Improving the uptake of pulmonary rehabilitation in patients with COPD : qualitative study of experiences and attitudes

Background
Pulmonary rehabilitation can improve the quality of life and ability to function of patients with chronic obstructive pulmonary disease (COPD). It may also reduce hospital admission and inpatient stay with exacerbations of COPD. Some patients who are eligible for pulmonary rehabilitation may not accept an offer of it, thereby missing an opportunity to improve their health status.

Aim
To identify a strategy for improving the uptake of pulmonary rehabilitation.

Design of study
Qualitative interviews with patients.

Setting
Patients with COPD were recruited from a suburban general practice in north-east Derbyshire, UK.

Method
In-depth interviews were conducted on a purposive sample of 16 patients with COPD to assess their concerns about accepting an offer of pulmonary rehabilitation. Interviews were analysed using grounded theory.

Results
Fear of breathlessness and exercise, and the effect of pulmonary rehabilitation on coexisting medical problems were the most common concerns patients had about taking part in the rehabilitation. The possibility of reducing the sensation of breathlessness and regaining the ability to do things, such as play with their grandchildren, were motivators to participating.

Conclusion
A model is proposed where patients who feel a loss of control as their disease advances may find that pulmonary rehabilitation offers them the opportunity to regain control. Acknowledging patients' fears and framing pulmonary rehabilitation as a way of ‘regaining control’ may improve patient uptake.

COPD results in a reduction in UCP3 long mRNA and UCP3 protein content in types I and IIa skeletal muscle fibers.

Purpose: Findings recently have shown coupling protein-3 (UCP3) content to be decreased in the skeletal muscle of patients with chronic obstructive pulmonary disease (COPD). Uncoupling protein-3 mRNA exists as two isoforms: long (UCP3L) and short (UCP3S). The UCP3 protein is expressed the least in oxidative and the most in glycolytic muscle fibers. Levels of UCP3 have been associated positively with intramyocellular triglyceride (IMTG) contents in conditions of altered fatty acid metabolism. As a source for muscle free fatty acid metabolism, IMTG is decreased in COPD. The current study completely characterized all the parameters of UCP3 expression (ie, UCP3L and UCP3S mRNA expression in whole muscle samples) and UCP3 protein content as well as IMTG content in the different fiber types in patients with COPD and healthy control subjects.

Methods: Using real-time polymerase chain reaction, UCP3 gene expression was quantified. Skeletal muscle fiber type and UCP3 protein and IMTG content were measured using immunofluorescence and Oil red oil staining, respectively.

Results: The findings showed that UCP3L mRNA expression was 44% lower (P < .005) in the patients with COPD than in the control subjects, whereas the UCP3S mRNA content was similar in the two groups. As compared with control subjects, UCP3 protein content was decreased by 89% and 83% and the IMTG content by 64% and 54%, respectively, in types I and IIa fibers (P < .0167) of patients with COPD, whereas they were unchanged in IIx fibers.

Conclusions: The reduced UCP3 and IMTG content in the more oxidative fibers may be linked to the altered muscle fatty acid metabolism associated with COPD. Further studies are required to determine the exact role and clinical relevance of the reduced UCP3 content in patients with COPD.

Airway clearance of apoptotic cells in COPD

Apoptosis of bronchial epithelial cells and the phagocytic clearance of these cells by alveolar macrophages (a process termed efferocytosis) are integral processes leading to repair of airway epithelial injury. Efferocytosis allows for the removal of apoptotic material with minimal inflammation and prevents the development of secondary necrosis and ongoing inflammation. Defective efferocytosis and the increased presence of apoptotic cells have been identified in the airways of subjects with chronic obstructive pulmonary disease (COPD). There are three major potential causes for this accumulation of apoptotic cells: (i) increased apoptosis per se as a result of an increase in apoptotic mediators, (ii) defects in the recognition of apoptotic cells by AM and (iii) failure to clear the unwanted cells by the process of efferocytosis. The implications of these processes in COPD and novel treatment strategies aimed at improving clearance of apoptotic cells form the focus of the present review.

Zinc and zinc transporters in macrophages and their roles in efferocytosis in COPD

Our previous studies have shown that nutritional zinc restriction exacerbates airway inflammation accompanied by an increase in caspase-3 activation and an accumulation of apoptotic epithelial cells in the bronchioles of the mice. Normally, apoptotic cells are rapidly cleared by macrophage efferocytosis, limiting any secondary necrosis and inflammation. We therefore hypothesized that zinc deficiency is not only pro-apoptotic but also impairs macrophage efferocytosis. Impaired efferocytic clearance of apoptotic epithelial cells by alveolar macrophages occurs in chronic obstructive pulmonary disease (COPD), cigarette-smoking and other lung inflammatory diseases. We now show that zinc is a factor in impaired macrophage efferocytosis in COPD. Concentrations of zinc were significantly reduced in the supernatant of bronchoalveolar lavage fluid of patients with COPD who were current smokers, compared to healthy controls, smokers or COPD patients not actively smoking. Lavage zinc was positively correlated with AM efferocytosis and there was decreased efferocytosis in macrophages depleted of Zn in vitro by treatment with the membrane-permeable zinc chelator TPEN. Organ and cell Zn homeostasis are mediated by two families of membrane ZIP and ZnT proteins. Macrophages of mice null for ZIP1 had significantly lower intracellular zinc and efferocytosis capability, suggesting ZIP1 may play an important role. We investigated further using the human THP-1 derived macrophage cell line, with and without zinc chelation by TPEN to mimic zinc deficiency. There was no change in ZIP1 mRNA levels by TPEN but a significant 3-fold increase in expression of another influx transporter ZIP2, consistent with a role for ZIP2 in maintaining macrophage Zn levels. Both ZIP1 and ZIP2 proteins were localized to the plasma membrane and cytoplasm in normal human lung alveolar macrophages. We propose that zinc homeostasis in macrophages involves the coordinated action of ZIP1 and ZIP2 transporters responding differently to zinc deficiency signals and that these play important roles in macrophage efferocytosis.

Validation of the 12-item partners in health scale to measure patient self-management behaviour and knowledge in Dutch patients with COPD

The 12-item Partner in Health (PIH) scale was developed in Australia to measure self-management behaviour and knowledge in patients with chronic diseases. The scale has undergone several changes since first published. Our study aim was to validate the latest PIH in Dutch COPD patients.The 12 items of the PIH are scored on a self-rated 9-point Likert scale (range: 0-8; higher scores indicate better self-management), providing total and subscale scores (knowledge, coping, recognition and management of functions, adherence to treatment).We used forward-backward translation of the latest version of the Australian PIH. Dimensionality and reliability analyses were performed to investigate the psychometric properties, and to determine whether the Dutch PIH replicated the same four subscales of self-management as the original PIH.Reanalysis of the original PIH validation study (186 Australian patients with chronic diseases) showed a single scale. Two scales (1. knowledge and coping; 2. recognition and management of symptoms, adherence to treatment) were found for the Dutch PIH (118 Dutch COPD patients). The correlation between the two Dutch scales was 0.43. The lower-bound of the reliability of the total scale was 0.81 (Australian PIH) and 0.84 (Dutch PIH).Different scale structures were found for the original Australian and the Dutch PIH. Our results did not support the 4-scale structure reported previously. To increase comparability and generalisability of our findings, the scale structure of the revised Australian PIH needs to be investigated further. Meanwhile, we advise using the PIH total score or two subscale scores when assessing COPD patients.

Construct validity of the Dutch version of the 12-item Partners in Health scale : measuring self-management behaviour and knowledge in COPD patients

The 12-item Partner in Health (PIH) scale was developed in Australia to measure self-management behaviour and knowledge in patients with chronic diseases. The scale has undergone several changes since first published. Our study aim was to validate the latest PIH in Dutch COPD patients.The 12 items of the PIH are scored on a self-rated 9-point Likert scale (range: 0-8; higher scores indicate better self-management), providing total and subscale scores (knowledge, coping, recognition and management of functions, adherence to treatment).We used forward-backward translation of the latest version of the Australian PIH. Dimensionality and reliability analyses were performed to investigate the psychometric properties, and to determine whether the Dutch PIH replicated the same four subscales of self-management as the original PIH.Reanalysis of the original PIH validation study (186 Australian patients with chronic diseases) showed a single scale. Two scales (1. knowledge and coping; 2. recognition and management of symptoms, adherence to treatment) were found for the Dutch PIH (118 Dutch COPD patients). The correlation between the two Dutch scales was 0.43. The lower-bound of the reliability of the total scale was 0.81 (Australian PIH) and 0.84 (Dutch PIH).Different scale structures were found for the original Australian and the Dutch PIH. Our results did not support the 4-scale structure reported previously. To increase comparability and generalisability of our findings, the scale structure of the revised Australian PIH needs to be investigated further. Meanwhile, we advise using the PIH total score or two subscale scores when assessing COPD patients.