scholarly journals Massive Ovarian Growth in a Woman With Severe Insulin-Resistant Polycystic Ovary Syndrome Receiving GnRH Analogue

2019 ◽  
Vol 104 (7) ◽  
pp. 2796-2800 ◽  
Author(s):  
Prapti Singh ◽  
Ariela Agress ◽  
Vanessa Kasarah Madrigal ◽  
Clara Magyar ◽  
Nora Ostrzega ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Gnrh Analogue ◽  
Ovary Syndrome ◽  
Severe Insulin Resistance ◽  
Antral Follicles

Abstract Context Ovarian hyperandrogenism from polycystic ovary syndrome (PCOS) and hyperinsulinemia from insulin resistance are modulators of ovarian follicle development. We report on a woman with PCOS and hyperandrogenism and severe insulin resistance from metabolic syndrome who received long-term GnRH analogue therapy preceding bilateral salpingo-oophorectomy for massive ovarian enlargement. Ovarian histological examination showed proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas, demonstrating a unique link between hyperinsulinemia and granulosa cell mitogenesis. Case Description A 30-year-old woman with PCOS with hyperandrogenism, severe insulin resistance from metabolic syndrome, and nonalcoholic steatohepatitis experienced abdominal pain from bilaterally enlarged ovaries. She had previously experienced a pulmonary embolism while taking oral contraceptives and hepatotoxicity from metformin and spironolactone therapies. Long-term GnRH analogue therapy to induce pituitary desensitization to GnRH successfully decreased gonadotropin-dependent steroidogenesis without improving insulin resistance. Despite GnRH analogue therapy, progressive ovarian enlargement in the presence of hyperinsulinemia from worsening metabolic function eventually required bilateral salpingo-oophorectomy for removal of massively enlarged ovaries. Histological examination showed both ovaries contained proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas. Conclusions In women with PCOS and hyperinsulinemia from severe insulin resistance due to metabolic syndrome, granulosa cell proliferation within antral follicles can occur despite long-term GnRH analogue therapy, implicating hyperinsulinemia as a granulosa cell mitogen in the absence of gonadotropin-dependent ovarian function.

Prevalence of the metabolic syndrome in women with a previous diagnosis of polycystic ovary syndrome: long-term follow-up

2011 ◽  
Vol 96 (5) ◽  
pp. 1271-1274 ◽  
Author(s):  
Miriam Hudecova ◽  
Jan Holte ◽  
Matts Olovsson ◽  
Anders Larsson ◽  
Christian Berne ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Previous Diagnosis ◽  
Long Term Follow Up

scholarly journals Insulin resistance in relation to clinical, endocrine and metabolic profile of infertile women with polycystic ovary syndrome

2021 ◽  
Vol 14 (1) ◽  
pp. 1-6
Author(s):  
Shakeela Ishrat ◽  
Marufa Hossain ◽  
Subrata Kumar Biswas
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Waist Circumference ◽  
Polycystic Ovary Syndrome ◽  
Body Mass ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Infertile Women ◽  
Significant Difference

The objective of this study is to explore how hyperinsulinemia and insulin resistance relate to the clinical, endocrine and metabolic factors in the infertile women with polycystic ovary syndrome. This study was conducted on 121 consecutive infertile women with polycystic ovary syndrome attending the Infertility unit from January 2017 to December 2017. They were divided into two groups: insulin resistant and insulin sensitive. There was significant difference in body mass index and waist circumference between the two groups. Serum lipids were not associated with insulin resistance. Hyperinsulinemia was significantly associated with metabolic syndrome. Reducing body mass index and waist circumference may improve insulin resistance in infertile women with polycystic ovary syndrome. Screening the infertile women with polycystic ovary syndrome for hyperinsulinemia and insulin resistance and subsequent counseling is recommended to address the long-term risks of metabolic syndrome.

Obesity in relation to clinical, endocrine and metabolic parameters in infertile women with polycystic ovary syndrome: the South Asian perspective

2021 ◽  
Vol 20 (4) ◽  
pp. 864-870
Author(s):  
Shakeela Ishrat ◽  
Marufa Hossain
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Waist Circumference ◽  
Polycystic Ovary Syndrome ◽  
South Asian ◽  
Polycystic Ovary ◽  
Metabolic Parameters ◽  
The South ◽  
Ovary Syndrome ◽  
Infertile Women

Background: Polycystic ovary syndrome (PCOS) affects 5-10% of reproductive age women and it is a common cause of infertility in young women. Most of the infertile women with PCOS are overweight or obese. Obesity or excess fat aggravates the endocrine and metabolic dysfunction in women with PCOS. Weight management is the first line measure advised to infertile PCOS women who are overweight or obese. The objective of the study was to explore the association of obesity with the clinical, endocrine and metabolic parameters in infertile women with polycystic ovary syndrome in Bangladesh. Methodology: This was a cross sectional study of 126 consecutive infertile women with polycystic ovary syndrome attending the Infertility unit of the Department of Obstetrics and Gynecology at Bangabandhu Sheikh Mujib Medical University from January 2017 to December 2017.Obesity groups were defined by BMI thresholds specific for the South Asian population. Results: The mean body mass index (BMI) was 26.58±3.18 kg/m2and mean waist circumference was 91.07±9.5 cm. There was highly significant association of obesity with waist circumference and fasting insulin. BMI at or above 25kg/m2 was significantly associated with acanthosis nigricans, hyperandrogenemia and hyperinsulinemia, whereas BMI at or more than 23kg/m2 was significantly associated, in addition, with insulin resistance and metabolic syndrome. Conclusion: Obesity is associated with hyperandrogenemia, hyperinsulinemia, insulin resistance and metabolic syndrome in infertile women with polycystic ovary syndrome. Bangladesh Journal of Medical Science Vol.20(4) 2021 p.864-870

Polycystic ovary syndrome: reproductive aspects

2011 ◽  
pp. 1229-1234
Author(s):  
Sophie Catteau-Jonard ◽  
Cécile Gallo ◽  
Didier Didier
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Therapeutic Approaches ◽  
Women Of Reproductive Age ◽  
Ovary Syndrome ◽  
Common Cause ◽  
The Metabolic Syndrome

The polycystic ovary syndrome (PCOS) is the most common cause of anovulation and hyperandrogenism in women, affecting between 5 and 10% of women of reproductive age worldwide (1). Although this difficult topic in endocrine gynaecology is under extensive research, controversies still remain about the pathophysiology, diagnosis, and therapy of PCOS. The PCOS phenotype can be structured in three components: manifestations of anovulation, hyperandrogenism, and the metabolic syndrome (of which hyperinsulinaemia secondary to insulin resistance is the central abnormality). The latter two are addressed in other chapters. Our knowledge about the mechanism of disturbed folliculogenesis in PCOS that is responsible for its reproductive aspects has much increased these last years, thus opening new avenues for the diagnostic and therapeutic approaches.

Obesity, hormonal and metabolic abnormalities in adolescent girls with polycystic ovary syndrome

2013 ◽  
Vol 154 (31) ◽  
pp. 1226-1234
Author(s):  
László Ságodi ◽  
Béla Lombay ◽  
Ildikó Vámosi ◽  
László Barkai
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Polycystic Ovary Syndrome ◽  
Adolescent Girls ◽  
Polycystic Ovary ◽  
Metabolic Abnormalities ◽  
Ovary Syndrome

Introduction: Polycystic ovary syndrome is associated with metabolic abnormalities, such as dyslipidemia, obesity, glucose intolerance, which are also components of the metabolic syndrome. Central obesity and insulin resistance appear to play an important role in the pathogenesis of polycystic ovary syndrome, perhaps via subsequent steroidogenic dysregulation. Aim: The aim of the authors was to assess metabolic and hormonal abnormalities in adolescent girls with polycystic ovary syndrome. Method: The study included 52 adolescents diagnosed with polycystic ovary syndrome based on the Rotterdam criteria. Anthropometric, hormonal and metabolic parameters were evaluated among all subjects. 20 healthy, age-matched, non-obese, regularly menstruating girls were used as controls. Of the 52 patients, 15 patients were born with low-birth-weight and 37 patients were born with normal birth weight. Oral glucose tolerance test was performed in all patients and controls. The age of patients was 16.8±3.1 years, and the age of controls was 16.95±2.1 years. Results: Among patients with polycystic ovary syndrome the prevalence of overweight and obesity was 35% (n = 18), while impaired fasting glucose occurred in one patient, impaired glucose tolerance in 8 patients, insulin resistance in 25 patients and metabolic syndrome in 12 patients. Serum triglyceride levels in patients and controls were 1.4±0.8 and 0.9±0.3 mmol/l, respectively (p<0.05), while fasting blood glucose, total cholesterol, HDL and LDL cholesterol were not different in the two groups. Metabolic abnormalities and obesity were more severe and more frequent in patients with low-birth-weight compared to those born with normal weight. There was a negative correlation between birth weight and body mass index SDS values and a positive correlation between fasting insulin levels and body mass index SDS (r = 0.37) in patients born with low-birth-weight. Conclusions: Abnormal glucose metabolism is frequently present in adolescents with polycystic ovary syndrome. It is possible that early diagnosis of polycystic ovary syndrome in adolescences may prevent some of the long-term complications associated with this syndrome. Orv. Hetil., 2013, 154, 1226–1234.

scholarly journals Polycystic Ovary Syndrome, Insulin Resistance, and Obesity: Navigating the Pathophysiologic Labyrinth

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Joselyn Rojas ◽  
Mervin Chávez ◽  
Luis Olivar ◽  
Milagros Rojas ◽  
Jessenia Morillo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Main Culprit ◽  
Exact Etiology

Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine-metabolic disorder that implies various severe consequences to female health, including alarming rates of infertility. Although its exact etiology remains elusive, it is known to feature several hormonal disturbances, including hyperandrogenemia, insulin resistance (IR), and hyperinsulinemia. Insulin appears to disrupt all components of the hypothalamus-hypophysis-ovary axis, and ovarian tissue insulin resistance results in impaired metabolic signaling but intact mitogenic and steroidogenic activity, favoring hyperandrogenemia, which appears to be the main culprit of the clinical picture in PCOS. In turn, androgens may lead back to IR by increasing levels of free fatty acids and modifying muscle tissue composition and functionality, perpetuating this IR-hyperinsulinemia-hyperandrogenemia cycle. Nonobese women with PCOS showcase several differential features, with unique biochemical and hormonal profiles. Nevertheless, lean and obese patients have chronic inflammation mediating the long term cardiometabolic complications and comorbidities observed in women with PCOS, including dyslipidemia, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. Given these severe implications, it is important to thoroughly understand the pathophysiologic interconnections underlying PCOS, in order to provide superior therapeutic strategies and warrant improved quality of life to women with this syndrome.

scholarly journals The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
White Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Obstructive Sleep ◽  
The Impact

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.

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