Objective:To evaluate the relationship between obesity and asthma. Methods:This was a preliminary cross-sectional analysis involving 925 subjects with mild-to-moderate or severe asthma evaluated between 2013 and 2015. Obesity was defined on the basis of body mass index (BMI) and abdominal circumference. We collected clinical, laboratory, and anthropometric parameters, as well as pulmonary function test results and data regarding comorbidities. The subjects also completed asthma control and quality of life questionnaires. Results:Obese individuals had a significantly higher number of neutrophils in peripheral blood than did nonobese individuals (p = 0.01). Among the obese individuals, 163 (61%) had positive skin-prick test results, as did 69% and 71% of the individuals classified as being overweight or normal weight, respectively. Obese individuals showed lower spirometric values than did nonobese individuals, and 32% of the obese individuals had uncontrolled asthma, a significantly higher proportion than that found in the other groups (p = 0.02). Conclusions:Obese individuals with asthma seem to present with poorer asthma control and lower pulmonary function values than do nonobese individuals. The proportion of subjects with nonatopic asthma was higher in the obese group. Our results suggest that obese individuals with asthma show a distinct inflammatory pattern and are more likely to present with difficult-to-control asthma than are nonobese individuals.

Older subjects with asthma have low odds of atopic and eosinophilic phenotypes, whereas they present high odds of irreversible airway obstruction and severe asthma.

BackgroundThe relationship between smoking, household pollution, dual exposure and severity of asthma in adults has not been sufficiently studied. We examined and compared the effects of cigarette smoking, domestic wood burning pollution and dual exposure (tobacco and wood burning) upon asthma severity in adults.MethodsThis was a cross-sectional study performed with 452 individuals with mild to moderate asthma and 544 patients with severe asthma (previously untreated). Smoking and exposure to wood smoke were identified and quantified through questionnaires to evaluate current and/or previous exposure; objective determination of cigarette exposure was obtained through the measurement of urinary cotinine. Asthma control was evaluated through Asthma Control Questionnaire; and severity was classified according to the Global Initiative for Asthma criteria. Subjects were grouped according to exposure type into 4 groups: smokers, household pollution, dual-exposure and no-exposure. Chi square, Mann–Whitney, and Kruskal–Wallis tests were used for comparisons between groups.ResultsOut of 996 included individuals, 78 (7.8%) were exposed to cigarette smoking alone, 358 (35.9%) to household pollution alone, 155 (15.6%) to the two exposures combined and 405 (40.7%) were not exposed. Compared to unexposed individuals, exposure to household pollution resulted in poorer asthma control, higher proportion of severe asthma, and worse indicators of lung function. The double-exposed individuals were worse off in all the evaluated parameters, and they were significantly worse than subjects with single exposure to household air pollution in relation to asthma severity and lung function. These subjects were predominantly females, older, with longer residence time in rural areas, lower income and lower schooling levels. Multivariate analysis showed that exposure to household pollution and double exposure were predictive factors associated with lack of control and increased severity of asthma.ConclusionsExposure to household pollution is associated with poorer control, greater severity, and poorer pulmonary function; double-exposed individuals have a greater risk of severe asthma and decreased lung function than those exposed only to household pollution.

Background: Asthma is a syndrome with multiple phenotypes. Peripheral blood eosinophil counts might be the ideal biomarker to identify subjects with eosinophilic asthma. It is available, inexpensive, and it is associated with eosinophilia in sputum. Objective: The aim of this study was to evaluate whether blood eosinophilia is associated with asthma severity and to evaluate whether blood eosinophilia is associated with lack of control of asthma symptoms and airway obstruction. Methods: Case control study. The cases were subjects recruited from a cohort of patients with severe asthma, in Salvador-BR, demanding continuous inhaled corticosteroids and LABA. There were two control groups: 1) subjects with mild/moderate asthma, 2) subjects with no asthma. Subjects enrolled in the study answered questionnaires, had their blood and stool samples collected, performed spirometry and SPT. We established a cutoff ≥ 260 cells/mm3 for blood eosinophilia. Results: We evaluated 544 subjects in the case group, 452 subjects with mild to moderate asthma and 450 subjects with no asthma. The subjects of the case group had higher odds of presenting the eosinophilic phenotype in comparison to subjects with mild to moderate asthma [OR 1.60 95CI(1.19-2.16)] and no asthma [OR 3.93; 95CI(2.90-5.33)]. The eosinophilic phenotype, according to blood count, is associated with uncontrolled asthma [OR 1.56; 95CI(1.06-2.28)], but it is not associated with airway obstruction [OR 0.87; 95CI(0.61-1.24)]. Conclusion: We conclude that the blood eosinophilia is a biomarker associated with asthma severity and poor symptom control, but we found no association with reduced lung function.

Background: Asthma prevalence is 339 million globally. 'Severe asthma' (SA) comprises subjects with uncontrolled asthma despite proper management. Objectives: To compare asthma from diverse ethnicities and environments. Methods: A cross-sectional analysis of two adult cohorts, a Brazilian (ProAR) and a European (U-BIOPRED). U-BIOPRED comprised of 311 non-smoking with Severe Asthma (SAn), 110 smokers or ex-smokers with SA (SAs) and 88 mild to moderate asthmatics (MMA) while ProAR included 544 SA and 452 MMA. Although these projects were independent, there were similarities in objectives and methodology, with ProAR adopting operating procedures of U-BIOPRED. Results: Among SA subjects, age, weight, proportion of former smokers and FEV 1 pre-bronchodilator were similar. The proportion of SA with a positive skin prick tests (SPT) to aeroallergens, the scores of sino-nasal symptoms and quality of life were comparable. In addition, blood eosinophil counts (EOS) and the % of subjects with EOS > 300 cells/μl were not different. The Europeans with SA however, were more severe with a greater proportion of continuous oral corticosteroids (OCS), worse symptoms and more frequent exacerbations. FEV 1 /FVC pre-and post-bronchodilator were lower among the Europeans. The MMA cohorts were less comparable in control and treatment, but similar in the proportion of allergic rhinitis, gastroesophageal reflux disease and EOS >3%. Conclusions: ProAR and U-BIOPRED cohorts, with varying severity, ethnicity and environment have similarities, which provide the basis for global external validation of asthma phenotypes. This should stimulate collaboration between asthma consortia with the aim of understanding SA, which will lead to better management.