Background: Recurrent implantation failure (RIF) poses a major challenge in assisted reproductive technologies, with thin endometrium (≤7 mm) being a frequently observed yet poorly understood condition. Emerging evidence implicates nuclear factor-kappa B (NF-κB), a key transcription factor in inflammatory signaling, in impaired endometrial receptivity. However, its clinical relevance and prognostic value for live birth outcomes still need to be fully elucidated. Objective: We aim to evaluate the expression levels of endometrial NF-κB in patients with RIF and thin endometrium and to determine its potential as a predictive biomarker for live birth outcomes following IVF treatment. Methods: In this prospective case–control study, 158 women were categorized into three groups: Group 1 (RIF with thin endometrium, ≤7 mm, n = 52), Group 2 (RIF with normal endometrium, >7 mm, n = 38), and fertile controls (n = 68). NF-κB levels were assessed using ELISA and immunohistochemical histoscore. Pregnancy outcomes were compared across groups. ROC analysis and multivariable logistic regression were performed to assess the predictive value of NF-κB. Results: NF-κB expression was significantly elevated in Group 1 compared to Group 2 and controls (p = 0.0017). ROC analysis identified a cut-off value of 7.8 ng/mg for live birth prediction (AUC = 0.72, sensitivity 74%, specificity 75%). Multivariable analysis confirmed NF-κB is an independent predictor of live birth (p = 0.045). Histological findings revealed increased NF-κB staining in luminal and glandular epithelial cells in the thin endometrium group. Conclusions: Increased endometrial NF-κB expression is associated with thin endometrium and reduced live birth rates in RIF patients. NF-κB may serve not only as a biomarker of pathological inflammation but also as a prognostic tool for treatment stratification in IVF. Based on findings in the literature, the therapeutic targeting of NF-κB may represent a promising strategy to improve implantation outcomes.

Pentraxin-3 (PTX-3) is a multibiological protein involved in cumulus cell expansion, fertilization, and implantation. This study was designed to analyze how circulating PTX-3 levels change in women with polycystic ovary syndrome (PCOS). A total of 50 Turkish participants, 35 of whom had PCOS and 15 of whom were fertile, were included in the study. Patients in the PCOS group were divided into 4 different phenotypes according to the NIH criteria (phenotypes A–D). The number of patients in phenotype A was the highest 13 (37.1%). In the calculations made without phenotyping, the serum ptx3 levels of the PCOS group were found to be significantly lower compared to the fertile control group (3.32 ± 0.73 ng/mL vs 4.97 ± 1.29 ng/mL; P < .001). The ptx3 value of phenotypes A and B was significantly lower than phenotype D (P = .008 and P = .009, respectively). When the phenotypes were compared with the fertile control group, the PTX-3 levels of phenotypes A and B were significantly lower than the fertile group. Although the ptx3 levels of phenotypes C and D were lower than the fertile group, the difference did not reach statistical significance. This is the first study to investigate serum ptx3 levels by phenotype in PCOS. While serum PTX-3 levels decreased in phenotypes A and B, ptx3 levels in phenotypes C and D were similar in fertile patients.

Objective: To investigate the relationship between follicular fluid pentraxin 3 (PTX-3) levels and ovarian response, embryo quality, and insulin resistance (IR) in patients with polycystic ovary syndrome (PCOS) undergoing IVF/ICSI. Methods: A total of 130 women were enrolled and categorized into three groups: lean PCOS ( n = 43), overweight PCOS ( n = 42), and unexplained infertility (UEI, n = 45). Patients with endocrine disorders, chronic inflammatory diseases, or recent hormonal therapy (within 3 months) were excluded. Follicular fluid (FF) and serum PTX-3 levels were measured using ELISA. Subgroup analyses were performed according to BMI and HOMA-IR status. Correlations between FF PTX-3 and clinical, hormonal, and embryological parameters were assessed. ROC curve analysis and multivariate linear regression were used to evaluate the diagnostic and predictive value of FF biomarkers for follicular output rate (FORT). Results: FF PTX-3 levels were significantly higher in both lean (23.31 ± 1.33 ng/mL) and overweight PCOS patients (12.54 ± 1.05 ng/mL) compared to UEI controls (7.01 ± 0.54 ng/mL; p = 0.029). Notably, PTX-3 remained elevated in lean PCOS despite a lower BMI, supporting its role in intrinsic ovarian inflammation. FF PTX-3 showed significant positive correlations with total testosterone ( r = 0.580), AFC ( r = 0.598), and oocyte count ( r = 0.532), but was inversely associated with high-quality embryo number ( r = − 0.482), 2PN count ( r = − 0.312), and FORT ( r = − 0.418). ROC analysis demonstrated moderate diagnostic performance of PTX-3 for predicting suboptimal FORT (AUC = 0.77; cut-off: 20.4 ng/mL). In multivariate analysis, FF PTX-3 (β = − 0.65, p = 0.001), TSG-6 (β = − 0.42), and ITI (β = − 0.37) were independent negative predictors of FORT, while AFC was positively associated. Conclusion: Elevated follicular PTX-3 levels are linked to hyperandrogenism and ovarian reserve in PCOS, but may impair embryo quality and functional follicular response. PTX-3 may serve as a potential biomarker of ovarian inflammation and compromised oocyte competence, independent of BMI or systemic insulin resistance.

Aim: To evaluate maternal serum copeptin levels and their predictive value for preterm birth in women with threatened preterm labor.Materials and Methods: This prospective study included 100 pregnant women (50 with threatened preterm labor, 50 controls) between 28–34 weeks. The threatened preterm labor group was subdivided into term (n=28) and preterm (n=22) deliveries. Copeptin levels were measured by enzyme immunoassay and analyzed using ROC curves.Results: Copeptin levels were significantly higher in women who delivered preterm (1.82±0.29 ng/mL) compared to term (1.22±0.40 ng/mL) and controls (0.97±0.34 ng/mL) (p

Polycystic ovary syndrome (PCOS) is frequently accompanied by dermatological manifestations related to hyperandrogenism, insulin resistance, and adipose tissue inflammation. Acne vulgaris (AV) is among its most common cutaneous findings, yet the role of adipokines remains unclear. Adipsin and isthmin-1 (Ism1) are emerging adipokines involved in metabolic regulation and inflammation. This study aimed to evaluate serum adipsin and Ism1 levels in women with PCOS and AV according to acne severity.This case–control study included 45 women with PCOS and AV and 45 age-matched controls without PCOS or acne. Acne severity was graded as mild, moderate, or severe using the Investigator Global Assessment (IGA) scale. Serum adipsin and Ism1 were measured by ELISA. Demographic, metabolic, and endocrine parameters were compared, and correlations were assessed using Spearman analysis. Compared with controls, women with PCOS had lower adipsin and higher Ism1 levels (p