Preeclampsia (PE) is a severe and highly prevalent pregnancy complication with a complex pathogenesis involving multiple pathological processes. Studies have demonstrated that the expression levels and functions of certain specific chemokines and their receptors are significantly different between pregnant women with PE and normal pregnant women. These abnormalities can be cooperatively regulated through multiple signaling pathways, disrupting the immune tolerance homeostasis at the maternal-fetal interface and inducing local immune microenvironment disturbances. Simultaneously, they interfere with normal placental vascular development and remodeling, and significantly inhibit the migration, invasion and infiltration capabilities of trophoblast cells. Consequently, they contribute to impaired spiral artery remodeling, placental hypoperfusion and ischemic-hypoxic injury, excessive activation of systemic inflammatory responses, and vascular endothelial dysfunction, ultimately participating in and mediating the onset and progression of PE. This review summarizes recent research advances regarding the role of chemokines and their receptors in the pathogenesis of PE, aiming to provide a theoretical basis and new insights for the diagnosis and treatment of PE.

The preterm birth rate in twin pregnancies is 47.6%-69.0%, with the late preterm birth rate ranging from 33.0% to 59.8%, which is significantly higher than in singleton pregnancies. The use of antenatal corticosteroids (ACS) before 34 weeks of gestation can effectively reduce complications such as neonatal mortality, but its application in late preterm birth is controversial, especially in twin pregnancies. Most studies support that ACS can reduce respiratory complications such as respiratory distress syndrome in late preterm neonates from twin pregnancies. However, some studies find no clear association between them, and the effect is inferior to that in singleton pregnancies. The long-term impact of ACS on the neurological development of late preterm infants from twin pregnancies is not yet clear. Some evidence suggests a possible increased risk of cognitive developmental delays, attention deficits, and hyperactivity disorders. Animal experiments have also verified the potential neuroinjury mechanisms of ACS. Concurrently, ACS may increase the risk of hypoglycemia in late preterm infants from twin pregnancies, and hypoglycemia also has a potential association with long-term neurodevelopmental abnormalities. Currently, there is a lack of consensus in both domestic and international guidelines regarding the routine use of ACS in late preterm twin pregnancies, with most recommending individualized decision-making.

Miscarriage is a common complication during pregnancy with a high incidence and complex etiology. Thyroid peroxidase antibody (TPOAb) positivity serves as an independent risk factor for miscarriage. It can directly damage the placenta via mechanisms such as immune inflammation and oxidative stress, independent of thyroid function, ultimately leading to miscarriage. Furthermore, TPOAb positivity can induce subclinical hypothyroidism (SCH). When they coexist, a vicious cycle of immune damage and thyroid hormone insufficiency can significantly exacerbate the risk of miscarriage. Levothyroxine (L-T₄) is the primary medication for treating SCH during pregnancy. However, its efficacy in preventing miscarriage and improving live birth outcomes remains controversial, particularly in patients with isolated TPOAb positivity or mild SCH, where the benefits are unclear. The optimal timing of intervention and dosing regimen also require further optimization. Future research should focus on precise risk stratification and early intervention strategies to provide evidence-based medical support for clinical practice.

Objective: To compare the performance of multiple machine learning algorithms in developing predictive models for neonatal hypoglycemia (NH), with the aim of early identification of high-risk pregnant women likely to deliver neonates with hypoglycemia. Methods: A retrospective analysis was conducted on 286 pregnant women admitted to Shanxi Children's Hospital from January 2021 to July 2025. Participants were randomly allocated into a training set (n=200) and a test set (n=86) at a 7:3 ratio. The primary outcome measure was the occurrence of NH. Feature selection was performed using univariate analysis, LASSO regression, and the Boruta algorithm. Predictive models were constructed based on the selected features, and Bootstrap cross-validation was applied for model validation. Results: Through univariate analysis, LASSO regression, and Boruta feature selection, pre-pregnancy body mass index, gestational weight gain,mode of delivery,gestational diabetes mellitus, hypertensive disorders of pregnancy, antenatal corticosteroid therapy for fetal lung maturation, neonatal birth weight,and preterm birth were identified as influencing factors for NH (P<0.05). In the training set, the AUC values for the random forest, decision tree, support vector machine, and Logistic regression models were 0.967, 0.943, 0.800, and 0.955, respectively; the corresponding values in the test set were 0.921, 0.860, 0.882, and 0.910, respectively. A comprehensive comparison of performance metrics across both the training and test sets demonstrated that the random forest model achieved superior overall performance. Conclusions: The random forest model can be applied to predict the risk of NH occurrence and demonstrates considerable clinical utility.

Congenital factor Ⅺ deficiency is a rare autosomal recessive inherited disease. Physiological changes during pregnancy may aggravate coagulation abnormalities, increasing the risk of intrapartum and postpartum hemorrhage and posing a serious threat to maternal and fetal safety. We report a case of a 32-year-old patient at 39⁺¹ weeks of gestation who was found to have prolonged activated partial thromboplastin time (APTT) during pregnancy. Congenital factor Ⅺ deficiency was confirmed by coagulation factor assays. Through multi-disciplinary team consultation, fresh frozen plasma transfusion was administered to correct the coagulation function. Successful vaginal trial of labor was achieved under close monitoring, with favorable maternal and neonatal outcomes. Coagulation function screening during pregnancy and etiological identification of abnormalities are crucial. For patients with congenital coagulation factor deficiency, individualized diagnosis and treatment plans should be developed for the perinatal period, and multidisciplinary collaborative management can effectively ensure maternal and neonatal safety.

This case report describes a 22-year-old primigravida admitted at 40⁺¹ weeks of gestation for delivery. Due to arrest of labor, an emergency cesarean section was performed. Postoperatively, the patient developed recurrent high fever, respiratory symptoms, and manifestations of heart failure. Through multi-disciplinary team consultation, a definitive diagnosis was established: puerperal infection complicated by bacterial pneumonia, and peripartum cardiomyopathy with cardiac insufficiency induced by severe infection. Treatment consisted of antibiotic therapy with Piperacillin-Tazobactam combined with minocycline, and anti-heart failure management centered on Sacubitril-Valsartan, metoprolol, and diuretics. The patient's infection was effectively controlled, and her cardiac function along with related parameters returned to normal. The patient was discharged on postoperative day 15 following recovery. Severe infection is a significant risk factor for triggering perinatal cardiomyopathy. For pregnant women presenting with complex and critical postpartum complications, early recognition, timely initiation of the multidisciplinary collaborative approach, and implementation of individualized comprehensive treatment are crucial for successful management and improved prognosis.

In recent years, the incidence of gynecological malignancies such as cervical cancer, endometrial cancer, and ovarian cancer has been increasing, gradually extending to younger populations and posing a serious threat to women's life and health. Although standardized treatments have benefited some patients, challenges such as strong tumor heterogeneity, high rates of recurrence and metastasis, and drug resistance persist, resulting in suboptimal overall prognosis. There is an urgent need to identify novel molecular targets for precise therapy and prognostic evaluation. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is a molecule that maintains cellular membrane homeostasis and lipid metabolic balance. It is highly expressed in cervical cancer, endometrial cancer, and ovarian cancer, promoting tumor cell proliferation, migration, and invasion through pathways such as phospholipid metabolism, epithelial-mesenchymal transition, ferroptosis, and cholesterol metabolism. LPCAT1 is closely associated with high tumor invasiveness, metastasis, and poor prognosis. In-depth investigation into the molecular mechanisms and clinical applications of LPCAT1, particularly inhibitory strategies targeting LPCAT1, is expected to provide important support for early diagnosis, prognosis evaluation, and targeted therapy of gynecological malignancies.

The application value of epigenetic biomarkers in the precision screening of cervical cancer is becoming increasingly prominent. Among these, the aberrant methylation of paired box gene 1 (PAX1) and junctional adhesion molecule 3 (JAM3) serves as a key epigenetic event during the malignant transformation of host cells. It can objectively reflect the abnormal transformation state of cervical epithelial cells, establishing itself as a biomarker for the early diagnosis of cervical cancer. PAX1 exerts tumor-suppressive role by inhibiting multiple carcinogenic pathways such as Wnt/β-catenin, and its methylation is a sensitive indicator in the early stages of carcinogenesis. JAM3 is closely related to epithelial barrier function and tumor invasion and metastasis, with its methylation level significantly increasing with disease progression. The combined methylation testing of these two genes exhibits high sensitivity and specificity, significantly outperforming traditional cytological methods. It not only enables precise and early identification but also effectively triages individuals who test positive in primary HPV screening, reducing unnecessary referrals for colposcopy. Furthermore, this test is applicable to the "self-sampling" mode, which helps improve screening accessibility in primary care and resource-limited settings. Additionally, combined PAX1/JAM3 methylation testing can predict the risk of pathological upgrading after cervical conization, guiding individualized therapeutic decisions. In the future, multi-center, large-sample clinical studies are needed to further establish standardized cut-off values for PAX1/JAM3 methylation. This combined testing is expected to be integrated as a core technology into cervical cancer screening guidelines, promoting a major shift in cervical cancer screening from "population-based screening" to a model of "individualized precision prevention and control."

The p53-abnormal (p53abn) subtype is the molecular subtype with the worst prognosis in endometrial cancer. Its immune microenvironment exhibits significant suppressive features, including functional exhausion of CD8+ T cells, enrichment of regulatory T cells, and polarization toward M2-type macrophages. Although this subtype generally demonstrates low tumor mutational burden and high chromosomal instability, resulting in weak immunogenicity, a subset of cases show high expression of programmed death-ligand 1 (PD-L1) and are enriched in T cells, displaying heterogeneity as 'hot tumors'. In terms of treatment, immune checkpoint inhibitors as monotherapy have limited efficacy. However, multiple phase Ⅲ clinical trials have confirmed that combining immunotherapy with chemotherapy, anti-angiogenic agents, or poly (ADP-ribose) polymerase (PARP) inhibitors can significantly improve patient outcomes, particularly in advanced or recurrent cases. This review summarizes the research progress on the characteristics of the immune microenvironment and immunotherapy strategies for p53abn endometrial cancer, providing theoretical foundations and practical reference for clinical precision subtyping, immunotherapy decision-making, and optimization of combination regimens.

The incidence of endometrial cancer (EC) continues to rise, posing a serious threat to women's health and challenging conventional classification and treatment approaches. Kinesin family member 18B (KIF18B), as a member of the kinesin superfamily, plays a pivotal role in mitotic cell division and chromosome segregation. KIF18B is aberrantly overexpressed in various malignancies, including EC, and its expression level is significantly correlated with adverse clinicopathological features and worse overall survival in EC patients. Mechanistically, KIF18B regulates cell cycle progression by activating signaling pathways such as Wnt/β-catenin and PI3K/Akt/mTOR, induces epithelial-mesenchymal transition (EMT), maintains cancer stem cell properties, and participates in shaping an immunosuppressive tumor microenvironment, thereby synergistically driving the initiation and progression of EC. With the increasing adoption of EC molecular classification in clinical practice, the potential association of KIF18B with different molecular subtypes offers novel perspective for its application as a prognostic biomarker and a subtype-specific therapeutic target. Based on the core function of KIF18B in chromosome segregation and the evidence for selective lethality of its homologous protein KIF18A in chromosomally unstable (CIN) cells, KIF18B may harbor targeting potential in the p53-abnormal（p53abn） subtype, and it could influence the efficacy of immune checkpoint inhibitors by remodeling the immune microenvironment in the mismatch repair-deficient（MMRd） subtype. This review systematically summarizes the biological characteristics, of KIF18B, its expression regulatory network and oncogenic mechanisms in EC, its potential association with EC molecular subtypes, and discusses the challenges and future directions for its clinical translation, aiming to provide a novel theoretical foundations and research direction for the precise diagnosis and targeted therapy of EC.

Ovarian cancer is the malignancy with the highest mortality rate in the female reproductive system. Surgery combined with chemotherapy is the primary therapeutic regimen, but the disease is prone to recurrence and the development of platinum resistance. The tumor immune microenvironment plays a crucial role in its pathogenesis, immune evasion, and therapeutic resistance. The immune microenvironment of ovarian cancer is highly heterogeneous, comprising immune cells, stromal cells, and significantly heterogeneous malignant tumor cells. Different cellular subpopulations influence patient prognosis through complex regulatory mechanisms. Key functional mechanisms involve critical immune evasion pathways such as the programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) axis, as well as cytokine/exosome-mediated intercellular communication, and microenvironment-mediated therapeutic resistance. Current research techniques include single-cell RNA sequencing, spatial transcriptomics, and other multi-omics technologies combined with bioinformatics analysis. Experimental models include murine models, patient-derived xenograft models, and three-dimensional (3D) in vitro models. Therapeutic strategies targeting the tumor immune microenvironment primarily involve immune checkpoint inhibitors, adoptive cell therapy, and interventions targeting immunosuppressive cells. Combination therapies show greater potential for clinical application. Future research should focus on integrating multi-level data, developing novel multi-target therapeutic strategies, and advancing personalized treatment approaches to provide more effective therapeutic options for patients with ovarian cancer.

This report presents a case of pulmonary metastasis from placental site trophoblastic tumor (PSTT) treated with chemotherapy combined with thoracoscopic surgery. The patient presented to the Cancer Hospital of Dalian University of Technology (our hospital) with a 15-day history of hemoptysis and elevated human chorionic gonadotropin (hCG) following previous surgery for PSTT. Chest CT revealed multiple solid nodules in both lungs, with the largest located in the left lower lobe. The patient had previously undergone laparoscopic resection of uterine mass, bilateral ovarian cystectomy, and hysteroscopic resection of endometrial lesion at another hospital due to uterine mass, ovarian mass, and intrauterine occupancy. Postoperative pathological examination confirmed PSTT (uterine mass, intrauterine occupancy). After receiving 7 cycles of chemotherapy in our hospital, the patient underwent transabdominal total hysterectomy, bilateral salpingectomy, and bilateral ovarian mass resection under general anesthesia in the gynecology department. A follow-up chest CT five months postoperatively showed enlargement of the left lower lobe nodule compared to the preoperative scan. Subsequently, the patient underwent single-port thoracoscopic left lower lobectomy under general anesthesia in the thoracic surgery department. Postoperative hCG levels were regularly monitored and remained within the normal range through December 2025, and chest CT revealed no significant abnormal nodules.

46, XY pure gonadal dysgenesis (PGD) is a rare disorder of sex development. Patients have a female social gender and a 46,XY karyotype. The primitive streak gonads are prone to malignant germ cell tumors. This report describes a 16-year-old phenotypic female with 46, XY PGD who presented with lower abdominal pain. Imaging revealed a solid pelvic mass. Postoperative pathology confirmed stage ⅠC2 left ovarian dysgerminoma and bilateral ovarian gonadoblastomas. The clinical manifestations of this condition include primary amenorrhea and delayed puberty with poor development of secondary sexual characteristics, elevated gonadotropin (follicle-stimulating hormone, luteinizing hormone) levels, and decreased sex hormone (estradiol, testosterone, anti-Müllerian hormone) levels. The imaging features of gonadoblastoma are variable-sized masses containing multiple nodular calcifications. The imaging features of dysgerminoma are large masses exhibiting multiple fibrovascular septa and marked heterogeneous enhancement. Once a diagnosis of 46, XY PGD is established, prophylactic bilateral gonadectomy should be performed as early as possible, at least before the onset of puberty, to prevent the development of malignant gonadal germ cell tumors.

A Collision tumor refers to the coexistence of two or more primary tumors of distinct histological origins in the same anatomical site without mutual transition. We report a rare case of an advanced high-grade endometrial stromal sarcoma coexisting synchronously with endometrioid adenocarcinoma. The patient was a 51-year-old female admitted with lower abdominal distension and pain. Imaging revealed a large solid pelvic mass accompanied by multiple organ metastases, invasion of the inferior vena cava, and suspected tumor thrombus. Postoperative pathology confirmed high-grade endometrial stromal sarcoma (stage ⅣB) combined with well-differentiated endometrioid adenocarcinoma. Genetic testing indicated a TP53 mutation. Despite undergoing cytoreductive surgery and adjuvant chemotherapy, the patient developed recurrence at the vaginal stump and widespread tumor progression approximately two months after surgery. Through analysis of this case and literature review, we suggest that for pelvic tumors presenting with complex imaging features, extremely rapid clinical progression, and extensive involvement, the possibility of rare pathological combinations should be considered. This case also highlights the urgent need to develop individualized therapeutic strategies based on molecular subtyping to improve the prognosis of such patients.

Cervical cystic adenomyoma is a rare subtype of adenomyosis. Its pathological characteristics include the formation of cystic lesions containing old hemorrhage, surrounded by smooth muscle within the cervical myometrium. The condition lacks specific clinical manifestations and often presents with refractory dysmenorrhea, pelvic pain, or menstrual irregularities. Its imaging findings are varied, making preoperative diagnosis difficult. A case of cervical cystic adenomyoma in a 24-year-old unmarried woman is reported. The patient presented with progressive dysmenorrhea for 16 months. MRI revealed a multilocular cystic lesion in the anterior cervix, with hyperintense internal content (on T2-weighted images), clear septations between cysts, and no communication with the uterine cavity. Cystoscopy combined with laparoscopic excision of the cervical lesion was performed. Chocolate-like old blood was found within the cyst. Postoperative pathological examination confirmed the diagnosis of cervical cystic adenomyoma. The patient received adjuvant therapy with a gonadotropin-releasing hormone agonist (GnRH-a) for three cycles after surgery. Follow-up at six months showed no recurrence, and dysmenorrhea was significantly relieved. The experience from this case suggests that combining preoperative MRI assessment, meticulous laparoscopic excision, and postoperative adjuvant GnRH-a therapy can safely and effectively eliminate the lesion while preserving the patient's fertility.

Recurrent cervical cancer with spontaneous vesicoenteric fistula formation is extremely rare. Its clinical presentation is insidious and easily confused with radiation- or inflammation-induced fistulas. We report a 52-year-old female who presented with painless gross hematuria more than one year after radical hysterectomy for cervical cancer. Imaging revealed a right pelvic wall mass invading the bladder and ileum, along with multiple metastases in the retroperitoneal, mediastinal, and left supraclavicular lymph nodes. PET/CT showed air within the bladder. Combined with CT and MRI findings, a vesicoenteric fistula was strongly suspected. After admission, the patient underwent bilateral internal iliac artery embolization for hemostasis followed by laparoscopic exploration, which confirmed a 5 cm-diameter fistula between the ileum (130 cm distal to the ligament of Treitz) and the posterior bladder wall. One-stage surgery comprising partial small-bowel resection, bladder repair, sigmoid colostomy, and percutaneous nephrostomy was performed. Postoperative pathology confirmed metastatic poorly differentiated squamous cell carcinoma. Immunohistochemistry showed a programmed death-ligand 1 (PD-L1) combined positive score (CPS) of 5 and epidermal growth factor receptor (EGFR) (3+). After surgery, the patient received Serplulimab combined with albumin-bound Paclitaxel plus Carboplatin, and imaging evaluation indicated tumor shrinkage with stable disease (SD). This case highlights that unexplained hematuria or fecaluria in advanced cervical cancer should raise suspicion of a neoplastic complex fistula. Early surgical intervention combined with individualized immunotherapy combined with chemotherapy can rapidly relieve symptoms and control disease, providing a reference for the comprehensive management of similar critical cases.

Premature ovarian insufficiency (POI) is an endocrine disorder characterized by a decline of ovarian function before the age of 40, primarily presenting as menstrual irregularities, decreased estrogen levels, diminished ovarian reserve, and reduced fertility. The pathogenesis of POI is complex, involving multiple factors such as genetics, immunity, metabolism, and environment. Studies indicate that the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway plays a critical role in regulating follicular development, proliferation and apoptosis of granulosa cells (GCs), oxidative stress, and inflammatory response. Dysregulation of this pathway is closely associated with the occurrence and progression of POI. Multiple studies have shown that Chinese medicine monomers and compound formulations can improve the ovarian microenvironment, inhibit apoptosis in GCs, and promote follicular development and maturation by modulating the PI3K/Akt signaling pathway, thereby delaying the decline of ovarian function. This review summarizes the mechanisms of the PI3K/Akt signaling pathway in POI and the research progress on Chinese medicine monomers and compound formulations in treating POI through regulation of this pathway, aiming to provide new insights for the treatment of POI with traditional Chinese medicine.

Endometrial fibrosis (EF) is a critical pathological basis for gynecological conditions such as infertility and abnormal menstruation. It is often induced by intrauterine procedures and recurrent infections, and current therapeutic approaches have limited efficacy with a high recurrence rate. In recent years, exosomes, as key mediators of intercellular communication, have demonstrated significant source-dependent bidirectional regulatory roles in the progression of EF. Stem cell-derived exosomes primarily exert antifibrotic effects. By carrying bioactive molecules such as microRNAs, long non-coding RNAs, and proteins, they regulate core signaling pathways including transforming growth factor-β/Smad, Yes-associated protein, and connective tissue growth factor. This regulation inhibits epithelial-mesenchymal transition, myofibroblast activation, and excessive deposition of the extracellular matrix. Simultaneously, they modulate processes like ferroptosis and autophagy, suppress inflammatory responses, and promote angiogenesis, thereby effectively improving the endometrial microenvironment and repairing its structure and function. In contrast, exosomes derived from damaged endometrium or ectopic lesions frequently carry profibrotic molecules, activating inflammatory cascades and accelerating fibrosis progression. Non-coding RNAs and protein biomarkers derived from exosomes show abnormal expression in body fluids such as serum and intrauterine lavage fluid, holding significant potential for non-invasive diagnosis. Exosomes are expected to become novel tools and targets for the precise diagnosis and treatment of EF.

Cervical cancer, the fourth most common malignant tumor among women globally, is closely associated with persistent infection by high-risk human papilloma virus (HR-HPV). The vaginal microbiome (VMB) and its metabolites are key factors influencing the outcome of HR-HPV infection and the progression of cervical lesions. Under healthy conditions, a Lactobacillus-dominant VMB maintains an acidic vaginal environment through the secretion of lactic acid, releases hydrogen peroxide (H₂O₂) and bacteriocins to inhibit HPV adsorption and replication, and simultaneously regulates innate and adaptive immunity to promote viral clearance. Conversely, VMB dysbiosis can induce chronic inflammation by activating nuclear factor-κB (NF-κB), damage the vaginal epithelial barrier, and accelerate lesion progression. Metabolites such as lactic acid and short-chain fatty acids are involved in the pathological process by modulating immune cell function and inflammatory pathways. In current VMB-based intervention strategies, approaches such as probiotic supplementation and traditional Chinese medicine can effectively restore microbial balance, enhance immune responses, and improve the rate of HPV clearance.

Hysteroscopy is a gynecological endoscopic surgery that highly relies on the operator's fine tactile perception and force control capabilities. However, traditional hysteroscopic virtual reality (VR) simulators commonly lack crucial haptic feedback, which constrains the improvement of training effectiveness. In response to this common challenge, it is particularly important to analyze the core value of haptic feedback in hysteroscopic simulation training from three dimensions: spatial navigation, tissue property discrimination, and force control of energy-based instruments. At the technical pathway level, by referencing the mature haptic feedback technologies from the fields of laparoscopy and stomatology, this study systematically reviews the limitations of multi-degree-of-freedom (DOF) force feedback robotic arms and customized integrated systems in the hysteroscopic context. Consequently, it proposes that developing specialized micro-force feedback systems compatible with mainstream VR platforms is a superior technical pathway. Cross-domain evidence-based research indicates that the introduction of haptic feedback can significantly enhance operational proficiency, decision-making accuracy, and teaching quality in hysteroscopic surgery training. In the future, a visuo-haptic fusion simulation training system should be constructed based on high-fidelity biomechanical modeling and with real-time haptic rendering as the interactive core, through multidisciplinary collaboration，which is expected to fundamentally reshape the training model for minimally invasive surgery professionals in obstetrics and gynecology.

Objective: To evaluate the therapeutic efficacy of transcranial direct current stimulation (tDCS) on endometriosis (EMs)-related pain and explore its potential mechanism involving the nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3) inflammasome pathway. Methods: From January 2024 to June 2025, 40 patients with EMs-related chronic pelvic pain admitted to Beijing Chao-Yang Hospital, Capital Medical University were selected and randomly divided into a tDCS group (n=20) and a sham stimulation control group (n=20) using a random number table. The tDCS group received stimulation with the anode placed over the F3 area and the cathode over the contralateral supraorbital Fp2 area, with a current intensity of 2 mA, once daily for 20 minutes per session, for 10 consecutive days. The sham stimulation control group had electrode placed in identical position as the tDCS group, but with a current intensity of 0 mA. Pain levels were assessed using the visual analogue scale (VAS) before treatment and 10 days after treatment completion. Serum levels of the downstream factors of NLRP3 inflammasome activation, interleukin-1β (IL-1β), IL-18 and lactate dehydrogenase (LDH), were measured by enzyme-linked immunosorbent assay (ELISA) before and 10 days after treatment. Data analysis was performed using GraphPad Prism 5.0 software. Results: There were no statistically significant differences between the two groups in age, gravidity, parity, or baseline VAS scores (all P>0.05). After treatment, the VAS score in the tDCS group was significantly lower than that in the sham stimulation control group (t=8.953, P<0.001). ELISA results showed that serum levels of IL-1β, IL-18, and LDH in the tDCS group were significantly lower than those in the sham stimulation control group after treatment (all P<0.05). Correlation analysis revealed that in the tDCS group, the post-treatment VAS score was significantly positively correlated with serum IL-1β (r=0.512, P=0.021) and LDH levels (r=0.580, P=0.007), but not with IL-18 levels (P=0.073). No significant correlations were observed before treatment (all P>0.05). Conclusions: tDCS effectively alleviate EMs-related pain. Its mechanism may be related to the inhibition of NLRP3 inflammasome activation, reduction in the release of downstream pro-inflammatory cytokines, and attenuation of pyroptosis. Furthermore, the degree of pain relief after treatment is directly associated with the reduction in inflammatory factors and cellular damage indicatiors.

This report presents a rare case of end-stage renal disease (ESRD) with abnormally elevated β-human chorionic gonadotropin (β-hCG), analyzes its clinical characteristics, diagnostic considerations, and the potential mechanism underlying β-hCG elevation, aiming to raise awareness of non-pregnancy and non-neoplastic β-hCG elevation in ESRD patients. The patient is a 35-year-old woman who had been on maintenance hemodialysis (MHD) for more than 7 years and was admitted due to amenorrhea lasting over 6 months. Laboratory tests showed elevated serum β-hCG. Gynecological ultrasound showed no signs of pregnancy. Ectopic pregnancy was initially suspected but ruled out after comprehensive evaluation. Based on literature review, the β-hCG elevation was considered to result from reduced renal clearance caused by ESRD. The patient continued MHD treatment with regular β-hCG monitoring and developed no new symptoms. This case indicates that when β- hCG is elevated in ESRD patients, it is essential to first exclude common etiologies such as pregnancy and neoplasms through detailed history, imaging, and laboratory examinations, while also considering the impact of renal failure on β-hCG metabolism. Clinicians should broaden diagnostic thinking to avoid misdiagnosis and promote precise diagnosis and management of complications in ESRD.