Abstract

According to the available literature, there is a clear suggestion that atopy and airway hyperresponsiveness are genetically determined. Current knowledge suggests that many genes are involved in the clinical expression of these clinical entities. However, it must be established whether the genes for these two traits are acting completely independently of each other. Atopy by itself can be defined in several ways ( see below ) and atopy can express itself in different organs (e.g., skin, nose, and airways). Hence, it is questionable whether there exists one gene for atopy or whether there exist many genes that may interact, resulting in different disease expressions. Twin studies have suggested that part of the genetic background for hay fever and asthma is similar (1, 2). Asthma and rhinitis coexist frequently, suggesting a common heritable origin. There are, however, also some arguments to suggest that some genes may be responsible for asthma, and others for atopy. A study in a London population showed that only 23% of patients with seasonal allergic rhinitis also experienced wheezing (3). Furthermore, Dold and coworkers (4) showed that having a relative with atopic dermatitis or rhinitis alone does not constitute a risk factor for children to develop asthma. But having a parent with asthma significantly increased the risk for development of asthma in the child. The study separately analyzed families with single allergic diseases of one parent and showed that only asthma, and not allergic rhinitis, is a predisposing factor for asthma in the offspring. Finally, children with two family members with an identical type of allergy had the highest risk of developing that specific type of allergy. This might suggest that there are more genes necessary for the expression of different allergies.

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