Endometriosis

Polycystic ovary syndrome (PCOS) is characterized by a constellation of clinical symptoms that include irregular menses due to chronic oligo-ovulation, phenotypic features of hyperandrogenism, and obesity The term “polycystic ovary” refers to ovarian morphology with increased ovarian stroma and a ring of cortical follicles Core biochemical features include hyperandrogenism and insulin resistance The pathogenesis of PCOS remains a topic of debate Treatment of PCOS typically focuses on mitigating the impact of hyperandrogenism, insulin resistance, and chronic oligo-ovulation and restoring fertility when desired

/pdf/polycystic-ovary-syndrome-1tb4ywt6qn.pdf

Polycystic ovary syndrome.

Due to the comprehensive examination of 50 patients with ovarian polycystosis the authors suggested that ultrasound, laparoscopic, hormonal and endometrial parameters should be employed as diagnostic criteria.

Diagnostic criteria for polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic disorders in premenopausal women. Heterogeneous by nature, PCOS is defined by a combination of signs and symptoms of androgen excess and ovarian dysfunction in the absence of other specific diagnoses. The aetiology of this syndrome remains largely unknown, but mounting evidence suggests that PCOS might be a complex multigenic disorder with strong epigenetic and environmental influences, including diet and lifestyle factors. PCOS is frequently associated with abdominal adiposity, insulin resistance, obesity, metabolic disorders and cardiovascular risk factors. The diagnosis and treatment of PCOS are not complicated, requiring only the judicious application of a few well-standardized diagnostic methods and appropriate therapeutic approaches addressing hyperandrogenism, the consequences of ovarian dysfunction and the associated metabolic disorders. This article aims to provide a balanced review of the latest advances and current limitations in our knowledge about PCOS while also providing a few clear and simple principles, based on current evidence-based clinical guidelines, for the proper diagnosis and long-term clinical management of women with PCOS.

Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment

Cosponsoring associations The American Society for Reproductive Medicine, the European Society of Endocrinology, and the Pediatric Endocrine Society. This guideline was funded by the Endocrine Society. Objective To formulate clinical practice guidelines for the diagnosis and treatment of functional hypothalamic amenorrhea (FHA). Participants The participants include an Endocrine Society-appointed task force of eight experts, a methodologist, and a medical writer. Evidence This evidence-based guideline was developed using the Grading of Recommendations, Assessment, Development, and Evaluation approach to describe the strength of recommendations and the quality of evidence. The task force commissioned two systematic reviews and used the best available evidence from other published systematic reviews and individual studies. Consensus process One group meeting, several conference calls, and e-mail communications enabled consensus. Endocrine Society committees and members and cosponsoring organizations reviewed and commented on preliminary drafts of this guideline. Conclusions FHA is a form of chronic anovulation, not due to identifiable organic causes, but often associated with stress, weight loss, excessive exercise, or a combination thereof. Investigations should include assessment of systemic and endocrinologic etiologies, as FHA is a diagnosis of exclusion. A multidisciplinary treatment approach is necessary, including medical, dietary, and mental health support. Medical complications include, among others, bone loss and infertility, and appropriate therapies are under debate and investigation.

/pdf/functional-hypothalamic-amenorrhea-an-endocrine-society-41ufivbujp.pdf

Functional Hypothalamic Amenorrhea: An Endocrine Society Clinical Practice Guideline

Criteria, prevalence, and phenotypes of polycystic ovary syndrome

Androgen excess (AE) is a key feature of polycystic ovary syndrome (PCOS) and results in, or contributes to, the clinical phenotype of these patients. Although AE will contribute to the ovulatory and menstrual dysfunction of these patients, the most recognizable sign of AE includes hirsutism, acne, and androgenic alopecia or female pattern hair loss (FPHL). Evaluation includes not only scoring facial and body terminal hair growth using the modified Ferriman–Gallwey method but also recording and possibly scoring acne and alopecia. Moreover, assessment of biochemical hyperandrogenism is necessary, particularly in patients with unclear or absent hirsutism, and will include assessing total and free testosterone (T), and possibly dehydroepiandrosterone sulfate (DHEAS) and androstenedione, although these latter contribute limitedly to the diagnosis. Assessment of T requires use of the highest quality assays available, generally radioimmunoassays with extraction and chromatography or mass spectrometry preceded by liquid or gas chromatography. Management of clinical hyperandrogenism involves primarily either androgen suppression, with a hormonal combination contraceptive, or androgen blockade, as with an androgen receptor blocker or a 5α-reductase inhibitor, or a combination of the two. Medical treatment should be combined with cosmetic treatment including topical eflornithine hydrochloride and short-term (shaving, chemical depilation, plucking, threading, waxing, and bleaching) and long-term (electrolysis, laser therapy, and intense pulse light therapy) cosmetic treatments. Generally, acne responds to therapy relatively rapidly, whereas hirsutism is slower to respond, with improvements observed as early as 3 months, but routinely only after 6 or 8 months of therapy. Finally, FPHL is the slowest to respond to therapy, if it will at all, and it may take 12 to 18 months of therapy for an observable response.

Androgen excess: Investigations and management

Introduction: Polycystic ovary syndrome (PCOS) is a hormonal and metabolic disorder affecting 5 to 20% of reproductive-aged women worldwide that results in androgen excess, menstrual dysfunction an...

Genetics of polycystic ovary syndrome

Polycystic ovarian syndrome (PCOS) is known as one of the most frequent endocrine diseases in women worldwide. However, this term does not completely capture the diversity of clinical signs associated with this syndrome e.g., menstrual irregularity and clinical features of androgen excess, which are though commonplace in women with PCOS, they are not included under the definition of PCOS, limited to polycystic ovarian morphology (PCOM). Utilizing the most globally accepted criterion used today in the diagnosis of PCOS, the authors of this article review and discuss the historical and current context of evidence as well as their limitations. This review addresses the phenotypic approach and age-dependent aspects of PCOS in adolescents, adult and peri/postmenopausal women, as presented in the NIH (1990, 2012), Rotterdam (2003), AE-PCOS Society (2006) consensuses and in the latest evidence-based international guideline (2018). Global data on the epidemiology of PCOS, including prevalence and distribution of polycystic ovarian syndrome phenotypes, is also analyzed in the article. Lastly, the authors discuss the importance and current need to perform more epidemiological studies focused on PCOS.

Criteria, phenotypes and prevalence of polycystic ovary syndrome.

Context Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic abnormality with a worldwide prevalence of 4% to 21%, depending on diagnostic criteria. The National Institutes of Health (NIH) is the largest single funding agency in the world; it invests nearly $30.0 billion annually in biomedical research. Evidence acquisition Using the NIH Research Portfolio Online Reporting tool, we searched for all grants awarded by the NIH for PCOS and three other disorders with similar degrees of morbidity and similar or lower mortality and prevalence [rheumatoid arthritis (RA), tuberculosis (TB), and systemic lupus erythematosus (SLE)]. Evidence synthesis We compared funding by the NIH for PCOS, RA, TB, and SLE research for the years 2006 to 2015, inclusive. Conclusion PCOS, compared with RA, TB, and SLE, was relatively less funded (total mean 10-year funding was $215.12 million vs $454.39 million, $773.77 million, and $609.52 million, respectively). Funding for PCOS was largely provided by one NIH Institute/Center (ICs) vs at least two ICs for SLE and RA; more individual Research Project Grants were awarded for RA, SLE, and TB than for PCOS, whereas PCOS funding was more likely to be through General Clinical Research Centers Program or Specialized Centers Program awards. Our data suggest that PCOS research may be underfunded considering its prevalence, economic burden, metabolic morbidity, and negative impact on quality of life. Greater education of NIH leaders, including those at the National Heart, Lung, and Blood Institute and National Institutes of Diabetes and Digestive and Kidney Diseases; other federal and state agency leads; elected leaders; and the general public by professional societies, the scientific community, and patient advocates regarding this disorder is needed.

Walidah Walker

Papers

Criteria, prevalence, and phenotypes of polycystic ovary syndrome

Androgen excess: Investigations and management

Genetics of polycystic ovary syndrome

Criteria, phenotypes and prevalence of polycystic ovary syndrome.

Perspectives on Polycystic Ovary Syndrome: Is Polycystic Ovary Syndrome Research Underfunded?