Screening for Bacterial Vaginosis Prior to Delivery: A Cost-Effectiveness Study.

OBJECTIVE: The objective of this study was to compare the cost and effectiveness of three strategies for screening and/or treating bacterial vaginosis (BV) during pregnancy prior to delivery: (1) the current standard of care was neither test nor treat for BV (Treat None); (2) test all patients for BV at 36 weeks' gestation; treat if positive (Test Treat); and (3) treat all patients undergoing cesarean delivery with intravenous metronidazole at time of surgery (Treat All Cesarean). Effectiveness was defined as avoidance of postpartum surgical site infection (SSI). STUDY DESIGN: A decision analytic cost-effectiveness model was designed from a third-party payer perspective using clinical and cost estimates obtained from the literature, American College of Surgeons National Surgical Quality Improvement Program participant use file (2005-2019), 2019 National Vital Statistics, Medicare costs, and wholesale drug costs. Cost estimates were inflated to 2020 U.S. dollars. For this study, effectiveness was defined as avoidance of postpartum SSIs. RESULTS: The base case analysis that is the current standard of care of not routinely testing and treating patients for BV (Treat None) was the most expensive and least effective strategy, with a mean cost of $59.16 and infection rate of 3.71%. Empirically treating all patients for BV without testing (Treat All Cesarean) was the most effective and the least expensive strategy, with a mean cost of $53.50 and an infection rate of 2.75%. Testing all patients for BV and treating those positive for BV (Test Treat) was also relatively inexpensive and effective, with an infection rate of 2.94% and mean cost of $57.05. Compared with Treat None, we would expect the Treat All Cesarean strategy to reduce the infection rate by 26%. CONCLUSION: These findings suggest that treating pregnant patients with intravenous metronidazole at time of cesarean delivery could be an effective and cost-saving strategy. Testing and treating for BV could also be considered a reasonable strategy, as it has the added benefit of preserving antibiotic stewardship. In no analysis was the standard of care strategy of neither testing nor treating for BV before delivery the preferred strategy. KEY POINTS: · BV colonization may increase surgical site infection risk after cesarean section.. · Treatment of BV before or during delivery may be cost-saving strategies as treatment could prevent costs associated with infection.. · Further study is needed to best balance the risk of surgical site infection with antibiotic stewardship..

Outcomes and Complications for Concurrent Hernia Repair Among Women Undergoing Hysterectomy.

OBJECTIVE: To assess whether concurrent hernia repair at time of hysterectomy is associated with increased complications. METHODS: In this retrospective cohort study, patients who underwent hysterectomy and hysterectomy with concurrent hernia repair were queried using the American College of Surgeons' National Surgical Quality Improvement Program participant use file (2005-2019). Propensity score matching was performed 1:1 with respect to preoperative and operative characteristics. Outcomes were operation time, length of stay (LOS), and major and minor complications. A secondary analysis of patients who underwent hysterectomy for malignancy was performed. RESULTS: A total of 369,010 patients underwent hysterectomy, and 5,071 of those underwent hysterectomy with concurrent hernia repair. After propensity score matching, there were 5,071 patients in each arm. Hysterectomy with concurrent hernia repair had a longer operation time by 46 minutes (95% CI 42.6-49.6; P <.001) and longer LOS after surgery by 0.71 days (95% CI 0.59-0.84; P <.001). Hysterectomy with concurrent hernia repair was associated with a 21.9% higher risk (15.6% vs 12.8%; 95% CI 1.11-1.34, P <.001) of major complications and was associated with a 34.5% higher risk (7.4% vs 5.5%; 95% CI 1.16-1.56, P <.001) of minor complications. In subgroup analyses, there was no significant increase in risk among patients with body mass indexes (BMIs) lower than 40, those who were younger than age 40 years or older than age 60 years, and those with tobacco use, diabetes, or a minimally invasive surgical approach. For patients undergoing hysterectomy for malignancy, hysterectomy with concurrent hernia repair was associated with a 32-minute longer operation time (95% CI 25.2-38.8; P <.001) and a 0.35-day longer LOS (95% CI 0.04-0.67, P =.027), but there was no significant difference in major and minor complications. CONCLUSION: Hysterectomy with concurrent hernia repair is associated with increased operation time, LOS, and risk of major and minor complications compared with hysterectomy without hernia repair. The subgroup analyses suggest that hysterectomy with concurrent hernia has a similar complication risk as hysterectomy without hernia repair in select populations, such as those with BMIs lower than 40 or with known malignancy.

An obstetrician-gynecologist's review of hernias: risk factors, diagnosis, prevention, and repair.

Management of obstetrical and gynecologic patients with hernias poses challenges to providers. Risks for hernia development include well-described factors that impair surgical wound healing and increase abdominal pressure. Among the diverse populations cared for by obstetricians and gynecologists, pregnant patients and those with gynecologic malignancies are at the highest risk for hernia formation. This article provides an overview of the existing literature, with a focus on patients cared for by obstetrician-gynecologists and commonly encountered preoperative and intraoperative scenarios. We highlight scenarios when a hernia repair is not commonly performed, including those of patients undergoing nonelective surgeries with known or suspected gynecologic cancers. Finally, we offer multidisciplinary recommendations on the timing of elective hernia repair with obstetrical and gynecologic procedures, with attention to the primary surgical procedure, the type of preexisting hernia, and patient characteristics.

Treatments and outcomes in high-risk gestational trophoblastic neoplasia: A systematic review and meta-analysis.

BACKGROUND: High-risk gestational trophoblastic neoplasia (GTN) is rare and treated with diverse approaches. Limited published institutional data has yet to be systematically reviewed. OBJECTIVES: To compile global high-risk GTN (prognostic score ≥7) cohorts to summarise treatments and outcomes by disease characteristics and primary chemotherapy. SEARCH STRATEGY: MEDLINE, Embase, Scopus, ClinicalTrials.gov and Cochrane were searched through March 2021. SELECTION CRITERIA: Full-text manuscripts reporting mortality among ≥10 high-risk GTN patients. DATA COLLECTION AND ANALYSIS: Binomial proportions were summed, and random-effects meta-analyses performed. MAIN RESULTS: From 1137 records, we included 35 studies, representing 20 countries. Among 2276 unique high-risk GTN patients, 99.7% received chemotherapy, 35.8% surgery and 4.9% radiation. Mortality was 10.9% (243/2236; meta-analysis: 10%, 95% confidence interval [CI] 7-12%) and likelihood of complete response to primary chemotherapy was 79.7% (1506/1890; meta-analysis: 78%, 95% CI: 74-83%). Across 24 reporting studies, modern preferred chemotherapy (EMA/CO or EMA/EP) was associated with lower mortality (overall: 8.8 versus 9.5%; comparative meta-analysis: 8.1 versus 12.4%, OR 0.42, 95% CI: 0.20-0.90%, 14 studies) and higher likelihood of complete response (overall: 76.6 versus 72.8%; comparative meta-analysis: 75.9 versus 60.7%, OR 2.98, 95% CI: 1.06-8.35%, 14 studies), though studies focused on non-preferred regimens reported comparable outcomes. Mortality was increased for ultra-high-risk disease (30 versus 7.5% high-risk; meta-analysis OR 7.44, 95% CI: 4.29-12.9%) and disease following term delivery (20.8 versus 7.3% following molar pregnancy; meta-analysis OR 2.64, 95% CI: 1.10-6.31%). Relapse rate estimates ranged from 3 to 6%. CONCLUSIONS: High-risk GTN is responsive to several chemotherapy regimens, with EMA/CO or EMA/EP associated with improved outcomes. Mortality is increased in patients with ultra-high-risk, relapsed and post-term pregnancy disease.

Diversity and transparency in gynecologic oncology clinical trials.

PURPOSE: Clinical trials advance the standard of care for patients. Patients enrolled in trials should represent the population who would benefit from the intervention in clinical practice. The aim of this study was to assess whether clinical trials enrolling patients with gynecologic cancers report racial and ethnic participant composition and to examine the level of diversity in clinical trials. METHODS: Using ClinicalTrials.gov, we identified clinical trials enrolling patients with ovarian, uterine/endometrial, cervical, vaginal, and vulvar cancers from 1988 to 2019. Race and ethnicity data were extracted from participant demographics. Descriptive statistics on race, ethnicity, cancer type, location, study status, and sponsor type were calculated. Among trials which reported race and/or ethnicity, sub-analyses were performed on composition of race and ethnicity by funding source, location, and completed study status. RESULTS: A total of 1,882 trials met inclusion criteria; only 179 trials (9.5%) reported race information. Of these, the racial distribution of enrollees was 66.9% White, 8.6% Asian, 8.5% Black/African American, 0.4% Indian/Alaskan Native, 0.1% Native Hawaiian/Pacific Islander, 1.0% more than one race, and 14.5% unknown. Only 100 (5.3%) trials reported ethnicity. Except for trials enrolling patients with cervical cancer which enrolled 65.2% White and 62.1% Non-Hispanic/Latino/a patients, enrollees in trials for other gynecologic cancers were over 80% White and 88% Non-Hispanic/Latino/a. Industry funded trials enrolled higher proportions of White (68.4%) participants than non-industry funded trials (57.5%). Domestic trials report race (11.5%) and ethnicity (7.6%) at higher rates than international trials (6.9% and 2.3%, respectively). Reporting of race (1.7% vs. 13.9%) and ethnicity (1.7% vs. 11.1%) has increased over time for patients enrolled in 2000 vs. 2018. CONCLUSION: Less than 10% of trials enrolling patients with gynecologic malignancies report racial/ethnic participant composition on ClinicalTrials.gov. Accurate reporting of participant race/ethnicity is imperative to ensuring minority representation in clinical trials.

Stress hormones are associated with inflammatory cytokines and attenuation of T-cell function in the ascites from patients with high grade serous ovarian cancer.

Mounting evidence suggests that chronic stress and subsequent distress can promote ovarian cancer progression. These altered psychological states have been linked to sustained release of stress hormones, activation of the ß-adrenergic receptors in ovarian cancer cells, and induction of pro-tumoral signaling pathways. In addition, data suggest that chronic stress promotes an inflammatory landscape highlighted by increased infiltration of tumor-associated macrophages into the ovarian tumor microenvironment (TME). In ovarian cancer, ascites is a unique TME comprised of tumor, and immune cells, which secrete pro-tumoral cytokines and chemokines that modulate tumor-associated immunity. However, our knowledge about how stress hormones impact the ascites TME remains limited. We hypothesized that the ascites harbors measurable levels of stress hormones, and accumulation of these in the ascites generates a pro-tumorigenic, inflammatory, and immunosuppressive TME. We evaluated ascites samples from 49 patients with high grade serous ovarian cancer (HGSOC) and quantified cortisol and stress hormones metabolites, metanephrine (MN), and normetanephrine (NMN) in all samples. We also measured 38 individual cytokines in the ascites, including several pro-inflammatory cytokines, such as IL-6, which were positively correlated to MN or NMN levels of those samples. Conversely, we found cortisol levels were negatively correlated to several pro-inflammatory cytokines. As T-cells are integral to the TME and our analyses identified cytokines in the ascites known to modulate T-cell function, we characterized ascites-derived T-cells and assessed the impact of stress hormones on the T-cell phenotype. Our data show an altered CD4+/CD8+ T-cell ratio and a heterogeneous expression of exhaustion markers in T-cells from the ascites, while ascites-derived CD8+ T-cells exposed to epinephrine had decreased co-expression CD38 and Granzyme B. To extend these findings to animal models, we subjected ovarian cancer-bearing mice to daily restraint stress, which resulted in increased tumor growth in two models. Congruent with our human analyses, we detected corticosterone, MN, and NMN in the ascites from tumor-bearing mice, and these stress hormones correlated with several inflammatory cytokines. Moreover, daily restraint stress leads to increased CD4+PD-1+/CD8+PD-1+ T-cell ratio in the ovarian tumor microenvironment. Overall, these data highlight a role of stress hormones in the ascites TME as a driver of tumor-associated inflammation, T-cell suppression, and disease progression.