[Treatment of pregnancy in a previous caesarean section scar with uterine artery embolization: analysis of 60 cases].

OBJECTIVE: To evaluate the security and effectiveness of uterine artery embolization (UAE) in treatment of pregnancy in uterine caesarean scar compared with medicine treatment. METHODS: Sixty patients with pregnancies in uterine caesarean scar were divided into medicine group (n = 31) that received intravenous injection of methotrexate (MTX) 100 mg once or MTX 20 mg once a day for 5 days as the first course, received the second course when the serum beta-human chorionic gonadotropin (HCG) decreased to the level as < 50%, and then underwent uterine curettage; and UAE group (n = 29) that underwent catheterization into the left uterine artery and then uterine curettage 48h after the successful embolization. The bleeding volume during suction curettage, side effects, admission day, and menstruation recover time were recorded. RESULTS: The hospital stay of the UAE group was (14.4 +/- 1.67) days, significantly shorter than that of the medicine group [(39.3 +/- 4.71) days, P < 0.05]. No patient had to receive hysterectomy in the UAE group but 2 in the medicine group underwent hysterectomy. Seven patients showed liver dysfunction and 8 patients had nausea and slight vomit in the medicine group, and 15 patients with fever and 10 with light post-embolization syndromes were found in the UAE group. Menstruation resumed normal in all patients of the 2 groups one or two months later. CONCLUSION: With the advantage of low risk of heavy bleeding and shorter admission day, UAE is safe and effective in treatment of pregnancy in uterine caesarean scar.

Risk factors for intraoperative hemorrhage at evacuation of a cesarean scar pregnancy following uterine artery embolization.

OBJECTIVE: To determine risk factors associated with massive uterine bleeding during dilation and suction curettage (D&C) after uterine artery embolization (UAE) for the treatment of cesarean scar pregnancy (CSP). METHODS: Data from 128 CSP patients treated with D&C after UAE were analyzed to assess risk factors associated with massive uterine bleeding (blood loss 500mL or more) during D&C after UAE. RESULTS: In total, 15 CSP patients had massive bleeding during D&C after UAE. Univariate analysis showed that a greater gestational age (GA), a larger CSP mass size, a thinner myometrium at the implantation site, a GA of 8weeks or more, a CSP mass diameter of 6cm or more, and evidence of fetal heartbeat were risk factors for massive bleeding (P<0.05). In a binary logistic regression analysis, GA of 8weeks or more and CSP mass diameter of 6cm or more remained as the only significant risk factors for massive bleeding (OR 11.49 [95% CI 1.08-122.13] and OR 96.59 [95% CI 6.20-150.57], respectively; P<0.05). CONCLUSION: For CSP masses with a GA of 8weeks or more and a diameter of 6cm or more, the outcome of surgical evacuation after UAE tends to be unsatisfactory.

Low-dose mifepristone increases uterine expression of aquaporin 1/aquaporin 2 at the time of implantation.

BACKGROUND: The aim of this study was to investigate the mechanism by which low-dose mifepristone serves as an antiimplantation contraceptive drug. A human endometrial explant system was used to study the effects of low-dose mifepristone (65 nmol/L and 200 nmol/L) on expression of the water channel family aquaporins, aquaporin-1 and aquaporin-2 (AQP1/AQP2), at the time of implantation. STUDY DESIGN: Endometrial samples from 17 normally cycling patients at the "window of implantation" were treated with different concentrations of mifepristone. The protein and mRNA expression of AQP1/AQP2 in the endometrium was examined using immunohistochemistry (IHC) and reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. RESULTS: The IHC and RT-PCR analyses demonstrated that expression of AQP1/AQP2 was increased by mifepristone in a dose-dependent manner, with the highest AQP1/AQP2 expression levels detected in subjects treated with 200-nmol/L mifepristone. CONCLUSION: Low-dose mifepristone may negatively regulate implantation by increasing AQP1/AQP2 protein and mRNA expression. The findings from this study provide further evidence to support the potential contraceptive activity of low-dose mifepristone.

Low-dose mifepristone increases uterine natural killer cell cytotoxicity and perforin expression during the receptive phase.

OBJECTIVE: To investigate the immunologic mechanism by which low-dose mifepristone serves as an anti-implantation contraceptive drug. DESIGN: In vitro study. SETTING: University hospital and research laboratory. PATIENT(S): Fifteen normally cycling patients at the "window of implantation." INTERVENTION(S): A human endometrial explant system was used to study the effects of low-dose mifepristone (65 and 200 nmol/L) on uterine natural killer (uNK) cells. Endometrial samples were treated with different concentrations of mifepristone. MAIN OUTCOME MEASURE(S): The cytotoxicity of uNK cells to K562 target cells and the expression of perforin (PFN) by uNK cells were examined using a methyl thiazolyl tetrazolium (MTT) assay and double immunohistochemistry, respectively. RESULT(S): Both uNK cell cytotoxicity and expression of PFN were increased after treatment with 65 or 200 nmol/L mifepristone, and these effects were dose-dependent. CONCLUSION(S): Mifepristone may negatively regulate implantation by increasing the cytotoxicity of uNK cells, and this increased cytotoxicity may result from increased PFN expression. These findings provide further evidence to support the potential contraceptive activity of low-dose mifepristone.

The effect of mifepristone on the peripheral blood natural killer cell's cytotoxicity and expression of CD94/NKG2A and NKG2D during the implantation phase.

OBJECTIVE: To investigate the effect of mifepristone on peripheral blood natural killer cell's (pbNK) cytotoxicity and the expression of the inhibitory receptor CD94/NKG2A and the activated receptor NKG2D on pbNK cells. DESIGN: In vitro study. SETTING: University hospital and research laboratory. PATIENT(S): Twenty healthy nonpregnant women. INTERVENTION(S): Detected the cytolytic activity of pbNK to K562 target cells; measured the expression of CD94/NKG2A and NKG2D on pbNK. MAIN OUTCOME MEASURE(S): Cytotoxicity of pbNK was detected by Methyl thiazolyl tetrazolium. The expression of CD94/NKG2A and NKG2D receptor on pbNK cells were detected by flow cytometry. RESULT(S): The NK cell cytotoxicity and the expression of inhibitory receptor CD94/NKG2A during the proliferative phase (81.71 +/- 11.5, 86.6 +/- 9.0) was significantly higher than the secretory phase (60.16 +/- 19.2, 60.15 +/- 31.0). The NK cells cytotoxicity, after being treated with mifepristone and the expression of inhibitory receptor CD94/NKG2A on pbNK cells treated with 200 nmol/L mifepristone, were significantly increased. Mifepristone had no effect on the expression of activating receptor NKG2D. CONCLUSION(S): These data suggest that Mifepristone maybe exert its anti-implantation function by increasing NK cytotoxicity. The increasing NK cytotoxicity of mifepristone is not related to CD94/NKG2A and NKG2D. In the secretory phase down-regulated CD94/NKG2A, NKG2D, and NK cytotoxicity may benefit with embryo implantation.

Mifepristone as an anti-implantation contraceptive drug: roles in regulation of uterine natural killer cells during implantation phase.

PROBLEM: To investigate the immunological mechanism of low-dose mifepristone acting as a contraceptive at the level of the endometrium. METHOD OF STUDY: Endometrial explants were cultured in vitro with or without mifepristone treatment for 24 hr. Some tissues were fixed and immunostained for CD56, while other tissues were dissociated and cells analysed by three colour flow cytometry for CD3, CD56 and CD16. RESULTS AND CONCLUSION: Results showed a significant increase in the number of CD56(+) natural killer (NK) cells and the percentages of CD3(-) CD56(+) CD16(-) NK cell subset in the tissue treated with mifepristone, while the percentage of CD3(-) CD56(+) CD16(+) NK cell subset remained unaffected. It shows that low-dose mifepristone increases the number of CD56(+) NK cells and the percentage of CD3(-) CD56(+) CD16(-) NK subset in receptive endometrium and provides new insights into the immunological mechanism of low-dose mifepristone as an anti-implantation contraceptive drug.