Hypoxia-ischaemia is involved in the pathogenesis of vulvar lichen sclerosus.
BACKGROUND
Lichen sclerosus (LS) is a chronic inflammatory skin disease, the pathogenesis of which is poorly understood.


OBJECTIVE
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)-1alpha 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-1alpha was not found in LS or control tissue.


CONCLUSIONS
HI is involved in the pathogenesis of vulvar LS.
Li
Y-Z
YZ
Department of Integrated Traditional Chinese and Western Medicine, Qilu Hospital, Shandong University, Jinan, China.
Wu
Y
Y
Zhang
Q-H
QH
Wang
Y
Y
Zhen
J-H
JH
Li
S-L
SL
D000328:Adult; D014408:Biomarkers, Tumor; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000150:complications*; D007150:Immunohistochemistry; D007511:Ischemia / Q000150:complications*; D046529:Microscopy, Electron, Transmission; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology; D011230:Precancerous Conditions / Q000209:etiology / Q000473:pathology; D012016:Reference Values; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D007724:Vulvar Lichen Sclerosus / Q000209:etiology* / Q000473:pathology
D014408:Biomarkers, Tumor; D042461:Vascular Endothelial Growth Factor A