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  Table of Contents    
Year : 2019  |  Volume : 36  |  Issue : 3  |  Page : 267-268  

Inflammatory phenotypes of severe asthma in India

1 Department of Medicine and Pulmonary Medicine, BR Singh Hospital and Centre for Medical Education and Research, Kolkata, West Bengal, India
2 Department of Pathology, BR Singh Hospital and Centre for Medical Education and Research, Kolkata, West Bengal, India

Date of Web Publication24-Apr-2019

Correspondence Address:
Dr. Angira Dasgupta
Department of Medicine and Pulmonary Medicine, BR Singh Hospital and Centre for Medical Education and Research, Kolkata, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/lungindia.lungindia_502_18

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How to cite this article:
Dasgupta A, Ade V, Dutta J, Dasgupta G. Inflammatory phenotypes of severe asthma in India. Lung India 2019;36:267-8

How to cite this URL:
Dasgupta A, Ade V, Dutta J, Dasgupta G. Inflammatory phenotypes of severe asthma in India. Lung India [serial online] 2019 [cited 2020 Jul 12];36:267-8. Available from: http://www.lungindia.com/text.asp?2019/36/3/267/256934


Severe asthma is a heterogeneous disease that warrants accurate phenotyping for optimal disease control since standard guideline-based treatment may not be effective in this subgroup of asthmatics.[1],[2] The purpose of phenotyping is to provide an insight into the mechanism (high Th2 vs. low Th2) driving the disease and direct treatment accordingly. Among others, sputum quantitative assay is a well-established method for measuring the cellular nature of airway inflammation and even for titrating doses of corticosteroids.[3] Although this method has been variously criticized for its need for a wet laboratory, adequate training, and patients not being able to produce sputum despite induction, this remains the most specific and accurate method for phenotyping airway diseases so far.[3] Further, this is the only noninvasive method which measures the inflammatory cells directly from the airways whereas most other methods (blood eosinophils and fraction of exhaled nitric oxide) do not.

We used sputum quantitative assay (Hamilton protocol) along with other clinical and blood parameters to phenotype 100 consecutive severe asthma patients who attended the severe asthma clinic of a referral hospital in eastern India.[2],[4] The mean age of the cohort was 50.93 (standard deviation [SD]: 15.46) years. There were 57% males. The mean duration of disease was 15.18 (SD: 10.62) years. A history of allergy was present in 62%, family history of asthma was present in 32%, and 16% of the participants were smokers. There were associated sinus disease and a history of pneumonia in 47% and 32% patients, respectively. The mean prebronchodilator forced expiratory volume in 1 s was 1.06 L (47% predicted). Sixty-four percent of the participants were atopic with a raised serum immunoglobulin E.

The most common inflammatory phenotype in our cohort (sputum report available in 72 patients) was neutrophilic (59%) which is only modestly higher than earlier reports.[1] Among them, 13% had raised total cell count indicating bacterial infection and need for antibiotic therapy. The remaining had isolated neutrophilia (46%). This latter group is known to respond poorly to corticosteroids and thus needs further research for identifying possible drivers of neutrophilia.[5]

The eosinophil phenotype comprised 26% of participants while mixed pattern and paucigranulocytic sputum were present in 11% and 3%, respectively. The eosinophilic phenotype was present in 64% of participants when a blood eosinophil count of >300 cells/cu mm was used as the cutoff. Thus, a discordance between blood eosinophilia and sputum eosinophilia [Figure 1] existed which indicates that mere finding of eosinophils in blood may not be reflective of the presence of activated eosinophils in the airways. Further, India has a greater prevalence of parasitic infections than most other countries which might necessitate using a greater cutoff for blood eosinophils. This, given the recent availability of specific anti-eosinophil agents, needs urgent attention.
Figure 1: Scatter plot showing poor correlation between blood eosinophils and sputum eosinophil counts

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While being limited by a cross-sectional design, this is the first report of the inflammatory phenotypes of severe asthma from the Indian subcontinent. The various phenotype prevalences are only modestly different from those in other countries[1],[2] and iterate the need to set up “state of art” severe asthma clinics for accurate phenotyping, especially when asthma is severe and biologics are contemplated.

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There are no conflicts of interest.

   References Top

Moore WC, Bleecker ER, Curran-Everett D, Erzurum SC, Ameredes BT, Bacharier L, et al. Characterization of the severe asthma phenotype by the National Heart, Lung, and Blood Institute's Severe Asthma Research Program. J Allergy Clin Immunol 2007;119:405-13.  Back to cited text no. 1
Chung KF, Wenzel SE, Brozek JL, Bush A, Castro M, Sterk PJ, et al. International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma. Eur Respir J 2014;43:343-73.  Back to cited text no. 2
Pizzichini E, Pizzichini MM, Efthimiadis A, Evans S, Morris MM, Squillace D, et al. Indices of airway inflammation in induced sputum: Reproducibility and validity of cell and fluid-phase measurements. Am J Respir Crit Care Med 1996;154:308-17.  Back to cited text no. 3
Nair P, Dasgupta A, Brightling CE, Chung KF. How to diagnose and phenotype asthma. Clin Chest Med 2012;33:445-57.  Back to cited text no. 4
Nair P, Hargreave FE. Measuring bronchitis in airway diseases: Clinical implementation and application: Airway hyperresponsiveness in asthma: Its measurement and clinical significance. Chest 2010;138:38S-43S.  Back to cited text no. 5


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