摘要
Several primarily symmetric skin diseases may, on rare oc- casions, manifest themselves more prominently along the embryonic migration pathways of cutaneous cell clones. Loss of heterozygosity along these lines of Blaschko resulting in hemizygosity or homozygosity of alleles predisposing for the disease is the most likely explanation for this phenomenon. Here, we report a case of severe Blaschko linear atopic dermatitis superimposed on a milder symmetric eruption of atopic eczema in a 36- year- old man with personal and familial history of allergy. Continuous transition of linear atopic eczema to linear vesicular (dyshidrotic) plantar eczema demonstrates the relationship between these two entities. Individuals such as our patient offer an opportunity to identify intraindividual genetic variations marking loci involved in the pathogenesis of atopy and atopic eczema.
Several primarily symmetric skin diseases may, on rare oc- casions, manifest themselves more prominently along the embryonic migration pathways of cutaneous cell clones. Loss of heterozygosity along these lines of Blaschko resulting in hemizygosity or homozygosity of alleles predisposing for the disease is the most likely explanation for this phenomenon. Here, we report a case of severe Blaschko linear atopic dermatitis superimposed on a milder symmetric eruption of atopic eczema in a 36- year- old man with personal and familial history of allergy. Continuous transition of linear atopic eczema to linear vesicular (dyshidrotic) plantar eczema demonstrates the relationship between these two entities. Individuals such as our patient offer an opportunity to identify intraindividual genetic variations marking loci involved in the pathogenesis of atopy and atopic eczema.
