In reply:
I appreciate the efforts taken by the author of the letter from Chest Research Foundation, Pune, who has responded to our article.1 First of all, I could not understand the meaning of the sentence “Prior studies have reported that plasma glutathione peroxidase levels were significantly elevated in plasma than males.” I believe that the author of the letter wants to reflect higher serum glutathione peroxidase levels in females as compared with males. Females showing higher serum glutathione peroxidase activity (256.4 ± 10.4 U/L vs 222.8 ± 15.6 U/L, P < .05) than males have been reported by Rush and Sandiford.2 However, the possibility of attributing the higher glutathione peroxidase activity measured in our study1 is attributable to a predominantly female rather than male population, as suggested by the author, may not be relevant. What we have highlighted in this study is a difference in the levels of glutathione peroxidase in the control group (50.95 ± 15.30 U/L) as compared with the COPD group (89.73 ± 27.84 U/L). In this study, even if both the COPD group and control group had consisted of equal numbers of males and females, the mean difference between the COPD group and control group would have been the same and led to the same conclusions. Taking more females into the control group and COPD group to match the number of males might have slightly increased the glutathione peroxidase levels in both groups, but the mean difference probably would still remain almost the same. This article was not aimed at establishing the normal reference range of glutathione peroxidase, yet I agree with the author that equal numbers of males and females in the study groups would have been better.
I agree with the comment of the author that prior studies have reported poor correlation of respiratory symptoms and lung function data in subjects with asthma. The same results may be found for COPD patients. Since none of the control subjects in this study had respiratory problems or lung diseases or were receiving inhaled bronchodilators or corticosteroids, spirometry for lung function data in the normal group was not conducted. This was in accordance with the guidelines of the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society.3
The author of the letter has pointed out that these studies reported that smokers have higher C-reactive protein levels compared with nonsmokers and suggested that it would have been interesting to see a comparison within the healthy and COPD subgroups (ie, healthy nonsmokers vs healthy smokers and smokers in the COPD group vs nonsmokers in the COPD group). I fully agree with the author that smokers have higher C-reactive protein levels. I further want to inform the author that this had already been done, and all of this information was provided while replying to a reviewer's comments during publication of the article, since the same query was expressed by one of the reviewers. However, the comparison is given once again along with glutathione peroxidase levels, as desired by the author, in Table 1.
Levels of Glutathione Peroxidase and C-Reactive Protein in Smokers and Nonsmokers of COPD and Control Groups
I have the same opinion as that of the author regarding the correlation of ferroxidase activity of ceruloplasmin and glutathione peroxidase with lung function. We wished the correlation would have been included in our article. However, the main focus in our article1 was about explaining the cutoff, area under the curve, specificity, and sensitivity of individual markers and combination of markers and setting the condition for the clinician to rule in or rule out COPD. However, in agreement with the author of the letter, it would have been interesting to see the correlation as suggested, but this was not done because it was not the objective of our article. Such correlation studies, taking into consideration the different spirometric parameters with all of the 6 different markers in both the smoker and nonsmoker categories within the COPD and control groups as well as in the entire COPD and control groups can be systematically discussed separately.
Footnotes
Mr Ambade has disclosed no conflicts of interest.
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