The diagnosis of PCOS is based on the Rotterdam guidelines: chronic anovulation, hyperandrogenism (biologic or clinical) and polycystic ovaries on ultrasound. Two of these three criteria are ...sufficient for making diagnosis of PCOS. However, one characteristic that is often associated to PCOS (obesity with severe insulin resistance and metabolic alteration regarding glucose metabolism and lipid pattern) has remained out of the current classification of PCOS. Because of this, patients with different metabolic and cardiovascular risk may be included in the same phenotype, and it makes more difficult to establish clear strategies of follow-up and treatment of the patients with increased risks, and also may hide genetic or environmental differences between PCOS patients. Our recent study has shown that metabolic alterations are linked to the weight and not to the Rotterdam phenotypes. Because of this, we suggest a new classification of PCOS phenotypes that divides each Rotterdam phenotype in obese (ob) or lean (l) sub-phenotype. An improved classification of PCOS may be essential for permitting new progress in our understanding of pathogenesis and treatment of PCOS (or of the different disorders that are part of PCOS).
Objective To evaluate the clinical and endocrine differences between main polycystic ovary syndrome (PCOS) phenotypes. Design To evaluate clinical and hormone parameters in a large group of ...consecutive women with PCOS diagnosed according Rotterdam criteria and divided according their phenotype. Setting University department of medicine. Patient(s) Three hundred eighty-two consecutive women with PCOS and 85 ovulatory controls. Intervention(s) Evaluation of clinical and hormone parameters. Main Outcome Measure(s) Blood levels of gonadotropins, testosterone, sex-hormone–binding globulin, dehydroepiandrosterone sulfate, 17α-hydroxyprogesterone, progesterone, glucose, and insulin, and calculation of the free androgen index and insulin sensitivity. Result(s) The severe PCOS phenotype (hyperandrogenism, chronic anovulation, and polycystic ovaries: type I classic PCOS) was the most common phenotype in 53.9% of the patients. The phenotype of 8.9% of patients was characterized by hyperandrogenism and chronic anovulation but normal ovaries (type II classic PCOS). The two phenotypes of classic PCOS had similar clinical and endocrine characteristics, but the patients with polycystic ovaries had a higher luteinizing hormone/follicle-stimulating hormone (LH/FSH) ratio. Ovulatory PCOS was relatively common (28.8% of PCOS patients) and presented milder clinical and endocrine alterations than the classic PCOS phenotypes. The normoandrogenic phenotype was relatively uncommon. These patients had a normal body mass index, insulin sensitivity, and free androgen index but showed increased levels of LH and LH/FSH ratio. Conclusion(s) Ovulatory PCOS represents the mild form of classic PCOS, but the normoandrogenic phenotype, although part of the spectrum, may represent a different disorder or have a different pathogenetic pathway.
Objective To quantify the magnitude and pattern of low-density lipoprotein (LDL) cholesterol and nonhigh-density lipoprotein (HDL) cholesterol levels in women with polycystic ovary syndrome (PCOS) ...versus control women. Design Systematic review and meta-analysis of lipid levels in published cross-sectional studies worldwide where PCOS women and controls were examined and sampled. Main Outcome Measure(s) Differences in plasma lipids (including triglycerides, HDL-cholesterol, LDL-cholesterol, and nonHDL-cholesterol) in PCOS versus control subjects were calculated. Comparisons were made with and without body mass index (BMI) matching. Result(s) Triglyceride levels were 26 mg/dL (95% confidence interval CI 17–35) higher and HDL-cholesterol concentrations 6 mg/dL (95% CI 4–9) lower in women with PCOS. Also, LDL-cholesterol and nonHDL-cholesterol concentrations were higher in PCOS: by 12 mg/dL (95% CI 10–16) and 19 mg/dL (95% CI 16–22), respectively. With BMI matching, LDL-cholesterol and nonHDL-cholesterol were still higher in PCOS: by 9 mg/dL (95% CI 6–12) and 16 mg/dL (95% CI 14–19), respectively. LDL-cholesterol and nonHDL-cholesterol differences were greater with National Institutes of Health criteria 15 mg/dL (95% CI 13–17) and 21 mg/dL (95% CI 16–25), respectively versus Rotterdam criteria 8 mg/dL (95% CI 5–12) and 17 (95% CI 13–22), respectively. Conclusion(s) Dyslipidemia is common in PCOS. Beyond known alterations in triglycerides and HDL-cholesterol, women with PCOS have higher LDL-cholesterol and nonHDL-cholesterol, regardless of BMI. We recommend that all women with PCOS be screened for dyslipidemia, including LDL-cholesterol and nonHDL-cholesterol determinations, for effective cardiovascular risk prevention.
Objective To review all available data and recommend a definition for polycystic ovary syndrome (PCOS) based on published peer-reviewed data, whether already in use or not, to guide clinical ...diagnosis and future research. Design Literature review and expert consensus. Setting Professional society. Patients None. Intervention(s) None. Main Outcome Measure(s) A systematic review of the published peer-reviewed medical literature, by querying MEDLINE databases, to identify studies evaluating the epidemiology or phenotypic aspects of PCOS. Result(s) The Task Force drafted the initial report, following a consensus process via electronic communication, which was then reviewed and critiqued by the Androgen Excess and PCOS (AE-PCOS) Society AE-PCOS Board of Directors. No section was finalized until all members were satisfied with the contents, and minority opinions noted. Statements were not included that were not supported by peer-reviewed evidence. Conclusion(s) Based on the available data, it is the view of the AE-PCOS Society Task Force that PCOS should be defined by the presence of hyperandrogenism (clinical and/or biochemical), ovarian dysfunction (oligo-anovulation and/or polycystic ovaries), and the exclusion of related disorders. However, a minority considered the possibility that there may be forms of PCOS without overt evidence of hyperandrogenism, but recognized that more data are required before validating this supposition. Finally, the Task Force recognized and fully expects that the definition of this syndrome will evolve over time to incorporate new research findings.
A limited number of publications have assessed the prevalence of hypertension (HTN) in polycystic ovary syndrome (PCOS) patients with inconclusive results. Since in general populations the occurrence ...of hypertension is related to age per se, we investigated the prevalence (P) / relative risk (RR) of HTN in pooled patients with PCOS, vs control population among reproductive age women with PCOS, compared to menopause/aging patients.
PubMed, Scopus, ScienceDirect, web of science, and Google scholar were systematically searched for retrieving observational studies published from inception to April 2019 investigating the HTN in patients with PCOS. The primary outcome of interest was pooled P and RR of HTN in reproductive and menopausal/aging women with PCOS compared to control population.
The pooled prevalence of HTN in reproductive and menopausal/aging women with PCOS was higher than in the control population (Pooled P: 0.15, 95% CI: 0.12-0.18 vs. Pooled P: 0.09, 95% CI: 0.08-0.10) and (Pooled P: 0.49, 95% CI: 0.28-0.70 vs. Pooled P: 0.40, 95% CI: 0.22-0.57), respectively. Compared to the control population, pooled relative risk (RR) of HTN patients was increased only in reproductive age PCOS (1.70-fold, 95% CI: 1.43-2.07) but not in menopausal/aging patients who had PCOS during their reproductive years. The same results were obtained for subgroups of population-based studies. Meta-regression analysis of population-based studies showed that the RR of HTN in reproductive age PCOS patients was 1.76-fold than menopausal/aging PCOS patients (P = 0.262).
This meta-analysis confirms a greater risk of HTN in PCOS patients but demonstrates that this risk is increased only in reproductive age women with PCOS, indicating that after menopause, having a history of PCOS may not be as an important predisposing factor for developing HTN.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Ovarian and Adrenal Hyperandrogenism CARMINA, ENRICO
Annals of the New York Academy of Sciences,
December 2006, Letnik:
1092, Številka:
1
Journal Article
Recenzirano
: Because in normal women androgens are secreted in almost equal quantities by both adrenals and ovaries, for many years many studies have tried to distinguish the source of androgen excess. ...However, in the last 10–15 years, the diagnoses of ovarian or adrenal hyperandrogenism have almost disappeared. This is due to the lack of specificity of dynamic tests as well as to the emphasis given on clinical information and ovarian sonography for the diagnosis of hyperandrogenic syndromes. However, determination of the source of increased androgens may still be useful for improving the classification and the understanding of androgen excess disorders. The aim of this review is to examine the source of androgen excess in the three more common androgen excess disorders: polycystic ovary syndrome (PCOS), idiopathic hyperandrogenism; and nonclassic 21‐hydroxylase deficiency (NCAH). The ovary is the main androgen source in PCOS and idiopathic hyperandrogenism while adrenal androgen secretion is prevalent in NCAH. However, androgen secretion from more than one source is common in all main forms of hyperandrogenism as is the case in 70–80% of patients with NCAH, in 35% of women with PCOS, and in 50% of patients with idiopathic hyperandrogenism. Secondary PCOS is the main cause of ovarian androgen excess in nonclassic 21‐hydroxylase deficiency while adrenal hyperandrogenism in PCOS and idiopathic hyperandrogenism is probably the consequence of multiple factors including hyperinsulinemia, altered cortisol metabolism, and increased ovarian steroid production. The clinical image is not generally affected by the source of androgen excess. However, hyperandrogenic patients with increased dehydroepiandrosterone sulfate (DHEAS) tend to have lower body weight and insulin levels and a better metabolic profile.
In spite of the widespread use of lifestyle modifications programs, many patients with PCOS are obese and prevalence of obesity in PCOS remains high. In this study, we present the data on the use of ...semaglutide, an incretin mimetic drug, in obese PCOS patients who were unresponsive to a lifestyle modification program. Twenty-seven obese patients with a diagnosis of PCOS, who did not reduce their body weight by a lifestyle modification program, were included in this study and treated by semaglutide, 0.5 mg subcutaneously once a week. After three months of treatment, an improvement in body weight with a mean decrease in body weight of 7.6 kg and a mean BMI loss of 3.1 was observed, while very few side effects were reported. Almost 80% of the studied obese PCOS patients obtained at least a 5% decrease in their body weight. Only a few patients (22%) obtained a decrease in body weight lower than 5% and were considered non-responsive to semaglutide, at least at the used doses. These patients presented a more severe obesity than responsive patients. Independently of results on body weight, and in patients who did not obtain a 5% decrease in their body weight, insulin basal values decreased, and HOMA-IR improved. Fasting blood glucose normalized in 80% of semaglutide-treated IFG PCOS women. In patients who were responsive to semaglutide (weight loss > 5%), the treatment was continued for additional three months. Weight loss slowed but continued and, at the end of the six months of therapy, the mean body weight loss was 11.5 kg and mean BMI reduced from 34.4 to 29.4. A total of 80% of responsive patients normalized menstrual cycles. In conclusion, treatment with semaglutide, at low doses, significantly reduces body weight in almost 80% of obese PCOS patients who were unresponsive to a previous lifestyle plan. It is often associated with the normalization of menstrual cycles, and these important results are obtained with very few side effects.
Polycystic ovarian syndrome (PCOS) may present with different clinical patterns and the anovulatory phenotype may not be the most common. Data suggest that anovulation in PCOS is not the consequence ...of increased androgen ovarian secretion but rather of a severe derangement of early follicle development. Other mechanisms may be operative in subgroups of patients and may contribute to the arrest of follicle growth and anovulation. At least 50% of anovulatory patients with PCOS become ovulatory in their late reproductive age. There is also evidence that menopause may occur later in women with PCOS. Finally, a strategy for treatment of infertility in PCOS is presented.
It is well known that a subgroup of women with PCOS present an excessive adrenal androgen production, generally associated with ovarian hyperandrogenism. In the past, it has been impossible to ...correlate adrenal hyperandrogenism to any clinical or hormonal pattern of PCOS. However, adrenal androgens are strictly dependent on age and their blood values reduce by 40% in patients moving from their twenties to thirties. Due to this, serum DHEAS values are strongly influenced by the age distribution of studied populations. To avoid this bias, in this study we retrospectively analyzed the clinical and hormonal data of PCOS women in their twenties (age between 20 and 29 years). Data of 648 young hyperandrogenic women with PCOS were evaluated. Serum DHEAS was increased in a third (33%) of studied patients and was associated with higher values of testosterone (T) and androstenedione (A). In each phenotype, patients with high DHEAS had higher values of T and A than patients with normal DHEAS of the same phenotype. Therefore, a DHEAS increase is generally part of a generalized higher androgen production in a subgroup of PCOS patients, independently of the finding of anovulatory or ovulatory cycles or of polycystic or normal ovaries. However, our study showed some important differences between PCOS phenotypes. A lower prevalence of increased DHEAS in A phenotype PCOS patients who generally have the highest androgen levels, versus non-classic (B or C) PCOS phenotypes, was observed. It was also found that patients with A phenotype PCOS present significantly lower BMI and serum insulin than patients with normal DHEAS of the same phenotype while, in patients with the B or C phenotype, the opposite occurs. We conclude that adrenal hyperandrogenism is more common in patients with non-classic (B and C) phenotypes of PCOS and is generally part of a generalized higher production of androgens in a subgroup of PCOS patients. However, other factors may increase the adrenal androgen production and influence the clinical expression of the syndrome. More studies in large, selected for age, populations of PCOS women with different phenotypes are needed.
Polycystic Ovary Syndrome (PCOS) represents a heterogeneous disorder and, using Rotterdam diagnostic criteria, four main phenotypes (A, B, C, and D) have been distinguished. However, it remains ...unclear whether lean versus obesity status influences findings in the various phenotypes of women with PCOS. 274 women with PCOS were consecutively assessed. Among these women, there were 149 with phenotype A, 24 with phenotype B, 94 with phenotype C, and 7 with phenotype D. We found normal body weight to be very common (65%) in phenotype C patients, common (43%) in phenotype A and D patients, and less represented (but still 25%) in phenotype B patients. Obesity was common in phenotype B (54%) and phenotype A (33%) patients and uncommon in phenotype C (only 11%) and phenotype D (14%) patients. Obese and lean patients of each phenotype were compared. Compared to the phenotype C PCOS patients, both phenotype A and B patients had higher total testosterone circulating values and higher luteinizing hormone/follicle stimulating hormone (LH/FSH) ratio (p < 0.01) while anti-Mullerian hormone (AMH) levels were higher only in phenotype A PCOS patients. Instead, in the three obese PCOS phenotypes no differences in serum insulin, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) calculation, and lipid blood values were observed. Analysis of data of lean patients gave similar results. Compared to the phenotype C PCOS patients, both phenotype A and B patients had higher total testosterone circulating values and higher LH/FSH ratio (p < 0.01) while AMH levels were higher only in phenotype A PCOS patients. However, no differences were observed in the circulating insulin levels, HOMA-IR calculation, or blood lipids between the three groups of lean PCOS patients. We conclude that Rotterdam phenotypes express the differences between PCOS patients in terms of ovulatory pattern and androgen secretion but fail to differentiate between obese patients with altered metabolic patterns and lean patients with normal metabolic patterns. A new classification of PCOS patients is needed and it should consider the influence of body weight on the metabolic patterns of PCOS patients.
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