No clinical meaningful differences were found between treatment conditions in the primary outcome measures health-related quality of life and disability. However, this is the first long-term RCT that has shown that PMT improves BA in patients with chronic pain and shows good effect size and a significant decrease for catastrophizing.

Abstract-The construct validity and construct responsiveness of the performance scale of the Canadian Occupational Performance Measure (COPM) was measured in 87 newly admitted patients with chronic pain attending an outpatient rehabilitation clinic. At admission and after 12 wk, patients completed a COPM interview, the Pain Disability Index (PDI), and the RAND 36-Item Health Survey (RAND-36). We determined the construct validity of the COPM by correlations between the COPM performance scale (COPM-P), the PDI, and the RAND-36 at admission. Construct responsiveness was assessed by calculating the correlations between the change scores (n = 57). The COPM-P did not significantly correlate with the PDI (r = 0.260) or with any subscale of the RAND-36 (r = 0.007 to 0.248). Only a moderate correlation was found between change scores of the COPM-P and PDI (r = 0.380) and weak to moderate correlations were found between change scores of the COPM-P and the RAND-36 (r = 0.031 to 0.388), with the higher correlations for the physical functioning, social functioning, and role limitations (physical) subscales. In patients with chronic pain attending our rehabilitation program, the COPM-P measures something different than the RAND-36 or PDI. Therefore, construct validity of the COPM-P was not confirmed by our data. We were not able to find support for the COPM-P to detect changes in occupational performance.

Self-efficacy beliefs are an important psychosocial determinant of pain behavior and predict the outcome of pain management programs. Participants in these programs are challenged to live a life as normal as possible despite the pain. In view of the continuous presence of pain, self-efficacy measurement should take this into account. The Pain Self-Efficacy Questionnaire (PSEQ) asks participants to take the pain into account when rating their self-efficacy beliefs. In the present study, this questionnaire is examined on its psychometric qualities. The study also examines self-efficacy as an independent predictor of outcome measures after controlling for pain intensity. 278 chronic pain patients participate in this study, divided into two samples. Exploratory and confirmatory factor analysis supported a 1-factor solution. Internal consistency was excellent, and test-retest reliability was adequate. Regression analysis showed that pain self-efficacy was an independent predictor of disability and quality of life after controlling for pain intensity. Furthermore, the PSEQ discriminated between workers and nonworkers, and between patients who used medication and those who did not.

BA might be an important target of treatment to improve the multidisciplinary treatment outcome in chronic pain patients. Furthermore, PMT is an intervention that seems to provide its benefits through improving BA and may be especially beneficial for patients with low BA.

Idiopathic pulmonary fibrosis (IPF) has a detrimental prognosis despite antifibrotic therapies to which individual responses vary. IPF pathology is associated with oxidative stress, inflammation and increased activation of SRC family kinases (SFK). This pilot study evaluates individual responses to pirfenidone, nintedanib and SFK inhibitor saracatinib, markers of redox homeostasis, fibrosis and inflammation, in IPF-derived human bronchial epithelial (HBE) cells. Differentiated HBE cells from patients with and without IPF were analyzed for potential alterations in redox and profibrotic genes and pro-inflammatory cytokine secretion. Additionally, the effects of pirfenidone, nintedanib and saracatinib on these markers were determined. HBE cells were differentiated into a bronchial epithelium containing ciliated epithelial, basal, goblet and club cells. NOX4 expression was increased in IPF-derived HBE cells but differed on an individual level. In patients with higher NOX4 expression, pirfenidone induced antioxidant gene expression. All drugs significantly decreased NOX4 expression. IL-6 (p = 0.09) and IL-8 secretion (p = 0.014) were increased in IPF-derived HBE cells and significantly reduced by saracatinib. Finally, saracatinib significantly decreased TGF-β gene expression. Our results indicate that treatment responsiveness varies between IPF patients in relation to their oxidative and inflammatory status. Interestingly, saracatinib tends to be more effective in IPF than standard antifibrotic drugs.

No abstract