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"Ovaries"
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Effects of Vitamin D3 Treatment on Polycystic Ovary Symptoms: A Prospective Double-Blind Two-Phase Randomized Controlled Clinical Trial
Background/Objectives: Vitamin D deficiency is common in women with polycystic ovary syndrome (PCOS) and may be associated with metabolic and endocrine disorders as well as ovulatory dysfunction. Vitamin D supplementation may improve ovarian dysfunction and follicular development by effecting gene expression. The aim of the present study was to investigate the effects of vitamin D supplementation in women with PCOS through a prospective, randomized, two-phase, parallel design, placebo-controlled trial. Methods: We assessed the impact on ovarian morphology, cycle length, and ovulatory dysfunction. Transvaginal ultrasonography (TVUS) examinations and clinical laboratory assessments were conducted at the baseline, and again after 12 and 24 weeks. The participants received vitamin D (30,000 IU/week) or a placebo (without concurrent metformin use) for 12 weeks, supplemented with calcium, followed by an additional 12 weeks of vitamin D treatment. Results: The treatment resulted in improvements in ovarian morphology and regularity of menstrual cycles in more than half of the patients. Additionally, vitamin D3 was associated with a significant increase in the ovulation rate. A statistically significant reduction in mean testosterone levels was observed in the subgroup of patients with an LH/FSH ratio greater than 2. Conclusions: Our results suggest that vitamin D3 treatment could function as either a standalone or an adjunctive therapy in the management of PCOS.
Journal Article
466 Laparoscopic management of huge ovarian cyst; novel technique
This is a case of 35 years old patient who presented with a massive ovarian mass. She underwent fertility-preserving ovarian cystectomy. The technique describes how to manage such ovarian masses while maintaining cancer hygiene and limitation of spillage risks.
Journal Article
305 A rare case of borderline brenner tumor
ObjectivesTo report a case of borderline Brenner tumorMethodsCase report and literature reviewResultsA 70-year old woman had lower abdominal pain and was found to have a large tumor in the pelvic cavity which had both cystic and solid leisions by ultrasonography and MRI. We underwent a surgery of total hysterectomy, bilateral salpingo-oophorectomy, omentum resection, pelvic and para-aortic lymph node dissection according to a frozen section diagnosis of borderline or malignant tumor of the ovary. The final pathological diagnosis was borderline Brenner tumor, StgaeIC3, which shows an exuberant papillary transitional cellular component with mild nuclear atypia lined by mucinous columnar epithelium without invasion to the stroma. There is no recurrent and metastasis at postoperative 3 months.ConclusionsBorderline Brenner tumor of the ovary is a rare tumor, which has only about 30 case reports of published English literatures. At present, we don’t have enough knowledge about the characteristics of the tumor to decide appropriate treatment. Additional collection of data of this tumor is necessary to establish diagnosis and treatment.
Journal Article
Beneficial effects of apigenin on ovarian histological changes and angiogenesis gene expression in rat model of polycystic ovary syndrome
Polycystic ovary syndrome (PCOS) is the most common heterogeneous reproductive disorder and can affect approximately 10% of women of reproductive age. Abnormal vasculogenesis is a common event in polycystic ovary syndrome. This study planned to evaluate the antiangiogenic role of apigenin in ovarian histology, gene expression, and vascular density and stability in an experimental model of PCOS. Twenty-eight rats weighing 180–250 g were divided into 4 groups. Seven rats in the control group remain intact and without treatment. In 21 rats, an ovary polycystic model with a single injection of estradiol valerate was established. The PCOS rats were treated with vehicle, apigenin 10, or apigenin 20 mg/kg in three different PCOS groups for 14 days. At the end, a histological assessment of the ovaries was performed to determine collagen density and follicle counting. The endothelial or periendothelial cells were determined by immunohistochemical assay, and angiogenesis gene expression was determined using molecular assessments. Apigenin treatment partially restored follicular development, decreased the number of cysts, and increased corpora lutea in PCOS rats. Also, apigenin decreased the collagen density in the polycystic ovaries. However, apigenin administration mitigated ovarian angiogenesis by a reduction in endothelial and periendothelial cell numbers. A decrease in VEGF and VEGF R2 (kinase insert domain receptor, KDR) expressions was found after the treatment of rats with apigenin. Conclusively, our data revealed that apigenin improves ovarian histological alterations and follicular dynamics in polycystic ovary rats. The effect is partially mediated by suppression of the VEGF signaling system and reduction in endothelial and periendothelial cell proliferation.
Journal Article
Melatonin refines ovarian mitochondrial dysfunction in PCOS by regulating the circadian rhythm gene Clock
Mitochondrial dysfunction is present in the ovaries of patients with polycystic ovary syndrome (PCOS). Melatonin (MT) has shown promise in treating PCOS by improving mitochondrial dysfunction, though the underlying mechanisms remain unclear. In this study, we first assessed the levels of proteins associated with mitochondrial autophagy and dynamics in ovary granulosa cells (GCs) of PCOS patients and in the ovaries of DHEA-induced PCOS mice. We found abnormal expression of these proteins, indicating the presence of mitochondrial dysfunction in PCOS ovaries. Notably, the expression of the circadian gene Clock and melatonin synthetic enzymes were also decreased in the ovaries of PCOS patients. Studies have suggested a potential role of circadian rhythm genes in the pathogenesis and progression of PCOS. We subsequently observed that pretreatment with MT could ameliorate the abnormal levels of mitochondrial-related proteins, reverse the low expression of CLOCK, and reduce pyroptosis in PCOS ovaries. Given the potential interaction between MT and Clock, we focused on whether exogenous MT improves mitochondrial dysfunction in PCOS ovaries by regulating the expression of the circadian gene Clock. Through in vitro culture of the human ovarian granulosa cell line KGN, we further found that when CLOCK levels were inhibited, the beneficial effects of MT on abnormal mitochondrial autophagy, disturbed mitochondrial dynamics, and mitochondrial dysfunction in PCOS ovaries were not significant, and there was no notable improvement in ovary GCs pyroptosis. Our study suggests that MT may improve ovary mitochondrial dysfunction by regulating circadian gene Clock while also reducing GCs pyroptosis in PCOS.
Journal Article
The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited
Polycystic ovary syndrome (PCOS) was hypothesized to result from functional ovarian hyperandrogenism (FOH) due to dysregulation of androgen secretion in 1989–1995. Subsequent studies have supported and amplified this hypothesis. When defined as otherwise unexplained hyperandrogenic oligoanovulation, two-thirds of PCOS cases have functionally typical FOH, characterized by 17-hydroxyprogesterone hyperresponsiveness to gonadotropin stimulation. Two-thirds of the remaining PCOS have FOH detectable by testosterone elevation after suppression of adrenal androgen production. About 3% of PCOS have a related isolated functional adrenal hyperandrogenism. The remaining PCOS cases are mild and lack evidence of steroid secretory abnormalities; most of these are obese, which we postulate to account for their atypical PCOS. Approximately half of normal women with polycystic ovarian morphology (PCOM) have subclinical FOH-related steroidogenic defects. Theca cells from polycystic ovaries of classic PCOS patients in long-term culture have an intrinsic steroidogenic dysregulation that can account for the steroidogenic abnormalities typical of FOH. These cells overexpress most steroidogenic enzymes, particularly cytochrome P450c17. Overexpression of a protein identified by genome-wide association screening, differentially expressed in normal and neoplastic development 1A.V2, in normal theca cells has reproduced this PCOS phenotype in vitro. A metabolic syndrome of obesity-related and/or intrinsic insulin resistance occurs in about half of PCOS patients, and the compensatory hyperinsulinism has tissue-selective effects, which include aggravation of hyperandrogenism. PCOS seems to arise as a complex trait that results from the interaction of diverse genetic and environmental factors. Heritable factors include PCOM, hyperandrogenemia, insulin resistance, and insulin secretory defects. Environmental factors include prenatal androgen exposure and poor fetal growth, whereas acquired obesity is a major postnatal factor. The variety of pathways involved and lack of a common thread attests to the multifactorial nature and heterogeneity of the syndrome. Further research into the fundamental basis of the disorder will be necessary to optimally correct androgen levels, ovulation, and metabolic homeostasis.
Journal Article