Environmental factors, such as obesity, appear to exacerbate the underlying genetic predisposition. Table 1.
An Update on Polycystic Ovary Syndrome – touchENDOCRINOLOGY
Clinical presentation of PCOS. Hirsutism is defined as a score of 8 or more on the modified Ferriman—Gallwey index 7.
Later, in , the Rotterdam Consensus 9 introduced the polycystic ovary appearance PCO on ultrasound as a new criterion to be added to the two previous criteria of the NIH, and the diagnosis requires two out of these three criteria. Table 2.
Diagnostic criteria for PCOS. Other causes for anovulation should also been excluded. In consequence, new phenotypes have arisen in addition to the classic phenotype, in which patients present hyperandrogenism and oligomenorrhea with or without PCO on ultrasound.
PCO has been defined as the presence of 12 or more follicles of mm or ovarian volume greater than 10 cm 3 9. However, with the new equipment, it is possible to visualize and count small follicles of less than 2 mm nowadays Therefore, the consequence of the improved ovarian imaging is the revaluation of the current follicle number threshold, and the probable increase in the number of follicles to more than follicles per ovary and per age classes to better define PCOS 11 , In turn, morphological ovarian changes are not exclusive of PCOS, and the presence of PCO in non-hirsute women with normal cycles is not negligible, varying from 2.
In addition, while the inclusion of a non-hyperandrogenic phenotype of the diagnosis of PCOS is still controversial, some authors consider the presence of PCO as being itself a sign of hyperandrogenism. Clinical characterization also changes throughout the lifespan, especially during the post-menarche years and in the menopause transition. PCOS is a persistent challenge to the clinician, as the phenotype of the syndrome can vary widely. This is still more evident during the post-pubertal period, as signs and symptoms of PCOS overlap with normal puberty. There is a relatively high rate of menstrual irregularity and anovulatory cycles in this period, as well as some difficulties in interpreting clinical and biochemical evidence of hyperandrogenism: acne is a very common complaint during adolescence, alopecia is a rare phenomenon in girls, and hirsutism is sometimes borderline and aggravates slowly.
Uncertainty also regards the significance of polycystic ovarian morphology on ultrasound: microcysts are often seen even before menarche.
Polycystic ovary syndrome
Because of these uncertainties, and the fact that the majority of ultrasound examinations in adolescent girls is abdominal and not transvaginal, the diagnosis of PCOS in adolescents needs all three Rotterdam criteria, and not only two However, even if the diagnosis cannot be confirmed and needs to be postponed, individual manifestations hirsutism, irregular menses should be treated. In menopausal transition, there may be an amelioration of clinical features. In fact, there is a trend towards more regular cycles and improvement on hirsutism with aging This is in part due to the well-known decrease in androgen secretion from the third for the fifth decade of life that occurs in normal women 20 , and has been also reported in PCOS 13 , 19 , In addition, ovarian volume decreases along with pre-menopause and menopause transition, as previously reported Thus, alterations in ovarian volume and morphology may be less evident in PCOS during menopausal transition, and PCO criteria are not useful after menopause.
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In fact, no specific clinical presentation during menopause has been established, and the diagnosis of PCOS is, in general, confirmed before this period, based on the history of oligomenorrhea and hyperandrogenism. Additionally, clinical or biochemical hyperandrogenism appearing in previously normal peri- or post-menopausal women should be carefully investigated in order to screen them for androgen-secreting tumors.
Obesity is a prevalent characteristic of PCOS 9 , 23 , ranging from The presence of obesity may exacerbate the metabolic and reproductive disorders associated with the syndrome 28 , including insulin resistance, dyslipidemia, and metabolic syndrome 23 , 29 - In addition, PCOS women present higher risk for type 2 diabetes 13 , PCOS is also associated with a clustering of cardiovascular risk factors 10 , 13 , 29 , 33 , However, there is no definitive evidence for increased cardiovascular events, nor data showing that PCOS alone leads to increased cardiovascular risk independent of associated risk factors.
Polycystic Ovary Syndrome (PCOS)
In fact, more rigorous cohort studies of long-term cardiovascular outcomes and clinical trials of risk factor modification are required for women with PCOS. In addition, evidence suggests clinical phenotypes are related with different metabolic risks Table 3. In this sense, insulin resistance seems to be a specific feature of the classic phenotype and, to a lesser extent, of the ovulatory phenotype 29 , 35 , Non-hyperandrogenic phenotype behave as a separate group that is metabolically similar to non-PCOS women 15 , Table 3.
Clinical features of different phenotypes. Insulin resistance and compensatory hyperinsulinemia is an important factor in maintaining hyperandrogenemia by acting directly on theca cells inducing excess androgen production. Insulin also acts as a co-gonadotropin, increasing the effect of LH on ovarian androgen secretion.
In consequence, both insulin and androgens act on the liver inhibiting SHBG secretion, leading to increased free and bioactive androgen circulating levels and making clinical hyperandrogenism worse. In addition, insulin resistance plays a central role on the pathophysiology of metabolic syndrome and on the cardiovascular risk in PCOS women. However, insulin resistance is a common, but not universal feature of PCOS, and treatment should be directed to the consequences rather than to insulin resistance per se The main interventions to minimize cardiovascular and metabolic risks in PCOS are lifestyle changes, pharmacological therapy, and bariatric surgery Table 4.
Lifestyle modification is the first form of therapy combining behavioral reduction of psychosocial stressors , dietary, and exercise management. Frequently, however, it will be necessary to add an insulin-sensitizing drug ISD to the treatment.
Metformin and thiazolidinediones pioglitazone are the main available ISD. However, due to the eventual weight gain and cancer risks of thiazolidinediones, the prescription of these drugs has been limited to diabetic patients and will not be discussed here. Table 4. Treatment of metabolic comorbidities in PCOS. Its main action is in the liver, with suppression of gluconeogenesis and hepatic glucose output, but it also enhances peripheral insulin action, and reduces glucose absorption from the digestive tract, with no significant direct effect on pancreatic insulin production Metformin also directly inhibits thecal androgen production In women with PCOS, treatment with metformin has been shown to ameliorate the cardiometabolic profile by improving insulin sensitivity, lowering blood glucose and androgen levels and possibly by its effects on body weight 41 - These effects of metformin are more potent when it is combined with lifestyle intervention Medications are also available to treat symptoms such as excessive hair growth, irregular periods and fertility problems.
This involves using heat or a laser to destroy the tissue in the ovaries that's producing androgens, such as testosterone. Page last reviewed: 1 February Next review due: 1 February More than half of these women do not have any symptoms. What causes polycystic ovary syndrome PCOS? FAQ Policy. About this book The field of androgen excess disorders has advanced substantially since the original publication of this book. Show all. From the reviews: " Richard, Jr.
Keta et al. Idiopathic Hirsutism Pages Carmina, Enrico. Jeffrey et al. Show next xx. Recommended for you.