Adjuvants to prevent reformation of adhesions following adhesiolysis for Asherman syndrome: a systematic review and meta-analysis.

Two international guidelines published on the management of Asherman syndrome (AS) have made recommendations on various adjuvant methods to prevent intrauterine reformation. Nevertheless, the effectiveness of these methods when used in primary or secondary prevention settings is different. Our aim is to assess the effectiveness of various adjuvant methods for the secondary prevention of intrauterine adhesions (IUAs). Articles were considered eligible if they included subjects with AS before surgery and compared a chosen method with either a control or a comparison group (using another method). The primary outcome was the IUA reformation rate at follow-up hysteroscopy. A total of 29 studies [15 randomised controlled trials (RCTs) and 14 cohort studies] were included. Adhesion reformation with various methods to prevented IUA reformation when compared with controls were: second-look hysteroscopy: [risk ratio (RR): 0.21, 95% confidence interval (CI): 0.05-0.90 (p = 0.02)]; intrauterine contraceptive device: RR: 0.64, 95% CI: 0.36-1.12 (p = 0.12); continuous intrauterine balloon: RR: 0.18, 95% CI: 0.05-0.68 (p = 0.01); intermittent intrauterine balloon: RR: 0.50, 95% CI: 0.31-0.80 (p = 0.004); anti-adhesion gel: RR: 0.80, 95% CI: 0.58-1.10 (p = 0.17); amnion graft: RR: 0.63, 95% CI: 0.44-0.91 (p = 0.01).

[Expression of cyclin D1 and p16 protein in vulvar white lesion].

OBJECTIVE: To investigate the relationship between cell cycle protein (cyclin D1 and p16) expression and vulvar white lesion. METHODS: Biopsies from 34 cases with vulvar white lesion, including 12 cases with lichen sclerosus (LS), 18 with squamous hyperplasia (SH) and 4 SH accompanied with LS, were examined for protein expression of cyclin D1 and p16 using immunohistochemical techniques. Normal vulvar tissues from 11 patients with other benign gynecologic diseases were used as control. RESULTS: Fifty-six percent of patients with vulvar white lesion were immunopositive for cyclin D1 protein, which was significantly higher than that of control group (9%, P < 0.05); but there was no significant difference between LS (58%) and SH patients (50%, P > 0.05) in expression of cyclin D1 protein. Immunopositive expression of p16 protein in patients was 6%, with no significant difference from the control group (0, P > 0.05). CONCLUSIONS: Cyclin D1 and p16 are important factors modulating cell cycle. The interrupt of balance between these two factors derived from abnormal expression of cyclin D1 may be one of the causes of vulvar white lesion.