The clinimetric properties of the World Health Organization Disability Assessment Schedule II in early inflammatory arthritis

OBJECTIVE: To assess the clinimetric properties of a new health-related quality of life (HRQOL) instrument, the World Health Organization Disability Assessment Schedule II (WHODAS II), in patients with early inflammatory arthritis. METHODS: Internal consistency as well as criterion, construct, and discriminative validity of the WHODAS II were assessed in 172 patients with early inflammatory arthritis who completed the WHODAS II, the Medical Outcomes Study Short Form 36 (SF-36), and other measures of disease severity, functioning, pain, depression, and resource use. Test-retest reliability of the WHODAS II was assessed by having a subset of 20 patients complete the WHODAS II a second time, 1 week after the first assessment. RESULTS: The WHODAS II had high internal consistency (Cronbach's alpha = 0.96 for patients working or in school and 0.93 for patients not working or in school). Test-retest intraclass correlation coefficients of the WHODAS II total score and subscales ranged from 0.82-0.96. The WHODAS II total score was strongly correlated with the SF-36 physical component score (Kendall's tau-b 0.51, P < 0.001) and moderately correlated with the SF-36 mental component score (tau-b 0.43, P < 0.001). WHODAS II correlations with disease outcomes ranged from Kendall's tau-b 0.15-0.55. The WHODAS II significantly differentiated between every aspect of disease severity assessed with the exception of measures of health resource use. CONCLUSION: The WHODAS II is a valid and reliable measure of HRQOL in cross-sectional studies of patients with early inflammatory arthritis. Research is still required to investigate potential item redundancy and determine its usefulness in longitudinal studies.     

Aerosolized metaproterenol in the treatment of asthmatics with severe airflow obstruction. Comparison of two delivery methods

The bronchodilator response to metaproterenol delivered by metered-dose inhaler (MDI) with a spacer device (Aerochamber [A]) and by jet nebulizer was studied in 44 asthmatic patients who presented to the emergency department with acute severe (FEV1 less than 50 percent predicted) airflow obstruction. The delivery method was randomized, double-blinded and placebo controlled. The A group received one puff of metaproterenol every five minutes for a total of three puffs (1.95 mg). The jet nebulizer group received 15 mg of metaproterenol by continuous nebulization over ten minutes. Only about 2.75 mg of the original 15 mg delivered by jet nebulizer was calculated to be available for inhalation due to the inefficiencies of the delivery system. The mean percentage of improvement in FVC and FEV1 in the A group was 33.5 and 49.0 percent, respectively. The mean percentage of improvement in FVC and FEV1 in the jet nebulizer group was 22.8 and 33.0 percent, respectively. There was no significant difference in the mean percentage of improvement values between the two groups. We were unable to demonstrate a difference in bronchodilator response to metaproterenol delivered by MDI-A and jet nebulizer in emergency department asthmatics with acute severe airflow obstruction.     

Diverse mechanisms underlying the regulation of ion channels by carbon monoxide

Carbon monoxide (CO) is firmly established as an important, physiological signalling molecule as well as a potent toxin. Through its ability to bind metal-containing proteins, it is known to interfere with a number of intracellular signalling pathways, and such actions can account for its physiological and pathological effects. In particular, CO can modulate the intracellular production of reactive oxygen species, NO and cGMP levels, as well as regulate MAPK signalling. In this review, we consider ion channels as more recently discovered effectors of CO signalling. CO is now known to regulate a growing number of different ion channel types, and detailed studies of the underlying mechanisms of action are revealing unexpected findings. For example, there are clear areas of contention surrounding its ability to increase the activity of high conductance, Ca²⁺-sensitive K⁺ channels. More recent studies have revealed the ability of CO to inhibit T-type Ca²⁺ channels and have unveiled a novel signalling pathway underlying tonic regulation of this channel. It is clear that the investigation of ion channels as effectors of CO signalling is in its infancy, and much more work is required to fully understand both the physiological and the toxic actions of this gas. Only then can its emerging use as a therapeutic tool be fully and safely exploited.

Linked Articles

This article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-6     

Magnetic field interactions between current consumer electronics and cardiac implantable electronic devices

Journal of Interventional Cardiac Electrophysiology - Ablation index (AI) is a radiofrequency lesion quality marker. The AI value that allows effective and safe pulmonary vein isolation (PVI) is...     

Oxygen cost of exercise is increased in heart failure after accounting for recovery costs

STUDY OBJECTIVES: The oxygen cost during exercise has been reported to be decreased in patients with congestive heart failure (CHF), implying an increased efficiency (lower oxygen uptake [VO(2)] per Watt [VO(2)/W]); however, these studies ignored the oxygen debt that is increased in heart failure. SUBJECTS: The primary aim of this research was to evaluate the total oxygen cost (work VO(2)/W) during exercise and recovery in patients with heart failure as compared with healthy adults. DESIGN AND PATIENTS: We performed a retrospective analysis comparing the exercise VO(2)/W, the recovery VO(2)/W, the work VO(2)/W, and the VO(2)/W relationship above and below the ventilatory threshold (VT) in 11 healthy control subjects and 45 patients with CHF. RESULTS: The exercise VO(2)/W was decreased by 29% (p < 0.0001) in patients with CHF; however, the recovery VO(2)/W was increased by 167% (p < 0.0001) and the work VO(2)/W was increased by 14% in patients with CHF (p = 0.014). The VO(2)/W slope increased above the VT (+ 27%, p = 0.0017) in both normal subjects and patients with CHF, suggesting a decrease in efficiency above the VT. There was an inverse correlation (r = 0.646, p < 0.0001) between exercise VO(2)/W and recovery VO(2)/W, implying that subjects with a low exercise VO(2)/W were not efficient but rather accumulated a large oxygen debt that was repaid following completion of exercise. CONCLUSIONS: Heart failure is associated with lower exercise VO(2)/W; however, the patient with heart failure is not efficient, but rather accumulating a large oxygen debt (recovery VO(2)/W) that is repaid following exercise. In addition, the work VO(2)/W (including both exercise and recovery) is increased in patients with heart failure in comparison to control subjects, and correlates inversely with the percentage of predicted VO(2). The large recovery VO(2)/W is likely due to impaired oxygen delivery to exercising muscle during exercise. The increase in the work VO(2)/W is probably due to changes in skeletal muscle fiber type that occur in patients with heart failure (type I to type IIb).