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Objective: This study aims to assess the efficacy of laparoscopic modified uterine incision pressure repair in treating type II-III cesarean scar pregnancy (CSP). Methods: A total of 20 patients diagnosed with type II-III CSP and admitted to the Affiliated Hospital of Guizhou Medical University between April 2021 and May 2023 were enrolled. The patients were divided into two groups: the study group (Group A), consisting of newly treated surgical patients, and the control group (Group B), including patients with type II-III CSP treated by doctors of similar grade and surgical experience (non-novel). Various parameters, including age, menopause duration, pregnancy and delivery history, cesarean section frequency, preoperative human chorionic gonadotropin (HCG) levels, pregnancy sac size, HCG turnover time, operation duration, intraoperative blood loss, blood transfusion requirements, and hospitalization costs, were compared. Results: When comparing mean age, menopause duration, preoperative HCG levels, pregnancy and cesarean section frequencies, pregnancy sac size, and HCG turnover time, no statistically significant differences were observed (P > .05). The number of transfusions and hospitalization costs in Group A were lower than in Group B, although the differences were not statistically significant (P > .05). However, operative time, intraoperative bleeding, and hospitalization costs were significantly lower in Group A compared to Group B (P < .05). Conclusions: The laparoscopic modified uterine incision pressure repair method demonstrated clinical value with its advantages of short operation time, reduced bleeding, lower costs, and rapid recovery for type II-III CSP.
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BACKGROUND: Recurrent pregnancy loss (RPL) is associated with variable causes. Its etiology remains unexplained in about half of the cases, with no effective treatment available. Individuals with RPL have an irregular iron metabolism. In the present study, we identified key genes impacting iron metabolism that could be used for diagnosing and treating RPL. METHODS: We obtained gene expression profiles from the Gene Expression Omnibus (GEO) database. The Molecular Signatures Database was used to identify 14 gene sets related to iron metabolism, comprising 520 iron metabolism genes. Differential analysis and a weighted gene co-expression network analysis (WGCNA) of gene expression revealed two iron metabolism-related hub genes. Reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry were used on clinical samples to confirm our results. The receiver operating characteristic (ROC) analysis and immune infiltration analysis were conducted. In addition, we analyzed the distribution of genes and performed CellChat analysis by single-cell RNA sequencing. RESULTS: The expression of two hub genes, namely, CDGSH iron sulfur domain 2 (CISD2)and Cytochrome P450 family 17 subfamily A member 1 (CYP17A1), were reduced in RPL, as verified by both qPCR and immunohistochemistry. The Gene Ontology (GO) analysis revealed the genes predominantly engaged in autophagy and iron metabolism. The area under the curve (AUC) demonstrated better diagnostic performance for RPL using CISD2 and CYP17A1. The single-cell transcriptomic analysis of RPL demonstrated that CISD2 is expressed in the majority of cell subpopulations, whereas CYP17A1 is not. The cell cycle analysis revealed highly active natural killer (NK) cells that displayed the highest communications with other cells, including the strongest interaction with macrophages through the migratory inhibitory factor (MIF) pathway. CONCLUSIONS: Our study suggested that CISD2 and CYP17A1 genes are involved in abnormal iron metabolism, thereby contributing to RPL. These genes could be used as potential diagnostic and therapeutic markers for RPL.