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Hypoxia–ischaemia is involved in the pathogenesis of vulvar lichen sclerosus
Author(s) -
Li Y.Z.,
Wu Y.,
Zhang Q.H.,
Wang Y.,
Zhen J.H.,
Li S.L.
Publication year - 2009
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/j.1365-2230.2009.03571.x
Subject(s) - lichen sclerosus , hypoxia (environmental) , pathogenesis , medicine , ischemia , dermatology , pathology , chemistry , oxygen , organic chemistry
Summary Background. Lichen sclerosus (LS) is a chronic inflammatory skin disease, the pathogenesis of which is poorly understood. Aim. To evaluate the role of hypoxia–ischaemia (HI) in vulvar LS. Methods. Samples from five patients with vulvar LS and five control subjects were collected for analysis by transmission electron microscopy (TEM) to reveal the ultrastructural changes of organelles and dermal blood capillaries. Samples from 37 patients with vulvar LS and 12 control subjects were collected for immunohistochemistry to detect the expression of vascular endothelial growth factor (VEGF) and the hypoxia markers hypoxia‐inducible factor (HIF)‐1α and glucose transporter (Glut)‐1. Results. Using TEM, the mitochondria of basal cells and vascular endothelial cells in vulvar LS tissue were found to be swollen with loss of cristae, and the rough endoplasmic reticulum had luminal swelling and ribosomal detachment. Damage to vascular endothelial cells, disorganization of capillary architecture and loss of capillaries were also seen. By immunohistochemistry, moderate to intense staining of VEGF was seen in almost 90% of control sections vs. about 55% of LS sections. Glut‐1 expression was negative or weak in 75% of control sections vs. moderate to very strong in about 80% of vulvar LS sections. Nuclear staining of HIF‐1α was not found in LS or control tissue. Conclusions. HI is involved in the pathogenesis of vulvar LS.