ObjectiveTo assess the impact of home telemonitoring on health service use and quality of life in patients with severe chronic lung disease.DesignRandomised crossover trial with 6 months of standard best practice clinical care (control group) and 6 months with the addition of telemonitoring.Participants68 patients with chronic lung disease (38 with COPD; 30 with chronic respiratory failure due to other causes), who had a hospital admission for an exacerbation within 6 months of randomisation and either used long-term oxygen therapy or had an arterial oxygen saturation (SpO2) of <90% on air during the previous admission. Individuals received telemonitoring (second-generation system) via broadband link to a hospital-based care team.Outcome measuresPrimary outcome measure was time to first hospital admission for an acute exacerbation. Secondary outcome measures were hospital admissions, general practitioner (GP) consultations and home visits by nurses, quality of life measured by EuroQol-5D and hospital anxiety and depression (HAD) scale, and self-efficacy score (Stanford).ResultsMedian (IQR) number of days to first admission showed no difference between the two groups—77 (114) telemonitoring, 77.5 (61) control (p=0.189). Hospital admission rate at 6 months increased (0.63 telemonitoring vs 0.32 control p=0.026). Home visits increased during telemonitoring; GP consultations were unchanged. Self-efficacy fell, while HAD depression score improved marginally during telemonitoring.ConclusionsTelemonitoring added to standard care did not alter time to next acute hospital admission, increased hospital admissions and home visits overall, and did not improve quality of life in chronic respiratory patients.Trial registration numberNCT02180919 (ClinicalTrials.gov).
Acetaminophen is one of the most commonly used drugs for the safe and effective treatment of pain and fever. Acetaminophen works by lowering cyclo-oxygenase products preferentially in the central nervous system, where oxidant stress is strictly limited. However, the precise mechanism of action for acetaminophen on cyclo-oxygenase activity is debated. Two theories prevail. First, it is suggested that acetaminophen selectively inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3. Second, it is suggested that acetaminophen has no affinity for the active site of cyclo-oxygenase but instead blocks activity by reducing the active oxidized form of cyclo-oxygenase to an inactive form. Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with IL-1beta) to show that acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells. However, acetaminophen, unlike nonsteroidal anti-inflammatory drugs (NSAIDs), cannot inhibit activity in broken cell preparations. The inhibitory effects of acetaminophen were abolished by increasing intracellular oxidation conditions with the cell-permeable hydroperoxide t-butylOOH. Similarly the inhibitory effects of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen and naproxen were significant reduced by t-butylOOH. By contrast, the inhibitory effects of indomethacin or diclofenac, which also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected by t-butylOOH. These observations dispel the notion that cyclo-oxygenase-3 is involved in the actions of acetaminophen and provide evidence that supports the theory that acetaminophen interferes with the oxidation state of cyclo-oxygease. Moreover, they suggest for the first time that the inhibitory effects of some NSAIDs, including the newly introduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe part of their inhibitory actions to effects on oxidation state of cyclo-oxygenase. Our data with t-butylOOH and NSAIDs illustrates an, as yet, undeveloped therapeutic window for the "cyclo-oxygenase inhibitor". Specifically, combining active site selectively with actions on enzyme oxidation state would allow for a broader range of tissue selective drugs.
Recent data have suggested that regular consumption of nonsteroid anti-inflammatory drugs (NSAIDs), particularly selective inhibitors of cyclo-oxygenase-2 (COX-2), is associated with an increased risk of thrombotic events. It has been suggested that this is due to NSAIDs reducing the release from the endothelium of the antithrombotic mediator prostaglandin I2 as a result of inhibition of endothelial COX-2. Here, however, we show that despite normal human vessels and endothelial cells containing cyclo-oxygenase-1 (COX-1) without any detectable COX-2, COX-1 in vessels or endothelial cells is more readily inhibited by NSAIDs and COX-2-selective drugs than COX-1 in platelets (e.g., log IC50+/-SEM values for endothelial cells vs. platelets: naproxen -5.59+/-0.07 vs. -4.81+/-0.04; rofecoxib -4.93+/-0.04 vs. -3.75+/-0.03; n=7). In broken cell preparations, the selectivities of the tested drugs toward endothelial cell over platelet COX-1 were lost. These observations suggest that variations in cellular conditions, such as endogenous peroxide tone and substrate supply, and not the isoform of cyclo-oxygenase present, dictate the effects of NSAIDs on endothelial cells vs. platelets. This may well be because the platelet is not a good representative of COX-1 activity within the body as it produces prostanoids in an explosive burst that does not reflect tonic release from other cells. The results reported here can offer an explanation for the apparent ability of NSAIDs and COX-2-selective inhibitors to increase the risk of myocardial infarction and stroke.
AimsImproving quality of life (QoL) in heart failure patients is a key management objective. Validated health‐related QoL (HR‐QoL) measurement tools have been incorporated into clinical trials but not routinely into daily practice. The aims of this study were to investigate the acceptability and feasibility of implementing validated HR‐QoL instruments into heart failure clinics and to examine the impact of patient characteristics on HR‐QoL.Methods and resultsOne hundred and sixty‐three patients attending heart failure clinics at a UK tertiary centre were invited to complete three HR‐QoL assessments: the Minnesota Living with Heart Failure Questionnaire (MLHFQ); the EuroQoL 5D‐3L (EQ‐5D‐3L); and the Kansas City Cardiomyopathy Questionnaire (KCCQ) in that order. Data on patient demographics, co‐morbidities, New York Heart Association (NYHA) class, plasma B‐type natriuretic peptide (BNP), renal function, and left ventricular ejection fraction were recorded. 94% of patients attending clinic were willing to participate. The EQ‐5D‐3L had all questions answered by 92% of patients, compared with 86% and 51% for the MLHFQ and KCCQ, respectively. HR‐QoL significantly correlated with NYHA class using each tool (MLHFQ, r = 0.59; KCCQ, r = −0.61; EQ‐5D‐3L, r = −0.44, all P < 0.01). However, within each NYHA class, there was a widespread of HR‐QoL scores. There was no association between patient demographics, left ventricular ejection fraction, plasma B‐type natriuretic peptide, or renal function with HR‐QoL using any tool.ConclusionsHealth‐related QoL assessment by validated questionnaire was acceptable to patients and feasible to perform in routine practice. Although NYHA class correlated significantly with HR‐QoL scores, there was high variability in HR‐QoL within each NYHA class, highlighting its limitation as the sole assessment of HR‐QoL. Clinicians should encourage the assessment of HR‐QoL to facilitate patient‐centred care and make more specific use of HR‐QoL measurement tools.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.