© 2004 BMJ Publishing Group Ltd & British Thoracic Society
EDITORIAL
Pi MZ and COPD
Pi MZ and COPD: will we ever know?
Correspondence to:
Correspondence to:
Dr N Seersholm
Pulmonary Department Y, Gentofte Hospital, Niels Andersens Vej 65, DK-2900 Hellerup, Denmark; seersholm@dadlnet.dk
Based on the current evidence, there is no reason to believe that Pi MZ individuals have an increased risk of developing lung disease as long as they do not smoke
Keywords: chronic obstructive pulmonary disease;
1-antitrypsin; genetics; heterozygote
| The first 150 words of the full text of this article appear below. |
Is Pi MZ a risk factor for the development of chronic obstructive pulmonary disease (COPD)? That is the question many authors have tried to answer during the last decades, but the results of published studies are still conflicting.
A very high percentage of patients with COPD have been smokers, but not all smokers develop COPD. There must be other contributing factors and, with a Pi MZ prevalence of 35% in many Western countries, it is relevant to determine whether this genotype is an additional risk factor for COPD.1 Furthermore, if a dose-response relation exists, it is biologically plausible since plasma levels of
1-antitrypsin (AAT) are reduced to about 60% in Pi MZ subjects compared with those with the normal Pi MM genotype, and Pi Z individuals with very low levels of AAT have a significantly increased risk for emphysema.
There are a number of reasons for
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eLetters:
Read all eLetters
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- Morten Dahl
- Thorax Online, 2 Nov 2004 [Full text]
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