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Risk of new onset diabetes mellitus in patients with asthma or COPD taking inhaled corticosteroids.

A recent case-controlled study reported an increased risk of diabetes mellitus in patients treated with inhaled corticosteroids for asthma or COPD, versus age-matched controls.

OBJECTIVE: The purpose of the current study was to evaluate whether there was an increased risk of new onset diabetes mellitus or hyperglycaemia among patients with asthma or COPD treated with inhaled corticosteroids.

METHODS: A retrospective analysis evaluated all double-blind, placebo-controlled, trials in patients ≥4 years of age involving budesonide or budesonide/formoterol in asthma (26 trials; budesonide: n = 9067; placebo: n = 5926), and in COPD (8 trials; budesonide: n = 4616; non-ICS: n = 3643). A secondary dataset evaluated all double-blind, controlled trials in asthma involving the use of inhaled corticosteroids (60 trials; budesonide: n = 33,496; fluticasone: n = 2773).

RESULTS: In the primary asthma dataset, the occurrence of diabetes mellitus/hyperglycaemia adverse events (AEs) was 0.13% for budesonide and 0.13% for placebo (HR 0.98 [95% CI: 0.38-2.50], p = 0.96) and serious adverse events (SAEs) was 0% for budesonide and 0.05% for placebo. In the secondary dataset, the occurrence of diabetes/hyperglycaemia as AE and SAE was 0.19% and 0.03%, respectively. In the COPD dataset, the occurrence of diabetes mellitus/hyperglycaemia AEs was 1.3% for budesonide and 1.2% for non-ICS (HR 0.99 [95% CI: 0.67-1.46], p = 0.96) and SAEs was 0.1% for budesonide and 0.03% for non-ICS.

CONCLUSION AND CLINICAL RELEVANCE: Treatment with inhaled corticosteroids in patients with asthma or COPD was not associated with increased risk of new onset diabetes mellitus or hyperglycaemia.

Vascular Risk in Chronic Obstructive Pulmonary Disease: Role of Inflammation and Other Mediators.

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung condition that affects 3 million adult Canadians aged 40 years or older. Most patients have mild to moderate disease and as such have only modest symptoms of cough and breathlessness. However, many will go on to experience ischemic heart disease and stroke and die of cardiovascular complications rather than from their lung disease. Indeed, nearly 50% of all hospitalizations and 25% of all deaths in patients with mild to moderate COPD are cardiovascular system related.

Experimental and epidemiologic data from the past 20 years provide compelling evidence that chronic lung inflammation (related to COPD or exposure to irritants such as tobacco smoke or air pollution) contributes to atherosclerotic plaque progression and that acute inflammatory stimulus such as acute respiratory tract infections or acute exacerbations of COPD induce plaque rupture, leading to cardiovascular events.

In this paper, we provide an overview of the epidemiologic and experimental data linking COPD with cardiovascular disease and highlight the clinical implications of this linkage for clinicians who evaluate and manage patients with COPD, cardiovascular diseases, or both.

Does upper extremity exercise improve dyspnea in patients with COPD? A meta-analysis.

BACKGROUND: Although unsupported upper extremity exercise (UUEE) is recommended in the guidelines for pulmonary rehabilitation (PR), it is controversial whether UUEE improves dyspnea in patients with COPD. The present study conducted a meta-analysis of randomized controlled trials to clarify whether UUEE could improve dyspnea in COPD patients.

METHODS: A computerized search through PubMed and Embase (up to Mar 2012) was performed to obtain sample studies. Methodological quality was assessed using the PEDro scale. Weighted mean differences (WMDs), and 95% confidence intervals (CIs) were calculated and heterogeneity was assessed with the I(2) test. The overall effect sizes were compared with the minimum clinically important difference (MCID).

RESULTS: 240 patients from 7 studies were included in this meta-analysis. The mean PEDro score was 7.0 (SD = 1.7). The results indicated UUEE relieved dyspnea and arm fatigue during activities of daily living (ADL) (WMD = -0.58, -0.55 scores; 95% CI = -1.13 to -0.02, -1.08 to -0.01), however, the overall treatment effects were lower than the MCID of 1 unit for the Borg scale. There was no statistical significance for dyspnea and arm fatigue during intervention (WMD = -0.34, 0.24 scores; 95% CI = -0.78 to 0.09, -0.33 to 0.81).

CONCLUSIONS: UUEE can relieve dyspnea and arm fatigue in patients with COPD during ADL and should be included in the PR program, however, there is currently a lack of clinical evidence to support UUEE relieving dyspnea and arm fatigue. Further study is urgent to investigate these effects of UUEE.

The Inflammasome in Lung Diseases.

Inflammation, the process aimed at restoring homeostasis after an insult, can be more damaging than the insult itself if uncontrolled, excessive or prolonged. The inflammasome is an intracellular multimeric protein complex that regulates the maturation and release of proinflammatory cytokines of the IL-1 family in response to pathogens and endogenous danger signals.

Growing evidence indicates that the inflammasome plays a key role in the pathogenesis of both acute and chronic respiratory diseases. The inflammasome can be activated by the pathogens that account for the most prevalent infectious diseases of the respiratory tract, such as Influenza A virus, Streptococcus pneumoniae, Pseudomonas aeruginosa and Mycobacterium tuberculosis. The inflammasome also plays a role in the chronic inflammation of the airways of patients with asthma and COPD, as well as in the initiation and progression of the inflammatory process seen in pulmonary fibrosis.

The aim of this review is to summarize the most relevant points of the inflammasome activation in lung diseases.

[Recommendation concerning the microscopic classification of lung adenocarcinoma presented by International Association for the Study of Lung Cancer, American Thoracic Society, and European Respiratory Society].

Authors: Langfort R, Szołkowska M PMID: 22370977 [PubMed - indexed for MEDLINE] (Source: Pneumonologia i Alergologia Polska)

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