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   Table of Contents      
LETTER TO EDITOR
Year : 2019  |  Volume : 5  |  Issue : 3  |  Page : 156-157

COPD − The Future Lies in Phenotyping


Department of Pulmonary, Critical Care and Sleep Medicine, VMMC & Safdarjung hospital, New Delhi, India

Date of Submission12-Oct-2019
Date of Decision26-Oct-2019
Date of Acceptance28-Oct-2019
Date of Web Publication17-Dec-2019

Correspondence Address:
Dr. Pranav Ish
B1, Green Park Extension, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mamcjms.mamcjms_79_19

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How to cite this article:
Rathi V, Ish P. COPD − The Future Lies in Phenotyping. MAMC J Med Sci 2019;5:156-7

How to cite this URL:
Rathi V, Ish P. COPD − The Future Lies in Phenotyping. MAMC J Med Sci [serial online] 2019 [cited 2020 Apr 6];5:156-7. Available from: http://www.mamcjms.in/text.asp?2019/5/3/156/273291





Sir,

The new guidelines by global initiative for chronic obstructive lung disease (GOLD) 2019 have revolutionized the treatment practices of chronic obstructive pulmonary disease (COPD).[1]

To begin with, there is increased recognition of indoor biomass exposure, poverty, and HIV positivity to be important risk factors for COPD. Active case finding has been advocated. Importance of pneumococcal vaccine for reducing exacerbation has been discussed. But the phenomenal change is in approach to patient and treatment. The role of steroids has been clarified to a large extent.

The ABCD tool for classifying patients and treatments according to these groups has been adapted using same variables as GOLD 2018–Exacerbation history for severity (2 or 1 leading to hospital admission) and CAT score (>10) or modified medical research council (mMRC) grade (>2) for symptoms. This has to be done after a spirometric diagnosis and assessment of airflow limitation. Treatment of group A and B remains essentially same, but practically, they are a small subgroup of the COPD population in India. Also the option of shifting to dual bronchodilation in group B has been removed. The group C patients are also now recommended to be treated with a long-acting muscarinic antagonist (LAMA) with no further options. The group D has been stratified into possible phenotypes. There is an option to start LAMA alone like group C. If the patient is severely symptomatic (CAT > 20), dual bronchodilation is recommended. In patients with serum eosinophilia > 300 cells/microL, inhaled corticosteroids (ICS) with long-acting beta2 agonists (LABA) is recommended. This is an approach toward phenotyping COPD.

The conclusions drawn include a limited role of steroids in COPD − particularly in eosinophilic phenotype (generally asthma-COPD overlap) and recurrent exacerbations. The concept of risk over benefit of steroids is being revealed in other phenotypes.

The limitations of these guidelines are also many. Sputum eosinophilia is unavailable on a large scale in India, owing to difficulty in isolation of eosinophils in sputum. Serum eosinophilia has been considered less reliable. Besides, steroids are to be used when eosinophil count > 300 with one exacerbation per year and when eosinophil count > 100 with two exacerbations per year or one severe requiring hospitalization in the last year. Two different values create confusion and ultimately the decision relies on exacerbation history and clinical judgment.

The ECLIPSE study did try to evaluate biomarkers and potential phenotypes of COPD.[2] A modified approach in view of Indian population could include the following phenotypes:
  1. Non-exacerbators − treat with bronchodilators.[2]
  2. Exacerbators/bronchial asthma overlap/atopy − add inhaled steroids.[2]
  3. Emphysema − add mucolytics.[2]
  4. Upper lobe emphysema with poor exercise capacity and severe airflow limitation − add lung volume reduction surgery.[3]
  5. Bronchiectasis overlap − add postural drainage.
  6. Exacerbators on triple therapy/chronic bronchitis/severe obstruction − add roflumilast.[1]
  7. Exacerbators on triple therapy/chronic bronchitis/former smokers − add macrolides.[1]
  8. Alpha-1-antitrypsin deficiency with COPD and liver disease − add augmentation therapy.[4]
  9. COPD OSA overlap syndrome − add positive airway pressure therapy.
  10. COPD with cardiovascular and metabolic comorbidities − treat comorbidities to improve prognosis.[5]


In view of varied phenotypes and their different treatment options, phenotyping must be done at the time of the diagnosis prior to initiating appropriate therapy.[6] The need of the hour to develop classifications for phenotypes of COPD in India, similar to the efforts made for bronchial asthma.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
2019 GOLD report. Available at: https://goldcopd.org/gold-reports. [Accessed 1 June 2019].  Back to cited text no. 1
    
2.
Miravitlles M, Soler-Cataluña JJ, Calle M, Soriano JB. Treatment of COPD by clinical phenotypes: putting old evidence into clinical practice. Eur Respir J 2013;41:1252-6.  Back to cited text no. 2
    
3.
Miravitlles M, Calle M, Soler-Cataluña JJ. Clinical phenotypes of COPD: identification, definition and implications for guidelines. Arch Bronconeumol 2012;48:86-98.  Back to cited text no. 3
    
4.
Stoller JK, Aboussouan LS. A review of α1-antitrypsin deficiency. Am J Respir Crit Care Med 2012;185:246-59.  Back to cited text no. 4
    
5.
Lange P, Halpin DM, O’Donnell DE, MacNee W. Diagnosis, assessment, and phenotyping of COPD: beyond FEV₁. Int J Chron Obstruct Pulmon Dis 2016;11:3-12.  Back to cited text no. 5
    
6.
Siafakas N, Corlateanu A, Fouka E. Phenotyping before starting treatment in COPD? COPD 2017;14:367-4.  Back to cited text no. 6
    




 

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