LONDON, ENGLAND -- June 26, 1998 -- Cystic fibrosis is a common genetic disorder that often causes premature death. It is characterised by lung disease that leads to airway obstruction. People heterozygous (one dominant gene, one recessive) for certain gene mutations associated with cystic fibrosis may have increased susceptibility to the development of obstructive pulmonary disease.
Dr, Morten Dahl and colleagues from Denmark looked for an association between the common gene mutation F508 that causes cystic fibrosis and the risk of developing asthma. They report their findings in this week's issue of The Lancet.
The investigators enrolled 9,141 people aged 20 years or older from the general adult population of Copenhagen. They measured the largest volume of air the participants could breathe out in one second and the total amount of air they could breathe out in relation to the amount inhaled. They asked participants about any external factors, such as smoking or exposure to industrial fumes, that could have influenced the development of obstructive pulmonary disease. They also tested blood samples to find out whether participants were heterozygous carriers of the cystic-fibrosis mutation.
Significantly more people (nine percent) who were carriers of the F508 mutation had asthma symptoms compared with non-carriers. The risk of having asthma was increased two-fold if the heterozygous mutation was carried. Among those who already had airway obstruction, the capacity of the lungs was decreased and the ability to exhale impaired in people heterozygous for the cystic-fibrosis mutation compared with non-carriers.
"Cystic fibrosis F508 heterozygosity may be over-represented among people with asthma," the researchers write. "Individuals heterozygous for F508 may account for up to two percent of people with asthma in the general population."
They believe that even though the prevalence of asthma varies from country to country, their results could be applicable to many countries of the world.
Thanks to The Doctor's Guide to the Internet™ for the article
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