title: Combination of Diane-35 and Metformin to Treat Early Endometrial Carcinoma in PCOS Women with Insulin Resistance.
abstract: BACKGROUND
  Young women with polycystic ovary syndrome (PCOS) have a high risk of developing endometrial carcinoma. There is a need for the development of new medical therapies that can reduce the need for surgical intervention so as to preserve the fertility of these patients. The aim of the study was to describe and discuss cases of PCOS and insulin resistance (IR) women with early endometrial carcinoma while being co-treated with Diane-35 and metformin.
  
  
  METHODS
  Five PCOS-IR women who were scheduled for diagnosis and therapy for early endometrial carcinoma were recruited. The hospital records and endometrial pathology reports were reviewed. All patients were co-treated with Diane-35 and metformin for 6 months to reverse the endometrial carcinoma and preserve their fertility. Before, during, and after treatment, endometrial biopsies and blood samples were obtained and oral glucose tolerance tests were performed. Endometrial pathology was evaluated. Body weight (BW), body mass index (BMI), follicle-stimulating hormone (FSH), luteinizing hormone (LH), total testosterone (TT), sex hormone-binding globulin (SHBG), free androgen index (FAI), insulin area under curve (IAUC), and homeostasis model assessment of insulin resistance (HOMA-IR) were determined.
  
  
  RESULTS
  Clinical stage 1a, low grade endometrial carcinoma was confirmed before treatment. After 6 months of co-treatment, all patients showed normal epithelia. No evidence of atypical hyperplasia or endometrial carcinoma was found. Co-treatment resulted in significant decreases in BW, BMI, TT, FAI, IAUC, and HOMA-IR in parallel with a significant increase in SHBG. There were no differences in the FSH and LH levels after co-treatment.
  
  
  CONCLUSIONS
  Combined treatment with Diane-35 and metformin has the potential to revert the endometrial carcinoma into normal endometrial cells in PCOS-IR women. The cellular and molecular mechanisms behind this effect merit further investigation.
authors.affiliation: 1. Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China ; 2. Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.affiliation: 1. Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
authors.forename: Yan-Rong
authors.initials: YR
authors.lastname: Guo
authors.affiliation: 1. Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
authors.forename: Jin-Fang
authors.initials: JF
authors.lastname: Lin
authors.affiliation: 2. Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden ; 3. Department of Integrative Medicine and Neurobiology, State Key Lab of Medical Neurobiology, Shanghai Medical College and Institute of Acupuncture Research (WHO Collaborating Center for Traditional Medicine), Institute of Brain Science, Fudan University, Shanghai 200032, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Feng
authors.affiliation: 2. Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
authors.forename: Håkan
authors.initials: H
authors.lastname: Billig
authors.affiliation: 2. Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
authors.forename: Ruijin
authors.initials: R
authors.lastname: Shao
keywords: PCOS; endometrial carcinoma; insulin resistance; progesterone resistance; steroid hormone receptors