Uterine Anteroposterior Diameter Measured by Transvaginal Sonography is a Predictor for Dysmenorrhea in Patients With and Without Endometriosis: A Pilot Study.

PURPOSE: The aim of this study was to determine the correlation between uterine diameters and menstrual abdominal pain intensity in patients with and without endometriosis (EM), and the independent influence of EM on the pain intensity. METHODS: Uterine diameters and the diagnosis of adenomyosis were ascertained by transvaginal ultrasonography (TVS). Menstrual abdominal pain intensity was estimated by visual analog scale (VAS). Linear regression was used to figure out the impact of uterine diameters and EM on the VAS scores. Logistic regression was used to calculate the correlation between uterine diameters and the diagnosis of adenomyosis. The cutoff values of uterine anteroposterior diameter (AD) to predict dysmenorrhea (VAS ≥ 4) and the diagnosis of adenomyosis were determined by receiver operating characteristic curves. RESULTS: There were 220 patients with and 233 patients without EM included. Uterine AD independently correlated with the VAS scores in patients with (B = .230, P = .000) and without (B = .203, P = .000) EM. A uterine AD of 39.5 mm predicted dysmenorrhea in both groups. The presence of EM increased the VAS scores by 1.151 points when controlling for uterine diameters. Uterine AD also independently correlated with the diagnosis of adenomyosis under TVS in patients with (OR = 1.212, 95% CI = 1.130-1.301; P = .000) and without (OR = 1.192, 95% CI = 1.123-1.263; P = .000) EM. A uterine AD of 38.5 and 39.5 mm predicted the diagnosis of adenomyosis under TVS in patients with and without EM, respectively. CONCLUSIONS: Increased uterine AD, which is probably ascribed to adenomyosis, plays an important role in augmented menstrual abdominal pain intensity. Meanwhile, the presence of EM reinforces the pain.

Macrophage polarization in placenta accreta and macrophage-trophoblast interactions.

PROBLEM: Placenta accreta (PA) is defined by an abnormal invasion of placental trophoblasts into the myometrium, which can lead to serious postpartum complications. Macrophages play an important role in the regulation of trophoblast function. Both granulocyte colony-stimulating factor (G-CSF) and its receptor (granulocyte colony-stimulating factor receptor, G-CSFR) have effects on trophoblast invasion. However, the current understanding of G-CSF secretion, G-CSFR expression, abnormal polarization of decidual macrophages (dMϕ) in PA and the abnormal invasion of placental trophoblasts into the myometrium are limited. METHOD OF STUDY: The polarization of dMϕ in PA was analyzed by flow cytometry (FCM), and the expression of G-CSFR in placental trophoblasts in PA was evaluated by immunohistochemistry. In an in vitro co-culture model, we investigated the effects of HTR-8/SVneo trophoblasts cell line (HTR-8) on macrophage human monocyte cell line (THP-1) polarization and G-CSF secretion, and we also analyzed the effects of THP-1 cells, especially M2-like subtype, on primary trophoblasts and HTR-8 proliferation, invasion, and adhesion. FCM, transwell assays, adhesion assays, and proliferation assays were used in the above model. RESULTS: Compared with controls (n = 9), dMϕ showed significantly lower levels of M1 markers CD80 and CD86 and higher levels of the M2 markers CD163 and CD206, and G-CSFR expression of placental trophoblasts was increased in PA (n = 5). In vitro experiments showed that the trophoblast HTR-8 cell line induced polarization of THP-1 cells to an M2-like subtype and increased their secretion of G-CSF. Furthermore, IL-4/IL-13-induced M2-like THP-1 macrophages were able to increase the expression of G-CSFR, proliferation, invasion and adhesion of both primary trophoblasts and HTR-8 trophoblasts. CONCLUSIONS: There is an altered immune imbalance at the maternal-fetal interface in PA, which further may lead to abnormal trophoblast function. G-CSF and its receptors may play important roles in abnormal polarization of macrophages and abnormal invasion of trophoblasts.

A Comparison of Ultrasound Guided Curettage With and Without Uterine Artery Embolization on Controlling Intraoperative Blood Loss for a Cesarean Scar Pregnancy Treatment: Study Protocol for a Randomized Clinical Trial.

Introduction: Cesarean scar pregnancy affects 6% of all ectopic pregnancies in women with prior cesarean section, and there is currently no consensus on the optimal treatment. Options of surgical treatment have a risk of intraoperative blood loss; therefore, uterine artery embolization (UAE) has been considered as an option of reducing intraoperative blood loss. However, UAE may be overused in clinical practice, especially in China. We present this protocol for a randomized clinical trial investigating the necessity of performing UAE for cesarean scar pregnancy, in combination with surgical suction curettage, taking into account the different subtypes of cesarean scar pregnancy. We recently developed a risk-scoring system (QRS) to estimate intraoperative blood loss, with 93.8% sensitivity and 6.3% false negative. Through this randomized clinical trial, we will retrospectively validate the QRS score on predicting intraoperative blood loss. Methods and Analysis: We propose undertaking a randomized clinical trial sequentially recruiting 200 patients. All the patients will randomly receive ultrasound guided curettage with or without UAE. Data on the subtypes of cesarean scar pregnancy (Types 1 and II and III) detected by ultrasound will be collected before operation. The score on estimating intraoperative blood loss assessed by our recently developed quantitative risk-scoring system (QRS) will be collected before the operation. We will primarily compare the duration of the operation, intraoperative blood loss, and complications between the two groups. We will also retrospectively analyze the association of subtypes of cesarean scar pregnancy and the options of treatment and validate the QRS score. Outcomes of subsequent pregnancy within the 2-year follow-up will be secondary outcomes. Trial Registration Number: [website], identifier ChiCTR2100041654.