Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan.
Clin Exp Dermatol. 2018 Aug;43(6):703-707. doi: 10.1111/ced.13549. Epub 2018 May 23.
Although numerous infective agents, including varicella zoster virus (VZV), have been described in association with pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC), none has been identified consistently in these lesions. We sought to immunohistochemically identify VZV glycoprotein (g)E antigens in the vascular endothelium in PLEVA and PLC lesions, based on our previous observation that gE was detected in the vascular endothelium and eccrine unit up until 2 months and 2.5, respectively, years after herpes zoster (HZ) infection. In five of the six cases of PLEVA, VZV gE was identified in the endothelial cells and eccrine epithelium, as observed in HZ lesions, whereas VZV gE was detected in only one of seven patients with PLC. None of the patients with PLEVA who had VZV gE-positive vascular endothelial cells had experienced previous episodes of HZ. VZV may be one of the aetiological agents for PLEVA while other aetiological factors could exist in PLC.
虽然已经描述了许多感染因子，包括水痘带状疱疹病毒（VZV），与急性痘疮样苔藓糠疹（PLEVA）和慢性苔藓样糠疹（PLC）有关，但在这些病变中始终未发现一致的感染因子。基于我们之前的观察结果，即 gE 在带状疱疹（HZ）感染后 2 个月和 2.5 年内分别在血管内皮细胞和外分泌单位中检测到 gE，我们试图通过免疫组织化学方法在 PLEVA 和 PLC 病变的血管内皮细胞中鉴定 VZV 糖蛋白（g）E 抗原。在 6 例 PLEVA 中，有 5 例观察到 VZV gE 在血管内皮细胞和外分泌上皮细胞中，与 HZ 病变中观察到的情况相同，而在 7 例 PLC 患者中，只有 1 例检测到 VZV gE。在 VZV gE 阳性血管内皮细胞的 PLEVA 患者中，没有既往 HZ 发作的病史。VZV 可能是 PLEVA 的病因之一，而 PLC 可能存在其他病因。
