Level of Foxp3, DNMTs, methylation of Foxp3 promoter region, and CD4 + CD25 + CD127low regulatory T cells in vulvar lichen sclerosus.

This study is to investigate the pathogenesis of vulvar lichen sclerosus (VLS) by analyzing the level of Foxp3, DNMTs, methylation of Foxp3 promoter region, and CD4 + CD25 + CD127low Regulatory T cells (Tregs). This study enrolled 15 VLS patients and 25 controls. Lesional and extralesional vulvar skin tissues, normal vulvar skin tissues and peripheral blood were collected. Compared with the control group, Foxp3 protein in the lesional and extralesional skin of VLS group was significantly reduced. The levels of DNMT1 and DNMT3b proteins in lesional skin of VLS group were significantly increased. There was no difference in the total methylation rates of the promoter region of the Foxp3 gene. The methylation rates of CpG1, CpG4, CpG9, and CpG10 were significantly higher in lesional skin of VLS group than in control group. There was no correlation between the total methylation rates of 10 CpG sites and the level of Foxp3 and DNMT1 proteins; there was a positive correlation between Foxp3 and DNMT1 protein in lesional skin of VLS group (r = 0.675, p < 0.05), and a negative correlation (r = -0.665, p < 0.05) in extralesional skin of VLS group. However, there was no correlation of Foxp3 with DNMT3b. The number of CD4 + CD25 + CD127low Tregs VLS decreased significantly. The expression of Foxp3 protein and the quantity of CD4 + CD25 + CD127low Tregs in patients with VLS decreased, which may cause local or systemic abnormal immunosuppression of Tregs, leading to the occurrence of VLS. This may be related with methylation or DNMT1, which needs further verification.

The clinical characteristic differences between thrombosis-related edema and lymphedema following radiotherapy or chemoradiotherapy for patients with cervical cancer.

Thrombosis-related edema and lymphedema are two principal types of lower extremity edema results from radiotherapy alone or chemoradiotherapy for patients with cervical cancer. To characterize differences between them, a retrospective study was performed. We collected data including age, race, body weight, FIGO stage, histology type, platelet count, haemoglobin, time of definitely diagnosis, therapeutic regimen, edema type and which leg edema firstly occurred in. Of 40 patients who were eligible for this study, 32 were diagnosed as thrombosis-related edema and 8 diagnosed as lymphedema. The differences in patient age (p = 0.004), propotion of race (p = 0.021), the latent time (p = 0.002) and the mean platelet count (p = 0.019) were statistically significant. Among 32 patients with thrombosis-related edema, 34.4% were in stage II and 53.1% in stage III, 78.1% were squamous cell carcinoma. Among 8 patients with lymphedema, 87.5% were in stage II and 62.5% were squamous cell carcinoma. The differences were not statistically significant for weight (p = 0.94), histology type (p = 0.648), edema site (p = 0.236), haemoglobin (p = 0.088) between the two grouping patients. Although the small patient cohort is a limitation, the results suggest that the patients with thrombosis-related edema may have higher proportion, lower age, shorter latent edema time and more platelet count than those with lymphedema. Also, thrombosis-related edema was likely inclined to Uigur and lymphedema to Han race. We did not find statistical differences in weight, edema site, histology type and haemoglobin between patients with thrombosis-related edema and lymphedema.