1,721,004 research outputs found
The importance of diagnosing the Polycystic Ovary Syndrome
The polycystic ovary syndrome (PCOS) is an extremely common disorder that occurs in 4% to 7% of women of reproductive age. Although PCOS is known to be associated with reproductive morbidity and increased risk for endometrial cancer, diagnosis is especially important because PCOS is now thought to increase metabolic and cardiovascular risks. These risks are strongly linked to insulin resistance and are compounded by the common occurrence of obesity, although insulin resistance and its associated risks are also present in nonobese women with PCOS. Women with PCOS are at increased risk for impaired glucose tolerance, type 2 diabetes mellitus, and hypertension. Cardiovascular disease is believed to be more prevalent in women with PCOS, and it has been estimated that such women also have a significantly increased risk for myocardial infarction. Many lipid abnormalities (most notably low high-density lipoprotein cholesterol levels and elevated triglyceride levels) and impaired fibrinolysis are seen in women with PCOS. Early diagnosis of the syndrome and close long-term follow-up and screening for diabetes and cardiovascular disease are warranted. An opportunity exists for preventive therapy, which should improve the reproductive, metabolic, and cardiovascular risks
Use of fasting blood to assess the prevalence of insulin resistance in women with polycystic ovary syndrome
To determine the prevalence of insulin resistance (IR) in women with polycystic ovary syndrome (PCOS) using baseline fasting blood measurements of glucose and insulin. Prospective clinical study. Academic endocrinology unit in Palermo, Italy. Two hundred and sixty-seven women with PCOS, consecutively evaluated, and 50 consecutively selected ovulating controls. Fasting blood was obtained for glucose and insulin measurements from all women. For 60 women with PCOS and 20 controls an insulin tolerance test (ITT) was also performed. Assessment of normal and abnormal values for fasting insulin, glucose/insulin ratio, and the calculated indices of the homeostasis model assessment (HOMA), quantitative sensitivity check index (QUICKI), as well as Kitt (kinetic disappearance of glucose) values after ITT. Evaluation was performed of the ability to detect IR using these methods in obese and nonobese women with PCOS. Normal insulin sensitivity was defined by insulin levels 6.4, HOMA values of 0.333. In the entire PCOS groups, IR was diagnosed in 65.4% of women using glucose/insulin ratios and in 77% and 79.2% using HOMA and QUICKI. In obese women (body mass index >28 in 48% of group), IR was present in 76.7% as measured by glucose/insulin ratios but was significantly higher (95.3%) using values of either HOMA or QUICKI (P<.01). All indices correlated with Kitt values with QUICKI showing the best correlation. Insulin resistance was detected in approximately 80% of women with PCOS, and in 95% of obese women. The detection of IR is superior using the calculated indices HOMA and QUICKI. © 2004 by American Society for Reproductive Medicine
Does metformin induce ovulation in normoandrogenic anovulatory women?
Objective:
This study was undertaken to evaluate the efficacy of metformin in women with anovulation who do not have evidence for hyperandrogenism and classic polycystic ovary syndrome.
Study design:
A randomized trial of metformin (1500 mg daily) and placebo in 24 anovulatory women was undertaken for 3 months. Assessments of changes in hormone levels and insulin sensitivity were carried out. Abnormal ormonal values were defined by levels exceeding the range in normal ovulatory controls.
Results:
Anovulatory women had normal androgen levels and luteinizing hormone but had higher serum insulin and lower insulin sensitivity compared with controls. Over 3 months, there were 16 ovulatory cycles with metformin and only 4 with placebo (P<.05). Success of ovulation did not correlate with changes in androgen, insulin, or insulin sensitivity parameters.
Conclusion:
Metformin may be useful for inducing ovulation in anovulatory women who do not have hyperandrogenism. This effect may be independent of a lowering of androgen or insulin level
A 20-year follow-up of young women with Polycystic Ovary Syndrome
OBJECTIVE: To determine whether hormonal, metabolic, and anthropomorphic parameters change over 20 years in women with polycystic ovary syndrome (PCOS).
METHODS: One hundred ninety-three women with PCOS, aged 20–25 years, were diagnosed according to Rotterdam criteria, divided into four phenotypes (A–D), and followed at 5-year intervals for 20 years. Androgens, gonadotropins, insulin, glucose, body mass index, waist circumference, and ovarian volume were measured.
RESULTS: At diagnosis, 57% had classic features (phenotype A), 9% had classic features without ovarian findings (phenotype B), 26% had the ovulatory phenotype (C), and 7% were nonhyperandrogenic (D). After 10 years, androgens decreased (P<.05); at 15 years, waist circumference increased (P<.05); at 20 years, ovarian volume decreased (P<.01). Serum luteinizing hormone and follicle-stimulating hormone decreased nonsignificantly and fasting insulin and quantitative insulin-sensitivity check index were unchanged. Eighty-five women (44%) were ovulatory at 20 years, and 18 women (8%) could no longer be diagnosed as having PCOS.
CONCLUSION: After 20 years of follow-up in women with PCOS, androgens and ovarian volume decreased and there were more ovulatory cycles suggesting a milder disorder, whereas metabolic abnormalities persisted and waist circumference increased.
LEVEL OF EVIDENCE: I
Not all women diagnosed with PCOS share the same cardiovascular risk profiles
Although definitive and confirmatory data are lacking, women with polycystic ovary syndrome (PCOS) are considered to be at increased risk for cardiovascular and metabolic disease. In recent years, the diagnosis of PCOS has broadened considerably to result in several phenotypes. Here we review the evidence for cardiovascular and metabolic risks in PCOS in the classic disorder and the various phenotypes. We conclude that not all women with PCOS should be considered as being similar in terms of cardiovascular risk profiles
Insulin resistance in postmenopausal women with metabolic syndrome and the measurements of adiponectin, leptin, resistin and ghrelin
Objective: Metabolic syndrome (MBS) is a significant health care problem in postmenopausal
women and is driven largely by obesity. We wished to assess the prevalence of insulin resistance
(IR), diagnosed using practical methods, and whether several adipocyte factors (adiponectin,
leptin, resistin) or the gastric peptide ghrelin, associated with cardiovascular risk, might be
abnormal and may relate to IR.
Study design: We evaluated 37 obese postmenopausal women with MBS and 34 matched obese
premenopausal controls, as well as 14 non-obese premenopausal controls. We measured fasting
glucose and insulin, performed 75g 2 hr oral glucose tolerance and intravenous insulin tolerance
tests to assess IR, and measured fasting lipids, adiponectin, leptin, resistin and ghrelin.
Results: The kinetic decline in glucose after insulin (kITT) as a marker of IR was the most
frequently abnormal test (abnormal in 81%), with QUICKI, HOMA, and a modification of the
Matsuda-DeFronzo index (ISIM) abnormal in 76, 73, and 68%, respectively. The GIR was
abnormal in only 35% of subjects. Leptin and resistin were elevated and adiponectin and ghrelin
were decreased in the postmenopausal women, compared to both groups of premenopausal
controls. BMI correlated strongly with markers of insulin resistance as well as adipocytokine
values. After controlling for BMI, only leptin was predictive of ISIM.
Conclusion: Being overweight after menopause results in worsening IR and elevations in
adipocytokine levels. While BMI is the most important factor, abnormal adipocytokine secretion
may enhance IR and increase cardiovascular risk in postmenopausal women.
2006 Mosby, Inc. All rights reserved
Insulin resistance in postmenopausal women with metabolic syndrome and the measurements of adiponectin, leptin, resistin, and ghrelin
Mullarian-inhibiting substance reflects ovarian findings in women with polycystic ovary syndrome better than does inhibin-B
Objective: To investigate Müllerian-inhibiting substance (MIS) levels in women with polycystic ovary syndrome
(PCOS), as well as relationships to ovarian morphology, levels of inhibin B, and other reproductive hormones.
Design: Prospective clinical study.
Setting: Academic endocrinology centers in Palermo, Italy and New York.
Patient(s): Forty-six women with PCOS, recruited on the basis of the classic criteria of chronic anovulation and
hyperandrogenism, and 25 age-matched ovulatory controls.
Intervention(s): Fasting blood was obtained in all subjects in the early follicular phase (days 5–6) after
spontaneous or induced menses (in PCOS), and transvaginal ultrasounds were performed.
Main Outcome Measure(s): Assessment of values for luteinizing hormone (LH), testosterone (T), androstenedione
(A), estradiol (E2), inhibin B, MIS, fasting insulin, and the calculated quantitative sensitivity check index
(QUICKI), as well as assessments of ovarian volume and blood flow.
Result(s): Women with PCOS had higher LH, T, and A; higher insulin and lower QUICKI; and higher ovarian
volume and lower pulsatility index. Inhibin B concentrations were statistically significantly higher in PCOS
patients (70 8.0 vs. 40 3.4 pg/mL), as was MIS (6.7 0.9 vs. 4.6 0.5 ng/mL). Inhibin B had a statistically
significant direct correlation with levels of MIS (r 0.351). However, MIS, but not inhibin B, had a statistically
significant positive correlation with ovarian size (r 0.350); the reproductive hormones LH, T, A, and E2; and
insulin (r 0.249), independent of body mass index. Women with PCOS with the highest levels of MIS had
higher ovarian volumes and values of LH, T, A, and insulin.
Conclusion(s): Measurements of MIS reflect ovarian findings in PCOS better than levels of inhibin B and are
more frequently elevated. However, MIS lacks sensitivity for use as a diagnostic tool in PCOS. (Fertil Steril
2005;84:1685–8. ©2005 by American Society for Reproductive Medicine.
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