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Differential Diagnosis in a Primary Care Population with Presumed Airway Obstruction: A Real-Life Study

Asthma and chronic obstructive pulmonary disease (COPD) have major symptoms in common. However, the mode of the underlying chronic airway inflammation is different. There is still no single diagnostic test that can be considered a gold standard to distinguish asthma from COPD.

Objectives: To determine the diagnostic accuracy for asthma and COPD of a series of diagnostic steps in a population older than 40 years with probable obstructive airway disease (OAD) in primary care. Methods: In this prospective cohort study, patients without a certain diagnosis underwent a work-up, including office spirometry by their general practitioner (GP). They were then referred to a pulmonologist, and they had control visits with their GP. The diagnostic gain of subsequent steps was calculated for 2 endpoints, namely the specialist’s opinion and the GP’s final opinion.

Results: Up to 60% of the patients failed to consult with the pulmonologist. For this subgroup, the office spirometry induced significantly more diagnostic congruency than any other diagnostic step. The specialists rejected 44.5% of the diagnoses made by the GPs, including spirometry. High values of diagnostic gain were found after the office spirometry and after the specialist’s advice. Up to 25% of the population taking bronchodilators were judged not to suffer from OAD.

Conclusions: Office spirometry added significantly more to the diagnostic certainty of the GPs than questionnaires, history and clinical examination. A pulmonologist’s advice contributed more to diagnostic certainty than any other diagnostic step. Nevertheless, 26% of the diagnoses made by the chest physicians were reconsidered by the GPs.

Clinical, Physiological and Anti-Inflammatory Effect of Montelukast in Patients with Cough Variant Asthma

Cough variant asthma (CVA) is a phenotype of asthma presenting solely with coughing, characterized by airway hyperresponsiveness, eosinophilic inflammation and a cough response to bronchodilators. Leukotriene receptor antagonists (LTRAs) are antiasthma medications with anti-inflammatory and bronchodilatory properties. Although LTRAs exert antitussive effects in CVA, the mechanisms involved are unknown.

Objectives: This study aimed to clarify the antitussive mechanisms of LTRAs in CVA patients. Methods: We prospectively observed the effect of montelukast (10 mg) daily for 4 weeks in 23 consecutive nonsmoking adults with anti-inflammatory treatment-naive CVA. We evaluated, before and after treatment, the cough visual analogue scale (VAS), pulmonary function (spirometry and impulse oscillation), methacholine airway responsiveness, cough receptor sensitivity, expressed by the concentration of capsaicin inducing 2 or more (C2) and 5 or more (C5) coughs, sputum eosinophil counts and levels of inflammatory mediators, including cysteinyl leukotrienes, leukotriene B4, prostaglandin (PG) D2, PGE2, PGF2α and thromboxane B2. We compared the baseline characteristics of the patients based on the symptomatic response to montelukast, defined as a decrease in the cough VAS of >25% (n = 15) or ≤25% (n = 8).

Results: Montelukast significantly decreased the cough VAS (p = 0.0008), sputum eosinophil count (p = 0.013) and cough sensitivity (C2: p = 0.007; C5: p = 0.039), whereas pulmonary function, airway responsiveness and sputum mediator levels remained unchanged. Multivariate analysis showed that a better response to montelukast was associated solely with younger age (p = 0.032).

Conclusion: The antitussive effect of montelukast in CVA may be attributed to the attenuation of eosinophilic inflammation rather than its bronchodilatory properties.

Neutrophil Activation in Severe, Early-Onset COPD Patients versus Healthy Non-Smoker Subjects in vitro: Effects of Antioxidant Therapy

Neutrophils and oxidative stress have been implicated in the pathogenesis of COPD. Severe, early-onset COPD is characterized by a rapid decline in the lung function at an early age; however, nothing is known about neutrophil activation in COPD patients.

Objectives: The aim of this study was to evaluate peripheral blood neutrophil activation in severe, early-onset COPD patients versus healthy non-smokers and the effect of N-acetyl-L-cysteine (NAC) on neutrophil activation in vitro.

Methods: Neutrophils were isolated from 15 severe, early-onset COPD patients and 15 age-matched healthy subjects and stimulated with N-formyl- Met-Leu-Phe (fMLP) in the presence or absence of NAC (10 µM to 10 mM). Neutrophil chemotaxis, elastase release, reactive oxygen species (ROS), intracellular thiols and apoptosis were measured by Boyden chamber, spectrofluorometry, CMFDA and H2DCF-DA dyes and by annexin V-FITC, respectively.

Results: Chemotaxis of peripheral blood neutrophils from COPD patients in response to fMLP was 30% more increased than that observed in healthy subjects. Elastase release in response to fMLP was 2-fold higher in neutrophils from COPD patients versus healthy subjects. Intracellular thiol levels were 30% lower in COPD and ROS was approximately 30% higher in COPD versus healthy neutrophils. Spontaneous apoptosis showed no differences in both groups of patients and fMLP-induced apoptosis was higher in COPD. Pre-treatment with the antioxidant NAC effectively attenuated neutrophil chemotaxis, elastase release and ROS as well as effectively increased thiol levels in COPD.

Conclusions: Neutrophils in severe, early-onset COPD patients are highly activated and this is alleviated by NAC in vitro.

Neutrophil-Mediated Lung Damage: A New COPD Phenotype

No abstract available
Source: Respiration
Author : Stephan F. Van Eeden
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Effects of Adding Omalizumab, an Anti-Immunoglobulin E Antibody, on Airway Wall Thickening in Asthma

Omalizumab may inhibit allergic inflammation and could contribute to decreasing airway remodeling in patients with asthma.

Objective: The aim of this study was to assess the effects of omalizumab on airway wall thickness using computed tomography (CT).

Methods: Thirty patients with severe persistent asthma were randomized to conventional therapy with (n = 14) or without omalizumab (n = 16) for 16 weeks. The following airway dimensions were assessed by a validated CT technique: airway wall area corrected for body surface area (WA/BSA), percentage wall area (WA%), wall thickness (T)/√BSA, and luminal area (Ai)/BSA at the right apical segmental bronchus. The percentage of eosinophils in induced sputum, pulmonary function and the Asthma Quality of Life Questionnaire (AQLQ) were assessed as well.

Results: Treatment with omalizumab significantly decreased WA/BSA (p < 0.01), WA% (p < 0.01), and T/√BSA (p < 0.01), and increased Ai/BSA (p < 0.05), whereas conventional therapy resulted in no change. In the omalizumab group (n = 14), a significant decrease in the percentage of sputum eosinophils (p < 0.01), improved forced expiratory volume in 1 s (FEV1), and an improved AQLQ score were recorded. The changes in FEV1% predicted and sputum eosinophils were significantly correlated with  changes in WA% (r = 0.88, p < 0.001, and r = 072, p < 0.01, respectively).

Conclusions: These findings suggest that omalizumab reduced airway wall thickness and airway inflammation. Larger patient studies with longer-term follow-up are needed to show whether omalizumab can truly maintain improved airway wall dimensions.

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