Takahashi Yoshie, Rouan Fatima, Uitto Jouni, Ishida-Yamamoto Akemi, Iizuka Hajime, Owaribe Katsushi, Tanigawa Mizuko, Ishii Norito, Yasumoto Shinichiro, Hashimoto Takashi
Department of Dermatology, Kurume University School of Medicine, 67 Asahimachi, Kurume, Fukuoka 830-0011, Japan.
J Dermatol Sci. 2005 Feb;37(2):87-93. doi: 10.1016/j.jdermsci.2004.11.003. Epub 2004 Dec 22.
Epidermolysis bullosa simplex associated with muscular dystrophy is caused by plectin deficiency.
To report clinical, immunohistochemical, ultrastructural and molecular features of a 52-year-old Japanese patient affected with this disease, whose muscular disease had been followed-up for 27 years.
We performed histopathological study, immunofluorescence, electron microscopic study and mutation detection analysis for plectin.
The patient developed blisters and erosions followed by nail deformity on the traumatized regions from birth. The skin lesions were continuously developed to date. The histopathological study showed subepidermal blister. Electron microscopic study showed blister formation inside the basal cells at the level just above the attachment plaque of hemidesmosome. Immunofluorescence showed complete loss of staining to plectin. The mutation analysis using protein truncation test and DNA sequencing revealed a C-to-T transition at nucleotide position 7006 of the plectin cDNA sequence, which lead a novel homozygous nonsense mutation (R2319X).
From the above results, the diagnosis of epidermolysis bullosa simplex associated with muscular dystrophy was made. Slight muscular dystrophy was noticed at the age of 25 years. The muscular dystrophy gradually progressed and she could not walk at the age of 46 years. However, she can still breathe and swallow by herself. This is the patient of this disease with the longest follow-up, and may indicate the slow progress of muscular condition of this disease.
与肌肉营养不良相关的单纯性大疱性表皮松解症由网蛋白缺乏引起。
报告一名52岁患此病的日本患者的临床、免疫组化、超微结构和分子特征,该患者的肌肉疾病已随访27年。
我们对网蛋白进行了组织病理学研究、免疫荧光、电子显微镜研究和突变检测分析。
患者自出生起在受创伤部位出现水疱和糜烂,随后出现指甲畸形。皮肤病变持续发展至今。组织病理学研究显示表皮下水疱。电子显微镜研究显示在半桥粒附着斑上方水平的基底细胞内形成水疱。免疫荧光显示网蛋白染色完全缺失。使用蛋白截短试验和DNA测序进行的突变分析显示,网蛋白cDNA序列第7006位核苷酸发生C到T的转换,导致一个新的纯合无义突变(R2319X)。
根据上述结果,诊断为与肌肉营养不良相关的单纯性大疱性表皮松解症。25岁时发现轻度肌肉营养不良。肌肉营养不良逐渐进展,46岁时她无法行走。然而,她仍能自主呼吸和吞咽。这是该疾病随访时间最长的患者,可能表明该疾病肌肉状况进展缓慢。