AIMS/BACKGROUND:To explore the factors influencing sleep disorders in patients with polycystic ovary syndrome (PCOS) after ketogenic diet intervention and establish a predictive model. METHODS:Data of 220 PCOS patients undergoing ketogenic diet intervention at Beijing Shijitan Hospital, Capital Medical University, from January 2021 to December 2023 were retrospectively collected. Patients were randomly divided into the modelling group (132 patients) and the validation group (88 patients) in a 3:2 ratio. The modelling group was further divided into the sleep disorder group (56 patients) and the non-sleep disorder group (76 patients). Univariate and binary logistic regression analyses were conducted to determine the influencing factors of sleep disorders after administering a ketogenic diet intervention in patients with PCOS. The predictive model was constructed using SPSS, and analyses of receiver operating characteristic (ROC) curves, calibration curves and decision curve analysis (DCA) were performed in the R language to evaluate the clinical practicality of the model. RESULTS:In the modelling group, anxiety (odds ratio [OR] = 1.768, 95% confidence interval [CI]: 1.284-2.434, p < 0.001), depression (OR = 1.494, 95% CI: 1.193-1.872, p < 0.001), blood sugar status (impaired fasting glucose/tolerance) (OR = 5.278, 95% CI: 1.533-18.177, p = 0.008) and low-density lipoprotein cholesterol (LDL-c; OR = 1.619, 95% CI: 1.201-2.181, p = 0.002) were significant factors affecting sleep disorders. The prediction model incorporates these factors (X1-X4), and the model expression is Logit(P) = βConstant + (β1X1) + (β2X2) + (β3X3) + (β4X4). The calibration curve showed good agreement between predicted risks and actual risks. ROC analysis showed that the area under the curve was 0.9328 (95% CI: 0.892-0.954) for the modelling group and 0.8431 (95% CI: 0.777-0.899) for the validation group, both indicating that the model has high accuracy. DCA curves showed that the model has significant positive net benefits and good clinical utility. CONCLUSION:Anxiety, depression, blood sugar status and LDL-c are key factors influencing sleep disorders in patients with PCOS after ketogenic diet intervention. A prediction model featuring high accuracy and remarkable clinical utility was successfully established.

To assess the overall safety and effectiveness of the etonogestrel implant radiopaque in real-world clinical settings in China. A multicenter, prospective, single-arm, observational study was conducted in women (aged ≥ 18 years) across 31 centers in China (March 2016–July 2021). The implant was prescribed as part of routine clinical practice. Primary outcomes included overall safety and topical (local) safety profile; secondary outcomes included participant and physician satisfaction and contraceptive effectiveness of the etonogestrel implant. Of 1,901 women using the etonogestrel implant, 45.4

Unexplained recurrent pregnant loss (URPL) is associated with immune imbalance at the maternal-fetal interface. Decidual immune cells regulate the response of the maternal immune system to the fetus. However, the effect of decidual stromal cells (DSCs) and trophoblast cells on cytokine secretion by decidual NK cells remains unclear. In this study, we investigated the influence of JEG-3 cells and DSCs on the secretion of cytokines in dNK cells. Furthermore, we investigated whether or not cytokine secretion was regulated by the mitogen-activated protein kinase (MAPK) signaling pathway at the maternal-fetal interface. Our study showed that the secretions of both IFN-γ and TNF-α in dNK cells in URPL were significantly higher than those in normal pregnancy. In the coculture of JEG-3, DSCs, and dNK cells, IL-10 and IL-4 production increased in dNK cells during normal pregnancy; whereas IFN-γ and TNF-α production increased but IL-10 and IL-4 levels decreased during URPL. Furthermore, pretreatment with P38/MAPK inhibition significantly inhibited the secretion of NK1- and NK2-type cytokines in the coculture of the three types of cells. Our study elucidated the influence of trophoblasts and DSCs on the expression of cytokines in dNK cells in patients with URPL and uncovered a complicated crosstalk through the MAPK signal at the maternal-fetal interface.

Objective:This study aimed to investigate the role of immune inflammation in recurrent spontaneous abortions (RSA). Methods:In this study, decidua tissues from 12 patients were collected. These included six individuals with RSA in the RSA group and six in the control group. The differences in gene and metabolite expression in the decidua of the placenta between normal pregnancies and patients with RSA were compared using transcriptomic and metabolomic analyses. The differentially expressed genes and metabolites were further analyzed through functional enrichment analysis using high-throughput sequencing technology. Results:There was a significant upregulation of genes associated with immunity and inflammation in the RSA group compared to the control group. The TNF signaling pathway was upregulated in the RSA group. Inflammatory mediators were expressed at higher levels in the RSA group, and arachidonic acid metabolism was the most significant differential metabolite set. The regulation of inflammatory mediators of transient receptor potential (TRP) channels were enriched in RSA cases. The integrated analysis of the data further suggests that the immune-inflammatory response might be an important factor in RSA. The expression levels of genes related to inflammation and hypoxia in tissues from patients with RSA were verified using quantitative reverse transcription polymerase chain reaction (qRT-PCR), and this revealed that the expression of MARK10 and TNFAIP3 genes was significantly upregulated in samples from RSA patients compared to normal tissues. Conclusion:The findings suggest a strong association between immune-related inflammation and RSA. Addressing metabolic and inflammatory aspects in patients with RSA may potentially help enhance pregnancy outcomes.

Intrauterine growth retardation (IUGR) is a major cause of perinatal morbidity and mortality. Previous studies showed that 1-nitropyrene (1-NP), an atmospheric pollutant, induces placental dysfunction and IUGR, but the exact mechanisms remain uncertain. In this research, we aimed to explore the role of mitophagy on 1-NP-evoked placental progesterone (P4) synthesis inhibition and IUGR in a mouse model. As expected, P4 levels were decreased in 1-NP-exposed mouse placentas and maternal sera. Progesterone synthases, CYP11A1 and 3βHSD1, were correspondingly declined in 1-NP-exposed mouse placentas and JEG-3 cells. Mitophagy, as determined by LC3B-II elevation and TOM20 reduction, was evoked in 1-NP-exposed JEG-3 cells. Mdivi-1, a specific mitophagy inhibitor, relieved 1-NP-evoked downregulation of progesterone synthases in JEG-3 cells. Additional experiments showed that ULK1/FUNDC1 signaling was activated in 1-NP-exposed JEG-3 cells. ULK1 inhibitor or FUNDC1-targeted siRNA blocked 1-NP-induced mitophagy and progesterone synthase downregulation in JEG-3 cells. Further analysis found that mitochondrial reactive oxygen species (ROS) were increased and GCN2 was activated in 1-NP-exposed JEG-3 cells. GCN2iB, a selective GCN2 inhibitor, and MitoQ, a mitochondria-targeted antioxidant, attenuated GCN2 activation, FUNDC1-mediated mitophagy, and downregulation of progesterone synthases in JEG-3 cells. In vivo, gestational MitoQ supplement alleviated 1-NP-evoked reduction of placental P4 synthesis and IUGR. These results suggest that FUNDC1-mediated mitophagy triggered by mitochondrial ROS may contribute partially to 1-NP-induced placental P4 synthesis inhibition and IUGR.

剖宫产瘢痕妊娠( cesarean scar pregnancy,CSP)是指孕囊着床于既往子宫切口瘢痕处的一种特殊类型的异位妊娠,2016年中国《剖宫产术后子宫瘢痕妊娠诊治专家共识》[1]指出包块型CSP属于III型CSP的特殊类型,多见于CSP术后或流产后,子宫瘢痕处妊娠物残留并继续生长,伴凝血块或坏死机化组织而形成.

Our previous study showed 1-Nitropyrene (1-NP) exposure disrupted testicular testosterone synthesis in mouse, but the exact mechanism needs further investigation. The present research found 4-phenylbutyric acid (4-PBA), an endoplasmic reticulum (ER) stress inhibitor, recovered 1-NP-induced ER stress and testosterone synthases reduction in TM3 cells. GSK2606414, a protein kinase-like ER kinase (PERK) kinase inhibitor, attenuated 1-NP-induced PERK-eukaryotic translation initiation factor 2α (eIF2α) signaling activation and downregulation of steroidogenic proteins in TM3 cells. Both 4-PBA and GSK2606414 attenuated 1-NP-induced steroidogenesis disruption in TM3 cells. Further studies used N-Acetyl-L-cysteine (NAC) as a classical antioxidant to explore whether oxidative stress-activated ER stress mediated 1-NP-induced testosterone synthases reduction and steroidogenesis disruption in TM3 cells and mouse testes. The results showed NAC pretreatment mitigated oxidative stress, and subsequently attenuated ER stress, particularly PERK-eIF2α signaling activation, and downregulation of testosterone synthases in 1-NP-treated TM3 cells. More importantly, NAC extenuated 1-NP-induced testosterone synthesis in vitro and in vivo. The current work indicated that oxidative stress-caused ER stress, particularly PERK-eIF2α pathway activation, mediates 1-NP-downregulated steroidogenic proteins and steroidogenesis disruption in TM3 cells and mouse testes. Significantly, the current study provides a theoretical basis and demonstrates the experimental evidence for the potential application of antioxidant, such as NAC, in public health prevention, particularly in 1-NP-induced endocrine disorder.

BackgroundPercutaneous extra-pedicular kyphoplasty can achieve better clinical results than transpedicular kyphoplasty. However, lumbar segment artery injury as a disaster complication limits its clinical application.ObjectiveTo describe and evaluate a modified trajectory of kyphoplasty for the treatment of osteoporotic vertebral compression fractures (OVCF).MethodsEighty-one patients who underwent percutaneous kyphoplasty (PKP) for lumbar OVCF at our hospital between May 2017 and May 2021 were enrolled. The patients were divided into an observation group (via the superior pedicle approach) and a control group (via the transpedicular approach) according to the surgical trajectory. The surgical procedure was described in detail, and the imaging parameters were recorded. Preoperative and postoperative clinical data were collected for statistical analysis.ResultsPKP via the superior pedicle notch approach could offer large abduction and cranial inclination angles without serious complications. The rate of paravertebral leakage was significantly lower in the observation group than in the control group. Surgery with a superior pedicle notch approach had a shorter operative time and fewer fluoroscopies.ConclusionsPKP via the superior pedicle notch approach is a modified extra-pedicular approach for lumbar osteoporotic vertebral compression fractures. This trajectory is an easy-to-use target position because it enters the vertebral body directly. A shorter operative time and lower radiation exposure can enhance recovery after surgery.

Research question: Do overweight/obese women with PCOS with different uric acid concentrations show different effects after a ketogenic diet intervention? Design: The study involved women with PCOS with a body mass index (BMI) of >= 24 kg/m(2). Groups showing different uric acid concentrations were given ketogenic diet guidance for 12 weeks. Weight, BMI, body fat percentage, fasting blood glucose, triacylglyerols, total cholesterol, uric acid and other metabolism-related indexes were measured. Results: After 12 weeks of the ketogenic diet intervention, body weight (hyperuricaemia group: P=0.001; non-hyperuricaemia group: P<0.001), BMI (hyperuricaemia group: P = 0.025; non-hyperuricaemia group: P<0.001) and body fat percentage (hyperuricaemia group: P<0.001; non-hyperuricaemia group: P<0.001) were decreased in both groups. There was greater weight loss in the non-hyperuricaemia group (hyperuricaemia group 11.2 +/- 4.6 kg versus non-hyperuricaemia group 14.7 +/- 4.8 kg; P < 0.05). In the non-hyperuricaemia group, uric acid concentrations increased significantly after 6 weeks of the ketogenic diet intervention (week 0: 5.69 +/- 0.84 mg/dl versus week 6: 8.41 +/- 2.33 mg/dl; P < 0.001) and reached the concentrations of the hyperuricaemia group (week 6: 9.37 +/- 2.43 mg/dl; P > 0.05). Conclusions: A ketogenic diet intervention is beneficial for overweight/obese women with PCOS with different serum uric acid concentrations. Participants with normal basal uric acid concentrations showed a greater fluctuation of serum uric acid concentrations during the ketogenic diet intervention and had a greater weight loss.

目的 荟萃分析研究前次妊娠早孕期经过对于初产妇子痫前期(Preeclampsia,PE)发病风险的影响.方法 通过检索Pubmed、Cochrane Library以及Embase数据库2021年前的相关研究,纳入涉及前次早期妊娠经过与PE发病风险的相关文献,从中筛选出11篇文献进行Meta分析.用固定效应模型分析PE发病风险,采用Begg's检验和Egger检验分析发表偏倚.统计学软件采用STATA 15.0.结果 共11篇文献纳入Meta分析,均为回顾性研究即病例对照研究.结果 显示,对于初产妇而言,前次正常妊娠早孕期经过可能降低PE 的发病风险[比值比(odd ratio,OR)=0.86,95％置信区间(confidence interval,CI)=0.81-0.91,I2=47.4％],而既往自然流产史对于PE发病无保护作用(OR=1.00,95％CI=0.95-1.06,I2=29％).无明显发表偏倚.结论 前次妊娠早孕期正常经过或可降低PE发病风险,即妊娠早期可能已经产生"记忆",对未来的妊娠起到保护作用.

Numerous studies demonstrated that bleomycin (BLM) caused acute lung injury (ALI). This study explored the role of mitochondrial reactive oxygen species (ROS) on BLM-induced ALI and pulmonary epithelial ferroptosis. Male C57BL/6J mice were intratracheally injected with BLM (3.0 mg/kg). BEAS-2B cells, human bronchial epithelial cells, were cultured with BLM (10 μg/ml). Pulmonary MDA and 4-HNE, two markers of lipid peroxidation, were elevated in BLM-exposed mice. Oxidized lipids were upregulated in BLM-exposed BEAS-2B cells. Ferroptosis-characteristic ultrastructure, mainly disappearance of mitochondrial bilayer membrane structure and cristae, was observed in BLM-exposed pulmonary epithelium. Ferrostatin-1, a specific inhibitor of ferroptosis, attenuated BLM-evoked pulmonary lipid peroxidation, ferroptosis-characteristic mitochondrial ultrastructure and pulmonary epithelial death. The in vitro experiments showed that mitochondrial membrane potentials (MMPs) were decreased and mitochondrial ROS were increased in BLM-exposed BEAS-2B cells. Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, prevented BLM-induced MMP reduction and mitochondrial ROS elevation in BEAS-2B cells. The in vivo experiment found that MitoQ attenuated BLM-evoked GSH depletion and lipid peroxidation in mouse lungs. Moreover, MitoQ prevented BLM-induced ferroptosis-characteristic mitochondrial changes, pulmonary epithelial death and ALI. In conclusion, mitochondrial ROS are an initiator of BLM-induced pulmonary epithelial ferroptosis. Mitochondria-targeted antioxidants may be used as potential therapeutic agents for BLM-induced ALI.

目的 探讨流产后包块型宫角妊娠的治疗方法.方法 回顾性分析2016年2月至2022年2月在北京妇产医院治疗的16例流产后包块型宫角妊娠患者的临床资料,分析不同治疗方式的临床疗效.结果 ①16例患者中,腹腔镜下宫角切开术+子宫修补+宫腔镜检查2例;腹腔镜或B超监测下宫腔镜下宫角胚物切除术11例;药物保守治疗3例.所有患者均治疗成功,无失血性休克及子宫切除.②13例患者在宫腹腔镜下完成手术,无中转开腹,手术时间(48.1±10.5)min,术中出血量(57.3±30.0)mL,术后阴道流血时间(8.5±2.9)d,β-hCG恢复正常时间(14.5±6.4)d.③3例药物保守治疗的患者均未生育且均有输卵管手术史,术前血β-hCG(365.8±215.6)IU/L,病灶最大径线(2.7±0.6)cm;住院时间(12.7±4.7)d,β-hCG恢复正常时间(46.0±25.5)d,包块消失时间7～8个月.结论 流产后包块型宫角妊娠可根据个体化原则选择手术治疗或药物保守治疗,宫腹腔镜联合手术治疗是较安全、有效的治疗方法;如患者药物保守治疗意愿强烈,结合其妇科手术病史,血hCG<500 IU/L～1000 IU/L,包块<3 cm也可以考虑在严密监测下行药物保守治疗.

Abstract Backgrounds Pregnancy termination during the second trimester in patients with placenta previa and placenta accreta spectrum (PAS) is a complex and challenging clinical problem. Based on our literature review, there has been a relative increase in the number of such cases being treated by hysterotomy and/or local uterine lesion resection and repair. In the present study, a retrospective analysis was conducted to compare the clinical outcomes when different management strategies were used to terminate pregnancy in the patients with placenta previa and PAS. Methods A total of 51 patients who underwent pregnancy termination in the second trimester in Beijing Obstetrics and Gynecology Hospital between June 2013 and December 2018 were retrospectively analyzed in this study. All patients having previous caesarean delivery (CD) were diagnosed with placenta previa status and PAS. Results ① Among the 51 patients, 16 cases received mifepristone and misoprostol medical termination, 15 cases received mifepristone and Rivanol medical termination, but 1 of them was transferred to hysterotomy due to failed labor induction, another 20 cases were performed planned hysterotomy. There was no placenta percreta cases and uterine artery embolization (UAE) was all performed before surgery.② There were 31 cases who underwent medical termination and 30 cases were vaginal delivery. Dilation and evacuation (D&E) were used in 20 cases of medical abortion failure and in all 30 cases of difficult manual removal of placental tissue. ③ A statistically significant difference was found among the three different strategies in terms of gestational weeks, the type of placenta previa status, main operative success rate and β-HCG regression time (P < 0.05). ④ There were 4(7.8%) cases who were taken up for hysterectomy because of life-threatening bleeding or severe bacteremia during or after delivery and hysterotomy. The uterus was preserved with the implanted placenta partly or completely left in situ in 47(92.2%) cases. Combined medical and/or surgical management were used for the residual placenta and the time of menstrual recovery was 52(range: 33 to 86) days after pregnancy termination. Conclusions Terminating a pregnancy by vaginal delivery through medical induction of labor may be feasible if clinicians have an overall understanding of gestational age, the type of placenta previa status, the type of placenta accreta, and patients concerns about preserving fertility. A collaborative team effort in tertiary medical centers with a very experience MDT and combined application of multiple methods is required to optimize patient outcomes.

目的:探讨宫内宫外同时妊娠(HP)的临床诊断及治疗.方法:回顾性分析3例HP患者的临床资料,并文献复习.结果:2例自然受孕且在人工流产术后20+d及10+d发现HP;1例是IVF术后,稽留流产清宫手术前再次复查超声时发现同时合并异位妊娠.3例患者经过及时有效的治疗,预后良好.结论:对停经后出现腹痛或阴道出血的宫内早孕的女性,无论是IVF术后还是自然妊娠,均应排除异位妊娠的可能.早期诊断和及时治疗能维持良好的宫内妊娠结局及防止发生危及生命的严重并发症.

Purpose To examine the association of chronic endometritis (CE) with cervical incompetence (CI) in Chinese women with mid-trimester loss, and the impact of the presence of CE on the outcome of laparoscopic cervical cerclage (LCC). Methods This retrospective cohort study included a study group of 293 women with mid-trimester loss due to CI (group I) and a comparison group of 332 women with recurrent first-trimester miscarriage (group II). Immunohistochemical study using CD138 epitope for the diagnosis of CE was completed in all subjects. Pre-conception LCC was undertaken in 247 women in the study group (group I). The study was approved by Institutional Review Board (IRB) (number 2015FXHEC-KY005). Results The prevalence of CE in group I was 42%, significantly (P < 0.001) higher than that of 23.5% in group II. Among 247 women in group I, there were no significant difference in mid-trimester loss rate, preterm delivery rate and term delivery rate in women with and without CE (2.2, 12.0, 85.8% vs. 1.8, 10.1, 88.1% respectively) and between women with CE treated and not treated with antibiotics prior to conception (2.3, 9.3, 88.4% vs. 2.0, 14.3, 83.7% respectively). Conclusions Mid-trimester loss due to cervical incompetence is associated with chronic endometritis; However, the presence or not of CE and whether it was treated with antibiotics prior to conception did not appear to significantly influence the obstetric outcomes of women with CI after LCC.

Previous studies demonstrated that microcystin-leucine-arginine (MC-LR) disrupted testosterone (T) synthesis, but the underlying mechanisms are not entirely elucidated. This study aims to explore the role of reactive oxygen species (ROS)-mediated GCN2/eIF2α activation on MC-LR-induced disruption of testicular T synthesis. Male mice were intraperitoneally injected with MC-LR (0 or 20 μg/kg) daily for 5 weeks. Serum T was decreased in MC-LR-exposed mice (0.626 ± 0.122 vs 24.565 ± 8.486 ng/ml, P < 0.01), so did testicular T (0.667 ± 0.15 vs 8.317 ± 1.387 ng/mg protein, P < 0.01). Steroidogenic proteins including StAR, CYP11A1 and CYP17A1 were downregulated in MC-LR-exposed mouse testes and TM3 cells. Mechanistically, p-GCN2 and p-eIF2α were elevated in MC-LR-exposed TM3 cells. GCN2iB attenuated MC-LR-induced GCN2 and eIF2α phosphorylation in TM3 cells. Moreover, GCN2iB attenuated MC-LR-induced downregulation of steroidogenic proteins in TM3 cells. Further analysis found that cellular ROS were elevated and HO-1 was upregulated in MC-LR-exposed TM3 cells. PBN rescued MC-LR-induced activation of GCN2/eIF2α signaling in TM3 cells. Additionally, pretreatment with PBN attenuated MC-LR induced downregulation of steroidogenic proteins and synthases in TM3 cells. These results suggest that ROS-mediated GCN2/eIF2α activation contributes partially to MC-LR-caused downregulation of steroidogenic proteins and synthases. The present study provides a new clue for understanding the mechanism of MC-LR-induced endocrine disruption.

Aim To evaluate the effect of a ketogenic diet (KD) in women with polycystic ovary syndrome (PCOS) and liver dysfunction who were obese. Methods Women with PCOS and liver dysfunction who were obese were enrolled in this prospective, open-label, parallel-group, controlled pilot trial, and randomly received KD (KD group) or conventional pharmacological treatment (Essentiale plus Yasmin, control group) in a 1:1 ratio for 12 weeks. The primary endpoint was the liver function markers. Secondary endpoints included the menstrual cycle, anthropometric characteristics, body composition, hormonal levels, and metabolic biomarkers. Results Of the 20 eligible participants enrolled, 18 participants completed the study. The KD group reported a significant reduction in anthropometric characteristics and body composition from baseline to week 12 (all p < 0.05). In addition, there were significant reductions in menstrual cycle, plasma estradiol, and progesterone levels in two groups (all p < 0.05), but no significant between-group difference was observed. KD significantly reduced the liver function markers compared with control group (p < 0.05). The signs of fatty liver disappeared in six out of seven fatty liver participants in KD group after 12 weeks of intervention, while only one of 10 fatty liver participants in control group disappeared. Conclusions In addition to improving the menstrual cycle, KD had the additional benefits of reducing blood glucose and body weight, improving liver function, and treating fatty liver compared to traditional pharmacological treatment in women with PCOS and liver dysfunction who were obese.

1-Nitropyrene (1-NP) is a representative nitro-polycyclic aromatic hydrocarbon from diesel exhaust. Recently, we found that maternal 1-NP exposure caused fetal growth retardation and disturbed cognitive development in adolescent female offspring. To investigate long-term 1-NP exposure on spermatogenesis and steroidogenesis, male mice were exposed to 1-NP (1.0 mg/kg/day) by gavage for 70 days. There was no significant difference on relative testicular weight, number of testicular apoptotic cells and epididymal sperm count between 1-NP-exposed mice and controls. Although long-term 1-NP exposure did not influence number of Leydig cells, steroidogenic genes and enzymes, including STAR, P450scc, P45017α and 17β-HD, were downregulated in 1-NP-expoed mouse testes. Correspondingly, serum and testicular testosterone (T) levels were reduced in 1-NP-exposed mice. Additional experiment showed that testicular GRP78 mRNA and protein were upregulated by 1-NP. Testicular phospho-IRE1α and sliced xbp-1 mRNA, a downstream molecule of IRE1α, were elevated in 1-NP-exposed mice. Testicular phospho-PERK and phospho-eIF2α, a downstream molecule of PERK pathway, were increased in 1-NP-exposed mice. Testicular NOX4, a subunit of NAPDH oxidase, and HO-1, MDA, two oxidative stress markers, were increased in 1-NP-exposed mice. Testicular GSH and GSH/GSSG were decreased in 1-NP-exposed mice. These results suggest that long-term 1-NP exposure induces reactive oxygen species-evoked ER stress and disrupts steroidogenesis in mouse testes.

[This corrects the article DOI: 10.1155/2020/6247526.].

目的 探讨不同方式治疗Ⅱ型剖宫产瘢痕妊娠(cesarean scar pregnancy,CSP)的临床疗效.方法 回顾性分析2016年1月至2017年12月在北京妇产医院生殖调节科手术治疗的225例Ⅱ型CSP的临床资料,其中114例行宫腔镜手术(非介入球囊组),72例行宫腔镜手术联合子宫动脉栓塞术(uterine artery embolization,UAE)(介入组),39例行宫腔镜手术联合宫腔球囊压迫(球囊组),分析不同治疗方式的临床疗效.结果 ①3组在年龄、孕次、剖宫产次数、流产次数、距离前次剖宫产时间、孕囊处最薄肌层厚度及是否保胎方面比较,差异无统计学意义(P>0.05);但介入组在停经天数、孕囊大小、术前血人绒毛膜促性腺激素(human chorionic gonadotropin,hCG)值、宫腔积血率及活胎率方面高于非介入球囊组(P<0.05),术前血hCG值及孕囊大小在3组间差异有统计学意义(P<0.05).②介入组手术时间短且术后血hCG下降快,但术后血hCG恢复正常时间、月经恢复时间及住院时间长,差异均有统计学意义(P<0.05).结论 Ⅱ型CSP患者行宫腔镜手术,部分联合宫腔球囊压迫或UAE治疗疗效确切.大部分未予UAE治疗的Ⅱ型CSP患者术后恢复快.对有多个高危因素如停经天数长、孕囊较大、术前血hCG值高、活胎且有宫腔积血的Ⅱ型CSP患者优先考虑UAE.