© 2004 American Thoracic Society
ACE Gene Polymorphism in COPDFrom the Authors:We thank Gosker and colleagues for their interest in our article (1) and for presenting further data in this area. We assume that, as with our patients, ACE genotype was unrelated to disease severity as judged by lung function. We would make two comments: First, we agree entirely with the authors' comment that "one could speculate that I is associated with enhanced improvement and/or preservation of endurance and D with better improvement and/or preservation of muscle strength"; indeed there is a wealth of data to support this view (2–6). Second, the data they present supports a role for the D allele in preserving muscle function: peak workload among I-allele carriers was lower than those of DD genotype (statistical significance possibly representing lack of power). The greater rise in peak workload with training thus seems to have yielded final status remarkably similar between genotype groups. Such data might suggest that I-allele carriers had become the most detrained and therefore had the greatest capacity to improve with pulmonary rehabilitation. Clearly, exercise limitation in patients with cardiorespiratory disease is a multifactorial process and renin–angiotensin systems may be involved at a number of potentially conflicting levels. We would certainly agree that further work in this area is required to clarify the mechanisms involved.
Royal Brompton Hospital London, United Kingdom Acknowledgments N.S.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. J.P. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. E.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. A.H.N. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. W.D.-C.M. has received assistance for travel to international conferences from Schering-Plough, GlaxoSmithKline, Allen & Hanbury's, Boehringer-Ingelheim, and Bayer pharmaceutical companies. J.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. H.M. is a named inventor on a patent concerning the role of RAS in metabolic efficiency, but passed this at no personal gain to a university-based company. He receives a stipend of approximately £10,000 per year from Ark Therapeutics Ltd for consultancy work relating to the use of RAS manipulation in cancer, together with stock options. His department has received unrestricted educational grants from Aventis Pharmaceuticals over the past three years. M.I.P. has received fees for lecturing from the following companies that total £2,674 (approximately US$3,700) between 2000 and 2003: Astra Zeneca, Glaxo Smith Kline, Nutricia, and Cephalon. He has also attended professional meetings (ERS, ATS, APSS) as a guest of various companies including Glaxo Wellcome, Astra Zeneca, Cephalon, 3M, and Ciba. REFERENCES
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