Smoking and nonsmoking asthma: differences in clinical outcome and pathogenesis

Fatemeh Fattahi, Machteld N. Hylkema, Barbro N. Melgert, Wim Timens, Dirkje S. Postma, Nick H. T. ten Hacken*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Citations (Scopus)

Abstract

Expert Rev. Resp. Med. 5(1), 93-105 (2011) Cigarette smoking in asthma is frequently present and is associated with worsening of symptoms, accelerated lung-function decline, a higher frequency of hospital admissions, a higher degree of asthma severity, poorer asthma control and reduced responsiveness to corticosteroids. Furthermore, it is associated with reduced numbers of eosinophils and higher numbers of mast cells in the submucosa of the airway wall. Airway remodeling is increased as evidenced by increased epithelial thickness and goblet cell hyperplasia in smoking asthmatics. The pathogenesis responsible for smoking-induced changes in airway inflammation and remodeling in asthma is complex and largely unknown. The underlying mechanism of reduced corticosteroid responsiveness is also unknown. This article discusses differences between smoking and nonsmoking asthmatics regarding the clinical expression of asthma, lung function, response to corticosteroids, airway inflammation and remodeling processes. Possible pathogenetic mechanisms that may explain the links between cigarette smoking and changes in the clinical expression of asthma will be discussed, as well as the beneficial effects of smoking cessation.

Original languageEnglish
Pages (from-to)93-105
Number of pages13
JournalExpert review of respiratory medicine
Volume5
Issue number1
DOIs
Publication statusPublished - Feb-2011

Keywords

  • airway inflammation
  • airway remodeling
  • asthma
  • corticosteroid unresponsiveness
  • smoking
  • smoking cessation
  • OBSTRUCTIVE PULMONARY-DISEASE
  • INDUCED AIRWAY INFLAMMATION
  • INDUCED LUNG INJURY
  • QUALITY-OF-LIFE
  • CIGARETTE-SMOKING
  • ALVEOLAR MACROPHAGES
  • FOLLOW-UP
  • RISK-FACTORS
  • INHALED CORTICOSTEROIDS
  • INDUCED SPUTUM

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