The prevalence of benign breast disease in women with polycystic ovary syndrome: a review of a 12-year follow-up.

A cross-sectional study of benign breast disease (BBD) was conducted to determine the actual prevalence and follow-up importance of BBD among women with polycystic ovary syndrome (PCOS) in conjunction with an ongoing prospective cohort study. The present study involved a subset of the original group of 244 women with a diagnosis of PCOS and 244 control women matched by age and race. A total of 240 women (116 cases and 124 controls) were included in the present analysis. The majority of women in each group were Caucasians (93 and 96%, respectively). The median age was 46 years in the cases and 47 years in the controls. Screening mammography begins at the age of 40 and has been carried out in 69% of cases and 66% of controls since the study began. Family history of breast disease was observed in 27 cases of both the groups (p > 0.05). Neither fibrocystic breast disease, lump thickening, calcification, fibroadenoma, pain, redness, discharge nor hyperplasia showed a significantly higher prevalence rate in cases than in controls. Eleven (9%) women with PCOS and 21 (17%) controls underwent diagnostic or curative surgery (relative risk: 0.56). These results, in contrast to the previously published literature, do not allow us to conclude that there is a higher risk for BBD among women with PCOS, and the proportion of women with a positive family history of breast cancer was significantly greater in women with PCOS compared with controls. Our observation is that having PCOS does not appear to affect surgeons' decisions to remove BBD.

The relationship between C-reactive protein and carotid intima-media wall thickness in middle-aged women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with premature carotid atherosclerosis. C-Reactive protein (CRP) has been implicated as a vascular disease risk factor. The objective of this study was to determine whether elevated CRP is associated with increased carotid intima-media wall thickness (IMT) in PCOS women. Forty-seven PCOS patients and 59 similarly aged controls were screened for cardiovascular risk factors and concurrently underwent carotid ultrasonography (1996-1999). The main outcome measure was carotid IMT. CRP was significantly higher in PCOS patients than in controls (3.4 vs. 2.1 mg/dl; P = 0.002). In regression modeling, PCOS associated with IMT independently of CRP and age (P = 0.019). Body mass index reduced the association of PCOS and CRP with IMT and was also associated with IMT (P = 0.029). The CRP-IMT relationship was attenuated when either insulin or visceral fat was included in the PCOS-age-CRP model (P = 0.197 and P = 0.550, respectively). PCOS remained associated with IMT independent of insulin (P = 0.033) or visceral fat (P = 0.040). CRP does not appreciably mediate the effect of PCOS on IMT. Obesity partially explained the influence of PCOS and CRP on IMT. The effect of body mass index on the PCOS-IMT relationship was not completely determined by hyperinsulinemia or visceral fat, and might be mediated by other aspects of PCOS-related adiposity.

Evidence for an association between metabolic cardiovascular syndrome and coronary and aortic calcification among women with polycystic ovary syndrome.

Women with polycystic ovary syndrome (PCOS) exhibit an adverse cardiovascular risk profile, characteristic of the metabolic cardiovascular syndrome (MCS). The aim of this study was to determine the prevalence of coronary artery (CAC) and aortic (AC) calcification among middle-aged PCOS cases and controls and to explore the relationship among calcification, MCS, and other cardiovascular risk factors assessed 9 yr earlier. This was a prospective study of 61 PCOS cases and 85 similarly aged controls screened in 1993-1994 for risk factors and reevaluated in 2001-2002. The main outcome measures were CAC and AC, measured by electron beam tomography. Women with PCOS had a higher prevalence of CAC (45.9% vs. 30.6%) and AC (68.9% vs. 55.3%) than controls. After adjustment for age and body mass index, PCOS was a significant predictor of CAC (odds ratio = 2.31; P = 0.049). PCOS subjects were also 4.4 times more likely to meet the criteria for MCS than controls. High-density lipoprotein cholesterol and insulin appeared to mediate the PCOS influence on CAC. Interestingly, total testosterone was an independent risk factor for AC in all subjects after controlling for PCOS, age, and body mass index (P = 0.034). We conclude that women with PCOS are at increased risk of MCS and demonstrate increased CAC and AC compared with controls. Components of MCS mediate the association between PCOS and CAC, independently of obesity.

Dietary intake, physical activity, and obesity in women with polycystic ovary syndrome.

OBJECTIVE: To determine whether dietary intake and physical activity contribute to obesity in women with polycystic ovary syndrome (PCOS). DESIGN: Case-control study. SUBJECTS: A total of 84 cases and 79 neighborhood controls of similar age. MEASUREMENTS: Fasting insulin, body mass index (BMI, kg/m2), waist/hip ratio, Block Food Frequency Questionnaire, Paffenbarger Physical Activity Questionnaire. RESULTS: Although women with PCOS had a higher BMI than control women, an overall comparison of women with and without PCOS showed no significant difference in dietary intake. However, stratification by BMI revealed that lean women with PCOS reported significantly lower energy intake than lean women without PCOS. CONCLUSION: Differences in dietary intake and physical activity alone are not sufficient to explain differences in weight between women with and without PCOS. Further research is necessary to determine the relative contributions of lifestyle factors and metabolism to obesity in PCOS.

Assessment of the disturbances in metabolic homeostasis: a hypothesis of synergism.

Based on the hypothesis that a synergistic interaction between triiodothyronine (T(3)) and insulin contributes to abnormalities in glucose and other metabolic pathways, the mechanisms underlying the impairment of metabolic homeostasis (MH) and the development of type-2 diabetes (DM) were investigated via a proposed homeostatic model, [(FG*TG)/T3*FI)]. The MH model characterizes the relationship between T(3) and insulin and the levels of triglycerides (TG), fasting insulin (FI), and fasting glucose (FG) and is introduced as a clinical method to assess insulin sensitivity and the status of metabolic homeostasis in lieu of current screening models advocated by the by American Diabetic Association (ADA). The present study validated the hypothetical model in a sample of 110 African-American women.

Cardiovascular risk in women with polycystic ovary syndrome.

Compared with normal cycling women of similar age, women with polycystic ovary syndrome (PCOS) have an adverse lipid profile and an increased prevalence of Type II diabetes and hypertension. These woman also appear to have greater subclinical atherosclerotic disease, as demonstrated by greater carotid intimamedia wall thickness and higher levels of coronary calcification. Given the high prevalence of PCOS in the female population, this condition may potentially account for a significant proportion of the atherosclerotic heart disease observed in younger women. This article reviews the issues and uncertainties surrounding the PCOS-CHD association.

Polycystic ovary syndrome, androgen excess, and the impact on bone.

Polycystic ovary syndrome (PCOS) is a unique, natural model for the study of the influence of androgen excess on bone mass among women. Both thin and obese women develop PCOS, a presentation that allows for the evaluation of the effects of life-long obesity, alterations in body composition (central adiposity), and related metabolic abnormalities (hyperandrogenemia, hyperinsulinemia) on the skeleton. The relatively high prevalence of PCOS and its manifestation early in life render this disorder of particular importance in assessing the influence of androgens and androgen-estrogen balance on the attainment of maximal bone mass and subsequent development of osteoporosis later in life.

Evidence for association between polycystic ovary syndrome and premature carotid atherosclerosis in middle-aged women.

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder characterized by obesity, hyperandrogenism, and insulin resistance. An adverse lipid profile has also been observed in PCOS-affected women, suggesting that these individuals may be at increased risk for coronary heart disease at a young age. The objective of the present study was to evaluate subclinical atherosclerosis among women with PCOS and age-matched control subjects. A total of 125 white PCOS cases and 142 controls, aged >/=30 years were recruited. Collection of baseline sociodemographic data, reproductive hormone levels, and cardiovascular risk factors was conducted from 1992 to 1994. During follow-up (1996 to 1999), these women underwent B-mode ultrasonography of the carotid arteries for the evaluation of carotid intima-media wall thickness (IMT) and the prevalence of plaque. A significant difference was observed in the distribution of carotid plaque among PCOS cases compared with controls: 7.2% (9 of 125) of PCOS cases had a plaque index of >/=3 compared with 0.7% (1 of 142) of similarly aged controls (P=0.05). Overall and in the group aged 30 to 44 years, no difference was noted in mean carotid IMT between PCOS cases and controls. Among women aged >/=45 years, PCOS cases had significantly greater mean IMT than did control women (0.78+/-0.03 versus 0.70+/-0.01 mm, P:=0. 005). This difference remained significant after adjustment for age and BMI (P:<0.05). These results suggest that (1) lifelong exposure to an adverse cardiovascular risk profile in women with PCOS may lead to premature atherosclerosis, and (2) the PCOS-IMT association is explained in part by weight and fat distribution and associated risk factors. There may be an independent effect of PCOS unexplained by the above variables that is related to the hormonal dysregulation of this condition.