From the Department of Pulmonary Medicine (Drs Zuur-Telgen, Brusse-Keizer, VanderValk, and van der Palen) and the Department of Internal Medicine (Dr Zuur-Telgen), Medisch Spectrum Twente; Regional Laboratory of Public Health (Dr Hendrix) and the Department of Research Methodology, Measurement, and Data Analysis (Dr van der Palen), University of Twente; the Department of Pulmonary Medicine (Dr Kerstjens) and the Department of Medical Microbiology (Dr Hendrix), University Medical Centre Groningen, University of Groningen; and Groningen Research Institute for Asthma and COPD (GRIAC) (Dr Kerstjens).
CORRESPONDENCE TO: Maaike C. Zuur-Telgen, MD, Department of Pulmonary Medicine, Medisch Spectrum Twente, PO Box 50 000, 7500 KA Enschede, The Netherlands; e-mail: email@example.com
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.
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We would like to respond to the letter in which Mr Khorfan remarks that several steps are required before proadrenomedullin (proADM) can be accepted as a strong predictor of mortality in COPD. Indeed, as he suggests, before the cutoff value of proADM that was observed in our study can be used in clinical practice it needs to be validated. We already started the validation study in the Cohort of Mortality and Inflammation in COPD (COMIC). The determination of the cutoff has also been done in the COMIC study, but this was performed in only a subset of patients for whom a paired blood sample (in stable state and at hospitalization for an acute exacerbation of COPD) was available.1 In this validation study we obtained 490 blood samples in stable state and 101 blood samples at hospitalization for an acute exacerbation of COPD from 545 patients that did not participate in the already published analysis. In addition, we are validating the cutoff values as suggested by Stolz et al.2,3
We agree with Mr Khorfan that it would be interesting to analyze the incremental value of proADM to current multidimensional indexes for prediction of mortality in COPD, such as the BMI, airflow obstruction, dyspnea, and exercise capacity (BODE) index as he suggests. We hypothesize that proADM has additional value because it could reflect the systemic component of COPD, which is currently not sufficiently done in indexes such as the BODE. Stolz et al3 already showed that proADM plus BODE predicts mortality more accurately than BODE alone. We are currently completing the analyses on the incremental value of proADM to currently used indexes in a pooled assessment of two large European, prospective, observational cohort studies of patients with COPD in stable state. We believe that these additional steps will bring the use of proADM in the clinic even closer to implementation.
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