The preventable burden of productivity loss due to suboptimal asthma control: a population-based study.

Chest

Institute for Heart and Lung Health, Department of Medicine, University of British Columbia, Vancouver, BC, Canada; Centre for Clinical Epidemiology and Evaluation, University of British Columbia, Vancouver, BC, Canada.

Published: April 2014

Background: Productivity loss is an overlooked aspect of the burden of chronic health conditions. While modern guidelines emphasize achieving clinical control in asthma management, few studies have reported on the relationship between asthma control and productivity loss. We calculated the productivity loss that can be avoided by achieving and maintaining clinical control in employed adults with asthma.

Methods: We prospectively recruited a population-based random sample of adults with asthma in British Columbia, Canada. We measured productivity loss due to absenteeism and presenteeism using validated instruments, and ascertained asthma control according to the GINA (Global Initiative for Asthma) classification. We estimated the average gain in productivity for each individual if the individual’s asthma was controlled in the past week, by fitting two-part regression models associating asthma control and productivity loss, controlling for potential confounding variables.

Results: The final sample included 300 employed adults (mean age, 47.9 years [SD 12.0]; 67.3% women). Of these, 49 (16.3%) reported absenteeism, and 137 (45.7%) reported presenteeism. Productivity loss due to presenteeism, but not absenteeism, was associated with asthma control. A person with uncontrolled asthma would avoid $184.80 (Canadian dollars [CAD]) in productivity loss by achieving clinical control during a week, CAD$167.50 (90.6%) of which would be due to presenteeism. The corresponding value was CAD$34.20 for partially controlled asthma and was not statistically significant.

Conclusions: Our results indicate that substantial gain in productivity can be obtained by achieving asthma control. Presenteeism is more responsive than absenteeism to asthma control, and, thus, is a more important source of preventable burden.

Download full-text PDF

Source
http://dx.doi.org/10.1378/chest.13-1619DOI Listing

Publication Analysis

Top Keywords

productivity loss
32
asthma control
28
asthma
13
clinical control
12
productivity
10
control
10
preventable burden
8
loss
8
achieving clinical
8
control productivity
8

Similar Publications

Background: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).

View Article and Find Full Text PDF

Background: Alzheimer's disease (AD) is a neurodegenerative disorder without a cure. Targeting this multifactorial disease by repurposing FDA approved drugs serves as a faster mode of treatment due to its pre-established human safety. We tested terazosin (TZ), an a-1 adrenergic receptor (AR) antagonist and phosphoglycerate kinase-1 (PGK1) activator as having potential to treat AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Retromer Therapeutics, New York, NY, USA.

Background: Genetic studies have established that loss of function SORL1 gene variants are associated with Alzheimer's disease (AD). SORL1 encodes an endosomal trafficking receptor, SORLA, which regulates endosomal protein recycling through its interaction with the retromer core complex (consisting of VPS26, VPS35 and VPS29). Deficits in the levels and function of the SORLA-retromer complex are thought to underlie AD.

View Article and Find Full Text PDF

Background: Alzheimer's disease (AD) is the most common cause of age-related dementia, and the presence of amyloid-β (Aβ) plaques and tau-containing neurofibrillary tangles is associated with the neurodegeneration and cognitive impairment in this incurable disease. Growing evidence shows that epigenetic dysregulation through histone deacetylases (HDACs) plays a critical role in synaptic dysfunction and memory loss in AD, and HDACs have been highlighted as a novel class of anti-Alzheimer targets. Moreover, restoring Wnt/β-catenin signaling, which is greatly suppressed in AD brains, is a promising therapeutic strategy for AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Merck & Co., Inc., Rahway, NJ, USA.

Background: Recent anti-amyloid mAb trial results demonstrate slowing of Alzheimer's disease progression, but to date do not fully halt or reverse this progression. Optimization of anti-amyloid therapy (timing and duration of intervention, modality, combinations, biomarker guidance) is limited by incomplete understanding of the disease, such as relationship between amyloid and tau pathways. Mechanistic Alzheimer's progression modeling investigated how amyloid and tau pathologies are connected in driving progression.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!