PubMed · 13869321
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
G BIRATH. 1962-08-09. [Chronic bronchitis].. https://pubmed.ncbi.nlm.nih.gov/13869321/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: The impact of acute exacerbations of chronic bronchitis (AECB), a common consequence of chronic obstructive pulmonary disease (COPD), is extensive, with symptoms ranging from mild to life threatening. Health-related quality of life (HRQL) is impaired in patients with COPD, but little is known about the direct effect of exacerbations on HRQL. METHODS: MEDLINE and EMBASE literature searches were conducted; reference lists of identified articles were reviewed. RESULTS: Eighteen studies reporting the impact on HRQL of acute exacerbations were identified. Study design and patient population varied. Six studies evaluated HRQL once; only four studies used both generic and disease-specific HRQL measures. Cross-sectional studies reported HRQL decrements during exacerbations and suggested that HRQL is a good predictor of health care resource utilization. Pharmacological treatment led to within-group improvements following AECBs. Non-pharmacological intervention studies were small and inconclusive. Longitudinal studies, assessing pharmacological and non-pharmacological interventions, found that HRQL improved from exacerbation to recovery, with responsiveness depending on sensitivity of the measure. Frequency of exacerbations was a significant predictor of HRQL. CONCLUSIONS: Exacerbations lead to substantial reductions in HRQL, both in physical as well as other domains. Further research should assess the impact of specific treatment regimens and the timeline for the recovery process.
BACKGROUND: A study was undertaken to assess both oxidative stress and inflammation in the lungs of patients with chronic obstructive pulmonary disease (COPD) during severe and very severe exacerbations compared with those with stable COPD, healthy smokers, and non-smokers. Two sites within the lungs were compared: the large airways (in sputum) and the peripheral airways (by bronchoalveolar lavage (BAL)). METHODS: BAL fluid cell numbers and levels of tumour necrosis factor (TNFalpha) and interleukin (IL)-8 were measured as markers of airway inflammation and glutathione (GSH) levels as a marker of antioxidant status. Nuclear translocation of the pro-inflammatory transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein 1 (AP-1) were also measured by electromobility shift assay in BAL fluid leucocytes and lung biopsy samples. RESULTS: Influx of inflammatory cells into the peripheral airways during exacerbations of COPD was confirmed. Increased IL-8 levels were detected in BAL fluid from patients with stable COPD compared with non-smokers and healthy smokers, with no further increase during exacerbations. In contrast, IL-8 levels in the large airways increased during exacerbations. GSH levels were increased in the BAL fluid of smokers (444%) and patients with stable COPD (235%) compared with non-smokers and were reduced during exacerbations (severe 89.2%; very severe 52.3% compared with stable COPD). NF-kappaB DNA binding in BAL leucocytes was decreased in healthy smokers compared with non-smokers (41.3%, n = 9, p<0.001) but did not differ in COPD patients, whereas AP-1 DNA binding was significantly decreased during exacerbations of COPD. CONCLUSION: There is evidence of increased oxidative stress in the airways of patients with COPD that is increased further in severe and very severe exacerbations of the disease. This is associated with increased neutrophil influx and IL-8 levels during exacerbations.
Explore the source record for details and available documents.