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Comment on “Distinct Suppression of Prednisone on Endometrial Immune Cells in Women With Reproductive Failure” 对“强的松对生殖衰竭妇女子宫内膜免疫细胞的明显抑制”的评论。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-11-19 DOI: 10.1111/aji.70186
Jin Linxi, Luo Shiling, Zhao Hongli
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引用次数: 0
Study on the Effects of Doxycycline Treatment on Endometrial Microbiota and Pregnancy Outcomes in Chronic Endometritis 多西环素治疗对慢性子宫内膜炎子宫内膜菌群及妊娠结局影响的研究。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-11-18 DOI: 10.1111/aji.70184
Huanhuan Guo, Lili Chen, Lan Liu

Background

This study aimed to characterize the endometrial microbiota in patients with chronic endometritis (CE) after doxycycline treatment and to compare microbial profiles and pregnancy outcomes between treated CE patients and those without CE.

Methods

Fifty-two women undergoing frozen–thawed embryo transfer were enrolled. Based on histopathological findings before oocyte retrieval, patients were categorized into the CE treatment group or the non-CE group. CE patients received doxycycline (100 mg twice daily for 14 days). Endometrial tissue was collected 1 day before endometrial transformation and analyzed by 16S rRNA gene sequencing of the V3–V4 region using QIIME2. Clinical and microbiological outcomes were compared between the groups.

Results

The two groups showed no significant differences in age, body mass index, endometrial thickness, number of embryos transferred, or transfer protocol (p > 0.05). Infertility duration was significantly longer in the CE group (p < 0.05). Alpha-diversity analysis revealed lower microbial richness and diversity in the CE group (p < 0.05). Firmicutes abundance was significantly reduced (p = 0.0214), whereas Bacteroidetes and Planctomycetes were increased (p < 0.05). At the genus level, Lactobacillus remained dominant but was markedly decreased in the CE group (p = 0.0157), while Ralstonia and Methylobacterium were enriched (p < 0.05). The clinical pregnancy rate and biochemical pregnancy rate showed no significant differences between the groups (p > 0.05), but the live birth rate was significantly lower in the CE group (p = 0.036).

Conclusion

Despite histological resolution following doxycycline therapy, CE patients exhibited persistent dysbiosis characterized by decreased Lactobacillus and increased opportunistic taxa, which may impair endometrial receptivity and pregnancy outcomes. These findings suggest that antibiotic therapy alone may not fully restore microbial balance in CE, warranting further investigation into microbiota-targeted interventions to improve reproductive success.

背景:本研究旨在描述强力霉素治疗后慢性子宫内膜炎(CE)患者的子宫内膜微生物群特征,并比较接受过CE治疗和未接受CE治疗的患者的微生物特征和妊娠结局。方法:选取52例接受冷冻解冻胚胎移植的妇女。根据取卵前的组织病理学结果,将患者分为CE治疗组和非CE组。CE患者接受强力霉素治疗(100mg,每日两次,连续14天)。在子宫内膜转化前1天采集子宫内膜组织,使用QIIME2对V3-V4区16S rRNA基因测序进行分析。比较两组患者的临床和微生物学结果。结果:两组患者在年龄、体重指数、子宫内膜厚度、移植胚胎数、移植方式等方面差异无统计学意义(p < 0.05)。CE组不孕持续时间明显延长(p < 0.05)。α -多样性分析显示,CE组微生物丰富度和多样性较低(p < 0.05)。厚壁菌门丰度显著降低(p = 0.0214),拟杆菌门和植物菌门丰度显著升高(p < 0.05)。在属水平上,CE组乳酸杆菌仍占优势,但数量显著减少(p = 0.0157), Ralstonia和Methylobacterium数量显著增加(p < 0.05)。两组临床妊娠率、生化妊娠率差异无统计学意义(p < 0.05), CE组活产率显著低于对照组(p < 0.036)。结论:尽管在多西环素治疗后组织学得到改善,CE患者仍表现出持续的生态失调,其特征是乳酸杆菌减少和机会性类群增加,这可能损害子宫内膜容受性和妊娠结局。这些发现表明,单靠抗生素治疗可能无法完全恢复CE中的微生物平衡,因此需要进一步研究以微生物群为目标的干预措施以提高生殖成功率。
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引用次数: 0
Letter to the Editor: Efficacy of Lymphocyte Immunotherapy in the Treatment of Recurrent Pregnancy Loss From Alloimmunity: A Systematic Review and Meta-Analysis 致编辑的信:淋巴细胞免疫疗法治疗同种免疫引起的复发性妊娠丢失的疗效:一项系统综述和荟萃分析。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-11-17 DOI: 10.1111/aji.70185
Ida Behrendt Møller, Henriette Svarre Nielsen, Kilian Vomstein
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引用次数: 0
Mentha spicata and Its Bioactive Compound Carvone Ameliorate Metabolic Disturbance and Ovarian Dysfunction in Experimental Rat Model of PCOS by Suppression of SREBP1/TLR4-Dependent Pathway 薄荷及其生物活性化合物香芹酮通过抑制SREBP1/ tlr4依赖通路改善PCOS实验大鼠代谢紊乱和卵巢功能障碍
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1111/aji.70183
Comfort A. Oladele, Stephanie E. Areloegbe, Chidubem F. Emereonye, Kehinde S. Olaniyi

Problem

Polycystic ovarian syndrome (PCOS) is a common endocrine and metabolic disorder in women of child-bearing age, often linked to ovarian dysfunction and complications beyond infertility. However, its management remains suboptimal due to unclear etiology. Sterol Regulatory Element Binding Protein 1 (SREBP1) and Toll-like Receptor 4 (TLR4) have been implicated in lipid metabolism and immune responses, but their interaction with ovarian function in PCOS remains unclear. Mentha spicata (spearmint) traditionally recognized for its hormonal and metabolic benefits, and its bioactive component, carvone (CARV), exhibit potent antioxidant and anti-inflammatory properties.

Method of study

This study investigated the involvement of SREBP1/TLR4-dependent pathway in letrozole-induced PCOS rat model and assessed the therapeutic potential of Mentha spicata extract (MENT) and carvone. Eight-week-old female Wistar rats were divided into groups (n = 7), namely, Control, CARV, MENT, PCOS, PCOS+CARV, and PCOS+MENT groups. Administration of letrozole (1 mg/kg) for 3 weeks induced PCOS. Thereafter, rats were treated with MENT (100 mg/kg, po) and carvone (20 mg/kg, po) for 6 weeks.

Result

The PCOS rats exhibited elevated plasma testosterone, anti-Mullerian hormone, prolactin, sex hormone–binding globulin, luteinizing hormone, lipid profiles, insulin resistance (HOMA-IR), and ovarian inflammation (NF-κB)/lipid peroxidation (malondialdehyde), alongside reduced antioxidant levels (glutathione) and increased Galectin-3 expression. Furthermore, there was an upregulation of SREBP1 and TLR4. Treatment with MENT or carvone significantly reversed these systemic and ovarian abnormalities compared to PCOS group.

Conclusion

These findings suggest that M. spicata and carvone ameliorate metabolic disturbance and ovarian dysfunction in PCOS by suppressing SREBP1/TLR4 expression.

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌和代谢紊乱,通常与卵巢功能障碍和不孕症以外的并发症有关。然而,由于病因不明,其治疗仍不理想。甾醇调节元件结合蛋白1 (SREBP1)和toll样受体4 (TLR4)参与脂质代谢和免疫应答,但它们与PCOS卵巢功能的相互作用尚不清楚。传统上认为薄荷具有激素和代谢益处,其生物活性成分香芹酮(CARV)具有强大的抗氧化和抗炎特性。研究SREBP1/ tlr4依赖通路在来曲唑诱导的PCOS大鼠模型中的作用,并评估薄荷提取物(menta spicata extract, MENT)和香芹酮的治疗潜力。将8周龄雌性Wistar大鼠分为Control组、CARV组、MENT组、PCOS组、PCOS+CARV组和PCOS+MENT组(n = 7)。给予来曲唑(1mg /kg) 3周诱导多囊卵巢综合征。此后,大鼠分别给予MENT (100 mg/kg, po)和香芹酮(20 mg/kg, po)治疗6周。结果PCOS大鼠血浆睾酮、抗苗勒管激素、催乳素、性激素结合球蛋白、促黄体生成素、血脂、胰岛素抵抗(HOMA-IR)、卵巢炎症(NF-κB)/脂质过氧化(丙二醛)水平升高,抗氧化剂(谷胱甘肽)水平降低,半乳糖凝集素-3表达升高。此外,SREBP1和TLR4表达上调。与PCOS组相比,经MENT或香芹酮治疗可显著逆转这些系统和卵巢异常。结论spicata和香芹酮通过抑制SREBP1/TLR4的表达,改善PCOS患者的代谢紊乱和卵巢功能障碍。
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引用次数: 0
Response of Bovine Uterine Microbiota to Staphylococcus aureus Infection 牛子宫微生物群对金黄色葡萄球菌感染的反应。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-11-04 DOI: 10.1111/aji.70178
Zhiqiang Li, Xiaolian Zhang, Lingwei Peng, Yi Fang, Hongyu Liu, Yang Zhou, Jun Wang, Wenfa Lu

Background

Endometritis is a highly prevalent reproductive disorder in cows, causing serious adverse effects on reproductive performance, which brings huge economic losses to the livestock industry. Staphylococcus aureus is detected in a high proportion of endometritis pathogens (alone or in combinations of infections). Uterine microbial composition plays an important role in endometritis.

Object and Method

In order to determine the role of S. aureus in endometritis, we established an endometritis model using this bacterium and utilized metagenomics to detect the structure and function of the bovine uterine microbiota.

Results

We found that S. aureus infection significantly increased the relative abundance of bacteria such as Escherichia coli, Trueperella pyogenes, and Streptococcus spp., while reducing the relative abundance of Akkermansia and Prevotella bacteria. The functions of microorganisms in the uterus are mainly manifested in metabolic levels, including carbohydrate metabolism, amino acid metabolism, energy metabolism, and lipid metabolism processes. The number of genes continues to increase with the duration of S. aureus infection, which disrupts the balance that maintains the bovine uterine flora.

Conclusion

This study provides a descriptive analysis of changes in the uterine microbiota of cows infected with S. aureus, which contributes to a new understanding of uncultured or unidentified pathogenic bacteria.

背景:子宫内膜炎是奶牛高发的一种生殖疾病,严重影响奶牛的繁殖性能,给畜牧业带来巨大的经济损失。金黄色葡萄球菌在子宫内膜炎病原体中检测到的比例很高(单独或合并感染)。子宫微生物组成在子宫内膜炎中起重要作用。目的和方法:为了确定金黄色葡萄球菌在子宫内膜炎中的作用,我们利用该细菌建立了子宫内膜炎模型,并利用宏基因组学技术检测牛子宫微生物群的结构和功能。结果:我们发现金黄色葡萄球菌感染显著增加了大肠埃希菌、化脓性真佩菌、链球菌等细菌的相对丰度,降低了阿克曼氏菌和普雷沃氏菌的相对丰度。子宫内微生物的功能主要表现在代谢水平,包括碳水化合物代谢、氨基酸代谢、能量代谢和脂质代谢过程。随着金黄色葡萄球菌感染的持续时间,基因的数量继续增加,这破坏了维持牛子宫菌群的平衡。结论:本研究提供了金黄色葡萄球菌感染奶牛子宫菌群变化的描述性分析,有助于对未培养或未鉴定的病原菌有新的认识。
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引用次数: 0
Neutrophils at the Maternal-Fetal Interface: Agents of Protection or Destruction? 中性粒细胞在母胎界面:保护或破坏代理人?
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-10-30 DOI: 10.1111/aji.70181
Sallie L. Fell, Sydney M. Nemphos, James E. Prusak, Amitinder Kaur, Jamie O. Lo, Jennifer A. Manuzak

Neutrophils, traditionally recognized for their role in innate immunity, have emerged as a key cell population at the maternal-fetal interface, during both uncomplicated and pathological pregnancies. Neutrophil effector functions, including phagocytosis, neutrophil extracellular trap formation, and degranulation, can play protective roles, such as preventing infection and facilitating tissue remodeling during pregnancy. However, these effector functions may also contribute to excessive inflammation, tissue damage, and adverse pregnancy outcomes in the context of sterile inflammation or maternal infection, underscoring the dual nature of neutrophils at the maternal-fetal interface. In this review, we examine the paradoxical nature of neutrophils at the maternal-fetal interface. Further, the protective and deleterious roles of neutrophils during pregnancy are evaluated in the context of bacterial, viral, and parasitic infections. Insights from this review are anticipated to inform basic and clinical research aimed at identifying neutrophils or neutrophil components as biomarkers and therapeutic targets in obstetric conditions and infectious diseases during pregnancy.

中性粒细胞,传统上被认为在先天免疫中起作用,已经成为母胎界面的关键细胞群,在非并发症和病理性怀孕期间。中性粒细胞效应功能,包括吞噬、中性粒细胞胞外陷阱形成、脱颗粒等,在妊娠期间可起到预防感染、促进组织重塑等保护作用。然而,在无菌炎症或母体感染的情况下,这些效应功能也可能导致过度炎症、组织损伤和不良妊娠结局,强调了中性粒细胞在母胎界面的双重性质。在这篇综述中,我们研究了中性粒细胞在母胎界面的矛盾性质。此外,中性粒细胞在怀孕期间的保护和有害作用在细菌,病毒和寄生虫感染的背景下进行评估。本综述的见解预计将为基础和临床研究提供信息,旨在确定中性粒细胞或中性粒细胞成分作为妊娠期间产科疾病和感染性疾病的生物标志物和治疗靶点。
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引用次数: 0
Development of a Preterm Birth Risk Prediction Model Based on CCL28 Biomarker Selection and Multidimensional Data Integration 基于CCL28生物标志物选择和多维数据集成的早产风险预测模型的建立。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-10-30 DOI: 10.1111/aji.70175
Yingying Li, Ning Xu, Jie Zhang, Guocheng Liu

Aim

This study aimed to identify potential biomarkers for preterm birth (PTB) and construct a multidimensional risk prediction model integrating clinical and proteomic data, with a focus on CCL28.

Materials and Methods

Pregnant women were enrolled and categorized into PTB and term birth (TB) groups. Plasma and placental samples were analyzed using OLINK proteomics, ELISA, and immunohistochemistry. Logistic regression and nomogram modeling were employed to assess predictive markers, while ROC curve analysis was used to evaluate model performance.

Results

Proteomic analysis revealed significantly lower CCL28 levels in PTB compared to TB (p < 0.01), which was validated by ELISA (p < 0.0001). Immunohistochemistry confirmed reduced CCL28 expression in PTB placental tissue. Multivariate logistic regression identified CCL28 as an independent predictor of PTB (OR = 0.150, p = 0.01). The developed nomogram, incorporating CCL28 levels and clinical variables, demonstrated strong predictive ability (AUC = 0.841).

Conclusion

CCL28 was identified as a key biomarker for PTB prediction. The integrated prediction model enhanced early risk assessment, providing a valuable tool for targeted clinical interventions in high-risk pregnancies.

目的:以CCL28为研究对象,寻找早产儿(PTB)的潜在生物标志物,构建整合临床和蛋白质组学数据的多维风险预测模型。材料与方法:纳入孕妇,并将其分为PTB组和足月分娩组。血浆和胎盘样本采用OLINK蛋白质组学、ELISA和免疫组织化学进行分析。采用Logistic回归和nomogram建模评估预测指标,ROC曲线分析评估模型性能。结果:蛋白质组学分析显示PTB的CCL28水平明显低于TB (p < 0.01), ELISA验证了这一点(p < 0.0001)。免疫组化证实PTB胎盘组织CCL28表达降低。多因素logistic回归发现CCL28是PTB的独立预测因子(OR = 0.150, p = 0.01)。综合CCL28水平和临床变量,所建立的nomogram预测能力强(AUC = 0.841)。结论:CCL28是预测肺结核的关键生物标志物。该综合预测模型增强了早期风险评估,为高危妊娠的针对性临床干预提供了有价值的工具。
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引用次数: 0
Reframing Endometriosis: Interplay of NETs, Macrophages, and Lymphocytes at the Crossroads of Disease Progression, Infertility, and Malignant Transformation 重构子宫内膜异位症:net、巨噬细胞和淋巴细胞在疾病进展、不孕症和恶性转化过程中的相互作用。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-10-27 DOI: 10.1111/aji.70179
Megha M. Anchan, Rahul Dutta

Endometriosis (ENDO) is a painful, chronic gynecological disease widely affecting women globally. While traditionally classified as a hormonal disorder, ENDO is now increasingly recognized as a multifaceted immune-mediated syndrome driven by chronic inflammation and immune tolerance. It is associated with painful symptoms, infertility, and potential malignant transformation. This study provides a comprehensive review of the immunological literature from electronic databases, focusing on the roles of innate and adaptive immune cell dysfunction in ENDO progression, including Neutrophil Extracellular Traps (NETs), macrophages, and lymphocytes. The pathology is governed by a dysregulated immunological landscape, specifically involving elevated NETs, the prevalence of immunosuppressive M2 macrophages, and compromised Natural Killer (NK) cell and T lymphocyte activity. These elements establish a tumor-like microenvironment through the activation of immune checkpoints and metabolic reprogramming. The chemokine IL-8 is highlighted as a central catalyst promoting NETosis and inflammation, driving fibrosis, lesion invasiveness, and reproductive failure. These immune circuits may also contribute to the risk of Endometriosis-Associated Ovarian Cancers. Reframing ENDO through this immunological paradigm provides an integrated model that incorporates its inflammatory, fibrotic, and carcinogenic features. This understanding reveals promising, non-hormonal therapeutic strategies targeting NETs, macrophage modulators, and immunological checkpoints for disease management and fertility preservation.

子宫内膜异位症(ENDO)是一种广泛影响全球妇女的疼痛性慢性妇科疾病。虽然传统上被归类为激素失调,但ENDO现在越来越被认为是一种由慢性炎症和免疫耐受驱动的多方面免疫介导综合征。它与疼痛症状、不孕和潜在的恶性转化有关。本研究对来自电子数据库的免疫学文献进行了全面回顾,重点关注先天和适应性免疫细胞功能障碍在ENDO进展中的作用,包括中性粒细胞胞外陷阱(NETs)、巨噬细胞和淋巴细胞。病理是由失调的免疫环境控制的,特别是涉及NETs升高,免疫抑制M2巨噬细胞的流行,自然杀伤细胞(NK)细胞和T淋巴细胞活性受损。这些元素通过激活免疫检查点和代谢重编程建立了类似肿瘤的微环境。趋化因子IL-8被强调为促进NETosis和炎症,驱动纤维化,病变侵袭性和生殖衰竭的中心催化剂。这些免疫回路也可能增加子宫内膜异位症相关卵巢癌的风险。通过这种免疫范式重新构建ENDO提供了一个整合其炎症、纤维化和致癌特征的综合模型。这一认识揭示了针对NETs、巨噬细胞调节剂和免疫检查点的有希望的非激素治疗策略,用于疾病管理和生育保护。
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引用次数: 0
Immunological Dynamics in PCOS T Cell Exhaustion TIGIT Upregulation Regulated by METTL3-Mediated N6 RNA Methylation mettl3介导的N6 RNA甲基化调控PCOS T细胞衰竭的免疫动力学
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-10-25 DOI: 10.1111/aji.70180
Zhaowei Cai, Rongju Liu, Li Zhao, Liling Zhou, Qingyang Li, Hongmei He

Problem

Polycystic ovary syndrome (PCOS) stands as a multifaceted endocrine disorder with implications beyond reproductive health, encompassing metabolic and immunological dimensions. This study delves into the immunological alterations within T cells in a murine PCOS model, unraveling novel insights into the molecular mechanisms contributing to T cell dysfunction.

Method of Study

A PCOS model was established in mice, followed by isolating T cells. Isolated T cells were activated by anti-CD3 and anti-CD28 antibodies. Cytokine levels were determined by enzyme-linked immunosorbent assay (ELISA) assay, and carboxyfluorescein succinimidyl ester (CFSE) dye was utilized for proliferation detection. Flow cytometry was utilized for analyzing exhaustion markers. RNA methylation analysis was determined by methylated RNA immunoprecipitation (Me-RIP) assay.

Results

In the PCOS mouse model, T cells exhibited a state of exhaustion, including impaired activation, reduced cytokine secretion, and decreased proliferative capacity. Particularly, the expression of T cell immunoreceptor with Ig and ITIM domain (TIGIT) molecules on the surface of T cells was significantly increased, which was associated with T cell exhaustion. The stability of TIGIT mRNA was enhanced due to the increased level of N6 RNA methylation, in which the methyltransferase-like 3 (METTL3) methyltransferase played a key role. Experiments showed that by inhibiting N6-methyladenosine (M6A) methylation or knocking out METTL3, the activation phenotype of PCOS T cells could be reversed, and cytokine secretion and proliferative capacity could be restored.

Conclusions

Although acknowledging study limitations, such as the murine model's partial recapitulation of human PCOS complexity, this research provides a foundation for future investigations into the specific molecular mechanisms governing T cell function and potential therapeutic targets within the N6 RNA methylation pathway.

多囊卵巢综合征(PCOS)是一种多方面的内分泌紊乱,其影响超出了生殖健康,包括代谢和免疫方面。本研究深入研究了小鼠PCOS模型中T细胞的免疫学改变,揭示了促进T细胞功能障碍的分子机制的新见解。研究方法建立小鼠PCOS模型,分离T细胞。分离的T细胞被抗cd3和抗cd28抗体激活。采用酶联免疫吸附法(ELISA)检测细胞因子水平,采用羧荧光琥珀酰亚胺酯(CFSE)染色法检测细胞增殖。利用流式细胞术分析衰竭标志物。采用甲基化RNA免疫沉淀(Me-RIP)法测定RNA甲基化分析。结果在PCOS小鼠模型中,T细胞表现出衰竭状态,包括活化受损,细胞因子分泌减少,增殖能力下降。特别是T细胞表面Ig和ITIM结构域(TIGIT)分子的T细胞免疫受体表达显著增加,这与T细胞衰竭有关。由于N6 RNA甲基化水平的增加,TIGIT mRNA的稳定性增强,其中甲基转移酶样3 (METTL3)甲基转移酶发挥了关键作用。实验表明,通过抑制n6 -甲基腺苷(M6A)甲基化或敲除METTL3,可逆转PCOS T细胞的活化表型,恢复细胞因子分泌和增殖能力。尽管承认研究的局限性,例如小鼠模型部分再现了人类多囊卵巢综合征的复杂性,但本研究为未来研究控制T细胞功能的特定分子机制和N6 RNA甲基化途径中的潜在治疗靶点提供了基础。
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引用次数: 0
Prognostic Value of Systemic Immune-Inflammation Index in Patients With Gynecological Tumors: A Systematic Review and Meta-Analysis 妇科肿瘤患者全身免疫炎症指数的预后价值:系统综述和荟萃分析。
IF 2.4 3区 医学 Q3 IMMUNOLOGY Pub Date : 2025-10-22 DOI: 10.1111/aji.70170
Feng Guo, Hao Peng, Hao Hu, Jia Liu

This meta-analysis (MA) systematically evaluated the application value of systemic immune-inflammation index (SII) in the prognosis of patients with gynecological tumors. Electronic databases including PubMed, Embase, Cochrane Library, Web of Science, Elsevier, and Wiley were searched for randomized controlled trials (RCTs) of SII according to inclusion and exclusion criteria, with the search period extending from the inception of the databases to November 2024. Clinical outcomes included overall survival (OS), disease-free survival (DFS), progression-free survival (PFS), and distant metastasis-free survival (DMFS). The quality of the included articles was assessed adopting the Cochrane systematic review method, and MA was conducted adopting Stata 17.0 software. A total of eight studies (10 trials) were included, with high SII having an observable negative impact on OS [Tau2 = 0.20, 95% confidence interval (CI): 1.30–2.58; Z = 3.47, p = 0.0005]. High SII had an observable negative impact on DFS and PFS (Tau2 = 0.08, 95% CI: 1.25–1.97; Z = 3.89, p = 0.0001). High SII had an observable negative impact on DMFS (95% CI: 1.20–1.86; Z = 3.54, p = 0.0004). The MA results indicate that a high SII index predicts poor survival outcomes in patients with gynecological tumors and is an effective indicator for prognosis in clinical practice.

本meta分析(MA)系统评价全身免疫炎症指数(SII)在妇科肿瘤患者预后中的应用价值。检索PubMed、Embase、Cochrane Library、Web of Science、Elsevier和Wiley等电子数据库,按照纳入和排除标准检索SII的随机对照试验(RCTs),检索时间从数据库建立之初至2024年11月。临床结果包括总生存期(OS)、无病生存期(DFS)、无进展生存期(PFS)和无远处转移生存期(DMFS)。采用Cochrane系统评价法评价纳入文献的质量,采用Stata 17.0软件进行meta分析。共纳入8项研究(10项试验),高SII对OS有可观察到的负面影响[Tau2 = 0.20, 95%可信区间(CI): 1.30-2.58;Z = 3.47, p = 0.0005]。高SII对DFS和PFS有明显的负面影响(Tau2 = 0.08, 95% CI: 1.25-1.97; Z = 3.89, p = 0.0001)。高SII对DMFS有明显的负面影响(95% CI: 1.20-1.86; Z = 3.54, p = 0.0004)。MA结果提示,高SII指数预示着妇科肿瘤患者的生存结局较差,是临床判断预后的有效指标。
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引用次数: 0
期刊
American Journal of Reproductive Immunology
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