© 2007 American Thoracic Society
SERPINE2 and COPDFrom the Authors:We appreciate Dr. Kauffmann's positive comments about the results from the SERPINE2 genetic association analysis in our article (1), and confirm that detailed descriptions of the study populations were not provided in the article. Manuscripts which describe the epidemiological characterization of these cohorts are either under review or in preparation currently. Although it is expected that these articles will provide answers to most of Dr. Kauffmann's concerns, we will try here to answer the key questions raised in her letter.
In the International COPD Genetics Network (ICGN), we recruited subjects with known chronic obstructive pulmonary disease (COPD) as probands based on the spirometric and smoking criteria described in our article (1). The probands were recruited from pulmonary and medical clinics and hospital admissions; they were not identified by general population screening. Probands and siblings with severe A detailed manuscript on the ascertainment, demographics, and phenotypic characterization of ICGN subjects is under review, and hence additional details are not included in this reply. Since we used family-based association analyses in the ICGN subjects, population stratification is not an issue. We did not analyze the data in a country-specific manner because of power concerns. A detailed manuscript on the gender differences in this population is also in preparation. Among the 973 patients with COPD of the Norwegian case-control population, 189 were recruited from the Horduland County Community Health Survey, while the rest were recruited from a registry at Haukeland University Hospital, Bergen. Among the 956 smokers without COPD (controls) from the Norwegian case-control population, 735 were recruited from the Horduland County Community Health Survey, while the rest were volunteers. The characterization of the Horduland County Community Health Survey has been previously reported (see Reference 2 for details), and we are preparing an epidemiology manuscript with details about the current case-control collection. We hope that this additional information will assist in the interpretation of our genetic association analysis results.
GlaxoSmithKline, Research Triangle Park, North Carolina
University of Bergen, Bergen, Norway
Cambridge Institute for Medical Research, Cambridge, United Kingdom
Brigham and Women's Hospital, Boston, Massachusetts FOOTNOTES Conflict of Interest Statement: S.G.P. is a full-time employee of GlaxoSmithKline (GSK). G.Z. is a full-time employee of GSK. A.G. has no financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.A.L. has received a grant of $1,562,500 from GSK to recruit patients in a multicenter study to identify biomarkers in COPD. E.K.S. received an honorarium for a talk on COPD genetics in 2006, and grant support and consulting fees from GSK for two studies of COPD genetics; he received an honorarium from Wyeth for a talk on COPD genetics in 2004; he received an honorarium from Bayer for a symposium at the ERS meeting in 2005; he received an honorarium from Astra-Zeneca for a talk at the Lund Symposium in 2007. REFERENCES
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1-antitrypsin deficiency were excluded. A total of 3,096 eligible individuals were recruited into the study between June 2000 and April 2003 (1,156 probands and 1,940 siblings). A subset of the total ICGN study population comprising 1,910 subjects was included in the SERPINE2 genetic association analysis. The ICGN was a cohort of subjects newly collected to identify genes that predispose smokers to COPD. In this family-based collection, all available siblings who met the smoking criteria (>5 pack-years) were contacted to participate, but data regarding refusals to participate were not collected. Demographic details on the probands and siblings used in the SERPINE2 analyses are provided in Table 1 of our article (