelines. The prevalence of snoring was significantly higher in asthmatic children (35.5%) than controls (15.7%) and the prevalence of a positive PSQ was significantly higher in asthmatic children (25.9%) than controls (10.6%) (P < 0.001 for both). The effect of asthma was "dose-dependent" as children with more severe asthma had increased odds ratios for snoring and a positive PSQ. On multivariate analysis, there were significant interactions of gender with asthma and age with gender. A positive modified PSQ along with measures of socioeconomic status and age were the only independent predictors of abnormal Child Behavior Checklist scores and score classifications. There was a higher prevalence of SDB in asthmatic children compared to non-asthmatic children and the prevalence of SDB increased with increasing asthma severity. In multivariate analysis the role of asthma was much less clear as it predicted a positive PSQ in girls but not boys. SDB, but not asthma, was an independent predictor of behavioral problems.

Asthma during pregnancy in a population-based study--pregnancy complications and adverse perinatal outcomes.

BackgroundAsthma is one of the most common chronic diseases, and prevalence, severity and medication may have an effect on pregnancy. We examined maternal asthma, asthma severity and control in relation to pregnancy complications, labour characteristics and perinatal outcomes.MethodsWe retrieved data on all singleton births from July 1, 2006 to December 31, 2009, and prescribed drugs and physician-diagnosed asthma on the same women from multiple Swedish registers. The associations were estimated with logistic regression.ResultsIn total, 266 045 women gave birth to 284 214 singletons during the study period. Maternal asthma was noted in 26 586 (9.4%) pregnancies. There was an association between maternal asthma and increased risks of pregnancy complications including preeclampsia or eclampsia (adjusted OR 1.15; 95% CI 1.06–1.24) and premature contractions (adj OR 1.52; 95% CI 1.29–1.80). There was also a significant association between maternal asthma and emergency caesarean section (adj OR 1.29; 95% CI 1.23–1.34), low birth weight, and small for gestational age (adj OR 1.23; 95% CI 1.13–1.33). The risk of adverse outcomes such as low birth weight increased with increasing asthma severity. For women with uncontrolled compared to those with controlled asthma the results for adverse outcomes were inconsistent displaying both increased and decreased OR for some outcomes.ConclusionMaternal asthma is associated with a number of serious pregnancy complications and adverse perinatal outcomes. Some complications are even more likely with increased asthma severity. With greater awareness and proper management, outcomes would most likely improve.

Predictors for the development of progressive severity in new-onset adult asthma

A proportion of patients with adult-onset asthma have severe disease. Risk factors for an increase in asthma severity are poorly known. We sought to identify predictors for the development of severe asthma in adults. A cohort of 200 adults with new-onset asthma was prospectively followed for 2 years. At baseline, patients underwent a comprehensive assessment of clinical, functional, and inflammatory parameters. After 2 years, change in asthma severity was assessed by using the Global Initiative for Asthma score (range, 1-4), which is based on asthma control (Asthma Control Questionnaire), lung function (FEV1), and inhaled corticosteroid requirement. ANOVA and multiple regression equations were used in the analysis. One hundred twenty-eight patients completed 2 years of follow-up. Seventeen (13.3%) patients had an increase in asthma severity, whereas 53 (41.4%) patients had a decrease. A lower postbronchodilator FEV1/forced vital capacity ratio and a higher number of cigarette pack years smoked at baseline were significantly associated with an increase in asthma severity at follow-up. Multiple regression equations showed that only the number of cigarette pack years smoked was independently associated with an increase in asthma severity, with an odds ratio of 1.4 (95% CI, 1.02-1.91) for every 10 pack years smoked. A history of cigarette smoking in patients with new-onset adult asthma predicts an increase in asthma severity during the first 2 years of the disease in a dose-dependent manner.

The chitinase-like protein YKL-40 is not a useful biomarker for severe persistent asthma in children

BackgroundThe chitinase-like protein YKL-40 is thought to play a role in inflammation and tissue remodeling. In adults with severe asthma, YKL-40 is expressed in the airway and YKL-40 levels are elevated in the serum. ObjectiveTo compare YKL-40 levels in children with severe persistent asthma with those in adults with severe persistent asthma and to determine whether YKL-40 levels correlate with increasing asthma severity in childhood asthma. MethodsIn this prospective, cross-sectional study, 23 adults and 19 children with severe persistent asthma, 23 children with moderate persistent asthma, and 19 children with mild persistent asthma were enrolled. The following data were collected on each patient: spirometry, exhaled nitric oxide, percutaneous skin testing results to aeroallergens, peripheral eosinophils, serum IgE levels, and serum YKL-40 levels. ResultsCompared with adults, children with severe persistent asthma had significantly lower YKL-40 levels, higher values for forced vital capacity and forced expiration volume in 1 second, higher serum IgE levels, and higher exhaled nitric oxide levels. YKL-40 levels did not correlate with increasing asthma severity in the pediatric cohort. ConclusionSevere persistent asthma in childhood is not associated with elevated YKL-40 levels, unlike in adults with severe persistent asthma. YKL-40 is not a useful biomarker for asthma severity in childhood asthma.

Agonist-induced β2-adrenoceptor desensitization and downregulation enhance pro-inflammatory cytokine release in human bronchial epithelial cells

It is not clear whether increased asthma severity associated with long-term use of β2-adrenoceptor (β2-AR) agonists can be attributed to receptor degradation and increased inflammation. We investigated the cross-talk between β-AR agonist-mediated effects on β2-AR function and expression and cytokine release in human bronchial epithelial cells. In 16HBE14o− cells grown in the presence and absence of β-AR agonists and/or antagonists, the β2-AR density was assessed by radioligand binding; the receptor protein and mRNA was determined using laser scanning cytometer and RT-PCR; cAMP generation, the cytokines IL-6 and IL-8 release were determined using AlphaScreen Assay and ELISA, respectively. Isoprenaline (ISO) and salbutamol (Salbu) induced a concentration- and time-dependent significant decrease in β2-AR density. Both Salbu and ISO reduced cAMP generation in a concentration-dependent manner while in same cell culture the IL-6 and IL-8 release was significantly enhanced. These effects were antagonized to a greater extent by ICI 118.551 than by propranolol, but CGP 20712A had no effect. Reduction of the β2-AR protein and mRNA could be seen when cells were treated with ISO for 24 h. Our findings indicate a direct link between cytokine release and altered β2-AR expression and function in airway epithelial cells. β2-AR desensitization and downregulation induced by long-term treatment with β2-AR agonists during asthma may account for adverse reactions also due to enhanced release of pro-inflammatory mediators and should, thus, be considered in asthma therapy.

Treating severe allergic asthma with anti-IgE monoclonal antibody (omalizumab): a review.

Increased asthma severity is not only associated with enhanced recurrent hospitalization and mortality but also with higher social costs.Several cases of asthma are atopic in nature, with the trigger for acute asthma attacks and chronic worsening of inflammation being allergens inducing an immune, IgE mediated response.Anti-inflammatory treatments are effective for most of asthma patients, but there are subjects whose disease is incompletely controlled by inhaled or systemic corticosteroids and these patients account for about 50% of the healthcare costs of asthma.Omalizumab is a biological engineered, humanized recombinant monoclonal anti-IgE antibody developed for the treatment of allergic diseases and with clear efficacy in adolescent and adult patients with severe allergic asthma. The anti-IgE antibody inhibits IgE functions blocking free serum IgE and inhibiting their binding to cellular receptors. By reducing serum IgE levels and IgE receptor expression on inflammatory cells in the context of allergic cascade, omalizumab has demonstrated to be a very useful treatment of atopic asthma, improving quality of life of patients with severe persistent allergic asthma that is inadequately controlled by currently available asthma medications. Several trials have demonstrated that this therapy is well tolerated and significantly improves symptoms and disease control, reducing asthma exacerbations and the need to use high dosage of inhaled corticosteroids.

Diagnosis and management of eosinophilic asthma: a US perspective.

Eosinophilic asthma is now recognized as an important subphenotype of asthma based on the pattern of inflammatory cellular infiltrate in the airway. Eosinophilic asthma can be associated with increased asthma severity, atopy, late-onset disease, and steroid refractoriness. Induced sputum cell count is the gold standard for identifying eosinophilic inflammation in asthma although several noninvasive biomarkers, including fractional exhaled nitric oxide and periostin, are emerging as potential surrogates. As novel therapies and biologic agents become increasingly available, there is an increased need for specific phenotype-directed treatment strategies. Greater recognition and understanding of the unique immunopathology of this asthma phenotype has important implications for management of the disease and the potential to improve patient outcomes. The present review provides a summary of the clinical features, pathogenesis, diagnosis, and management of eosinophilic asthma.

Clinical significance of small airway obstruction markers in patients with asthma

The role of small airway obstruction in the clinical expression of asthma is incompletely understood. We tested the hypotheses that markers of small airway obstruction are associated with (i) increased asthma severity, (ii) impaired asthma control and quality of life and (iii) frequent exacerbations. Seventy-four adults with asthma and 18 healthy control subjects underwent impulse oscillometry (IOS), multiple breath inert gas washout (MBW), body plethysmography, single-breath determination of carbon monoxide uptake and spirometry. Patients completed the six-point Asthma Control Questionnaire (ACQ-6) and standardized Asthma Quality of Life Questionnaire [AQLQ(S)]. Asthma severity was classified according to the Global Initiative for Asthma (GINA) treatment steps. The putative small airway obstruction markers Sacin , resistance at 5 Hz minus resistance at 20 Hz (R5-R20) and reactance area (AX) were not independently associated with asthma severity, control, quality of life or exacerbations. In contrast, markers of total (R5) and mean airway resistance of large and small airways (R20) were significantly higher in the severe asthma group compared with the mild-moderate group (0.47 vs. 0.37, P < 0.05 for R5; 0.39 vs. 0.31, P < 0.01 for R20). The strongest independent contributors to ACQ-6 score were R20 and forced expiratory volume in one second (% pred.), and the strongest independent contributors to AQLQ(S) score were R20 and forced vital capacity (% pred.). A history of one or more exacerbations within the previous year was independently associated with R20. Previously reported markers of small airway obstruction do not appear to be independently associated with asthma disease expression. In contrast, the IOS parameter R20, a marker of mean airway resistance of both large and small airways, appears to have independent clinical significance. These observations require confirmation in prospective longitudinal studies.

Assessing asthma severity among children and adults with current asthma

Background: Asthma severity is a key indicator to assess asthma care and management. Severity status may vary over time. Assessing asthma severity periodically is important for monitoring the health and well-being of people with asthma. Objective: To assess population-based asthma severity and to identify related-risk factors among children and adults with asthma. Methods: We used the 2006–2010 BRFSS child and adult Asthma Call-back Survey. Asthma severity was classified as intermittent or persistent. We performed multivariate logistic regression to identify related-risk factors. Results: Overall, 63.8% of persons with asthma had persistent asthma. Persistent asthma was more prevalent among children aged 0–4 years (71.8%; prevalence rate ratio [PR] = 1.3). Among adults with current asthma, persistent asthma was more prevalent among those who were 45 years or older (aged 45–54: 69.4%; PR = 1.1, aged 55–64: 72.6%; PR = 1.2, and aged 65+: 77.8%; PR = 1.3); annual household incomes of <$15 000 (74.1%; PR = 1.1); and first diagnosed at age 55 years or older (first diagnosed at age 55–64: 80.4%; PR = 1.1, at age 65 + : 81.5%; PR = 1.1). The prevalence of persistent asthma was also higher among current smokers who were also exposed to secondhand smoke (SHS) (74.7%; PR = 1.1); and among those with Chronic Obstructive Pulmonary Disease (COPD) (77.1%; PR = 1.2). Conclusions: Nearly two-thirds of children and adults with asthma had persistent asthma. Identifying related-risk factors could help improve targeted interventions or strategies to reduce modifiable predictors (low income, smoking, and SHS) of increased asthma severity. Such strategies could improve asthma care and quality of life.

Linking obesity and asthma

A growing body of literature suggests that obesity has a significant impact on asthma risk, phenotype, and prognosis. Epidemiological studies have clearly demonstrated that asthma is more likely to occur in obese patients, and health status is impaired in obese individuals with asthma, with obese asthmatics experiencing more symptoms, worse quality of life, increased healthcare use, and increased asthma severity. However, obesity has well-described effects on lung function and mechanics that can lead to symptoms of dyspnea without causing the pathophysiologic changes of asthma. Adding to the challenges of evaluating this association, some studies have failed to demonstrate a robust relationship between obesity and traditional biomarkers of airway inflammation in adult asthmatics, leading to the conclusion that obesity does not necessarily worsen airway inflammation in asthma. In this regard, emerging data suggest that nonatopic mechanisms may be relevant in obese asthmatics, and that these mechanisms may have a direct impact on the response of obese asthmatics to asthma therapies, most notably inhaled glucocorticoids. This article will review selected aspects of the contributions of obesity-related airway and systemic inflammation to asthma, with a focus on the impact of obesity as a modifier of risk, prognosis, and therapeutic response in asthma.

Peripheral blood leukocyte counts as a marker of severity of functional lung impairment in OAD patients attending a tertiary care hospital in Manipur, India

Background: Systemic inflammation is associated with impaired lung function and inflammation is a part of Obstructive Airway Disease (OAD). Chronic obstructive pulmonary disease (COPD) and bronchial asthma are the two most common OAD. In view of this, the present study was done with the objective of determining the relationship between the various grades of severity of airway obstruction in COPD and asthma with blood leukocyte counts. Methods: A cross-sectional study enrolling 40 COPD & 25 asthmatic patients of both sexes. Lung function was studied by computerized spirometer (Helios 402) and blood leukocyte counts (absolute neutrophil count, absolute eosinophil count, absolute basophil count, absolute lymphocyte count and absolute monocyte count) were determined by using suitable diluting fluids. Results: Grading of COPD and asthma severity was done according to GOLD and GINA guidelines respectively based on FEV1% predicted. With the increase in severity of airway obstruction, FEV1 was found to decline in both the groups. Out of 40 COPD patients, 12.5 % of patients had mild, 20% had moderate, 40% had severe and 27.5% had very severe COPD. Out of 25 asthma patients, 48% had mild, 32% had moderate and 20% had severe asthma. There was a significant increase in neutrophil count with the increase in COPD severity and with the increase in asthma severity, eosinophil count increases significantly. . Monocyte count was also increased with the decline in lung function in both the groups. Conclusion:Peripheral blood leukocyte counts are useful and can be used as an indirect & inexpensive marker of severity of functional lung impairment in OAD patients.