Single-chain antibodies are recombinant constructs comprising only the heavy- and light-chain variable domains tethered by a flexible peptide linker, representing the smallest intact antigen-binding fragment. Compared with full-length antibodies, single-chain antibodies exhibit lower molecular weight, superior tissue penetration, reduced immunogenicity, and facile genetic manipulation. High-affinity, high-specificity clones are routinely isolated from phage display, ribosome display, or alternative combinatorial libraries, followed by scalable production in Escherichia coli, yeast, or mammalian expression systems. Current translational research focuses on gynecologic tumors. For diagnostics, radionuclide-conjugated single-chain variable fragment (scFv) serves as molecular probes in positron emission tomography to enable accurate tumor localization and staging. Therapeutically, scFvs function as targeting moieties to deliver small interfering RNA, toxins, or chemotherapeutics, neutralize oncogenic ligands, or constitute recombinant immunotoxins and bispecific antibodies that simultaneously inhibit neoplastic growth and activate anti-tumor immunity. Their exceptional penetration confers unique advantages in poorly vascularized solid tumors and peritoneal metastatic deposits relative to conventional antibodies. Clinical transformation is nevertheless constrained by short serum half-life, limited stability, and potential immunogenicity. Future efforts directed toward protein-engineering optimisation, development of advanced delivery platforms, and theranostic integration will be pivotal for advancing precise management of gynecologic tumors.

Ovarian cancer is one of the malignant tumors with extremely high mortality in the female reproductive system. Its early symptoms are not obvious, and it is prone to misdiagnosis and missed diagnosis. More than 70% of patients are already in the advanced stage at the time of diagnosis, and the survival rate is relatively low. Currently, the sensitivity and specificity of common screening methods such as carbohydrate antigen 125 testing and transvaginal ultrasound examination in the early diagnosis of ovarian cancer are limited. In recent years, with the development of gene sequencing technology, molecular diagnosis has become an important means for the early detection of ovarian cancer. In particular, the detection based on circulating tumor DNA (ctDNA) has received extensive attention. CtDNA is a DNA fragment released by tumor cells into the blood, carrying tumor characteristics and capable of dynamically and real-time reflecting the tumor's status. The mutation detection and methylation pattern recognition of ovarian cancer based on ctDNA have significantly improved the detection sensitivity. In addition, the combination of ctDNA and machine learning methods has further increased the early detection rate of ovarian cancer. In the future, with the research on detection technology and large-scale population data, as well as the integration of multi-omics data, the application of ctDNA in the diagnosis and treatment of ovarian cancer will be greatly promoted, and the quality of patients' lives will be improved.

Due to the insidious early symptoms and limited screening methods of ovarian cancer, most patients are diagnosed at an advanced stage. Moreover, its high heterogeneity has led to an incomplete elucidation of the pathogenic mechanism. Ferroptosis, an iron-dependent non-apoptotic programmed cell death, is involved in the occurrence and development of ovarian cancer through processes such as reactive oxygen species accumulation and lipid peroxidation, and has become the focus of research on tumor intervention. Non-coding RNA (ncRNA) can participate in the ferroptosis process by regulating iron metabolism, lipid peroxidation, and antioxidant systems. Among them, long non-coding RNA (lncRNA), microRNA (miRNA), and circular RNA (circRNA) play specific roles in the regulation of ferroptosis in ovarian cancer. LncRNA targets key genes of ferroptosis through the competitive endogenous RNA (ceRNA) network, protein-protein interactions, or epigenetic modifications; circRNA adsorbs miRNA in the form of a molecular sponge, indirectly regulating the ferroptosis process, as well as the metastasis and drug resistance of ovarian cancer. The precise regulatory network composed of ncRNA targets the core nodes of ferroptosis, providing new molecular targets and research directions for the early diagnosis, individualized treatment, and prognostic evaluation of ovarian cancer.

Cervical cancer is a malignant tumor that seriously threatens women's health, and its occurrence is closely related to persistent infection of high-risk human papilloma virus (HR-HPV). Although the current screening strategies mainly based on cytology and HPV testing have reduced the burden of cervical cancer, the low specificity of HR-HPV testing has led to a large number of transient infected individuals being referred for unnecessary colposcopy, which has become a challenge in clinical practice. The p16/Ki-67 dual staining technique synchronously detects the co-expression of p16^INK4a and Ki-67 proteins through immunocytochemical methods, which can objectively identify the state of cell transformation driven by HR-HPV and provides an excellent solution for the triage management of HR-HPV positive individuals. A large amount of evidence shows that for the detection of high-grade cervical intraepithelial neoplasia (CIN2+), the dual staining technique not only has a sensitivity of over 90%, but its specificity (approximately 70%-85%) is significantly better than that of cytological triage. It can reduce colposcopy referrals by about 30%-50%. Moreover, its negative predictive value (>97%) supports extending the follow-up interval for negative individuals, thus optimizing the screening efficiency. The p16/Ki-67 dual staining technique, through accurate risk stratification, significantly reduces overdiagnosis and over-treatment while ensuring the detection rate of lesions. It has become one of the triage tools with the most evidence-based support in the optimization of cervical cancer screening strategies.

Primary ovarian epithelioid angiosarcoma is a rare and aggressive ovarian malignant tumor originating from endothelial cells. Its clinical symptoms are non-specific, making early diagnosis difficult. It progresses rapidly, has a high recurrence rate, is insensitive to traditional chemotherapy and radiotherapy, and has a poor prognosis. Surgical resection is the most definite treatment method. This paper reports a case of primary ovarian epithelioid angiosarcoma. The patient presented with abnormal uterine bleeding and lower abdominal pain for 3 months, which worsened in the last 2 days. Imaging examinations suggested a hypoechoic mass in the right adnexal area, and ovarian cancer was suspected. Pre-operative diagnosis considered the possibility of a rupture of an ovarian malignant tumor. Thus, a laparotomy was performed. During the operation, a cystic-solid mixed mass with a diameter of about 10 cm was found in the right adnexal area. The surface of the mass had abundant, thick blood vessels, the capsule was ruptured, and there was a small amount of active bleeding. Then, cytoreductive surgery for ovarian tumor was carried out. According to the pathological diagnosis, it was stage ⅢB primary ovarian epithelioid angiosarcoma. After 1 course of intravenous chemotherapy with 100 mg of cisplatin and 80 mg of doxorubicin, the patient did not receive treatment as scheduled for 50 days. When she was readmitted to the hospital, recurrence had occurred in multiple lesions in the lungs, pelvis, and abdominal cavity. The disease progressed rapidly, and the patient eventually died 3 months after the surgery.

Epithelioid trophoblastic tumor (ETT) is an exceedingly rare subset of gestational trophoblastic neoplasia (GTN) that typically arises in the lower uterine segment or cervix and is classically associated with a history of amenorrhea and only modestly elevated serum human chorionic gonadotropin (hCG). Because of its non-specific clinical presentation and the frequently low hCG levels, diagnosis is challenging and requires integrated evaluation of clinical history, morphology, and immunohistochemistry. We report a woman with prior amenorrhea who presented with acute life-threatening vaginal bleeding, a cervical mass, and low serum hCG. Owing to overlapping morphologic and immunophenotypic features with cervical carcinoma, the differential diagnosis was complex. After emergent uterine artery embolization, the patient underwent laparoscopic hysterectomy with bilateral salpingo-oophorectomy and achieved an excellent outcome. This case underscores the necessity of including ETT in the differential diagnosis of atypical cervical neoplasms to avoid misdiagnosis and ensure timely, effective therapy.

Low-grade appendiceal mucinous neoplasm (LAMN) is a rare and heterogeneous gastrointestinal tumor. When LAMN secretes mucin that spreads into the peritoneal cavity, forming pseudomyxoma peritonei (PMP) and involving the ovarian, its clinical manifestations and auxiliary examinations are highly similar to those of ovarian mucinous tumors with pelvic and abdominal metastasis, which can easily lead to preoperative misdiagnosis. LAMN complicated by PMP has a high risk of postoperative recurrence, and standardized treatment can improve the prognosis. Given that the treatment regimens for LAMN and ovarian mucinous tumors are different, early identification of the tumor origin is the key to treatment. We report a case of a patient with LAMN complicated by PMP initially presenting as an ovarian tumor. The patient presented with abdominal distension and abdominal pain. Preoperative imaging studies suggested an ovarian tumor. Intraoperative pathological diagnosis indicated a borderline mucinous ovarian tumor, while postoperative pathology confirmed LAMN involving the ovaries. The patient refused hyperthermic intraperitoneal chemotherapy. After one year postoperative surveillance, no recurrence or metastasis was observed. This case aims to provide a reference for the clinical management of cases with difficult differential diagnosis between ovarian tumors and LAMN, so as to avoid misdiagnosis and inappropriate treatment.

Benign multicystic peritoneal mesothelioma (BMPM) is an exceedingly rare peritoneal neoplasm characterized by a high recurrence rate and potential for malignant transformation. Preoperative diagnosis remains challenging; lesions are usually encountered incidentally during surgery. Optimal management is controversial, and long-term postoperative surveillance is mandatory. We describe two patients with BMPM confirmed by postoperative histopathology. Case 1: a pelvic mass was incidentally detected on gynecologic ultrasound performed for abdominal distension. Laparoscopic evacuation of loculated pelvic fluid, resection of a right para-tubal cyst, and adhesiolysis were performed; ultrasound at 2 months showed no residual disease, but the patient was subsequently lost to follow-up. Case 2: the patient had undergone surgery for BMPM in 2021; four years later, recurrence was identified during evaluation for failed oocyte retrieval. Multifocal cystectomy and bilateral tubal ligation were completed, followed by assisted reproductive technology; no gynecologic follow-up has since been recorded. Preoperative diagnosis of BMPM is difficult, and clinicians need to strengthen differentation from disease with similar imaging findings. BMPM should be considered when multiple cystic peritoneal lesions are observed. A detailed occupational and prior surgical history is essential to improve pre-operative diagnostic accuracy.

The typical manifestation of cervical cancer is irregular vaginal bleeding. However, in postmenopausal women, due to cervical atrophy, retraction of the transformation zone, and the possible endophytic growth of tumors, clinical symptoms are often atypical, and biopsy results are prone to false- negatives, increasing the risk of missed diagnosis. This paper reports a 69-year-old female patient who presented with lower abdominal pain. Imaging examinations showed a cystic mass of about 7 cm formed by hematometra in the uterus. Tumor markers were normal, and human papilloma virus 58 (HPV58) was positive. Cervical biopsy indicated chronic inflammation. Given the discrepancy between imaging and pathological results, a multi-disciplinary team decided to perform exploratory laparotomy after discussion. Intraoperative frozen-section examination diagnosed squamous cell carcinoma of the cervix. Subsequently, radical hysterectomy+ bilateral salpingo-oophorectomy + pelvic lymph node dissection were performed. Postoperative pathology confirmed moderately differentiated non-keratinizing squamous cell carcinoma. The tumor invaded more than two-thirds of the cervical stroma and involved the parametrium tissues. The final diagnosis was FIGO 2018 StageⅡB, and adjuvant chemoradiotherapy were required. After the operation, the patient received one course of chemotherapy with paclitaxel 240 mg (D1) combined with cisplatin 30 mg (D1-3). Currently, she is undergoing pelvic external beam radiotherapy with concurrent cisplatin 30 mg/week for radiosensitizer. Her condition remains stable, and she has been enrolled in the standardized follow-up management. By summarizing the clinical manifestations, imaging features, diagnosis, and treatment of this patient, this paper aims to remind clinicians that for postmenopausal women with unexplained hematometra, the possibility of endophytic cervical cancer should be alerted, providing a reference for the early identification and standardized management of similar cases.

Pelvic floor dysfunction (PFD) is a clinical syndrome mainly characterized by urinary incontinence, defecation dysfunction, and pelvic organ prolapse, which significantly affects the quality of patients' life. Internal rectal prolapse (IRP), as an important component of PFD, is closely related to the integrity of the pelvic floor support structure in terms of its grading. Current evidence shows that the degeneration of the pelvic floor support structures and the dysfunction of the levator ani muscle caused by PFD are the key driving factors for the occurrence and development of IRP. The grading of IRP is significantly correlated with the degree of pelvic floor injury. High-grade IRP (Grades Ⅲ-Ⅳ) is often accompanied by severe pelvic floor anatomical and functional abnormalities. Dynamic magnetic resonance defecography (DMRD) and high-resolution anorectal manometry (HR-ARM) are the key tools for objective grading and functional evaluation. In terms of treatment, low-grade IRP responds well to pelvic floor muscle training (PFMT), while high-grade IRP often requires surgical intervention. Currently, there is still a lack of a unified grading standard and support from prospective cohort studies in this field. In the future, efforts should be made to construct a standardized grading system through multi-center collaboration, integrating radiomics and artificial intelligence technologies to promote precision diagnosis and treatment.

Endometriosis (EMs) is a common gynecological disease. Traditional treatment methods have limitations such as high recurrence rates and damage to ovarian function. Mesenchymal stem cells (MSCs) have emerged as a novel therapeutic approach due to their multi-directional differentiation potential and immunomodulatory properties. This review summarizes the dual roles of MSCs in EMs: pathogenic MSCs drive disease progression through abnormal proliferation and fibrosis, while therapeutic MSCs exert effects through mechanisms such as immunomodulation and anti-angiogenesis. The review focuses on the progress of strategies such as stem cell transplantation, cell-free therapy, gene modification, and combination therapy, and analyzes the challenges in clinical translation, including drug delivery safety, long-term efficacy, and standardization issues. Future research should optimize the delivery system and improve the evaluation criteria to promote the clinical application of MSC therapy.

Endometriosis (EMs) is a common benign gynecological disease. Currently, the main treatment methods include drug therapy and surgical treatment, but both have certain limitations. Even after EMs surgery, long-term drug management is still required to prevent recurrence. Therefore, it is particularly important to explore new, effective, and well-tolerated drug treatment modalities. In recent years, drug delivery using nanotechnology has become a new approach for disease treatment. Nanomedicine has advantages such as targeting, improving pharmacokinetics, prolonging circulation time, increasing the bioavailability of poorly soluble drugs, and multi-mode integration, and has been successfully applied in the treatment of various tumor diseases. EMs also exhibits biological behaviors similar to those of tumor cells, so the strategies of applying nanomedicine in tumor treatment can be used in the treatment of EMs. Currently, the applications of nanomedicine in the treatment of EMs include antioxidant and anti-inflammatory therapies, pain treatment, immunotherapy, photothermal therapy, gene therapy, and multi-mode diagnosis and treatment. This review summarizes the relevant research on the application of nanomedicine in the treatment of EMs, providing new directions for clinicians in treating EMs.

Endometrial injury induced diseases such as thin endometrium, chronic endometritis, and intrauterine adhesions are the main diseases affecting female reproductive health, and their clinical treatment still faces bottlenecks. Platelet-rich plasma (PRP) therapy, as a regenerative medicine approach, shows broad prospects in the repair of endometrial injury and functional reconstruction by releasing various growth factors and cytokines. Studies have demonstrated that PRP can promote the proliferation of endometrial-derived mesenchymal stem cells, stimulate angiogenesis, inhibit the inflammatory response and fibrotic process, and regulate cell apoptosis, thereby increasing endometrial thickness, improving the immune microenvironment, reducing the risk of adhesion recurrence, and enhancing the pregnancy rate. However, the clinical application of PRP still faces many problems that need to be solved urgently, including the lack of unified standards for its preparation, the unclear individualized clinical application protocols, and the relatively limited research on its non-growth factor components. This review summarizes the preparation, mechanism of action and research progress of PRP in the repair of endometrial injury, aiming to provide new ideas and strategies for clinical treatment.

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease characterized by hyperandrogenemia, insulin resistance, ovulation disorders, and polycystic changes in the ovaries. Exosomes, as key mediators of intercellular communication, carry microRNAs (miRNAs) that play a crucial role in the pathogenesis of PCOS.Exosomal miRNAs participate in the glycolysis process of granulosa cells, improve energy metabolism disorders, affect the proliferation of granulosa cells and follicular development, and improve the local ovarian inflammation response by influencing macrophage polarization. Meanwhile, the abnormal expression of exosomal miRNAs is closely related to hyperandrogenemia, adipocyte differentiation, and insulin resistance. These findings reveal that exosomal miRNAs are involved in the occurrence and development of PCOS by regulating granulosa cell function, inflammatory response, hyperandrogenemia, and metabolic processes, providing new targets for its diagnosis and treatment.

Polycystic ovary syndrome (PCOS) is a prevalent endocrinopathy among reproductive-age women. Adipose-tissue dysfunction constitutes the pivotal axis linking reproductive-endocrine derangements to metabolic dysregulation; the resulting chronic low-grade inflammation and insulin resistance perpetuate a vicious cycle with hyperandrogenism. The adipose-tissue immune microenvironment in PCOS is markedly perturbed: an imbalance in M1/M2 macrophage polarization leads to extensive infiltration of pro-inflammatory M1 macrophages, and the newly identified inflammatory and metabolically activated macrophage (iMAM) subset may act as a key disease-progression driver. Metabolic disequilibrium traps adipose tissue in a loop of lipotoxicity and oxidative stress, while adipokine secretion is dysregulated, manifesting as aggravated leptin resistance and decreased adiponectin levels. These pathological changes seriously impair ovarian steroidogenesis, ovulation function, and endometrial receptivity, thereby compromising fertility. Among emerging therapeutic strategies, glucagon-like peptide-1 receptor agonists promote adipose-tissue browning and reestablish immune homeostasis, and exosomes derived from adipose mesenchymal stem cells deliver specific microRNAs for precise modulation, providing a theoretical basis for individualized interventions targeting the adipose-tissue microenvironment.

We report a case of a 50-year-old female patient with adenomyosis complicated by an intramural uterine abscess and pyosalpinx. The patient was admitted due to abdominal pain and fever. Laboratory examinations indicated severe infection (leukocyte count: 47.05×10⁹/L) and imaging revealed significant uterine enlargement. Following initial empirical antibiotic therapy (imipenem/cilastatin sodium), infectious parameters partially decreased. However, the abdominal pain intensified and ascites developed, raising suspicion of abscess rupture. Emergency exploratory laparotomy with total abdominal hysterectomy, bilateral salpingo-oophorectomy, pelvic adhesiolysis and enterolysis was performed. Intraoperative findings included purulent exudate in the pelvic cavity. Postoperative dissection of the uterine specimen confirmed multiple abscess cavities within the myometrium. Histopathological diagnosis was consistent with adenomyoma with superimposed infection and abscess formation. Postoperatively, based on etiological results, targeted antibiotic therapy and supportive care were continued, leading to successful infection control. This case highlights that adenomyosis may serve as a nidus for pelvic infection dissemination and the formation of deep intramural abscesses. For such complicated infections, if clinical condition deteriorates or abscess rupture is suspected despite potent antibiotic therapy, surgical intervention to control the source of infection is critical for successful management.

Oxidative stress is a key pathophysiological mechanism in preeclampsia. Therefore, antioxidant stress holds significant importance for the prevention and treatment of preeclampsia and its related complications. This paper systematically reviews the molecular mechanisms and pathophysiological significance of nuclear factor-erythroid 2-related factor 2 (Nrf2) in regulating oxidative stress in preeclampsia. Recent studies have found that the signaling pathway constituted by Nrf2 and its negative regulatory protein, Kelch-like ECH-associated protein 1 (KEAP1), is frequently dysregulated or functionally impaired in placental tissues of preeclampsia patients and in animal models. This impairment leads to the inhibited transcriptional activation of downstream antioxidant genes, such as heme oxygenase-1 and NAD(P)H:quinone oxidoreductase 1, thereby exacerbating placental oxidative damage. Further research indicates that Nrf2 not only regulates the gene expression profile driven by the antioxidant response element (ARE) but also participates in placental formation and remodeling by influencing vascular endothelial cell function and trophoblast apoptosis. Nrf2 is a key nodal molecule linking oxidative stress to the pathological progression of preeclampsia, and its activation status is closely associated with disease severity and progression.

Fetal growth restriction (FGR) is an important contributor of perinatal morbidity and mortality. Its pathogenesis is complex, involving multiple factors at the fetal, maternal, and placental levels. As a core organ for material exchange and endocrine regulation between the mother and the fetus, abnormal placental structure and function play a crucial role in the pathogenesis of FGR. In recent years, studies have revealed that the occurrence of FGR is not only accompanied by macroscopic morphological changes such as reduced placental volume and disrupted villous tree structure but is also deeply associated with dysfunctions in trophoblast proliferation and differentiation, leading to insufficient remodeling of the spiral arteries. Advances in epigenetics have shown that the occurrence of FGR is accompanied by abnormal genomic imprinting in the placenta, alterations in DNA methylation patterns, and dysregulated expression of various microRNAs. These changes can contribute to the development of FGR by regulating placental development, angiogenesis, and cellular stress responses. With the development of multi-omics, research on the placental etiology of FGR is deepening to more refined cellular and molecular levels. This review summarizes the research progress of placental morphology, cell functional studies, and epigenetics in FGR, aiming to enhance the understanding of its pathological mechanisms and provide a scientific basis for early identification and precise intervention.

Gestational diabetes mellitus (GDM) is a common metabolic disease during pregnancy. It not only increases the risk of preeclampsia, postpartum hemorrhage, and type 2 diabetes mellitus in pregnant women, but also makes the offspring prone to adverse outcomes. Neonatal respiratory distress syndrome (NRDS) is common in infants of mothers with GDM. Studies have shown that the pathological mechanisms of NRDS in infants of GDM mothers involve multiple interrelated pathways: oxidative stress caused by maternal hyperglycemia, systemic inflammatory response, disruption of pulmonary surfactant synthesis, and changes in epigenetic modifications. This review summarizes the latest progress in the mechanisms of NRDS in infants of GDM mothers, aiming to reduce the incidence of NRDS and improve perinatal health outcomes.

The etiology of recurrent spontaneous abortion (RSA) is complex and diverse. Among them, the immune disease antiphospholipid syndrome (APS), as a high-risk factor for thrombosis, mainly leads to adverse pregnancy outcomes through the immune-inflammatory thrombosis mechanism. APS mainly initiates the immune-inflammatory thrombosis cascade reaction through antiphospholipid antibodies (aPLs). That is, there is a functional imbalance among decidual natural killer cells, decidual macrophages, and regulatory T cells, and an excessive release of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), which damage the vascular endothelium. Subsequently, it activates signaling pathways such as Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and nuclear factor-κB (NF-κB), activates the complement system, damages the vascular endothelium, promotes local thrombosis, and leads to an imbalance in the immune microenvironment at the maternal-fetal interface. Therefore, based on the in-depth analysis of the pathological mechanism of immune-inflammatory thrombosis, this paper reviews the occurrence mechanism and clinical treatment progress of RSA caused by APS, aiming to provide reference for future research, a new entry point for implementing new diagnosis and treatment plans, and a theoretical basis and clinical practice reference for targeted drug diagnosis and treatment of RSA complicated with APS.

Objective: To analyze the clinical profiles of parturients with umbilical vascular thrombosis, to delineate early recognition markers and diagnostic-therapeutic protocols, and to provide evidence for optimizing maternal-fetal outcome. Methods: Clinical data of 6 parturients with umbilical vascular thrombosis managed at Shenzhen Guangming District People's Hospital were retrospectively reviewed. Results: Among the 6 cases, 5 cases exhibited abnormal antepartum cardiotocography (CTG). Prenatal ultrasound identified umbilical vascular thrombosis in 3 cases, all delivered by emergency cesarean section promoted by pathological CTG patterns. Within this subgroup, one fetus presented with a secondary single umbilical artery and one with markedly tight umbilical cord spirals; the latter received a complete course of antenatal corticosteroids for fetal pulmonary maturation after sonographic detection of umbilical arterial thrombosis at 31⁺¹ weeks, followed by emergency cesarean section at 34⁺⁴ weeks. In the remaining 3 cases, prenatal ultrasound revealed no umbilical vascular anomaly; 2 cases underwent emergency cesarean section for abnormal CTG and one had an elective cesarean section. All 6 neonates survived. Of the 5 parturient-neonate pairs screened for protein S and protein C activity, 4 mothers were deficient in protein S and 2 in protein C; 3 neonates were deficient in protein S and 5 in protein C. Conclusions: Whenever obstetric ultrasound indicates an altered umbilical vessel count, hyper-coiled umbilical cord, laboratory evidence of protein S or protein C deficiency, or abnormal CTG patterns, umbilical vascular thrombosis should be suspected. In preterm pregnancies with stable fetal status, expectant management under intensive surveillance may be considered.

Objective: To evaluate the predictive utility of serum insulin-like growth factor 1 (IGF1) and sex hormone-binding globulin (SHBG) for postpartum glucose metabolism outcomes in patients with gestational diabetes mellitus (GDM). Methods: 120 women with GDM in the third trimester (GDM group) and 120 healthy pregnant controls (control group) were recruited between June 2022 and October 2024. According to postpartum glucose status, the GDM cohort was subdivided into an abnormal outcome group (n=48) and a normal outcome group (n=72). Serum IGF1 and SHBG levels were quantified by enzyme-linked immunosorbent assay (ELISA). Baseline characteristics and biochemical parameters were compared between the GDM and control groups, and between the abnormal and normal outcome subgroups. Multivariate logistic regression was used to identify determinants of impaired postpartum glucose metabolism. Receiver operating characteristic (ROC) curve analysis assessed the predictive performance of serum IGF1 and SHBG, individually and in combination. Results: Serum IGF1 was higher and SHBG was lower in the GDM group than in the control group (both P<0.05). Women in the abnormal outcome subgroup exhibited higher triglyceride (TG) and IGF1 levels and lower serum SHBG levels compared with the normal outcome subgroup (all P<0.05). Both IGF1 and SHBG were independent predictors of postpartum glucose metabolism impairment (both P<0.05). The combined model of serum IGF1 and SHBG had a higher value in predicting abnormal postpartum glucose metabolism glucose in GDM patients than single indicators alone (both P<0.05). Conclusions: Elevated serum IGF1 and reduced SHBG are associated with abnormal postpartum glucose metabolism in GDM. Their combined measurement offers superior predictive accuracy for identifying women with high risk of persistent glucose dysregulation after delivery.

Transient neonatal myasthenia gravis (TNMG) has an insidious onset, and its clinical manifestations are non-specific, making it easily misdiagnosed. It mainly occurs as a complication of maternal myasthenia gravis (MG). A case of a child with maternal TNMG is reported. The main manifestations were dyspnea, hypotonia, dysphagia, and a weak cry. The child was positive for acetylcholine receptor (AChR) antibodies. Based on the clinical manifestations and the mother's history of MG, the child was diagnosed with TNMG. After comprehensive treatment including mechanical ventilation, intravenous injection of human immunoglobulin, pyridostigmine bromide, and anti-infection therapy, the child's symptoms gradually improved. The child was cured and discharged on the 30th day after admission. During the follow-up until 6 months of age, the child's growth and development were normal. Early identification of TNMG is crucial. After individualized comprehensive intervention, the prognosis of most patients is good.