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Introduction and Hypothesis
The objective of this study was to identify the predictors of postoperative voiding dysfunction in women following extensive vaginal pelvic reconstructive surgery.Methods
We enrolled 1,425 women who had pelvic organ prolapse of POP-Q stage III or IV and had undergone vaginal pelvic reconstructive surgery with or without transvaginal mesh insertion from January 2006 to December 2014. All subjects were required to complete a 72-h voiding diary, and the IIQ-7, UDI-6, POPDI-6 and PISQ-12 questionnaires. Urodynamic study was performed preoperatively and postoperatively.Results
Of the 1,425 women, 54 were excluded due to incomplete data, and 1,017 of the remaining 1,371 (74.2 %) had transvaginal mesh surgery and 247 (18 %) had concurrent midurethral sling insertion. Of 380 women (27.7 %) with preoperative voiding dysfunction, 37 (9.7 %) continued to have voiding dysfunction postoperatively. Of the remaining 991 women (72.3 %) with normal preoperative voiding function, 11 (1.1 %) developed de novo voiding dysfunction postoperatively. The overall incidence of postoperative voiding dysfunction was 3.5 % (48/1,371). Those with concurrent midurethral sling insertion were at higher risk of developing voiding dysfunction postoperatively (OR 3.12, 95 % CI 1.79?–?5.46, p?<?0.001). Diabetes mellitus, preoperative detrusor pressure at maximal flow (Dmax) <10 cm H2O and postvoid residual volume ≥200 ml were significant risk factors for the development of postoperative voiding dysfunction (OR 3.07, 1.84 and 2.15, respectively; 95 % CI 1.69?–?5.60, 1.39?–?2.91 and 1.10?–?3.21, respectively).Conclusions
Diabetes mellitus, concurrent midurethral sling insertion, preoperative Dmax <10 cm H2O and postvoid residual volume ≥200 ml in patients with advanced pelvic organ prolapse were risk factors for the development of postoperative voiding dysfunction after vaginal pelvic reconstructive surgery. Therefore, counseling is worthwhile before considering vaginal pelvic reconstructive surgery.Area covered: We describe the clinicopathological significance of MUC4, summarize mechanisms contributing to its deregulated expression, review preclinical studies aimed at inhibiting MUC4, and discuss how MUC4 overexpression provides opportunities for developing targeted therapies. Finally, we discuss the challenges for developing MUC4-based therapeutics, and identify areas where efforts should be directed to effectively exploit MUC4 as a therapeutic target for PC.
Expert opinion: Studies demonstrating that abrogation of MUC4 expression reduces proliferation and metastasis of PC cells and enhances sensitivity to therapeutic agents affirm its utility as a therapeutic target. Emerging evidence also supports the suitability of MUC4 as a potential immunotherapy target. However, these studies have been limited to in vitro, ex vivo or in vivo approaches using xenograft tumors in immunodeficient murine models. For translational relevance, MUC4-targeted therapies should be evaluated in murine models with intact immune system and accurate tumor microenvironment. Additionally, future studies evaluating MUC4 as a target for immunotherapy must entail characterization of immune response in PC patients and investigate its association with immunosuppression and survival. 相似文献