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Bram van den Borst, MD; Harry R. Gosker, PhD; Annemie M. W. J. Schols, PhD
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From NUTRIM School for Nutrition, Toxicology and Metabolism, Department of Respiratory Medicine, Maastricht University Medical Center+.

Correspondence to: Bram van den Borst, MD, NUTRIM School for Nutrition, Toxicology and Metabolism, Department of Respiratory Medicine, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands; e-mail: b.vdborst@maastrichtuniversity.nl


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(1):236. doi:10.1378/chest.10-2272
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To the Editor:

In response to the letter from Ahmad et al, we would like to clarify how we carefully dealt with BMI in our metaanalysis on pulmonary function in diabetes in our recent article in CHEST (August 2010).1 All the studies we included in our metaanalysis had a control group, and in almost every study BMI was already closely matched between the diabetes patients and control subjects by the original authors. Still, to exclude the potential influence of a relatively small difference in mean BMI between diabetes patients and control subjects, we analyzed whether the delta of the mean BMI between the groups was a source for between-study heterogeneity, which was proven not to be the case. Therefore, we concluded that the observed differences in pulmonary function indices between diabetes patients and controls were independent of BMI. This finding from our quantitative review is also supported by a recent narrative systematic review on pulmonary function specifically in type 2 diabetes.2

Ahmad et al directly link the lower pulmonary function in type 2 diabetes patients to systemic inflammation, for which no direct evidence exists. To the contrary, as we discussed, two large studies that sought a systemic inflammatory explanation for lower pulmonary function in diabetes failed to provide significant findings.3,4 It has yet to be elucidated whether the subclinically lower lung function associated with diabetes indeed forms a risk of progressive decline.

van den Borst B, Gosker HR, Zeegers MP, Schols AM. Pulmonary function in diabetes: a metaanalysis. Chest. 2010;1382:393-406. [CrossRef] [PubMed]
 
Klein OL, Krishnan JA, Glick S, Smith LJ. Systematic review of the association between lung function and Type 2 diabetes mellitus. Diabet Med. 2010;279:977-987. [CrossRef] [PubMed]
 
Yeh HC, Punjabi NM, Wang NY, et al. Cross-sectional and prospective study of lung function in adults with type 2 diabetes: the Atherosclerosis Risk in Communities (ARIC) study. Diabetes Care. 2008;314:741-746. [CrossRef] [PubMed]
 
Lee HM, Le TV, Lopez VA, Wong ND. Association of C-reactive protein with reduced forced vital capacity in a nonsmoking U.S. population with metabolic syndrome and diabetes. Diabetes Care. 2008;3110:2000-2002. [CrossRef] [PubMed]
 

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References

van den Borst B, Gosker HR, Zeegers MP, Schols AM. Pulmonary function in diabetes: a metaanalysis. Chest. 2010;1382:393-406. [CrossRef] [PubMed]
 
Klein OL, Krishnan JA, Glick S, Smith LJ. Systematic review of the association between lung function and Type 2 diabetes mellitus. Diabet Med. 2010;279:977-987. [CrossRef] [PubMed]
 
Yeh HC, Punjabi NM, Wang NY, et al. Cross-sectional and prospective study of lung function in adults with type 2 diabetes: the Atherosclerosis Risk in Communities (ARIC) study. Diabetes Care. 2008;314:741-746. [CrossRef] [PubMed]
 
Lee HM, Le TV, Lopez VA, Wong ND. Association of C-reactive protein with reduced forced vital capacity in a nonsmoking U.S. population with metabolic syndrome and diabetes. Diabetes Care. 2008;3110:2000-2002. [CrossRef] [PubMed]
 
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