A joint ERS/ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework

Juan Carlos Ivancevich Monday, 13 November 2017 23:32
 
George D. ThurstonHoward KipenIsabella Annesi-MaesanoJohn BalmesRobert D. BrookKevin CromarSara De MatteisFrancesco ForastiereBertil ForsbergMark W. FramptonJonathan GriggDick HeederikFrank J. KellyNino KuenzliRobert LaumbachAnnette PetersSanjay T. RajagopalanDavid RichBeate RitzJonathan M. SametThomas SandstromTorben SigsgaardJordi SunyerBert Brunekreef

Abstract

The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.

This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution.

 

Response to case report: Airway autoimmune responses in severe eosinophilic asthma following low-dose Mepolizumab therapy

Juan Carlos Ivancevich Sunday, 05 November 2017 19:55

Allergy, Asthma & Clinical Immunology 2017, 13:45 | Published on: 3 November 2017

I. J. Pouliquen, P. Howarth, D. Austin, G. Gunn, E. Meyer, R. G. Price and E. Bradford

To the Editor,

We read with interest the case report and accompanying discussion published by Mukherjee et al. (AACI 2017;13:2) of a 62-year old woman diagnosed with severe eosinophilic asthma. This clinical case presents a patient with progressive deterioration in FEV1 function since 2011 with no improvement observed while receiving OCS, hydroxyurea or imatinib therapy. On this background of deterioration, the patient entered the double-blind placebo controlled clinical trial MEA115575 and received mepolizumab 100 mg s.c. every 4 weeks. Further deterioration in FEV1 coincided with the (protocol defined) reduction in prednisolone during the study, and neither intravenous solumedrol nor pre-study prednisolone doses improved FEV1 to pre-study values. During the open-label mepolizumab extension study MEA115661 the patient’s clinical status was unchanged. In January 2015, 9 months after their last dose of mepolizumab, the patient further deteriorated whilst receiving azathioprine immunosuppressive therapy. This clinical case presentation clearly underlines the aggressive nature...

 

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Bronchial thermoplasty: When is it needed to treat asthma | Prof. Thomas B Casale

Juan Carlos Ivancevich Tuesday, 24 October 2017 13:58


Prognostic nomogram for inpatients with asthma exacerbation

Juan Carlos Ivancevich Thursday, 02 November 2017 11:25
Wakae Hasegawa,Yasuhiro Yamauchi Email author,Hideo Yasunaga,Hideyuki Takeshima,Yukiyo Sakamoto,Taisuke Jo,Yusuke Sasabuchi,Hiroki Matsui,Kiyohide Fushimi and Takahide Nagase

Abstract

Background

Asthma exacerbation may require a visit to the emergency room as well as hospitalization and can occasionally be fatal. However, there is limited information about the prognostic factors for asthma exacerbation requiring hospitalization, and no methods are available to predict an inpatient’s prognosis. We investigated the clinical features and factors affecting in-hospital mortality of patients with asthma exacerbation and generated a nomogram to predict in-hospital death using a national inpatient database in Japan.

Methods

We retrospectively collected data concerning hospitalization of adult patients with asthma exacerbation between July 2010 and March 2013 using the Japanese Diagnosis Procedure Combination database. We recorded patient characteristics and performed Cox proportional hazards regression analysis to assess the factors associated with all-cause in-hospital mortality. Then, we constructed a nomogram to predict in-hospital death.

Results

A total of 19,684 patients with asthma exacerbation were identified; their mean age was 58.8 years (standard deviation, 19.7 years) and median length of hospital stay was 8 days (interquartile range, 5–12 days). Among study patients, 118 died in the hospital (0.6%). Factors associated with higher in-hospital mortality included older age, male sex, reduced level of consciousness, pneumonia, and heart failure. A nomogram was generated to predict the in-hospital death based on the existence of seven variables at admission. The nomogram allowed us to estimate the probability of in-hospital death, and the calibration plot based on these results was well fitted to predict the in-hospital prognosis.

Conclusion

Our nomogram allows physicians to predict individual risk of in-hospital death in patients with asthma exacerbation.

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Asthma with bronchial hypersecretion: expression of mucins and toll-like receptors in sputum and blood

Juan Carlos Ivancevich Tuesday, 24 October 2017 12:44

Authors Crespo-Lessmann A, Mateus E, Torrejón M, Belda A, Giner J, Vidal S, Sibila O, Plaza V

Published 12 October 2017 Volume 2017:10 Pages 269—276

DOI https://doi.org/10.2147/JAA.S142200

Astrid Crespo-Lessmann,1 Eder Mateus,1,2Montserrat Torrejón,1 Alicia Belda,1 Jordi Giner,1Silvia Vidal,2 Oriol Sibila,1 Vicente Plaza,1

1Service of Pneumology, Hospital de la Santa Ceu i Sant Pau, Institute of Sant Pau Biomedical Research (IBB Sant Pau), Universitat Autònoma de Barcelona, Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), 2Department of Immunology, Hospital de la Santa Creu i Sant Pau, Institut d’Investigació Biomédica Sant Pau, Barcelona, Spain

Abstract: Asthma with bronchial hypersecretion is a type of asthma that is poorly studied. Its pathogenesis is not well understood, but is probably related to innate impaired immunity, particularly with toll-like receptors (TLRs) and secretory mucins (MUC).
Objectives: 1) Define the clinical and inflammatory phenotype of asthma with bronchial hypersecretion of mucus. 2) Compare the type of mucin present in induced sputum (IS) of patients with and without bronchial hypersecretion. 3) Determine the expression of TLRs in IS and blood of asthmatics with and without bronchial hypersecretion.
Materials and methods:
 Cross-sectional study which included 43 non-smoking asthmatic patients without bronchiectasis, 19 with bronchiectasis, and 24 without bronchial hypersecretion. All patients underwent the following: IS, spirometry, fractional exhaled nitric oxide, prick test, total immunoglobulin E (IgE), and blood albumin. Analysis of mucins was determined by ELISA and expression of TLR2 and TLR4 by flow cytometry. The level of asthma control was determined by the Asthma Control Test (ACT) questionnaire and quality of life was assessed by the reduced version of the Asthma Quality of Life Questionnaire (mini-AQLQ).
Results: Asthmatics with bronchial hypersecretion were significantly older (62.6 years vs 48.5 years; p=0.02); had greater severity (persistent severe asthma 94.7% vs 29.2%; p=0.000); a higher proportion of nasal polyposis (36.8% vs 8.3%; p=0.022); less control of asthma (73.7% vs 8.3%; p=0,000); a higher proportion of asthma with negative prick test (68.4% vs 16.6%; p=0.001), and lower levels of IgE (113.4 IU/mL vs 448 IU/mL; p=0.007), compared with asthmatics without bronchial hypersecretion. Significant differences were observed neither in the expression of  TLRs 2 and 4 in inflammatory cells of IS or peripheral blood, nor in the expression of mucins between both groups.
Conclusion: Asthma patients with bronchial hypersecretion have more severe and uncontrolled disease, with poor quality of life as well as a non-allergic inflammatory phenotype. Within the mechanisms involving these differences, it does not appear that mucins and TLRs play an important role.

Keywords: asthma, mucins, inflammation, induced sputum, toll-like receptor

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Editor: Juan C. Ivancevich, MD

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