POSTSCRIPT
Correspondence
Heme oxygenase 1 variations and lung function decline in smokers: proof of replication
1 Department of Epidemiology, University Medical Center Groningen, University of Groningen, the Netherlands
2 Department of Pulmonology, University Medical Center Groningen, University of Groningen, the Netherlands
Correspondence to:
Dr H M Boezen, Department of Epidemiology, University Medical Center Groningen, E3.29, PO Box 30.001, 9700 RB Groningen, The Netherlands; H.M.Boezen@epi.umcg.nl
Revised version received 14 February 2008
Accepted 17 February 2008
| The first 150 words of the full text of this article appear below. |
We provide supportive evidence for a role of the promoter polymorphism (GT-repeat) in heme oxygenase 1 (HO-1) in relation to lung function loss over time. This observation has been made by Guénégou and colleagues in a Caucasian population, and a call for replication of these results in a larger and independent cohort was made.1 The relevance of HO-1 has been widely acknowledged.2 Chronic obstructive pulmonary disease (COPD)—often a consequence of abnormally accelerated lung function decline3—has been widely studied in relation to HO-1 promoter GT-repeat, using a case–control approach. So far these studies provided contradictory findings.4–7
We genotyped the HO-1 GT-repeat in our Dutch general population based Vlagtwedde-Vlaardingen cohort (n = 1390, age median (range): 52 (35–79) years, 51% males, packyears median (range): 9 (0–262), 67.9% ever smokers), that was followed for 25 years (1965–1990) with forced expiratory volume in 1 s (FEV1) measurements every 3 years. We
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