Like other atopic conditions, AD has a strong genetic predisposition. As many as 6080% of patients with AD have a family history of a first-degree relative with AD, asthma or allergic rhinitis. In studies of twins, Rajka reported a much higher concordance for atopy in monozygotic twins, whereas AD alone revealed only a 50% concordance in both monozygotic and dizygotic twins. Rajka's data cast doubt on the strictly hereditary influence, yet underscore the importance of the combination of hereditary and environmental factors in the disease process. Numerous reports have suggested HLA associations among families with atopic disease in general and AD specifically. Based on genomic studies assessing for susceptibility loci for atopic dermatitis, multiple pathophysiologically relevant candidate genes have been identified including areas on chromosome 3q21, 1q21, 17q25, and 20p. An area on chromosome 5q31-33 that contains a clustered family of Th2 cytokine genes has been of particular interest. Other genetic variations reported in AD include a mutation in the promoter region of RANTES, a gain-of-function polymorphism in the a-subunit of the IL-4 receptor and IL-13 coding variants. These data are not definitive at present and suggest that a single set of genes is not responsible for atopic disease inheritance. Multiple patterns of disease inheritance such as autosomal dominance, autosomal-recessive and multifactorial inheritance have been found, emphasizing the obvious complexity of genetic influence on the disease process. Throughout all these studies, however, it is maintained that individuals from atopic families are at greater risk for development of atopic disease in some form.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.