Asthma-COPD overlap syndrome (ACOS)

What are known:

Asthma

  • Eosinophilic inflammation
  • Small airways disease
  • Bronchial hyper-responsiveness -> smooth muscle contraction & mucus secretion
  • Reversible bronchoconstriction

COPD

  • Neurophilic inflammation
  • Small and large airways disease
  • Inflammatory infiltrates -> smooth muscle contraction, mucus secretion (chronic bronchitis) & tissue breakdown (emphysema)
  • Irreversible bronchoconstriction

Why is there an entity called ACOS?

  • In asthma, with age, airway remodelling happens and eventually lead to features of COPD.
  • In COPD, reversible airway obstruction can happen, resembling asthma.

Recently, GINA and GOLD issued a joint document that describes ACOS as a clinical entity and proposes that clinicians should assemble the features for asthma and for COPD that best describe the patient and compare the number of features in favour of each diagnosis.

  • If similar number of features of asthma and COPD, then ACOS should be considered.

From this NEJM article, these are some of the points i concluded.

Bronchial hyper-responsiveness is also a RF for COPD

  • Surprise? Apparently bronchial hyper-responsiveness is associated with increased airway inflammation.
  • COPD patients with this has a more rapid FEV1 decline and therefore is a marker of severity.
  • Response to inhaled g/c also differs in COPD + bronchial hyperresponsiveness. The article does not mention how does it differ but it is fair to think that inhaled g/c doesn’t work as well in COPD compared to asthma.

Asthma can be irreversible/less reversible in chronic/severe disease.

  • Irreversibility DOES NOT therefore, exclude the diagnosis of asthma.

Airway obstruction in COPD can be reversible.

  • Another surprise fact. However, reversibility has no association with risk of exacerbation, death and FEV1 decline. In other words, a reversible COPD does not mean that it is a less severe COPD.

Atopy is a risk factor for both asthma and COPD.

  • The important thing is that if COPD patient has atopy, g/c may offer benefits.

Smokers with asthma may exhibit neutrophilic inflammation.

  • Absence of eosinophilia DOES NOT exclude the diagnosis of asthma.

Eosinophils may also present in COPD, even after the exclusion of bronchial asthma/atopy history and bronchial-hyperresponsiveness.

  • COPD patients with eosinophilia have better response to inhaled g/c in exacerbations and slower decline in FEV1 (although more exacerbations).
  • A little bit contradicting to point #1 but I think more exacerbations = more severe disease.
  • However, the good thing is they respond better to inhaled g/c (compared to the other COPDers without eosinophilia) and therefore FEV1 decline maybe delayed in this population (if inhaled g/c is given early).
  • The thing is that inhaled g/c is not the treatment in mild-moderate COPD and therefore this subtype of patients may have greater decline in FEV1 without early treatment with inhaled g/c.

Most importantly, no specific definition for ACOS exists.

  • Therefore, the authros believe that it is premature to recommend ACOS as a disease entity. Need criteria to better characterize the disease.

The authors’ opinions on treatment of asthma and signs of concomitant COPD & COPD and signs of concomitant asthma

  • Asthma + signs of concomitant COPD: inhaled g/c + bronchodilators therapy
  • COPD + signs of concomitant asthma: may benefit from inhaled g/c (due to the presence of airway hyperresponsiveness, reversibility and eosinophilia discussed above).

Learning points:

  1. Asthma and COPD can have overlapping features.
    – COPD can have airway hyper-responsiveness, reversibility, eosinopilia and atopy features.
    – Asthma can have neutrophilic inflammation (especially in smokers) and irreversibility (or less reversibility).
  2. Specific definition for ACOS does not exist (yet).
  3. Inhaled g/c can be used in COPD if there are features of asthma.

Reference

The Asthma–COPD Overlap Syndrome
Dirkje S. Postma, M.D., Ph.D., and Klaus F. Rabe, M.D., Ph.D.

N Engl J Med 2015; 373:1241-1249

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