Abstract

ObjectiveImpaired glucose metabolism, including insulin resistance, diabetes, and obesity, is a high-risk factor for the development of endometrial cancer (EC). Most previous studies evaluated the safety and effectiveness of fertility preservation (FP) for endometrial hyperplasia (EH) and EC patients were from the perspective of oncology or case reports. The study aims to evaluate the effect of glucose metabolic status on clinical pregnancy outcome of in vitro fertilization and embryo transfer (IVF-ET) in infertile patients with endometrial hyperplasia and early-stage endometrial cancer. MethodsThis retrospectively analysis included the data from patients who underwent IVF-ET after fertility preservation (FP) with endometrial hyperplasia and early-stage endometrial carcinoma, and primary infertile patients with normal endometrium (NE) but the fallopian tubal factors or pelvic adhesions who underwent IVF-ET during the same period as control group. All the patients were further divided into the following four subgroups: A: FP+ impaired glucose metabolism (IGM) (N = 20); B: FP+ normal glucose tolerance (NGT) (N = 29); C: NE+ IGM (N = 130); and D: NE+ NGT (N = 98). The main research outcome measure was the live birth rate (LBR) per embryo transfer (ET) cycle. Student's t-test or analysis of variance (ANOVA) was used for intergroup comparisons. The least significant difference (LSD) test was used for pairwise comparison between multiple groups. ResultsThe differences in anti-Mullerian hormones (AMH) and body mass index (BMI) between the four groups were significant. As BMI increased, the total dose of gonadotropin (Gn) during the controlled ovarian stimulation in the IGM group was significantly higher than that in the NGT group. The LBR was 16.7%, 26.3%, 41.6%, and 45.3% in the four subgroups (p = 0.033), respectively. By multivariate Logistic analysis, it was found that in FP group, IGM (OR = 1.501, 95% CI: 1.045–2.154, p = 0.028) was an independent risk factor for IVF-ET. ConclusionIGM was negatively affected by the LBR after endometrial complete response (CR) from early-stage endometrial cancer and endometrial hyperplasia. It was essential for the early detection and control of insulin resistance with metformin.

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