Costs of asthma in the United States: 2002-2007

Barnett, Stephen; Nurmagambetov, Tursynbek

doi:10.1016/j.jaci.2010.10.020

Cited by 535 publications

(386 citation statements)

References 57 publications

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“…Asthma presents a substantial economic and financial burden to industrialized and developing countries (2), with direct health care costs reaching approximately $50 billion annually in the United States alone (3). The management of asthma includes inhaled corticosteroids to combat inflammation and b2-agonist bronchodilators to reverse airway smooth muscle (ASM) bronchoconstriction.…”

mentioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

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The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor b1 (TGF-b1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-b1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-b1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-b1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-b1 as a potential therapeutic target for reducing asthma morbidity and mortality.

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mentioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

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“…Exacerbations, the worsening of asthma symptoms, are a growing public health concern, resulting in millions of missed work and school days and $50 billion in direct healthcare costs in the United States each year (3)(4)(5). Prior studies have examined environmental correlates of asthma exacerbations, including air quality measures (6)(7)(8), whereas others have considered the role of respiratory virus infections in triggering asthma exacerbation (9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

Respiratory virus transmission dynamics determine timing of asthma exacerbation peaks: Evidence from a population-level model

Eggo

Scott

Galvani

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Asthma exacerbations exhibit a consistent annual pattern, closely mirroring the school calendar. Although respiratory viruses-the "common cold" viruses-are implicated as a principal cause, there is little evidence to link viral prevalence to seasonal differences in risk. We jointly fit a common cold transmission model and a model of biological and environmental exacerbation triggers to estimate effects on hospitalization risk. Asthma hospitalization rate, influenza prevalence, and air quality measures are available, but common cold circulation is not; therefore, we generate estimates of viral prevalence using a transmission model. Our deterministic multivirus transmission model includes transmission rates that vary when school is closed. We jointly fit the two models to 7 y of daily asthma hospitalizations in adults and children (66,000 events) in eight metropolitan areas. For children, we find that daily viral prevalence is the strongest predictor of asthma hospitalizations, with transmission reduced by 45% (95% credible interval =41-49%) during school closures. We detect a transient period of nonspecific immunity between infections lasting 19 (17-21) d. For adults, hospitalizations are more variable, with influenza driving wintertime peaks. Neither particulate matter nor ozone was an important predictor, perhaps because of the large geographic area of the populations. The school calendar clearly and predictably drives seasonal variation in common cold prevalence, which results in the "back-to-school" asthma exacerbation pattern seen in children and indirectly contributes to exacerbation risk in adults. This study provides a framework for anticipating the seasonal dynamics of common colds and the associated risks for asthmatics.

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“…Although only 10% of patients have severe, uncontrolled, persistent asthma, these patients account for an estimated 80% of the economic burden of healthcare costs attributed to this disease (2,3). One key pathogenic feature is chronic airway inflammation stemming from the infiltration of eosinophils and Th2 cells into the airways (4) that contribute significantly to the immune response in asthma (5,6).…”

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confidence: 99%

Airway Inflammation after Bronchial Thermoplasty for Severe Asthma

et al. 2015

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Rationale: Bronchial thermoplasty is an alternative treatment for patients with severe, uncontrolled asthma in which the airway smooth muscle is eliminated using radioablation. Although this emerging therapy shows promising outcomes, little is known about its effects on airway inflammation.Objectives: We examined the presence of bronchoalveolar lavage cytokines and expression of smooth muscle actin in patients with severe asthma before and in the weeks after bronchial thermoplasty.Methods: Endobronchial biopsies and bronchoalveolar lavage samples from 11 patients with severe asthma were collected from the right lower lobe before and 3 and 6 weeks after initial bronchial thermoplasty. Samples were analyzed for cell proportions and cytokine concentrations in bronchoalveolar lavage and for the presence of a-SMA in endobronchial biopsies.Measurements and Main Results: a-SMA expression was decreased in endobronchial biopsies of 7 of 11 subjects by Week 6. In bronchoalveolar lavage fluid, both transforming growth factor-b 1 and regulated upon activation, normal T-cell expressed and secreted (RANTES)/CCL5 were substantially decreased 3 and 6 weeks post bronchial thermoplasty in all patients. The cytokine tumor-necrosisfactor-related apoptosis-inducing ligand (TRAIL), which induces apoptosis in several cell types, was increased in concentration both 3 and 6 weeks post bronchial thermoplasty.Conclusions: Clinical improvement and reduction in a-SMA after bronchial thermoplasty in severe, uncontrolled asthma is associated with substantial changes in key mediators of inflammation. These data confirm the substantial elimination of airway smooth muscle post thermoplasty in the human asthmatic airway and represent the first characterization of significant changes in airway inflammation in the first weeks after thermoplasty.

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Costs of asthma in the United States: 2002-2007

Cited by 535 publications

References 57 publications

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Respiratory virus transmission dynamics determine timing of asthma exacerbation peaks: Evidence from a population-level model

Airway Inflammation after Bronchial Thermoplasty for Severe Asthma

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