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Effect of One-Year Subcutaneous and Sublingual Immunotherapy on Clinical and Laboratory Parameters in Children with Rhinitis and Asthma: A Randomized, Placebo-Controlled, Double-Blind, Double-Dummy Study.

It has been reported that both sublingual (SLIT) and subcutaneous (SCIT) allergen-specific immunotherapy have clinical efficacy, yet there are rather few comparative placebo studies of children.

We aimed to investigate the clinical and immunological efficacy of mite-specific SLIT and SCIT versus a placebo in rhinitis and asthma in children.

Methods: The outcomes of this 1-year, randomized, placebo-controlled, double-blind, double-dummy study were symptom and medication scores, visual analog scores (VAS), titrated skin prick tests, nasal and bronchial allergen provocation doses, serum house dust mite-specific immunglobulin E (HDM-sIgE), sIgG4, IL-10 and IFN-γ levels.

Results: Clinical and laboratory parameters were evaluated in 30 patients. SCIT significantly diminished symptom and medication scores for rhinitis and asthma (p = 0.03 and p = 0.05 for rhinitis; p = 0.01 and p = 0.05 for asthma) and VAS. SLIT also reduced VAS, symptoms associated with rhinitis and asthma as well as medication usage for rhinitis, but this reduction was not significant when compared with the placebo. Skin reactivitiy to HDM and HDM-sIgE levels was reduced significantly in both immunotherapy groups. Serum IL-10 levels and nasal provocative doses increased significantly with both SCIT and SLIT. Nasal eosinophil increments after nasal challenge decreased with two treatment modes, but bronchial provocative doses and sputum eosinophil increments after bronchial challenge were reduced only with SCIT. In both treatment arms, there was no change in IFN-γ levels. Serum sIgG4 levels increased significantly only in the SCIT group.

Conclusion: Based on the limited number of patients at the end of the 1-year immunotherapy, the clinical efficacy of SCIT on rhinitis and asthma symptoms was more evident when compared with the placebo.

Nocturnal asthma.

The aim is to review pathophysiological mechanisms and treatment of nocturnal asthma.

RECENT FINDINGS: Physiologic changes accompanying sleep, as well as the nocturnal phase of circadian rhythms, may have an adverse effect on asthma control. Chronotherapeutic principles, which consider circadian variation in relevant biologic rhythms, may improve asthma outcomes. Administration of long-acting bronchodilators and inhaled corticosteroids which achieve maximum efficacy at night may improve nocturnal asthma. Comorbid conditions that may contribute to nocturnal asthma should be considered. The prevalence of obstructive sleep apnea is greater in a cohort of patients with severe asthma than in moderate asthma and in BMI and age matched nonasthmatic controls, suggesting a link between these diseases. A large trial concluded that esomeprazole did not improve asthma control even with comorbid acid reflux, questioning the importance of acid reflux in asthma. The role of polymorphisms of the β2-adrenergic receptor and their relationship with nocturnal asthma remain controversial.

SUMMARY: Sleep is a time of vulnerability to respiratory compromise, especially in asthma patients experiencing nocturnal exacerbations. This asthma phenotype is associated with poorer control, reduced sleep quality, daytime somnolence and increased morbidity and mortality. Nocturnal asthma is a common but under-recognized problem.

Inflammatory biomarkers in severe asthma.

Severe asthma remains a condition in search of deeper understanding and of newer effective therapies. Risk factors for developing severe asthma, phenotyping of disease, characterizing the inflammatory response and understanding of poor therapeutic responses to corticosteroids are important areas of research. The development of biomarkers for phenotypic diagnosis and prognostic reasons is important.

RECENT FINDINGS: Severe asthma has been defined as asthma that does not respond adequately to asthma medications, particularly corticosteroids, with continuing loss of control of asthma and future risk of exacerbations and side effects from corticosteroid therapy. This is a heterogeneous condition and cluster analyses have yielded phenotypes on the basis of age of onset of disease, sex, lung function, atopy and questionnaire data. Use of sputum eosinophil counts has further defined a group with persistent eosinophilic inflammation despite corticosteroid therapy, and a noneosinophilic group with uncontrolled asthma.

SUMMARY: Use of a single biomarker provides value in phenotyping and in predicting response to treatment but many more biomarkers such as those derived from -omic approaches remain to be used in the analysis. A systems biology approach to finding novel biomarkers is the way forward to stratify severe asthma so that appropriate and distinct therapies can be selected for each subtype.

Lung function is associated with arterial stiffness in children.

In older adults, an independent association exists between impaired lung function and cardiovascular disease. This interaction might be related to the effects of aging and/or smoking. In order to explore possible childhood antecedents to this association, we hypothesized that decreased lung function and vascular stiffness might be related, in early life.

OBJECTIVE: To determine the relationship between lung function and carotid augmentation index (AIx), a measure of vascular stiffness, in 8-year old children.

METHODS: Data on brachial blood pressure, lung function (FEV(1), FVC, FEV(1)/FVC, obtained by spirometry) and carotid AIx75 (AIx standardised to an arbitrary heart rate of 75 beats per minute, obtained by applanation tonometry) was available in 249 community-based 8-year old children. These healthy children had been subjects in a randomised controlled trial of two interventions (omega-3 fatty acid supplementation and house-dust mite avoidance) to prevent asthma. Smoking in pregnancy and childhood environmental tobacco smoke (ETS) exposure was prospectively collected by questionnaire. The association between lung function and carotid AIx75 was assessed in multivariate models that included sex, height, smoking status during pregnancy, ETS exposure and randomisation groups (house dust mite avoidance and dietary intervention) as covariates.

RESULTS: In the fully adjusted models, Carotid AIx75 was independently associated with FEV1 (standardised β = -0.17,b = -6.72, partial R(2) = .02, p = 0.03), FVC (standardised β = -0.29, b = -9.31, partial R(2) = 0.04, p<0.001) and FEV1/FVC (standardised β = .13, b = 18.4, partial R(2) = 0.02, p = 0.04).

CONCLUSION: Lower lung volumes are associated with increased vascular stiffness at an early age. The interaction between lung function and vascular stiffness may thus represent more than just age-related alterations in both the pulmonary and vascular systems.

Airflow limitation or static hyperinflation: which is more closely related to dyspnea with activities of daily living in patients with COPD?

Dyspnea while performing the activities of daily living has been suggested to be a better measurement than peak dyspnea during exercise. Furthermore, the inspiratory capacity (IC) has been shown to be more closely related to exercise tolerance and dyspnea than the FEV1, because dynamic hyperinflation is the main cause of shortness of breath in patients with COPD. However, breathlessness during exercise is measured in most studies to evaluate this relationship.PurposeTo evaluate the correlation between breathlessness during daily activities and airflow limitation or static hyperinflation in COPD.

Methods: We examined 167 consecutive outpatients with stable COPD. The Baseline Dyspnea Index (BDI) was used to evaluate dyspnea with activities of daily living. The relationship between the BDI score and the clinical measurements of pulmonary function was then investigated.

Results: The Spearman rank correlation coefficients (Rs) between the BDI score and the FEV1(L), FEV1(%pred) and FEV1/FVC were 0.60, 0.56 and 0.56, respectively. On the other hand, the BDI score also correlated with the IC, IC/predicted total lung capacity (TLC) and IC/TLC (Rs = 0.45, 0.46 and 0.47, respectively). Although all of the relationships studied were strongly correlated, the correlation coefficients were better between dyspnea and airflow limitation than between dyspnea and static hyperinflation. In stepwise multiple regression analyses, the BDI score was most significantly explained by the FEV1 (R2 = 26.2%) and the diffusion capacity for carbon monoxide (R2 = 14.4%) (Cumulative R2 = 40.6%). Static hyperinflation was not a significant factor for clinical dyspnea on the stepwise multiple regression analysis.

Conclusion: Both static hyperinflation and airflow limitation contributed greatly to dyspnea in COPD patients.

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