Metformin for endometrial hyperplasia

Clement, Naomi; Oliver, Thomas R. W.; Shiwani, Hunain; Sanner, Juliane Rf; Mulvaney, Caroline; Atiomo, William

doi:10.1002/14651858.cd012214.pub2

Cited by 24 publications

(24 citation statements)

References 41 publications

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“…A 2017 Cochrane systematic review reported on three studies that studied the effects of metformin on endometrial hyperplasia; only one of these studies compared the effects of progestin and metformin with progestin alone. 12 Since then, additional studies have been added to the literature, and have also examined outcomes for patients with atypical hyperplasia and those with endometrial carcinoma. Although atypical endometrial hyperplasia is a pre-cancerous disease state, there is significant overlap between patients with atypical hyperplasia and those found to have invasive carcinoma after hysterectomy.…”

Section: Highlightsmentioning

confidence: 99%

Outcomes of women treated with progestin and metformin for atypical endometrial hyperplasia and early endometrial cancer: a systematic review and meta-analysis

Chae-Kim

Garg

Gavrilova-Jordan

et al. 2021

Int J Gynecol Cancer

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ObjectiveProgestin therapy is the recommended fertility-sparing management of atypical endometrial hyperplasia or early-stage endometrial cancer in reproductive-aged women. Our objective was to evaluate disease relapse after progestin and metformin versus progestin therapy alone in patients with endometrial hyperplasia or cancer. Our secondary outcomes were disease remission, clinical pregnancy and live birth rate.MethodsA systematic review of the literature was conducted (MEDLINE, Web of Science, Cochrane Library, CINAHL, LILACS, clinicaltrials.gov) from inception to April 2021. Studies of reproductive-aged women with atypical endometrial hyperplasia or early endometrial cancer who received progestin and metformin or progestin alone for fertility-sparing management, were included in the review. Early endometrial cancer was defined as grade 1, stage 1 disease. Exclusion criteria included women with higher grade endometrial cancer and when conservative management was not for fertility-sparing purposes. Data are presented as odds ratios (ORs) and 95% confidence intervals (CIs) with fixed or random effects meta-analysis. Quality scoring was based on the Newcastle-Ottawa and Jadad scales.ResultsIn total, 271 reports were identified and six studies met the inclusion criteria. These studies included 621 women; 241 (38.8%) patients received combined therapy and 380 (61.2%) received progestin therapy alone. Relapse rates were lower for progestin and metformin than for progestin therapy alone (pooled OR 0.46, 95% CI 0.24 to 0.91, p=0.03). The remission rates were not different (pooled OR 1.35, 95% CI 0.91 to 2.00, p=0.14). Women who received progestin and metformin achieved pregnancy and live birth rates similar to those who received progestin therapy only (pooled OR 1.01, 95% CI 0.44 to 2.35, p=0.98; pooled OR 0.46, 95% CI 0.21 to 1.03, p=0.06).ConclusionFor reproductive-aged women with atypical endometrial hyperplasia or early endometrial cancer, progestin and metformin therapy compared with progestin therapy alone is associated with lower relapse rates, and similar remission, clinical pregnancy and live birth rates.PROSPERO registration numberCRD42020179069.disease remission,

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Section: Highlightsmentioning

confidence: 99%

Outcomes of women treated with progestin and metformin for atypical endometrial hyperplasia and early endometrial cancer: a systematic review and meta-analysis

Chae-Kim

Garg

Gavrilova-Jordan

et al. 2021

Int J Gynecol Cancer

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“…Endometrial hyperplasia is an abnormal thickening of endometrium due to excess estrogen exposure or low progesterone which counteracts the enhancing action of estrogen on growth. Due to the associated hormonal changes, it is most common in females who are postmenopausal or have reached the reproductive age (Clement et al 2017). It may also happen secondary to diabetes, overweight, hypertension, or polycystic ovary.…”

Section: Introductionmentioning

confidence: 99%

Melatonin reduced endometrial hyperplasia induced by estradiol in female albino rats

Abdel-Hamid

Zenhom²,

Toni³

2019

gpb

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Melatonin, the pineal gland hormone, plays a crucial role in regulation of neuroendocrine and defensive functions, free radicals neutralization, and suppresses angiogenesis, proliferation and cancer. The purpose of designing our study is to assess the effect of estradiol benzoate and its combination with melatonin on uteri of female albino rats. For 4 weeks, the present study was conducted on thirty six female rats separated into 3 groups: Control group (rats received the vehicle), EB group (rats were treated by estradiol benzoate (600 μg/kg intramuscular) for induction of endometrial hyperplasia), and EB+Mel group (rats were treated with estradiol benzoate (600 μg/kg) plus melatonin (50 µg/ml) added to drinking water. Melatonin administration reduced estradiol benzoate-induced endometrial hyperplasia and prevented the occurrence of atypia associated with a significant reduction in lipid peroxide level and NF-κB mRNA and a significant rise in immune-expression of caspase-3, interleukin-2 (IL-2) mRNA and total antioxidant levels in uterine tissues. The results demonstrated that melatonin reduced estradiol benzoate action on the endometrium.

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“…In our study, the endometrial glands of PCOS rats appeared to overgrowth even hyperplasia, not only the gland number increased but also the gland size enlarged. And when the rats underwent EX or MET treatment, the gland number decreased and the gland size narrowed, which inferred that either EX or MET could improve the endometrial hyperplasia that is a common pathological state in PCOS, and MET may have therapeutic bene ts for PCOS patients in endometrial hyperplasia, and some studies have already prompted or con rmed [12,13]. We have investigated that EX or MET in uenced the ovaries of PCOS rats, not only in the ovarian morphology but also in the ovarian reservation function [8,9], and similarly, in the endometrium of PCOS mice models, we also found EX or MET were able to y positive effect on endometrial glands in PCOS rats.…”

Section: Discussionmentioning

confidence: 99%

Exenatide Improves Endometrial Glands in PCOS Rats through AMPKα-SIRT1

Cai

et al. 2020

Preprint

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Exenatide can contribute to the therapeutic effect for PCOS patients in restoring menstrual cycles. To exploring endometrial tissue change in PCOS rats and the effects of exenatide on endometrial tissue, we carried out in vivo study of PCOS rat models. Method: PCOS rat models were obtained after DHEA treatment, and the corresponding parameters were measured to confirm the establishment of PCOS models. Hematoxylin-eosin (H&E) staining was performed to observe endometrium morphological change, and western blot and RT-PCR were performed to identify the alteration AMP-activated protein kinase (AMPKα) and SIRT1 proteins and the relative expression of SIRT1 mRNA in endometrial cellular after the intervention of exenatide (EX). Results: The endometrium of PCOS rats appeared to not only the gland number increased but also the gland size enlarged. When the PCOS rats underwent EX treatment, the gland number decreased and the gland size narrowed, the expression of AMPKα and SIRT1 protein increased, and the expression of SIRT1 mRNA level augmented. Conclusion: EX could decrease gland number and narrow gland size in PCOS rat endometrium which may be partly via AMPKα-SIRT1 pathway.

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Metformin for endometrial hyperplasia

Cited by 24 publications

References 41 publications

Outcomes of women treated with progestin and metformin for atypical endometrial hyperplasia and early endometrial cancer: a systematic review and meta-analysis

Outcomes of women treated with progestin and metformin for atypical endometrial hyperplasia and early endometrial cancer: a systematic review and meta-analysis

Melatonin reduced endometrial hyperplasia induced by estradiol in female albino rats

Exenatide Improves Endometrial Glands in PCOS Rats through AMPKα-SIRT1

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