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Lung function measurements in children - copsac

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who do not develop RSV bronchiolitis. The risk factors for neonatal lung <strong>function</strong> was studied <strong>in</strong><br />

the COPSAC cohort <strong>in</strong> a recent publication (29) and showed that high body mass <strong>in</strong>dex <strong>in</strong> newborns<br />

and mothers smok<strong>in</strong>g were associated with reduced lung <strong>function</strong>, also that parental atopic<br />

disease (mother’s or father’s eczema, urticaria or allergic rh<strong>in</strong>itis or father’s asthma) did not affect<br />

the neonatal lung <strong>function</strong> and bronchial responsiveness.<br />

In our study group of <strong>in</strong>fants less than 2 years of age the mean age of the <strong>in</strong>fants diagnosed with<br />

RSV bronchiolitis was 8 months (30), which is higher than reported by other study groups. Other<br />

studies have limited the group of <strong>in</strong>terest to <strong>children</strong> less than 12 months of age and accord<strong>in</strong>gly<br />

reported even lower age of RSV <strong>in</strong>fection (35, 62-65).<br />

The <strong>in</strong>cidence of bronchiolits (5%) was higher reported <strong>in</strong> most studies (1-3%) (5-7, 48, 66, 67).<br />

This suggests a genetic component <strong>in</strong> RSV bronchiolitis as all mothers had asthma. Predisposition<br />

to asthma and atopy has been associated with <strong>in</strong>creased risk of lower respiratory tract <strong>in</strong>fection and<br />

hospitalization for RSV <strong>in</strong>fection (64, 68, 69). Young et al (1995) found 7% of a cohort (253 <strong>in</strong>fants)<br />

with the diagnosis of bronchiolitis before 2 years of age (only 2 <strong>in</strong>fants were hospitalized and<br />

confirmed for RSV <strong>in</strong>fection); 71% had a family history of atopy (18). A tw<strong>in</strong> cohort study showed<br />

that the severity of RSV <strong>in</strong>fection was determ<strong>in</strong>ed partly by genetic factors (16%); family environment<br />

accounted for 73% and nonshared environment for 11% of the <strong>in</strong>dividual susceptibility to develop<br />

severe respiratory syncytial virus <strong>in</strong>fection (70, 71). A Danish case-control study has also<br />

supported that asthmatic disposition and wheez<strong>in</strong>g were strong determ<strong>in</strong>ants of subsequent respiratory<br />

syncytial virus hospitalization <strong>in</strong> <strong>children</strong>

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