Objective: To systematically review and meta-analyze evidence on surgical outcomes after uterine artery occlusion (UAO) at myomectomy. Design: Systematic review and meta-analysis. Setting: Not applicable. Patient(s): Twenty-six studies involving 2,871 patients located via database searches of MEDLINE, Embase, Web of Science, PubMed, clinicaltrials.gov, and cited references. Intervention(s): Intervention groups undergoing UAO at laparoscopic or abdominal myomectomy (UAOþM) (1,569 patients), and control groups undergoing myomectomy alone (1,302 patients). Main Outcome Measure(s): Primary outcome of surgical blood loss (estimated blood loss, transfusion rate, and change in hemoglobin values), and secondary outcomes including operative time, length of stay, conversion and complications rates, fibroid recurrence, and changes in fibroid-related symptoms. Result(s): The patients undergoing UAOþM had a statistically significant reduction in estimated blood loss (mean difference [MD] À103.7 mL; 95% confidence interval [CI], À126.5 to À80.8), blood transfusion (relative risk [RR] 0.24; 95% CI, 0.15-0.39), and change in hemoglobin values (MD À0.60 g/dL; 95% CI, À0.79 to À0.40) compared with controls. Using UAOþM prolonged operative times (MD 10.9 minutes; 95% CI, 3.5-18.2) but shortened the length of stay (MD À0.37 days; 95% CI, À0.62-0.11). Using UAOþM lowered the complication rates (RR 0.73; 95% CI, 0.52-1.00) to the threshold of statistical significance and reduced the risk of fibroid recurrence (RR 0.36; 95% CI, 0.16-0.83) compared with controls. Conclusion(s):Uterine artery occlusion at myomectomy is associated with decreased surgical blood loss and transfusion rate compared with control patients. However, further research is required on reproductive outcomes and the effect on ovarian reserve before routine use can be recommended in women desiring future fertility. (Fertil Steril Ò 2019;111:816-27. Ó2018 by American Society for Reproductive Medicine.) El resumen está disponible en Español al final del artículo.

No abstract

In order to advance the field of idiopathic OAB, more trials are needed that profile and test urgency outcomes in participants according to suspected underlying pathophysiology. Neurourol. Urodynam. 33:611-617, 2014. © 2014 Wiley Periodicals, Inc.

BackgroundFibulin-5 is an extracellular matrix glycoprotein that plays critical roles in vasculogenesis and embryonic development. Deletion of Fibulin-5 in mice results in enhanced skin vascularization and upregulation of the angiogenesis factor angiopoietin-1 (Ang-1), suggesting that Fibulin-5 functions as an angiogenesis inhibitor. In this study, we investigate the inhibitory effects of Fibulin-5 on Ang-1/TIE-2 receptor pathway signaling and cell survival in human endothelial cells.Methodology/Principal FindingsRecombinant wild-type and RGE-mutant Fibulin-5 proteins were generated through stable transfection of HEK293 and CHO cells, respectively. In vitro solid phase binding assays using pure proteins revealed that wild-type Fibulin-5 does not bind to Ang-1 or TIE-2 proteins but strongly binds to heparin. Binding assays using human umbilical vein endothelial cells (HUVECs) indicated that wild-type Fibulin-5 strongly binds to cells but RGE-mutant Fibulin-5, which is incapable of binding to integrins, does not. Pre-incubation of HUVECs for 1 hr with Fibulin-5 significantly increased caspase 3/7 activity, ERK1/2 phosphorylation, and expressions of the transcription factor early growth response 1 (EGR1) and the dual-specificity phosphatase 5 (DUSP5). Fibulin-5 also strongly attenuated Ang-1-induced TIE-2 and AKT phosphorylation, decreased Ang-1-induced expressions of the transcription factors Inhibitor of DNA Binding 1 (ID1) and Kruppel-like Factor 2 (KLF2), and reversed the inhibitory effect of Ang-1 on serum deprivation-induced cytotoxicity and caspase 3/7 activity.Conclusion/SignificanceWe conclude that Fibulin-5 strongly binds to the endothelial cell surface through heparin-sulfate proteoglycans and possibly integrins and that it exerts strong anti-angiogenic effects by reducing endothelial cell viability and interfering with the signaling pathways of the Ang-1/TIE-2 receptor axis.