膨胀纹后的线状局限性弹性组织变性：线状局限性弹性组织变性发病机制中瘢痕疙瘩修复过程的进一步证据。

Linear focal elastosis following striae distensae: further evidence of keloidal repair process in the pathogenesis of linear focal elastosis.

作者信息

Jeong Jin Seob, Lee Ji Yeoun, Kim Mi Kyeong, Yoon Tae Young

机构信息

Department of Dermatology, School of Medicine and Medical Research Institute, Chungbuk National University, Cheongju, Korea.

出版信息

Ann Dermatol. 2011 Oct;23(Suppl 2):S141-3. doi: 10.5021/ad.2011.23.S2.S141. Epub 2011 Oct 31.

DOI:10.5021/ad.2011.23.S2.S141

PMID:22148035

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3229050/

Abstract

Linear focal elastosis (LFE) is a rare dermal elastosis characterized by hypertrophic yellowish linear plaques and increased abnormal elastic tissues in the lumbosacral area. Although the pathogenesis of this disorder remains unknown, it may be associated with keloidal repair process (KRP) of elastic tissues in striae distensae (SD), because there have been some reported cases of LFE accompanied by SD. We herein report a 14-year-old boy with LFE following SD in the lumbar region. Our case supports the hypothesis of KRP in the pathogenesis of LFE. Immunohistochemical study for transforming growth factor-beta (TGF-β) was negative. Therefore, we assume that the pathogenesis of KRP in LFE is different from that of keloid development, which is the TGF-β signaling pathway.

摘要

线性局限性弹性组织变性（LFE）是一种罕见的皮肤弹性组织变性，其特征为腰骶部出现肥厚性淡黄色线性斑块以及异常弹性组织增多。尽管这种疾病的发病机制尚不清楚，但它可能与膨胀纹（SD）中弹性组织的瘢痕疙瘩样修复过程（KRP）有关，因为已有一些LFE伴有SD的病例报道。我们在此报告一名14岁男孩，其腰部SD后出现LFE。我们的病例支持KRP在LFE发病机制中的假说。转化生长因子-β（TGF-β）的免疫组织化学研究为阴性。因此，我们认为LFE中KRP的发病机制与瘢痕疙瘩形成的发病机制不同，后者是TGF-β信号通路。