Is the increase in asthma prevalence occurring in children without a family history of atopy?

Citation
Gl. Christie et al., Is the increase in asthma prevalence occurring in children without a family history of atopy?, SCOT MED J, 43(6), 1998, pp. 180-182
Citations number
20
Categorie Soggetti
General & Internal Medicine
Journal title
SCOTTISH MEDICAL JOURNAL
ISSN journal
00369330 → ACNP
Volume
43
Issue
6
Year of publication
1998
Pages
180 - 182
Database
ISI
SICI code
0036-9330(199812)43:6<180:ITIIAP>2.0.ZU;2-#
Abstract
We investigated the familial associations of asthma and atopic disease in a population in which the prevalence of asthma and atopy is increasing. Inte rviewer administered abbreviated family history questionnaires were applied in 416 families with a total of 1005 children ascertained through index ch ildren attending fracture and dressing clinics. The prevalence of reported asthma (22.5%), eczema (24%) and hayfever (20%) in the children was high bu t similar to previous studies in this population. Asthma was reported in 20 .8% of children of parents without a history of asthma and 18% of children of parents without any history of atopic disease. Logistic regression analy sis of outcomes in the index children showed increased risk of atopic disea se associated with parental history of the same atopic disease. The presenc e of an affected sibling was associated with an increased risk of eczema (O R 3.04 CI 1.83-5.05) or hayfever (OR 1.79 CI 0.97-3.3) but not asthma (OR 1 .18 CI 0.66-2.08). Increasing number of siblings was associated with reduce d risk although this was significant only for hayfever (OR 0.62 CI 0.41-0.8 6). Although the presence of affected relatives is associated with an incre ased risk of atopic disease the high prevalence of reported atopic disease, particularly asthma. in children of parents without a family history of at opic disease suggests that much of the increase in asthma prevalence is occ urring in children without a significant genetic predisposition. Childhood asthma developing in what would previously have been regarded as low risk f amilies may differ in its aetiology from classical atopic asthma.