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Exacerbations of severe asthma: a focus on steroid therapy.

Bronchial asthma remains one of the most common chronic diseases in the world; approximately 10% of patients shows exacerbations severe enough to be judged life-threatening, whereas around 2-20% of patients are admitted to the Intensive Care Unit (ICU).

Acute severe asthma is a dangerous condition where the deterioration of the asthmatic exacerbation usually progresses over days or weeks, although in a few patients over hours or even minutes. Morbidity and mortality are mainly related to the underestimation of the severity of the exacerbation, delay in referring to hospital and inadequate emergency treatment. The cornerstone measures of therapy for acute severe asthma are oxygen supplementation, as to achieve arterial saturation >90%, and repetitive or continuous administration of bronchodilators (short-acting inhaled β2-agonists and ipratropium bromide) and corticosteroids.

Despite extensive clinical experience in treatment of chronic asthma with steroids, there is considerable uncertainty about the accurate use of these agents for treatment of acute severe asthma in emergency settings.

How to match the optimal currently available inhaler device to an individual child with asthma or recurrent wheeze.

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Inhaled medications are the cornerstone of treatment in early childhood wheezing and paediatric asthma. A match between patient and device and a correct inhalation technique are crucial for good asthma control. The aim of this paper is to propose an inhaler strategy that will facilitate an inhaler choice most likely to benefit different groups of children.

The main focus will be on pressurised metered dose inhalers and dry powder inhalers. In this paper we will discuss (1) practical difficulties with the devices and with inhaled therapy and (2) the optimal location for deposition of medicines in the lungs, and (3) we will propose a practical and easy way to make the best match between the inhaler device and the individual patient. We hope that this paper will contribute to an increased likelihood of treatment success and improved adherence to therapy.

The use of β2-agonist therapy before hospital attendance for severe asthma exacerbations: a post-hoc analysis.

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Patterns of inhaled β2-agonist therapy use during severe asthma exacerbations before hospital attendance are poorly understood.

AIMS: To assess β2-agonist use prior to hospital attendance.

METHODS: We undertook an exploratory post hoc analysis of data from a 6-month clinical trial of 303 patients randomised to combination budesonide/formoterol inhaler according to a Single combination inhaler as Maintenance And Reliever Therapy regimen ('SMART') or fixed-dose budesonide/formoterol with salbutamol as reliever ('Standard'). Patterns of β2-agonist use for 14 days before hospital attendance with a severe asthma exacerbation were determined by electronic monitoring of inhaler use.

RESULTS: There were 22 hospital attendances in 16 patients during the study. Seven and nine hospital attendances were eligible for analysis in the SMART and Standard groups, respectively. In both regimens, β2-agonist use increased before hospital attendance, with a median (range) maximum daily number of actuations of 14 (9 to 63) budesonide/formoterol in SMART and 46 (6 to 95) salbutamol in Standard with 4 (0 to 10) budesonide/formoterol actuations on the day of maximal salbutamol use. There was delay in obtaining medical review despite high β2-agonist use, in 9/16 patients. Different patterns of use were observed, including repeated days of no inhaled corticosteroid despite marked salbutamol use, which occurred in 3/9 patients in the Standard group.

CONCLUSIONS: Delay in obtaining medical review in association with high β2-agonist use is common in patients before hospital presentation with severe exacerbations of asthma. The SMART regimen reduced nonadherence with inhaled corticosteroid therapy during severe exacerbations.

Cigarette smoking and lung obstruction among adults aged 40-79: United States, 2007-2012.

Data from the National Health and Nutrition Examination Survey, 2007-2012. During 2007-2012, 46.2% of adults aged 40-79 with lung obstruction currently smoked cigarettes. About 41% with mild and 55% with moderate or worse obstruction were current smokers. A similar percentage of men and women with lung obstruction, overall and at each level of severity, smoked cigarettes. A greater percentage of adults aged 40-59 with lung obstruction, overall and at each level of severity, smoked cigarettes than those aged 60-79.

Cigarette smoking among adults with lung obstruction varied by race and Hispanic origin and by severity of obstruction. The percentage of adults with lung obstruction, overall and at each level of severity, who smoked cigarettes declined with increasing education. Lung obstruction is characterized by blocked airflow, shortness of breath, and difficulty exhaling. The most common obstructive lung diseases are asthma and chronic obstructive pulmonary disease (COPD), which includes emphysema and chronic bronchitis. Approximately 15% of U.S. adults aged 40-79 have lung obstruction, with about one-third of those having moderate or worse obstruction (1). Smoking tobacco increases respiratory symptoms (2), lung function loss (3), and the rate of lung function decline (4-6). The benefits of smoking cessation are numerous for all adults (6) and especially for those with lung obstruction (5).

This report presents national estimates of cigarette smoking among adults with measured lung obstruction for the period 2007-2012.

House Dust Mites Induce Proliferation of Severe Asthmatic Smooth Muscle Cells via an Epithelium-dependent Pathway.

house.dust.mitesRationale: Asthma is a very frequent airway disease and asthma control determinants have been associated to indoor allergens sensitization. The most frequent allergens are the house dust mites (HDM), which act in vivo on bronchial epithelial layer. Severe asthma has also been associated to bronchial remodeling and more specifically to the increased mass of bronchial smooth muscle (BSM). However, the relationship between HDM stimulation of the bronchial epithelial layer and BSM remodeling is unknown.

Objectives: To evaluate whether epithelial stimulation with HDM induces BSM cell proliferation in severe asthmatics.

Methods: 22 severe asthmatics and 27 non asthmatic subjects were recruited. We have developed an in vitro culture model combining an epithelium layer in air liquid interface (ALI) interacting with BSM. We assessed BSM proliferation using BrdU incorporation. We explored the role of epithelium-derived mediators using RT-PCR and ELISA both in vitro and in vivo. Finally leukotrienes receptor expression was assessed both in vitro by flow cytometry and RT-PCR and ex vivo by laser micro dissection and RT-PCR.

Measurements and Main Results: We found that epithelial stimulation by HDM selectively increased the proliferation of asthmatic BSM cells and not that of non asthmatics. The mechanism involved an epithelial PAR-2 dependent production of leukotrienes C4 associated to an over-expression of leukotrienes receptor CysLTR1 by asthmatic BSM cells both in vitro and ex vivo.

Conclusions: This work demonstrates the selective role of HDM on BSM remodeling in severe asthmatic patients and points out different therapeutic targets at both epithelial and smooth muscle levels.

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