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Causes of Chronic Cough in Non-smoking Patients.

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Chronic cough is a common medical problem. The aim of the study was to analyze chronic cough causes in non-smoking patients and to search for demographic factors associated with different cough reasons. The etiology of cough was determined by medical history, diagnostic tests and response to specific treatment. Patients with significant abnormalities in the chest radiograph or spirometry were not included.

The study included 131 non-smoking patients; median age 54 years, 77 % female. The most frequent causes of cough were gastroesophageal reflux disease (GERD) (62 %) and upper airway cough syndrome (UACS) (46 %). Cough variant asthma and non-asthmatic eosinophilic bronchitis (NAEB) were diagnosed in 32 (25 %) and 19 (15 %) patients, respectively. Other cough causes were found in 27 patients (21 %). Asthma was a significantly more common cause of chronic cough in women than in men (31 % vs. 3 %, p = 0.005). A reverse relationship was demonstrated for UACS (39 % vs. 67 %, p = 0.01). Patients with chronic cough aged >50 yrs were more likely to be diagnosed with less common cough causes.

In conclusion, the most common chronic cough reasons are GERD and UACS. Asthma-related cough is diagnosed more frequently in females, while UACS-related cough is more frequent in males.

Pulmonary macrophages: key players in the innate defence of the airways.

Macrophages are the most numerous immune-cells present in the lung environment under homoeostatic conditions and are ideally positioned to dictate the innate defence of the airways. Pulmonary macrophage populations are heterogeneous and demonstrate remarkable plasticity, owing to variations in origin, tissue residency and environmental influences. Lung macrophage diversity facilitates considerable specialisation, aids efficient responses to environmental signals and allows rapid alterations in phenotype and physiology in response to a plethora of cytokines and microbial signals.

This review describes pulmonary macrophage origins, phenotypes, roles in diseases of the airways and implications for the treatment of respiratory disease.

Benefits of completing pulmonary rehabilitation in patients with asthma.

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Asthma affects 30 million Americans and results in reduced productivity and quality of life. Pulmonary rehabilitation (PR) is known to improve physical conditioning and exercise performance in chronic lung diseases such as COPD, however, few studies have examined its benefits in patients with asthma. We aimed to determine the benefits of PR in this population as well as the predictors of completion of therapy.

METHODS: We performed a retrospective review of data from patients with a diagnosis of asthma who participated in PR at our institution from 1996 to 2013. Nine hundred and nineteen patients participated in the program of whom 75 were referred with a primary diagnosis of asthma. Patients underwent physiologic testing and their symptoms and quality of life were assessed using validated questionnaires. For patients who completed PR (n = 37), data obtained at the initial and exit visit was compared. Characteristics of completers were compared to non-completers to determine predictors of successful completion.

RESULTS: Individuals with asthma completing PR had improvement from baseline to exit visit in Six Minute Walk Distance (326 vs. 390 feet; p < 0.0001), decreased body mass index (33 vs. 32 kg/m(2); p < 0.046), decreased Beck Depression Inventory scores (15 vs. 9; p < 0.0009), and increased Short Form-36 scores (345 vs. 445; p = 0.0005). In a multivariate logistic regression analysis, lower depression scores predicted completion (OR 1.08, 95% CI 1.02-1.15, p = 0.02).

CONCLUSION: Patients with asthma who completed PR had improvement in physical function and emotional well-being. Depression is a risk factor for non-completion of PR. Further research is needed to determine which patients will benefit most from therapy.

Recent advances in paediatric respiratory medicine.

This review highlights important advances in paediatric respiratory medicine since 2014, excluding cystic fibrosis. It focuses mainly on the more common conditions, bronchopulmonary dysplasia, bronchiolitis and preschool wheezing, asthma, pneumonia and sleep, and highlights some of the rarer conditions such as primary ciliary dyskinesia and interstitial lung disease (ILD).

TH2 and TH17 inflammatory pathways are reciprocally regulated in asthma.

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TH7Increasing evidence suggests that asthma is a heterogeneous disorder regulated by distinct molecular mechanisms. In a cross-sectional study of asthmatics of varying severity (n = 51), endobronchial tissue gene expression analysis revealed three major patient clusters: TH2-high, TH17-high, and TH2/17-low. TH2-high and TH17-high patterns were mutually exclusive in individual patient samples, and their gene signatures were inversely correlated and differentially regulated by interleukin-13 (IL-13) and IL-17A.

To understand this dichotomous pattern of T helper 2 (TH2) and TH17 signatures, we investigated the potential of type 2 cytokine suppression in promoting TH17 responses in a preclinical model of allergen-induced asthma. Neutralization of IL-4 and/or IL-13 resulted in increased TH17 cells and neutrophilic inflammation in the lung. However, neutralization of IL-13 and IL-17 protected mice from eosinophilia, mucus hyperplasia, and airway hyperreactivity and abolished the neutrophilic inflammation, suggesting that combination therapies targeting both pathways may maximize therapeutic efficacy across a patient population comprising both TH2 and TH17 endotypes.

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