Does Pelvic Organ Prolapse Quantification Examination D Point Predict Uterosacral Ligament Suspension Outcomes?

OBJECTIVES: The best predictors for postoperative anatomic apical success after transvaginal uterosacral ligament suspension remain unknown. The aim of this study was to determine if there is a correlation between the preoperative D point and anatomic outcomes for apical prolapse after 1 year. METHODS: This retrospective cohort study included subjects undergoing transvaginal uterosacral ligament suspension from 2008 through 2013 who had at least 1 year follow-up. Demographic information, preoperative and postoperative Pelvic Organ Prolapse Quantification (POPQ) examination measurements, need for retreatment or repeat surgery, and assessment of pelvic floor symptoms were reviewed. Postoperative apical success was defined as C point descent no more than one third into the vaginal canal. RESULTS: One hundred twenty-five women met inclusion criteria and had follow-up at 1 year or more. Concomitant procedures included anterior/posterior repair and midurethral sling. Mean follow-up time was 22.8 months (range, 12-63 months). At last follow-up, 96% met criteria for apical success. A more negative preoperative D point was significantly related to improved postoperative apical support, with each 1-cm descent in preoperative D point resulting in a postoperative C point that was 0.21 cm lower (P = 0.0005). Based on the receiver operating characteristic curve, a "cutoff" D point value of -4.25 (sensitivity, 0.8; specificity, 0.65) was determined to be a predictor of postoperative apical success at 1 year or more. CONCLUSIONS: The preoperative D point correlates with postoperative apical support, and a clinically meaningful relationship exists between the preoperative D point and anatomic apical success.

Epigenetic factors and autism spectrum disorders.

Autism is a complex neurodevelopmental disorder that has significant phenotypic overlap with several diseases, many of which fall within the broader category of autism spectrum disorders (ASDs). The etiology of the disorder is unclear and seems to involve a complex interplay of polygenic as well as environmental factors. We discuss evidence that suggests that epigenetic dysregulation is highly implicated as a contributing cause of ASDs and autism. Specifically, we examine neurodevelopmental disorders that share significant phenotypic overlap with ASDs and feature the dysregulation of epigenetically modified genes including UBE3A, GABA receptor genes, and RELN. We then look at the dysregulated expression of implicated epigenetic modifiers, namely MeCP2, that yield complex and varied downstream pleiotropic effects. Finally, we examine epigenetically mediated parent-of-origin effects through which paternal gene expression dominates that of maternal contributing to contrasting phenotypes implicated in ASDs. Such preliminary evidence suggests that elucidating the complex role of epigenetic regulations involved in ASDs could prove vital in furthering our understanding of the complex etiology of autism and ASDs.