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Authors’ response
  1. M Albers1,
  2. T Schermer1,
  3. Y Heijdra2,
  4. J Molema2,
  5. R Akkermans1,
  6. C van Weel1
  1. 1
    Department of General Practice, Radboud University Nijmegen Medical Centre, The Netherlands
  2. 2
    Department of Pulmonology, Radboud University Nijmegen Medical Centre, The Netherlands
  1. Professor C van Weel, Department of General Practice, 117-HAG, PO Box 9101, Nijmegen, The Netherlands; c.vanweel{at}

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We thank Quanjer et al for their detailed comments on our study. The decline in lung function is a key aspect of COPD. The DIMCA study has been one of the first that focused on patients in the early stage of COPD and collected data covering a period of 10 years. It is therefore important to review the quality and reliability of our data.

In response to the comments raised by Quanjer et al we would like to stress the following. Our paper1 reported on the first 5 years of follow-up of our study population. For the baseline and year 10 measurements, the same spirometer (Microspiro HI-298 spirometer; Chest Corporation, Japan) was used. Because a different spirometer was used at year 5 (Fukuda Sangyo spiro analyzer ST-250, Japan), equipment performance was assessed before as well as after lung function measurements in all participants had been completed. As we observed a systematic linear deviation in the lung function indices compared with the original spirometer, we considered it necessary to account for this. Further support for the reliability of our data was found in the follow-up of our study subjects. After 10 years, lung function was reassessed using the same spirometer that was used at baseline, and all assessments at year 10 were performed by the same lung function technician who performed the baseline assessments. We have now analysed the 10 year follow-up data and observed a further lung function decline that was fully in line with the pattern presented at year 5. Although the 10 year data have not been published to date (Mieke Albers thesis: COPD in primary care. Aspects of secondary prevention; chapters 6 and 7), the group of subjects without baseline abnormalities showed a decline in forced expiratory volume in 1 s (FEV1) amounting to 348 ml over the 10 year observation period. Over the 5 year period, this decline amounted to 197 ml. The decline in FEV1/vital capacity (VC) was 10.8% after 10 years of follow-up and 5.2% after 5 years of follow-up.

Given the quality of the measurements and consistency of the pattern over time, we do not think there are reasons to doubt our findings. Quanjer et al point to the use of FEV1/FVC. It is to be expected that our findings would have been arithmetically different had we used this ratio instead of the FEV1/VC ratio. But the systematic difference still leaves the prediction in decline intact. For that reason, we do not believe there were fundamental flaws in our study, although we agree that the decline is relatively high compared with findings in previous population cohorts. We have no explanation for this.

Quanjer et al are correct in that it would have been more appropriate to refer to the 1987 update of the American Thoracic Society statement on the standardisation of spirometry. At the time, this guideline served as the basis of procedures in the lung function laboratory of the University Lung Centre Dekkerswald, where all of our study subjects were measured.


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  • Competing interests:None declared.

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