Chronic cough is a major clinical problem. The causes of
chronic cough can be categorized into eosinophilic and noneosinophilic disorders, the former being comprised of
asthma, cough variant asthma (CVA), atopic
cough (AC) and non-asthmatic eosinophilic
bronchitis (NAEB).
Cough is one of the major symptoms of
asthma.
Cough in
asthma can be classified into three categories; 1) CVA:
asthma presenting solely with coughing, 2)
cough-predominant
asthma:
asthma predominantly presenting with coughing but also with
dyspnea and/or
wheezing, and 3)
cough remaining
after treatment with inhaled
corticosteroid (ICS) and beta2-agonists in patients with classical
asthma, despite control of other symptoms. There may be two subtypes in the last category; one is
cough responsive to anti-mediator drugs such as
leukotriene receptor antagonists and
histamine H1 receptor antagonists, and the other is
cough due to co-morbid conditions such as
gastroesophageal reflux. CVA is one of the commonest causes of chronic isolated
cough. It shares a number of pathophysiological features with classical
asthma with
wheezing such as atopy,
airway hyperresponsiveness (AHR), eosinophilic airway
inflammation and various features of
airway remodeling. One third of adult patients may develop
wheezing and progress to classical
asthma. As established in classical
asthma, ICS is considered the first-line treatment, which improves
cough and may also reduce the risk of progression to classical
asthma. AC proposed by Fujimura et al. presents with
bronchodilator-resistant dry
cough associated with an atopic constitution. It involves eosinophilic tracheobronchitis and
cough hypersensitivity and responds to ICS treatment, while lacking in AHR and variable airflow obstruction. These features are shared by non-asthmatic eosinophilic
bronchitis (NAEB). However, atopic
cough does not involve bronchoalveolar
eosinophilia, has no evidence of
airway remodeling, and rarely progresses to classical
asthma, unlike CVA and NAEB.
Histamine H1 antagonists are effective in atopic
cough, but their efficacy in NAEB is unknown. AHR of NAEB may improve with ICS within the normal range. Taken together, NAEB significantly overlaps with atopic
cough, but might also include milder cases of CVA with very modest AHR. The similarity and difference of these related entities presenting with
chronic cough and characterized by airway
eosinophilia will be discussed.