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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Polycystic Ovary Syndrome (PCOS) includes three phenotypic compartments, not always fully associated, consisting in hyperandrogenism, anovulation and metabolic syndrome, secondary to insulin resistance. The pathophysiological grounds lie upon two main components, i.e.: the theca-interstitial cell (TIC) and the granulosa cell (GC) dysregulations, the former accounting for hyperandrogenism and the latter for anovulation, and both of them being under the influence of hyperinsulinism. The former mainly results from an enzymatic overactivity, yielding an exaggerated output of androgens by the TIC, but the type(s) of enzymes as well as the genetic or adaptative nature of its (their) dysregulation are still controversial. The main consequence of the CG dysregulation is the follicular arrest just before the time of dominance. This might result from an intrinsic abnormality in CG, involving the IGFs and/or the Inhibin/Activin/Follistatin systems. Alternatively, the CTI might have deleterious effects on GC, mainly via the intra-ovarian hyperandrogenism. The latter should not be regarded any more as an atretogenic phenomenon. It is closely related to the two main morphological features of PCOS, i.e.: the stromal hyperplasia and the excessive follicular number.
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PMID:[Physiopathology of polycystic ovary syndrome]. 1045 84

The polycystic ovary syndrome (PCOS) is the most frequent endocrine disease in women of reproductive age. Hyperandrogenism, anovulation and metabolic syndrome are the cardinal features of PCOS. Hyperandrogenism results from a diffuse enzymatic hyperactivity at the theca-interstitial cell level. Anovulation is due to an impairment of the selection of a dominant follicle, while the number of smaller follicles is exaggerated. The molecular grounds of insulin resistance could be an increased Serine phosphorylation of the insulin receptor. The clinical classification of PCOS distinguishes three forms: the classic PCOS, where the three above mentioned features are present, the non classic PCOS and the asymptomatic PCOS, revealed by ultrasonography. Only the increased ovarian volume or surface (>11ml and> 5.5cm(2), respectively) must be viewed as a specific ultrasonic sign of PCOS. Cyproterone acetate remains the basic treatment of hyperandrogenism. The treatment of anovulation and infertility follows a consensual strategy. The insulin sensitizing treatment allows to decrease hyperandrogenism, to reverse the menstrual cycle irregularity and to obtain spontaneous or induced pregnancies.
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PMID:[Polycystic ovary syndrome]. 1113 21

A clinical, descriptive, and transversal study was conducted in a group of patients with chronic anovulation and sterility, to correlate insulin resistance, determined by the fasting glucose/insulin ratio, with body fat composition using anthropometrics parameters and the interaction of light near infrared region method, we studied 41 young patients with chronic anovulation and sterility. Based on their body mass index, all patients had obesity or overweight. Similarly, most of them presented with a percentage of body fat over the recommended limits. Forty percent of all studied patients had a fasting glucose/insulin ratio below 4.5, which corresponds to insulin resistance. The correlation between the percentage of body fat and fasting glucose/insulin ratio was significant, as was the correlation between body mass index and the percentage of body fat. We found overweight or obesity in the majority of our patients, and insulin resistance in almost half of them. Such disturbances were positively associated with the percentage of body fat and android distribution. Therefore, we recommend a routinely anthropometrics evaluation in these patients as well as fasting glucose/insulin ratio determination in order to act in an early stage over the natural history of metabolic syndrome, whose common denominator is insulin resistance.
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PMID:[Insulin-glucose ratio and body fat composition in patients with chronic anovulation and sterility]. 1201 50

The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype. Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and/or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.
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PMID:Obesity and the polycystic ovary syndrome. 1208 Apr 40

Polycystic ovary syndrome (PCOS) is a common heterogeneous disorder characterized by hyperandrogenism and chronic anovulation. The syndrome is frequently associated with an increased risk for insulin resistance and type 2 diabetes mellitus; obesity exacerbates insulin resistance and favors the progression from impaired glucose tolerance to diabetes in these patients. In young women, precocious pubarche and hyperinsulinemia are early manifestations of PCOS. The familial clustering of women with PCOS suggests that heredity is implicated in the origin of the syndrome. However, genetic approaches to its pathogenesis have been hampered by the heterogeneity of phenotypic features within families, and the lack of uniform criteria for diagnosis. Currently, PCOS is considered a polygenic trait that might result from the interaction of susceptibility and protective genomic variants under the influence of environmental factors. Both linkage analysis and association studies are valid tools for the study of the genetics of PCOS. Candidate genes for PCOS include those related to androgenic pathways and metabolic associations of the syndrome. More recently, genes encoding inflammatory cytokines have been identified as target genes for PCOS, as proinflammatory genotypes and phenotypes are also associated with obesity, insulin resistance, type 2 diabetes, PCOS, and increased cardiovascular risk. This paper reviews the candidate genes involved in the metabolic pathways that are altered in patients with PCOS. Despite a significant amount of research in this area, none of the genes studied so far has been identified as the PCOS susceptibility gene for the majority of cases. PCOS is the first component of the metabolic syndrome to be detected in many women, so the identification and correct diagnosis of PCOS has important preventive and therapeutic implications for the affected women and their families. In the future, new therapeutic approaches to PCOS will rely on knowing the genes, environmental influences, and etiologic mechanisms associated with the disorder.
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PMID:Genetic basis of metabolic abnormalities in polycystic ovary syndrome: implications for therapy. 1505 32

Insulin resistance is a central feature of polycystic ovary syndrome (PCOS). Hyperinsulinaemia contributes to anovulation, hyperandrogenism, infertility and early pregnancy loss in women with PCOS. Chronic hyperinsulinaemia also predisposes women with PCOS to increased risks of diabetes and cardiovascular events. Current data indicate that metformin, either as monotherapy or in combination with clomiphene in clomiphene-resistant patients, is an effective treatment for anovulation in PCOS. Initial evidence also suggests that insulin sensitizers may have a role in preventing early pregnancy loss. Of the available insulin-sensitizing agents, metformin has been the agent most frequently studied in PCOS, and has the least undesirable pregnancy safety profile. Ameliorating the metabolic syndrome associated with insulin resistance in PCOS with metformin may also prevent long-term cardiovascular and diabetes complications, pending further evidence. Based on these data, metformin should be a first-line therapy for women with PCOS.
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PMID:Should insulin-sensitizing drugs be used in the treatment of polycystic ovary syndrome? 1514 68

The polycystic ovary syndrome (PCOS), characterized by chronic anovulation and hyperandrogenism, has many features of metabolic syndrome and can be considered a metabolic disease. Approximately 50% of patients with PCOS are overweight or obese with abdominal fat accumulation. Some metabolic alterations and abdominal fat distribution have also been reported in lean women with PCOS. The aim of this study was to evaluate the effect, if any, of obesity on metabolic features, body composition and fat distribution in patients with PCOS. Body composition and abdominal fat distribution (evaluated by DEXA), waist circumference, blood pressure, lipid profile, glucose tolerance and homeostasis model assessment index were determined in 23 lean [mean age 23 +/- 5 yr, mean body mass index (BMI) 22 +/- 2 kg/m2] and 27 overweight-obese (mean age 21 +/- 5 yr, mean BMI 32 +/- 5 kg/m2) patients with PCOS and in 20 age- and weight-matched eumenorrhoic women. Patients exhibited slight but non-significant differences in metabolic parameters, waist circumference, blood pressure and total and abdominal fat content compared with weight-matched controls. None of the lean subjects suffered from metabolic syndrome according to the National Cholesterol Education Program--Adult Treatment Panel III (NCEP-ATPIII) criteria as opposed to 10 overweight-obese patients and three overweight-obese control subjects (37% and 33.3% of each subgroup, respectively). Our data do not show significant metabolic alterations in lean PCOS women. Results indicate that obesity seems to underpin the metabolic alterations exhibited by the overweight-obese patients. However, since women with PCOS are at increased cardiovascular risk, further studies are needed to evaluate metabolic alterations and body composition in these patients.
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PMID:Body composition, fat distribution and metabolic characteristics in lean and obese women with polycystic ovary syndrome. 1527 73

Polycystic ovary syndrome (PCOS) is characterised by anovulation, infertility and hyperandrogenism. The condition affects about 5-10% of women in the reproductive age group. Insulin resistance has proven to be a key factor in the pathogenesis of PCOS. There are several similarities between PCOS and the metabolic syndrome, and PCOS may be a risk factor for development of type 2 diabetes and cardiovascular disease. The treatment of PCOS has, so far, been focussed on treatment of the clinical signs and symptoms. Oral contraceptives have been the standard treatment. There is now a greater focus on the management of the metabolic consequences of PCOS, primarily through lifestyle intervention to achieve weight loss and increase physical activity. Metformin has proven to be effective in the management of the metabolic disturbances, anovulation and hirsutism and is now a widely accepted therapy. The thiazolidinediones (pio- and rosiglitazone), a novel class of insulin-sensitising agents, also seem to ameliorate the metabolic disturbances and clinical symptoms characterizing PCOS, but more randomised, controlled trials are needed before clinical guidelines can be determined.
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PMID:[Polycystic ovary syndrome. New pathophysiological discoveries--therapeutic consequences]. 1611 10

Polycystic ovary syndrome (PCOS) affects mostly young women causing chronic anovulation, hyperandrogenism, hirsutism and obesity with android pattern. The prevalence of the metabolic syndrome (abnormal glucose metabolism, dyslipidemia, hypertension and increased waist circumference) in PCOS is not defined although both have a common etiologic factor: insulin resistance. This retrospective study from medical records examined the presence of obesity and features of the metabolic syndrome in women with PCOS. The metabolic syndrome was defined as presence of two or more of the following signs: abnormal glucose metabolism, hypertriglyceridemia, low HDL, and hypertension. Thirty nine records of patients with PCOS were reviewed. The mean age was 29.4 years and the body mass index was 36 kg/m2. Hypertriglyceridemia was present in 43%, low HDL in 71%, hypertension in 36%, impaired glucose tolerance in 10% and diabetes mellitus type 2 in 37%. The metabolic syndrome was identified in 44% of sampled women with PCOS. These findings indicate that women with PCOS are at increased risk of diabetes mellitus type 2 at a young age. PCOS patients have higher prevalence of the metabolic syndrome than the rest of the population and thus are at increased risk of cardiovascular disease even if they don't develop diabetes mellitus type 2.
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PMID:Association between the polycystic ovary syndrome and the metabolic syndrome in Puerto Rico. 1632 83

The polycystic ovary syndrome (PCOS) is the most frequent cause of hyperandrogenism and anovulation in adult women as well as in adolescent girls. Since 2003 the diagnosis of PCOS has been based on the association of hyperandrogenism, oligoanovulation and polycystic ovary (PCO) morphology at ultrasound (at least 2 items out of 3). In adolescents however, PCOS features may be difficult to distinguish from the symptoms of the end of puberty. Moreover, transvaginal ultrasound examination is seldom possible, and it is difficult to get precise imaging of the ovaries by abdominal route. However, the diagnosis of PCOS in a hyperandrogenic and/or oligomenorrheic adolescent requires on the strict application of the Rotterdam criteria, as in adult women. Priority should be given to clinical features whereas pelvic ultrasound must be considered as optional. Few hormonal assays will serve mainly to make the differential diagnosis, in addition to clinical findings. Once established, the diagnosis of PCOS in an adolescent girl must lead to the detection of the metabolic syndrome by means of simple investigations. This will allow early prevention of its complications.
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PMID:[Rotterdam consensus in adolescent girls: which investigations and how to interpret them to make the diagnosis of PCOS?]. 1698 85


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