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Noneosinophilic asthma

S. Mukherjee, S. Baksi
European Respiratory Journal 2003 22: 188-189; DOI: 10.1183/09031936.03.00013803
S. Mukherjee
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S. Baksi
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To the Editors:

We read with interest the article by Buist 1 on similarities and differences between asthma and chronic obstructive pulmonary disease. We would like to make some comments on the nature of inflammation in asthma, which the author has mentioned to be predominantly eosinophilic. Patients have been noted to have severe asthma or suffer an exacerbation without an increase in the eosinophil population in the airways 2. Based on several studies from 1995 onwards with data on eosinophil levels (cut-off values 2–4%) on bronchial biopsy specimens, bronchoalveolar lavage fluid and sputum of asthmatic patients, the weighted mean proportion of subjects with eosinophilic inflammation was 51%, the rest being noneosinophilic asthma 3. In most of the studies with noneosinophilic asthma, the predominant cells were neutrophils associated with increased levels of interleukin‐8 4–6 and similar cellular and inflammatory profiles as in occupational asthma 2. Asthma of all grades of severity can have neutrophil dominance in the airways 3, thus establishing it as a variant of asthma, not just a marker of severity. This is unlikely to be the effect of inhaled corticosteroids as shown by two studies 2, 6.

Eosinophilc asthma is CD4/interleukin‐5 driven in response to an allergen, whereas neutrophilic asthma is usually mediated by interleukin‐8 triggered by viral infection, pollution or bacterial endotoxin 3. It is important to try to differentiate between these two groups, which may have implications on treatment, and it is tempting to postulate that inhaled corticosteroids will not be as effective in patients with noneosinophilic asthma. Future studies should be directed to prospectively evaluate any prognostic difference between these two groups of asthma.

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    References

    1. ↵
      Buist AS. Similarities and differences between asthma and chronic obstructive pulmonary disease: treatment and early outcomes. Eur Respir J 2003;21:Suppl. 39, 30s–35s.
      OpenUrl
    2. ↵
      Turner MO, Hussack P, Sears MR, Dolovich J, Hargreave FE. Exacerbations of asthma without sputum eosinophilia. Thorax 1995;10:1057–1061.
      OpenUrl
    3. ↵
      Douwes J, Gibson P, Pekkanen J, Pearce N. Non-eosinophilic asthma: importance and possible mechanisms. Thorax 2002;57:643–648.
      OpenUrlAbstract/FREE Full Text
    4. ↵
      Wenzel SE, Schwartz LB, Langmack EL, et al. Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. Am J Respir Crit Care Med 1999;160:1001–1008.
      OpenUrlCrossRefPubMedWeb of Science
    5. Gibson PG, Simpson JL, Saltos N. Heterogeneity of airway inflammation in persistent asthma: evidence of neutrophilic inflammation and increased sputum interleukin‐8. Chest 2001;119:1329–1336.
      OpenUrlCrossRefPubMedWeb of Science
    6. ↵
      Amin K, Ludviksdottir D, Janson C, et al. Inflammation and structural changes in the airways of patients with atopic and nonatopic asthma. Am J Respir Crit Care Med 2000;162:2295–2301.
      OpenUrlCrossRefPubMedWeb of Science
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    Noneosinophilic asthma
    S. Mukherjee, S. Baksi
    European Respiratory Journal Jul 2003, 22 (1) 188-189; DOI: 10.1183/09031936.03.00013803

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    Noneosinophilic asthma
    S. Mukherjee, S. Baksi
    European Respiratory Journal Jul 2003, 22 (1) 188-189; DOI: 10.1183/09031936.03.00013803
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