Login to your account

Username *
Password *
Remember Me

Blog With Right Sidebar

    Vous êtes ici :  
  1. Accueil
  2. Blog With Right Sidebar

Effects of budesonide/formoterol combination therapy versus budesonide alone on airway dimensions in asthma.

The mechanism by which budesonide/formoterol combination therapy exerts clinically beneficial effects appears to be related to increased anti-inflammatory activity and attenuation of aspects of airway remodeling in asthmatic patients.

Background and objective:  Combination therapy with inhaled corticosteroids and long-acting β(2) -agonists results in improved asthma symptom control compared with the use of inhaled corticosteroids alone. However, the effects of combination therapy on structural changes and inflammation of the airways are still unknown. The aim of this study was to compare the effects of budesonide/formoterol with those of budesonide alone on airway dimensions and inflammation in individuals with asthma.

Methods:  Fifty asthmatic patients were randomized to treatment with budesonide/formoterol (200/6 µg, two inhalations bd) or budesonide (200 µg, two inhalations bd) for 24 weeks. Airway dimensions were assessed using a validated CT technique, and airway wall area (WA) corrected for body surface area (BSA), percentage wall area (WA%), wall thickness (T)/√BSA, and luminal area (Ai)/BSA at the right apical segmental bronchus, were measured. The percentage of eosinophils in induced sputum, pulmonary function, and Asthma Quality of Life Questionnaires (AQLQ) were also evaluated.

Results:  There were significantly greater decreases in WA/BSA (P < 0.05), WA% (P < 0.001) and T/√BSA (P < 0.05), and increases in Ai/BSA (P < 0.05), in subjects treated with budesonide/formoterol compared to those treated with budesonide. The reduction in sputum eosinophils and increase in FEV(1) % were greater for subjects treated with budesonide/formoterol compared to those treated with budesonide alone. In the budesonide/formoterol group, the changes in WA% were significantly correlated with changes in sputum eosinophils and FEV(1) % (r = 0.84 and r = 0.64, respectively). There were improvements in the AQLQ scores after treatment with budesonide/formoterol.

Conclusions:  Budesonide/formoterol combination therapy is more effective than budesonide alone for reducing airway wall thickness and inflammation in individuals with asthma. © 2012 The Authors. Respirology © 2012 Asian Pacific Society of Respirology.

Severe asthma in childhood: recent advances in phenotyping and pathogenesis.

PURPOSE OF REVIEW: Children with severe asthma have a high degree of respiratory morbidity despite treatment with high doses of inhaled corticosteroids and are therefore very difficult to treat. This review will discuss phenotypic and pathogenic aspects of severe asthma in childhood, as well as remaining knowledge gaps.

RECENT FINDINGS: As a group, children with severe asthma have a number of distinct phenotypic features compared with children with mild-to-moderate asthma. Clinically, children with severe asthma are differentiated by greater allergic sensitization, increased exhaled nitric oxide, and significant airflow limitation and air trapping that worsens as a function of age. These findings are accompanied by structural airway changes and increased and dysregulated airway inflammation and oxidant stress which may explain the differential nature of corticosteroid responsiveness in this population. Because children with severe asthma themselves are a heterogeneous group, current efforts are focused on improved definition and sub-phenotyping of the disorder. Whereas the clinical relevance of phenotyping approaches in severe asthma is not yet clear, they may provide important insight into the mechanisms underlying the disorder.

SUMMARY: Improved classification of severe asthma through unified definitions, careful phenotypic analyses, and mechanism-focused endotyping approaches may ultimately advance knowledge and personalized treatment.

Maternal Asthma Medication Use and the Risk of Selected Birth Defects.

Approximately 4% to 12% of pregnant women have asthma; few studies have examined the effects of maternal asthma medication use on birth defects. We examined whether maternal asthma medication use during early pregnancy increased the risk of selected birth defects.

METHODS:National Birth Defects Prevention Study data for 2853 infants with 1 or more selected birth defects (diaphragmatic hernia, esophageal atresia, small intestinal atresia, anorectal atresia, neural tube defects, omphalocele, or limb deficiencies) and 6726 unaffected control infants delivered from October 1997 through December 2005 were analyzed. Mothers of cases and controls provided telephone interviews of medication use and additional potential risk factors. Exposure was defined as maternal periconceptional (1 month prior through the third month of pregnancy) asthma medication use (bronchodilator or anti-inflammatory). Associations between maternal periconceptional asthma medication use and individual major birth defects were estimated by using adjusted odds ratios (aOR) and 95% confidence intervals (95%CI).

RESULTS:No statistically significant associations were observed for maternal periconceptional asthma medication use and most defects studied; however, positive associations were observed between maternal asthma medication use and isolated esophageal atresia (bronchodilator use: aOR = 2.39, 95%CI = 1.23, 4.66), isolated anorectal atresia (anti-inflammatory use: aOR = 2.12, 95%CI = 1.09, 4.12), and omphalocele (bronchodilator and anti-inflammatory use: aOR = 4.13, 95%CI = 1.43, 11.95).

CONCLUSIONS:Positive associations were observed for anorectal atresia, esophageal atresia, and omphalocele and maternal periconceptional asthma medication use, but not for other defects studied. It is possible that observed associations may be chance findings or may be a result of maternal asthma severity and related hypoxia rather than medication use.

Severe asthma: from characteristics to phenotypes to endotypes.

Asthma, and severe asthma, in particular, is increasingly recognized as a heterogeneous disease. While traditional views of asthma have centered around a childhood onset disease with an allergic component, several large scale network studies are now confirming that severe asthma can present in multiple different ways, only 30-50% of which meet traditional childhood onset allergic criteria.

To understand the different groups better, initial studies have attempted to define phenotypes of severe asthma. A phenotype is defined as the integration of different characteristics that are the product of the interaction of the patient's genes with the environment. Both clinical and statistical approaches have identified at least 3-5 phenotypes of severe asthma. However, these phenotypes, in isolation, do not identify the immunopathology that makes these clinical phenotypes distinct or identifies a target population for a specific approach to therapy. As biological characteristics are identified, phenotypes should continue to evolve towards asthma endotypes.

The identification of these endotypes, either by matching biology, genetics and therapeutic responses to therapy with clinically or statistically defined phenotypes or through unbiased genetic and genomic approaches, remains limited. Moving forward, this integration of genetics, biology and clinical characteristics should substantially enhance our ability to effectively treat complex heterogeneous diseases, such as severe asthma.

Current treatment of severe asthma.

Severe asthma is considered a heterogeneous disease in which a variety of clinical, physiological and inflammatory markers determine disease severity. Pivotal studies in the last 5 years have led to substantial progress in many areas, ranging from a more accurate definition of truly severe, refractory asthma, to classification of the disease into distinct clinical phenotypes, and introduction of new therapies.

This review focuses on three common clinical phenotypes of severe asthma in adults (early onset severe allergic asthma, late onset non-atopic eosinophilic asthma, late onset non-eosinophilic asthma with obesity), and provides an overview of recent developments regarding treatment options that are best suited for each of these phenotypes.

Search

Search