Are sleep disorders associated with increased mortality in asthma patients?

Juan Carlos Ivancevich Friday, 25 November 2016 21:36
Kyu-Tae Han, Hong-Chul Bae, Sang Gyu Lee, Seung Ju Kim, Woorim Kim, Hyo Jung Lee, Yeong Jun Ju and Eun-Cheol Park
Contributed equally
 

Abstract

Background

South Korea has experienced problems regarding poor management of symptoms of asthma patients and remarkable increases in sleep disorders. However, few studies have investigated these issues. We examined the relationship between sleep disorders and mortality in asthma patients to suggest effective alternatives from a novel perspective.

Methods

We used data from the National Health Insurance Service (NHIS) National Sample Cohort 2004–2013, which included medical claims filed for 186,491 patients who were newly diagnosed with asthma during the study period. We performed survival analyses using a Cox proportional hazards model with time-dependent covariates to examine the relationship between sleep disorders and mortality in asthma patients.

Results

There were 5179 (2.78%) patients who died during the study period. Sleep disorders in patients previously diagnosed with asthma were associated with a higher risk of mortality (hazard ratio [HR]: 1.451, 95% confidence interval [CI]: 1.253–1.681). In addition, significant interaction was found between sleep disorders and Charlson comorbidity index.

Conclusions

Our findings suggest that an increased prevalence of sleep disorders in asthma patients increases the risk of mortality. Considering the worsening status of asthma management and the rapid growth of sleep disorders in South Korea, clinicians and health policymakers should work to develop interventions to address these issues. 

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Risk of asthma in patients with primary Sjögren’s syndrome: a retrospective cohort study

Juan Carlos Ivancevich Tuesday, 22 November 2016 14:06
Te-Chun ShenHsuan-Ju ChenChang-Ching WeiChia-Hung ChenChih-Yen TuTe-Chun HsiaChuen-Ming ShihWu-Huei HsuFung-Chang SungEmail author and Da-Tian Bau† This email address is being protected from spambots. You need JavaScript enabled to view it.

Abstract

Background

Sjögren’s syndrome (SS) has been associated with bronchial hyperresponsiveness and asthma; however, no population-based cohort study has been performed. We evaluated the risk of asthma in patients with primary SS in a nationwide population.

Methods

We conducted a retrospective cohort study using data from the National Health Insurance Research Database in Taiwan. The primary SS group included 4725 adult patients diagnosed between 2000 and 2006. Each patient was frequency-matched with four people without SS by sex, age and year of diagnosis. The occurrence and hazard ratio (HR) of asthma was monitored by the end of 2011.

Results

The overall incidence density of asthma was 1.62-fold higher in the primary SS group than in the non-SS group (9.86 vs. 6.10 per 1000 person-years), with a multivariable Cox proportional hazards model measured adjusted HR of 1.38 [95% confidence interval (CI) = 1.21–1.58]. Stratified analyses by sex, age group, and presence of comorbidity revealed that asthma incidences were all higher in the primary SS group than in the non-SS group, and the relative HRs of asthma associated with primary SS were significant in all subgroups.

Conclusion

Patients with primary SS are associated with an increased risk of developing asthma. We should pay more attention to this group of individuals and provide them with appropriate support.

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Anti-inflammatory potential of PI3Kδ and JAK inhibitors in asthma patients

Juan Carlos Ivancevich Monday, 14 November 2016 23:54
Thomas Southworth Email author, Jonathan Plumb, Vandana Gupta, James Pearson, Isabel Ramis, Martin D. Lehner, Montserrat Miralpeix and Dave Singh
 

Abstract

Background

Phosphatidylinositol 3-kinase delta (PI3Kδ) and Janus-activated kinases (JAK) are both novel anti-inflammatory targets in asthma that affect lymphocyte activation. We have investigated the anti-inflammatory effects of PI3Kδ and JAK inhibition on cytokine release from asthma bronchoalveolar lavage (BAL) cells and T-cell activation, and measured lung PI3Kδ and JAK signalling pathway expression.

Method

Cells isolated from asthma patients and healthy subjects were treated with PI3Kδ or JAK inhibitors, and/or dexamethasone, before T-cell receptor stimulation. Levels of IFNγ, IL-13 and IL-17 were measured by ELISA and flow cytometry was used to assess T-cell activation. PI3Kδ, PI3Kγ, phosphorylated protein kinase B (pAKT) and Signal Transducer and Activator of Transcription (STAT) protein expression were assessed by immunohistochemistry in bronchial biopsy tissue from asthma patients and healthy subjects. PI3Kδ expression in BAL CD3 cells was measured by flow cytometry.

Results

JAK and PI3Kδ inhibitors reduced cytokine levels from both asthma and healthy BAL cells. Combining dexamethasone with either a JAK or PI3Kδ inhibitor showed an additive anti-inflammatory effect. JAK and PI3Kδ inhibitors were shown to have direct effects on T-cell activation. Immunohistochemistry showed increased numbers of PI3Kδ expressing cells in asthma bronchial tissue compared to controls. Asthma CD3 cells in BAL expressed higher levels of PI3Kδ protein compared to healthy cells.

Conclusions

Targeting PI3Kδ or JAK may prove effective in reducing T-cell activation and the resulting cytokine production in asthma.

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Development of New Therapies for Severe Asthma

Juan Carlos Ivancevich Tuesday, 15 November 2016 04:46

Allergy Asthma Immunol Res. 2017 Jan;9(1):3-14. English.

  Open Access

Merritt L. Fajt and Sally E. Wenzel

Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh Asthma Institute at UPMC/University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. 

Abstract

Persistent asthma has long been treated with inhaled corticosteroids (CSs), as the mainstay of therapy. However, their efficacy in patients with more severe disease is limited, which led to the incorporation of poor response to ICSs (and thereby use of high doses of ICS) into recent definitions of severe asthma. Several studies have suggested that severe asthma might consist of several different phenotypes, each with ongoing symptoms and health care utilization, despite the use of high doses of ICS, usually in combination with a second or third controller. Several new therapies have been approved for severe asthma. Long-acting muscarinic agents have recently been approved as an additional controller agent and appear to improve lung function, although their effect on symptoms and exacerbations is less. Although bronchial thermoplasty (BT) has emerged as a therapy for severe asthma, little is understood regarding the appropriate selection of these patients. Considerable data have emerged to support the presence of a group of patients with severe asthma who have ongoing Type 2 inflammation. These patients appear to respond to targeted biologic approaches which are at the current time mostly investigational. In contrast, few effective therapies for patients with less or no evidence for Type 2 inflammation have emerged. Many new and exciting therapies are at the forefront for severe asthma therapy and, in conjunction with precision medicine approaches to identify the group of patients likely to respond to these approaches, will change the way we think about treating severe asthma.

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Air pollution, epigenetics, and asthma

Juan Carlos Ivancevich Tuesday, 08 November 2016 13:05

Hong Ji, Jocelyn M. Biagini Myers, Eric B. Brandt, Cole Brokamp, Patrick H. Ryan and Gurjit K. Khurana Hershey

Abstract

Exposure to traffic-related air pollution (TRAP) has been implicated in asthma development, persistence, and exacerbation. This exposure is highly significant as large segments of the global population resides in zones that are most impacted by TRAP and schools are often located in high TRAP exposure areas. Recent findings shed new light on the epigenetic mechanisms by which exposure to traffic pollution may contribute to the development and persistence of asthma. In order to delineate TRAP induced effects on the epigenome, utilization of newly available innovative methods to assess and quantify traffic pollution will be needed to accurately quantify exposure. This review will summarize the most recent findings in each of these areas. Although there is considerable evidence that TRAP plays a role in asthma, heterogeneity in both the definitions of TRAP exposure and asthma outcomes has led to confusion in the field. Novel information regarding molecular characterization of asthma phenotypes, TRAP exposure assessment methods, and epigenetics are revolutionizing the field. Application of these new findings will accelerate the field and the development of new strategies for interventions to combat TRAP-induced asthma.

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Editor: Juan C. Ivancevich, MD

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