© 2006 American Thoracic Society doi: 10.1164/rccm.2604009
Rebuttal by Dr. KraftProfessor Barnes has provided a cogent discussion asserting that asthma and chronic obstructive pulmonary disease (COPD) are distinct entities. Yet if this were entirely true, then why do almost half of our patients with obstructive lung disease exhibit characteristics of both diseases? While I agree with Dr. Barnes that we will continue to see patients who exhibit either "pure" asthma or "pure" COPD phenotypes, I propose that there are more similarities than differences between these two phenotypes. Clearly, more studies are needed specifically to address common mechanisms. As a matter of fact, Dr. Barnes illustrates this point rather well in the summary table he presents at the end of his discussion. I would like to address a few of his comments directly in my rebuttal.Dr. Barnes states that the peripheral airways are not involved in mild asthma but possibly are in severe asthma; this is in contrast to COPD, where the peripheral airways and parenchyma are routinely involved. We demonstrated in 1996 and 1999 that distal lung inflammation was present even in mild asthma, although inflammation was more pronounced in patients with moderate asthma. In fact, the presence of peripheral lung tissue eosinophils predicted the overnight decrement in lung function in both groups. With regard to physiology of the peripheral airways, we recently demonstrated that loss of elastic recoil exists even in mild asthma. These observations suggest that in asthma the distal lung is involved both pathologically and physiologically.
Dr. Barnes asserts that asthma and COPD are caused by different "genetic substrates." I would argue that very little is known about the genetics of either disease, so one cannot be dogmatic about their differences. Actually, Dr. Barnes supports my position by discussing the genetics of ADAM-33, where specific polymorphisms have been shown in both asthma and COPD. He further speculates that genes involving antioxidants and proteases may be involved in COPD, but presents no evidence other than Dr. Barnes also asserts that IgE levels are not elevated in COPD. I contend that Sherrill and colleagues have shown an inverse association between IgE levels and lung function in COPD, regardless of level. Another instructive study by Herland and colleagues looked at patients with obstructive lung disease recruited from primary care and specialists' practices. They found that the absence of atopy only identified 17% of the COPD population and 7% of the entire population of patients with obstructive lung disease in this cohort. They concluded that atopy does not distinguish COPD from asthma and that subjects studied in clinical trials do not represent real-world obstructive disease. A major implication is that if we only study those patients with classic asthma and COPD phenotypes in clinical trials, we will be missing a substantial proportion of the obstructive lung disease population. Furthermore, how will we explain the presentation of these patients with mixed disease? The Dutch hypothesis at least offers an option to explore what we see in real life in patients with obstructive lung disease. To close our minds to the possibility that obstructive diseases may have a common origin would be premature and even parochial. This article has been cited by other articles:
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1-antitrypsin deficiency, which affects fewer than 1% of patients. 
