Department of Dermatology, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany.
Eur J Dermatol. 2011 Mar-Apr;21(2):170-2. doi: 10.1684/ejd.2010.1247.
Dystrophic epidermolysis bullosa is a group of inherited skin blistering disorders caused by mutations in the COL7A1 gene coding for type VII collagen. More than 500 different COL7A1 mutations have been detected in dystrophic epidermolysis bullosa to date. Clarification of genotype-phenotype correlations is of particular importance for the development of novel therapeutic approaches. Here we report a female patient with mild dystrophic epidermolysis bullosa harbouring two compound heterozygous COL7A1 mutations, namely the intronic splice site mutation c.3832-2A > G and the glycine substitution p.G1347W. Our data extend the current knowledge on genotype-phenotype correlations in dystrophic epidermolysis bullosa.
营养不良型大疱性表皮松解症是一组由 COL7A1 基因突变引起的遗传性皮肤水疱病。迄今为止,已在营养不良型大疱性表皮松解症中发现了超过 500 种不同的 COL7A1 突变。阐明基因型-表型相关性对于开发新的治疗方法尤为重要。本文报道了一例携带 COL7A1 基因两个复合杂合突变的女性轻度营养不良型大疱性表皮松解症患者,分别为内含子剪接位点突变 c.3832-2A>G 和甘氨酸取代 p.G1347W。本研究结果扩展了目前对营养不良型大疱性表皮松解症的基因型-表型相关性的认识。