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American Journal of Respiratory and Critical Care Medicine Vol 174. pp. 1057, (2006)
© 2006 American Thoracic Society

Correspondence

Beyond the Dutch Hypothesis

From the Authors:

With regard to our recent Pro/Con editorial debate (1–4), we agree with Prof. Chhabra that the ventilatory response in chronic obstructive pulmonary disease (COPD) differs from that in severe asthma, but whether these differences are due to a reduction in ventilatory drive in COPD is not conclusive. The causes of hypercapnia in COPD are multifactorial and include increased physiologic dead space due to V/Q mismatching, higher resistive and elastic load of the respiratory muscles due to dynamic hyperinflation, and reduced gas exchange because of emphysema (5, 6). Although decreased ventilatory drive is not usually associated with asthma, a subset of patients with asthma exhibit a reduced ventilatory drive due to the inability to achieve full neural activation of the diaphragm with voluntary efforts (7).

In response to Dr. Hahn, we disagree about the role of atopy, as many studies have demonstrated a strong relationship between atopy and asthma (8), but this does not mean that other factors, such as infection, are not important. In COPD, bacterial load and serotype contribute to the decline in lung function (9). In asthma, several studies have shown that viral and bacterial infections can influence the presentation, severity, and persistence of asthma (10, 11). We agree that the genetic response to infection is critical and requires further investigation.

Monica Kraft

Duke University Medical Center, Durham, North Carolina

Peter J. Barnes

National Heart & Lung Institute Imperial College, London, United Kingdom

FOOTNOTES

Conflict of Interest Statement: M.K. received fees from GlaxoSmithKline (GSK) for consulting, from Astra-Zeneca, Boehringer-Ingelheim, Genentech, and Merck for participation in advisory board activities, and from Merck, GSK, Sepracor, and Genentech/Novartis for participation as a speaker at scientific meetings. She has received research funding from GSK, Altana, Genentech, Novartis, Boehringer-Ingelheim, Medicinova, and Merck for participation in clinical trials. P.J.B. has received research funding and lecture fees, and has served on Scientific Advisory Boards for GlaxoSmithKline, AstraZeneca, Boehringer-Ingelheim, Novartis, Altana, Pfizer, and Scios.

REFERENCES

  1. Kraft M. Asthma and chronic obstructive pulmonary disease exhibit common origins in any country! Am J Respir Crit Care Med 2006;174:238–240.[Free Full Text]
  2. Barnes PJ. Against the Dutch hypothesis: asthma and chronic obstructive pulmonary disease are distinct diseases. Am J Respir Crit Care Med 2006;174:240–243.[Free Full Text]
  3. Kraft M. Rebuttal by Dr. Kraft. Am J Respir Crit Care Med 2006;174:243–244.[Free Full Text]
  4. Barnes PJ. Rebuttal by Dr. Barnes. Am J Respir Crit Care Med 2006; 174:244.[Free Full Text]
  5. Begin P, Grassino A. Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991;143:905–912.[Medline]
  6. Sorli J, Grassino A, Lorange G, Milic-Emili J. Control of breathing in patients with chronic obstructive pulmonary disease. Clin Sci Mol Med 1978;54:295–304.[Medline]
  7. Allen GM, McKenzie DK, Gandevia SC, Bass S. Reduced voluntary drive to breathe in asthmatic subjects. Respir Physiol 1993;93:29–40.[CrossRef][Medline]
  8. Sherrill DL, Lebowitz MD, Halonen M, Barbee RA, Burrows B. Longitudinal evaluation of the association between pulmonary function and total serum IgE. Am J Respir Crit Care Med 1995;152:98–102.[Abstract]
  9. Sethi S, Maloney J, Grove L, Wrona C, Berenson CS. Airway inflammation and bronchial bacterial colonization in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006;173:991–998.[Abstract/Free Full Text]
  10. Hahn DL. Chlamydia pneumoniae, asthma and COPD: what is the evidence? Ann Allergy Asthma Immunol 1999;83:271–288.[Medline]
  11. Martin RJ, Kraft M, Chu HW, Berns EA, Cassell GH. A link between chronic asthma and chronic infection. J Allergy Clin Immunol 2001;107: 595–601.[CrossRef][Medline]




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Copyright © 2006 American Thoracic Society