© 1995 American Heart Association, Inc.
Articles |
Coronary Heart Disease Risk Factors in Women With Polycystic Ovary Syndrome
From the Department of Epidemiology (E.T., A.C., K.D., K.W., L.K.), Graduate School of Public Health, and the Department of Obstetrics, Gynecology, and Reproductive Sciences (D.G., S.B.), Magee-Womens Hospital, University of Pittsburgh, Pa.
Correspondence to Evelyn Talbott, DrPH, MPH, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto St, Pittsburgh, PA 15261. E-mail eo1@ vms.cis.pitt.edu.
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Abstract |
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Abstract The goal of the study was to compare cardiovascular heart disease risk factors in women with polycystic ovary syndrome (PCOS) and matched control subjects. Women with PCOS have risk factors, including anovulation, hyperandrogenism, and insulin resistance, that suggest a male coronary heart disease risk-factor profile. A total of 206 women with PCOS were recruited by using records from a large reproductive endocrinology practice. A clinical diagnosis of PCOS was made if there was a history of chronic anovulation in association with either clinical evidence of androgen excess (hirsutism) or if total testosterone level was >2 nm/L or the luteinizing hormone/follicle-stimulating hormone ratio was greater than 2. The overall response rate for cases was 76%. A control population was obtained by using a combination of area voters' registration tapes and directories of households. A control subject was matched to each case subject by age±5 years, race, and neighborhood. The response rate for recruitment of the first or second eligible control subject was 83.6%. The average age at initial interview was 35.9±7.4 years for case and 37.2±7.8 years for control subjects. Women with PCOS had significantly increased cardiovascular disease risk factors compared with control women. These included increases in body mass index, insulin, and triglyceride levels (P<.001), decreased total HDL and HDL2 levels (P<.01), and increased total cholesterol and fasting LDL levels, waist/hip ratio, and systolic blood pressure (P<.05). After controlling for age, body mass index, and other confounding variables, differences in total cholesterol, total HDL, HDL2, LDL cholesterol, and triglycerides were still significant between case and control subjects. These risk factors were especially elevated in PCOS women in the early premenopausal years compared with control women, indicating that women with PCOS should be monitored for early detection and considered for appropriate clinical interventions.
Key Words: coronary heart disease • polycystic ovary syndrome • risk factors • case-control study
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Introduction |
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Significant controversy exists about the primary pathophysiological defect in polycystic ovary syndrome (PCOS).1 There is now a broad consensus, however, that women with this condition are characterized by chronic anovulation in association with androgen excess, hyperinsulinemia, and alterations in gonadotropin secretion.1 2 The correlation between insulin and ovarian vein androgens is in the range of .88 to .99,3 and evidence suggests that the direction of causation is from insulin to androgens rather than the reverse: when androgens are reduced by a gonadotropin-releasing hormone analogue, insulin resistance remains in PCOS women,4 whereas pharmacological reduction of hyperinsulinemia leads to a reduction in androgen levels.5 Furthermore, reduction of hyperinsulinemia by weight loss in obese PCOS women is associated with a reduction in androgens and restoration of ovulatory menstrual cycles despite an unchanged gonadotropin profile as measured by luteinizing hormone (LH) level, pulsatility, and amplitude.6 Thus, insulin resistance appears to play a critical role in the pathophysiology of PCOS.1
Women with chronic anovulation, hyperandrogenism, hyperinsulinemia, and obesity have an increase in cardiovascular disease (CVD) risk factors.7 8 9 10 11 There have been few studies of the epidemiology of PCOS in free-living populations, however. Most investigations have used patients seen in outpatient clinics for infertility or irregular periods. Studies have generally used small numbers of women, varying definitions of PCOS, and different age criteria.
In 1985, Wild and colleagues7 found that women with PCOS had lower HDL levels, higher LDL/HDL ratios, and higher triglyceride levels than regularly menstruating women. More recently, Slowinska-Srzednicka et al8 have drawn attention to the role of insulin in the lipid abnormalities observed in hyperandrogenic women with PCOS. These investigators compared 27 women with PCOS and 22 eumenorrheic control subjects stratified by weight (obese and nonobese). Women with PCOS had significantly lower levels of HDL2 and higher levels of apoB and triglycerides. Multiple regression analysis within PCOS patients, after adjustment for age, body mass index (BMI), and sex steroids, revealed that fasting insulin was a significant explanatory variable for total triglyceride and apoA-1 levels. These results, which suggest that hyperinsulinemia independent of obesity may play a role in the lipid disturbances in PCOS, are supported by a 1992 study by Wild et al9 in which 31 women with evidence of androgen excess were treated for 3 months with a gonadotropin-releasing hormone agonist that suppressed ovarian estradiol and testosterone. Lipid profiles remained aberrant despite the sex steroid suppression and remained correlated with insulin resistance. It was concluded9 that lipoprotein abnormalities appeared to be associated more with insulin than with endogenous androgens or estrogens.
Dahlgren et al10 11 studied a retrospective cohort of 33 older women (mean age, 50 years) with ovarian histopathology typical of PCOS at wedge resection 22 to 31 years previously and 132 age-matched control subjects (mean age, 51.7±5.3 years). A total of 30% of PCOS women and 56% of control women had reached menopause. Compared with control subjects, PCOS patients had a higher prevalence of central obesity, diabetes, and hypertension and had higher basal serum insulin concentrations. The authors concluded that the increase in CVD and diabetes among PCOS patients should be viewed not only as a condition requiring treatment for anovulation and infertility but as a metabolic syndrome requiring ongoing medical surveillance.
Another approach to the study of hyperandrogenism and coronary artery disease (CAD) was conducted by Wild et al,12 who used a case series of 102 women with CAD consecutively evaluated between July 1986 and December 1987 via cardiac catheterization. Mean ages were 63.6 and 60.5 years for case and control subjects, respectively. A self-administered questionnaire was given to the study group concerning the distribution of body hair and prevalence of acne. No hormonal assays were obtained, nor was there a specific diagnosis of PCOS. A total of 52 women with and 50 women without CAD were noted, and twice as many case subjects as control subjects reported excess body hair.
In the present study, we seek to elaborate on these findings concerning the association between PCOS and CVD risk factors by using a matched case-control design with a larger sample than previously reported.
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Methods |
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Case Recruitment
Subjects with PCOS were recruited from two sources: previous (1970 through 1986) and current (1987 through 1990) academic practice records. Initially, the charts of 2777 women seen at Magee-Womens Hospital between 1970 and 1986 were reviewed. Magee-Womens Hospital is the regional center for gynecological and obstetric care. These records were obtained from the previous director of reproductive endocrinology (Dr David Archer) and reviewed by the authors (E. Talbott, D. Guzick, and A. Clerici). During the 1970s and early 1980s, the diagnosis of PCOS was mainly based on clinical findings, as biochemical parameters (ie, hormone assays) were not in widespread use. Therefore, a presumptive clinical diagnosis of PCOS was made if there was a history of chronic anovulation in association with either clinical evidence of androgen excess (hirsutism) or if total testosterone concentration was >2 nmol/L or the LH/follicle-stimulating hormone (FSH) ratio was greater than 2. Based on our review of the infertility clinic records in the charts of 2777 women in the 1970 through 1986 cohort, 10% (274) met the criteria for PCOS. Of these 274, 190 had hirsutism; 84 did not have hirsutism but had elevated testosterone (n=24), increased LH/FSH ratio (n=49), or both (n=11). The average number of years of follow-up was 14, and the current age of these women was 40.2 years. Detailed tracing efforts were employed for this population. A total of 235 (85.7%) were interviewed by telephone, 21 refused to be interviewed, 15 were not located, and 3 were deceased. Vital status was also verified through the National Death Index. It was determined that 152 (64.7%) lived within the greater Pittsburgh area (<50 miles), and 112 of these women (73.7%) participated in the clinical phase of our study.
The current group (1987 through 1990) comprised 204 women with PCOS
from the academic practice of the Division of Reproductive
Endocrinology at Magee-Womens Hospital. In general, the diagnosis of
PCOS was based on hormone parameters in this population. A total of 188
(92.2%) were interviewed by telephone, 12 refused to be interviewed,
and 4 could not be located at the time of analysis. Of these women,
140 (74.5%) lived in the greater Pittsburgh area, and 99 (70.7%) of
these participated in the clinical phase. The final case population is
shown in the Figure
. For both current and previous
cohorts, a total of 278 women lived within a 50-mile radius who were
eligible to participate in the clinical phase of the study; of these,
211 actually participated.
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Control Subject Recruitment
Age (±5 years)– and race-matched neighborhood control
subjects were selected by using a combination of voters' registration
tapes for 1992 for the greater Pittsburgh area and Cole's Cross
Reference Directory of households.13 The major sources of
control candidates were the Allegheny County and Westmoreland County
voters' registration tapes. A nonrepeating random selection process
was used that matched on date of birth, sex, race, and zip code of the
case subject. For each PCOS case subject, five control subjects were
randomly drawn, and a letter was then sent to the first person listed.
This letter explained the nature of the study and invited the person to
participate. A preaddressed, stamped postcard was included in the
letter. After 2 weeks, a follow-up letter was sent to the same
address.
All participants completed a telephone questionnaire conducted by a trained interviewer. Demographic information was collected regarding age at interview, date of birth, current marital status, occupation, and highest level of education attained. A detailed reproductive and gynecological history was obtained, including total number of pregnancies, live births, age at menarche, age at menopause (if applicable), reason for menopause (natural, surgical, drug-induced, etc), previous use of fertility medication (including type and duration), and use of oral contraceptives or hormone replacement therapy. A disease history was also obtained, including history of heart disease, cancer, and diabetes and treatment for hypertension. A positive history of myocardial infarction, stroke, angina, and other circulatory problems was documented. Surgical history included reproductive organ–related surgeries (hysterectomy, oophorectomy, or ovarian wedge resection) as well as nonreproductive organ–related surgeries. Self-reported height and weight were collected in the anthropometric section of the interview.
Upon completion of the telephone questionnaire, those participants residing within the greater Pittsburgh area were asked to participate in the clinical phase of our study by coming to Magee-Womens Hospital. Subjects were evaluated after a 12-hour fast. An additional questionnaire was administered on-site that included a repeat medical history, review of medication use, current medical practices, and family history of PCOS. Height was measured and rounded to the nearest half inch; weight was measured and rounded to the nearest half pound. Two measures each of waist and hip were collected, and the average value was recorded. Waist/hip ratio was calculated as the waist circumference divided by the hip circumference. Wrist circumference was measured for estimation of frame size. The subject's blood pressure was measured by using a random-zero sphygmomanometer, and the average of two values was recorded. A fasting blood sample was obtained for lipid and hormone assays.
Lipid and Lipoprotein Measurement
Serum concentrations of total cholesterol, total HDL cholesterol
(HDL-C), subfractions HDL2 and
HDL3, triglycerides, LDL, and VLDL were measured in
the Heinz Lipid Laboratory at the University of Pittsburgh. Total
cholesterol was determined by using the enzymatic method of Allain et
al.14 Duplicate samples with standards, control sera, and
serum calibrators were included in each run. The coefficient of
variation (CV) between runs was 1.3%.
HDL-C was determined after selective precipitation by heparin/manganese chloride and the removal by centrifugation of VLDL and LDL.15 The cholesterol was measured as described above for total cholesterol. Duplicate samples, standards, and control sera were included in each run. The CV between runs was 2.1%. After precipitation and removal of VLDL and LDL by heparin/manganese chloride as described above, the supernatant was mixed with dextran sulfate.16 The HDL2 precipitates and the HDL3 in the supernatant were then measured using the methods described above for cholesterol measurement. The HDL2 content was estimated by subtracting the HDL3 level from the total HDL content. Duplicate samples, standards, and control sera were included in each run. The CV between runs was 6.0%. LDL concentration was estimated by using the Friedewald formula.17 Triglycerides were determined by using the enzymatic procedure of Bucolo and David.18 The CV between runs was 1.7%. Blood for glucose and insulin determinations was obtained when the subjects were fasting. Plasma glucose was analyzed by using an enzymatic assay (Yellow Springs Glucose Analyzer, Yellow Springs Instruments) and plasma insulin by radioimmunoassay.
Hormone Assays
LH and FSH were measured by using an immunofluorometric assay
(Delfia, human LHSpec, human FSH, and prolactin; Wallac Inc). These
methods were chosen for their high degree of sensitivity and low sample
volume required (25 µL per determination). The intra-assay and
interassay CVs ranged between 2% to 4% and 7% to 9%, respectively,
for the three pituitary hormones. The sensitivity of both the LH and
FSH assays was 0.05 IU/L. Total testosterone, androstenedione, and
estradiol levels were determined by using a radioimmunometric assay
(Coat-A-Count, Diagnostic Products Corp). Testosterone and estradiol
levels were measured directly. Serum samples for the determination of
androstendione were first extracted with an ethyl acetate–hexane (3:2)
mixture, resuspended in the assay diluent, and then measured by
radioimmunoassay. Sensitivities for total testosterone, androstendione,
and estradiol were 0.04 ng/mL, 0.02 ng/mL, and 8 pg/mL, respectively.
These immunoassays exhibited CVs ranging from 3% to 4% and 9% to
13% for the intra-assay and interassay, respectively.
All data collected for this study were entered and verified by using SPSS data-entry software. Univariate analyses were performed by using SPSS FOR WINDOWS. Mean levels of selected CVD risk factors were compared by using Student's t tests in SPSS. Linear regressions were then performed on variables that remained significant (P<.05). To normalize the distribution of the triglyceride data, log transformations were performed before linear regression analyses were performed on the data by using SPSS FOR WINDOWS. SAS FOR WINDOWS was used for matched-pair conditional logistic regression analyses, with case-control status as the dependent variable.
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Results |
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Of the 478 women in the final cohort, 278 (58.2%) lived within 50 miles of the research facility; of these, 211 (75.9%) participated in the clinical portion of the study, 206 of whom are included in the matched-pair analyses. One hundred thirty (of 220) of the first eligible control subjects consented to participate. Fifty-four control subjects were obtained from the second eligible name, and the remaining 36 were obtained after three or more attempts. The response rate for recruitment of first or second eligible control subjects was 83.6%.
Sample Description
The mean age of the total cohort was 35.1±7.9 years. The women in
our study were white (n=388; 92.4%), black (n=17; 4.0%), or other
races (n=15; 3.6%). Almost two thirds of the case subjects were
currently married, 122 (29.0%) were never married, and 35 (8.4%) were
separated or divorced. Thirty-one percent obtained a high school
degree, and the remainder had some schooling beyond high school; almost
20% had received a college degree or higher. Approximately 23% of
case subjects with PCOS were current smokers.
Table 1 presents the age and race distribution of
all PCOS cases by source. The characteristics of the women who were
seen at Magee-Womens Hospital Clinic versus those who were interviewed
only on the telephone were very similar. The proportion of individuals
seen in the clinic on estrogen replacement or oral contraceptives was
41 (19.4%), compared with 33 (16.0%) in the telephone interview–only
group. Thirteen (6.2%) of the cases evaluated clinically and 16
(7.6%) of those not seen reported a surgical menopause. Corresponding
figures for natural menopause were 3 (1.5%) and 6 (2.8%),
respectively, for case and control subjects.
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A total of 206 control subjects who met the matching criteria also
visited the clinic. Table 2 shows selected
sociodemographic and reproductive factors for case subjects and matched
control subjects. Case subjects were 35.9±7.4 and control subjects
were 37.2±7.8 years at the time of the initial interview; 33.2% of
the case and 40.8% of the control subjects were over 40 years old at
the time of the interview.
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A similar proportion of case (88.4%) and control (86.0%) subjects reported that they were still menstruating. Surgical menopause occurred in 14 (7%) of PCOS patients and 21 (10%) of the control subjects. Similar rates of hysterectomy with bilateral oophorectomy were reported (case subjects, 5%; control subjects, 5.8%). Twenty percent of control and 18.1% of case subjects reported taking estrogen replacement or oral contraceptives. Presence of hirsutism or removal of unwanted hair from face or body was reported in 43% of the case and 13% of the control subjects (P<.01).
Case subjects weighed more than control subjects (176.9±49 versus
153.76±35.7 pounds, respectively, P<.001). Almost 50% of
the case and 27.8% of the control subjects weighed 170 pounds or more
(P<.01). Wrist circumference, a surrogate for frame size,
was 16 or greater in 62.8% of the case subjects and 34.4% of the
control subjects (P<.01). Shown in Table 3
are other anthropometric and hormonal parameters. Mean BMI and
waist/hip ratio were significantly higher among case than control
subjects (BMI, 30.5±8.3 versus 26.3±6.5, P<.001;
waist/hip ratio, 0.82±.14 versus 0.76±.07, P<.001).
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Mean total serum testosterone level was higher among case than control subjects (1.66 nmol/L versus 1.11, P<.0001). Serum samples from 28 case and 29 control subjects were selected randomly to compare the correlation of bioavailable testosterone to total testosterone; the results of the Spearman test indicated a highly significant correlation (r=.9241, P<.001). The mean LH value for PCOS case subjects under 40 years old was 12.5±1.4 mIU/mL compared with 7.7±1.3 mIU/mL for control subjects (P<.05).
BMI, waist/hip ratio, and insulin, which were significantly different
between case and control groups in univariate analysis, were
included in a multivariate matched-pair conditional logistic regression
with case-control status as the dependent variable. All three variables
were forced into the model. Waist/hip ratio was a significant predictor
(P=.045), followed by insulin, which was almost significant
(P=.075). BMI was highly correlated with these variables and
did not show a significant independent contribution. One SD for each
independent variable was used for the unit of risk for the odds ratios
in Table 4.
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Serum total cholesterol, LDL cholesterol (LDL-C), and triglyceride
levels were significantly higher for case than control subjects
(respectively, 195.4±33.5 versus 185.6±37.8 mg/dL, P<.01;
118.4±31.5 versus 110.7±34.6 mg/dL, P=.03; and 129.0±88.8
versus 85.9±63.4 mg/dL, P<.001) (Table 5).
HDL-C was lower in case than control subjects (51.1±14.5 versus
57.8±14.5 mg/dL, P<.0001). Fasting insulin levels among
case (23.5±17.9 µU/L) and control (13.6±8.7 µU/L) subjects
differed significantly (P<.0001). Mean systolic blood
pressure among case subjects was 113.6±14.3 mm Hg and among control
subjects, 110.3±12.7 mm Hg (P=.025). Mean diastolic
pressure was not significantly different. The prevalence of a mean
diastolic blood pressure 
90 mm Hg was 5.9% among case subjects and
3.3% among control subjects (NS).
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Sixteen case (8%) and 6 control (3%) subjects reported a history of hypertension as diagnosed by their physicians. Nine of the 16 (5%) were currently taking blood pressure medication versus 3 (2%) of the control subjects. One case and one control subject reported a history of insulin-dependent diabetes, and non–insulin-dependent diabetes was noted in 8 case subjects (4%).
A comparison of CVD risk factors by cross-sectional age strata for case
and control subjects (Table 6) showed higher levels of
CVD risk factors among PCOS patients at an earlier age than control
subjects, with differences decreasing with age.
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By using multiple regression analysis we determined whether
lipid levels and blood pressure were higher among PCOS patients than
control subjects after adjusting for other risk factors: BMI, fasting
insulin, age, and use of exogenous hormones and/or oral contraceptives.
PCOS women had significantly higher lipid levels than control subjects
after adjusting for potentially confounding variables. There were no
significant differences in blood pressure in the multiple regression
analysis (Table 7).
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Discussion |
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In this study, we have documented higher levels of total cholesterol, LDL-C, triglycerides, and insulin and lower levels of HDL-C, especially HDL2-C, among women with PCOS compared with matched control subjects. The PCOS patients were probably heterogeneous in terms of both etiology and clinical presentation. As noted, however, the risk-factor differences were robust and appear to have been little affected by variations in clinical presentation. There were also substantial differences in BMI and waist/hip ratio. However, even after adjusting for BMI and fasting insulin, the differences in risk factors between PCOS patients and matched control subjects persisted.
One of the most important observations is that the differences in risk factors between PCOS women and control subjects are generally stronger at earlier ages. This is probably due to an early onset of hormonal changes and obesity and possibly to the distribution of intra-abdominal fat among PCOS patients. The data presented, however, are cross-sectional; longitudinal follow-up will provide answers regarding the changes in risk factors over time, especially among the younger PCOS women.
One can argue that PCOS represents one of the best examples of syndrome X as defined by Reaven.19 According to our data, the risk factors in the PCOS women are probably elevated at an earlier age than among non-PCOS women. If the central obesity, hyperinsulinemia, and low HDL-C and high triglyceride levels noted in the PCOS cases are really a unique profile of risk factors of atherosclerosis and subsequent coronary heart disease in women, then women with PCOS should have much more atherosclerosis than control subjects, especially at younger ages. If the risk of atherosclerosis is primarily related to elevated LDL-C, then there is an alternative reason for a higher prevalence of atherosclerosis in PCOS patients. Comparison of the evaluation of the risk of atherosclerosis in relation to these different risk factors may provide an estimate of the independent contributions of LDL-C compared with the syndrome X profile.20 PCOS women in many ways present risk-factor characteristics found in younger men and also among older obese postmenopausal women. It will be important in the subsequent follow-up and evaluation to determine whether the clinical presenting characteristics of PCOS women are related to changes in risk factors or to the development of atherosclerosis.
The etiology of PCOS is still not fully understood. The possible
association with insulin metabolism and genetic variation (5-
reductase)21 22 are interesting and potentially very
important. The observation that at least some PCOS women
represent an autosomal dominant genetic disorder and that the
male counterpart is defined by premature baldness and central obesity
is of great interest.23 24 25 Male-pattern baldness and
central obesity are risk factors for CVD.19 23 It will be
very important to evaluate both male and female siblings for risk
factors for CVD in order to determine both familial aggregation of PCOS
in women and the counterpart male syndrome. The extent of CVD and other
aspects of atherosclerosis should be evaluated in these families.
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Acknowledgments |
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This work was supported through a grant from the National Institutes of Health (R01,HL4664-01A2).
Received October 27, 1994; accepted April 4, 1995.
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D. S. Guzick Do Cardiovascular Risk Factors in Polycystic Ovarian Syndrome Result in More Cardiovascular Events? J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1170 - 1171. [Full Text] [PDF]
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M. Corton, J. I. Botella-Carretero, J. A. Lopez, E. Camafeita, J. L. San Millan, H. F. Escobar-Morreale, and B. Peral Proteomic analysis of human omental adipose tissue in the polycystic ovary syndrome using two-dimensional difference gel electrophoresis and mass spectrometry Hum. Reprod., March 1, 2008; 23(3): 651 - 661. [Abstract] [Full Text] [PDF]
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O. Valkenburg, R. P. M. Steegers-Theunissen, H. P. M. Smedts, G. M. Dallinga-Thie, B. C. J. M. Fauser, E. H. Westerveld, and J. S. E. Laven A More Atherogenic Serum Lipoprotein Profile Is Present in Women with Polycystic Ovary Syndrome: A Case-Control Study J. Clin. Endocrinol. Metab., February 1, 2008; 93(2): 470 - 476. [Abstract] [Full Text] [PDF]
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 S. E. Riechman, R. D. Andrews, D. A. MacLean, and S. Sheather Statins and Dietary and Serum Cholesterol Are Associated With Increased Lean Mass Following Resistance Training J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2007; 62(10): 1164 - 1171. [Abstract] [Full Text] [PDF]
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L. J. Moran, M. Noakes, P. M. Clifton, G. A. Wittert, D. P. Belobrajdic, and R. J. Norman C-Reactive Protein before and after Weight Loss in Overweight Women with and without Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2007; 92(8): 2944 - 2951. [Abstract] [Full Text] [PDF]
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S. Hu, A. Leonard, A. Seifalian, and P. Hardiman Vascular dysfunction during pregnancy in women with polycystic ovary syndrome Hum. Reprod., June 1, 2007; 22(6): 1532 - 1539. [Abstract] [Full Text] [PDF]
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 M.L. Hendriks, J.C.F. Ket, P.G.A. Hompes, R. Homburg, and C.B. Lambalk Why does ovarian surgery in PCOS help? Insight into the endocrine implications of ovarian surgery for ovulation induction in polycystic ovary syndrome Hum. Reprod. Update, May 1, 2007; 13(3): 249 - 264. [Abstract] [Full Text] [PDF]
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T. Cascella, S. Palomba, L. Tauchmanova, F. Manguso, S. Di Biase, D. Labella, F. Giallauria, C. Vigorito, A. Colao, G. Lombardi, et al. Serum Aldosterone Concentration and Cardiovascular Risk in Women with Polycystic Ovarian Syndrome J. Clin. Endocrinol. Metab., November 1, 2006; 91(11): 4395 - 4400. [Abstract] [Full Text] [PDF]
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E. Diamanti-Kandarakis, T. Paterakis, K. Alexandraki, C. Piperi, A. Aessopos, I. Katsikis, N. Katsilambros, G. Kreatsas, and D. Panidis Indices of low-grade chronic inflammation in polycystic ovary syndrome and the beneficial effect of metformin Hum. Reprod., June 1, 2006; 21(6): 1426 - 1431. [Abstract] [Full Text] [PDF]
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 E. Yesilada, I. Sahin, H. Ozcan, I. H. Yildirim, S. Yologlu, and C. Taskapan Increased micronucleus frequencies in peripheral blood lymphocytes in women with polycystic ovary syndrome. Eur. J. Endocrinol., April 1, 2006; 154(4): 563 - 568. [Abstract] [Full Text] [PDF]
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S. Topcu, M. Caliskan, E. E. Ozcimen, D. Tok, A. Uckuyu, D. Erdogan, H. Gullu, A. Yildirir, H. Zeyneloglu, and H. Muderrisoglu Do young women with polycystic ovary syndrome show early evidence of preclinical coronary artery disease? Hum. Reprod., April 1, 2006; 21(4): 930 - 935. [Abstract] [Full Text] [PDF]
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K. Lakhani, W. Yang, A. Dooley, E. El-Mahdi, M. Sundaresan, S. McLellan, R. Bruckdorfer, A. Leonard, A. Seifalian, and P. Hardiman Aortic function is compromised in a rat model of polycystic ovary syndrome Hum. Reprod., March 1, 2006; 21(3): 651 - 656. [Abstract] [Full Text] [PDF]
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 M. E. Zanolin, F. Tosi, G. Zoppini, R. Castello, G. Spiazzi, R. Dorizzi, M. Muggeo, and P. Moghetti Clustering of Cardiovascular Risk Factors Associated With the Insulin Resistance Syndrome: Assessment by principal component analysis in young hyperandrogenic women Diabetes Care, February 1, 2006; 29(2): 372 - 378. [Abstract] [Full Text] [PDF]
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 C. C.W. Chan, M. W.L. Koo, E. H.Y. Ng, O.-S. Tang, W. S.B. Yeung, and P.-C. Ho Effects of Chinese Green Tea on Weight, and Hormonal and Biochemical Profiles in Obese Patients With Polycystic Ovary Syndrome--A Randomized Placebo-Controlled Trial Reproductive Sciences, January 1, 2006; 13(1): 63 - 68. [Abstract] [PDF]
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E. Tasali, E. Van Cauter, and D. A. Ehrmann Relationships between Sleep Disordered Breathing and Glucose Metabolism in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 36 - 42. [Abstract] [Full Text] [PDF]
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J. Vrbikova, K. Vondra, D. Cibula, K. Dvorakova, S. Stanicka, D. Sramkova, G. Sindelka, M. Hill, B. Bendlova, and J. Skrha Metabolic syndrome in young Czech women with polycystic ovary syndrome Hum. Reprod., December 1, 2005; 20(12): 3328 - 3332. [Abstract] [Full Text] [PDF]
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F. Orio Jr., S. Palomba, T. Cascella, B. De Simone, F. Manguso, S. Savastano, T. Russo, A. Tolino, F. Zullo, G. Lombardi, et al. Improvement in Endothelial Structure and Function after Metformin Treatment in Young Normal-Weight Women with Polycystic Ovary Syndrome: Results of a 6-Month Study J. Clin. Endocrinol. Metab., November 1, 2005; 90(11): 6072 - 6076. [Abstract] [Full Text] [PDF]
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K. Lakhani, A. Leonard, A.M. Seifalian, and P. Hardiman Microvascular dysfunction in women with polycystic ovary syndrome Hum. Reprod., November 1, 2005; 20(11): 3219 - 3224. [Abstract] [Full Text] [PDF]
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M. Kravariti, K. K. Naka, S. N. Kalantaridou, N. Kazakos, C. S. Katsouras, A. Makrigiannakis, E. A. Paraskevaidis, G. P. Chrousos, A. Tsatsoulis, and L. K. Michalis Predictors of Endothelial Dysfunction in Young Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5088 - 5095. [Abstract] [Full Text] [PDF]
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I. Tarkun, B. Cetinarslan, E. Turemen, T. Sahin, Z. Canturk, and B. Komsuoglu Effect of rosiglitazone on insulin resistance, C-reactive protein and endothelial function in non-obese young women with polycystic ovary syndrome Eur. J. Endocrinol., July 1, 2005; 153(1): 115 - 121. [Abstract] [Full Text] [PDF]
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A. Vryonidou, A. Papatheodorou, A. Tavridou, T. Terzi, V. Loi, I.-A. Vatalas, N. Batakis, C. Phenekos, and A. Dionyssiou-Asteriou Association of Hyperandrogenemic and Metabolic Phenotype with Carotid Intima-Media Thickness in Young Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2740 - 2746. [Abstract] [Full Text] [PDF]
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E. B. Kilicdag, T. Bagis, H. B. Zeyneloglu, E. Tarim, E. Aslan, B. Haydardedeoglu, and S. Erkanli Homocysteine levels in women with polycystic ovary syndrome treated with metformin versus rosiglitazone: a randomized study Hum. Reprod., April 1, 2005; 20(4): 894 - 899. [Abstract] [Full Text] [PDF]
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K Rautio, J S Tapanainen, A Ruokonen, and L C Morin-Papunen Effects of metformin and ethinyl estradiol-cyproterone acetate on lipid levels in obese and non-obese women with polycystic ovary syndrome Eur. J. Endocrinol., February 1, 2005; 152(2): 269 - 275. [Abstract] [Full Text] [PDF]
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F. Orio Jr., S. Palomba, T. Cascella, S. Di Biase, F. Manguso, L. Tauchmanova, L. G. Nardo, D. Labella, S. Savastano, T. Russo, et al. The Increase of Leukocytes as a New Putative Marker of Low-Grade Chronic Inflammation and Early Cardiovascular Risk in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 2 - 5. [Abstract] [Full Text] [PDF]
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E. O. Talbott, J. V. Zborowski, M. Y. Boudreaux, K. P. McHugh-Pemu, K. Sutton-Tyrrell, and D. S. Guzick The Relationship between C-Reactive Protein and Carotid Intima-Media Wall Thickness in Middle-Aged Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., December 1, 2004; 89(12): 6061 - 6067. [Abstract] [Full Text] [PDF]
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E. O. Talbott, J. V. Zborowski, J. R. Rager, M. Y. Boudreaux, D. A. Edmundowicz, and D. S. Guzick Evidence for an Association between Metabolic Cardiovascular Syndrome and Coronary and Aortic Calcification among Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., November 1, 2004; 89(11): 5454 - 5461. [Abstract] [Full Text] [PDF]
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I. Tarkun, B. C. Arslan, Z. Canturk, E. Turemen, T. Sahin, and C. Duman Endothelial Dysfunction in Young Women with Polycystic Ovary Syndrome: Relationship with Insulin Resistance and Low-Grade Chronic Inflammation J. Clin. Endocrinol. Metab., November 1, 2004; 89(11): 5592 - 5596. [Abstract] [Full Text] [PDF]
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F. Orio Jr., S. Palomba, T. Cascella, B. De Simone, S. Di Biase, T. Russo, D. Labella, F. Zullo, G. Lombardi, and A. Colao Early Impairment of Endothelial Structure and Function in Young Normal-Weight Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4588 - 4593. [Abstract] [Full Text] [PDF]
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D. S. Guzick Cardiovascular Risk in PCOS J. Clin. Endocrinol. Metab., August 1, 2004; 89(8): 3694 - 3695. [Full Text] [PDF]
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F. Orio Jr., S. Palomba, L. Spinelli, T. Cascella, L. Tauchmanova, F. Zullo, G. Lombardi, and A. Colao The Cardiovascular Risk of Young Women with Polycystic Ovary Syndrome: An Observational, Analytical, Prospective Case-Control Study J. Clin. Endocrinol. Metab., August 1, 2004; 89(8): 3696 - 3701. [Abstract] [Full Text] [PDF]
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R. S. Legro, E. Myers, and for the Reproductive Medicine Network Surrogate end-points or primary outcomes in clinical trials in women with polycystic ovary syndrome? Hum. Reprod., August 1, 2004; 19(8): 1697 - 1704. [Abstract] [Full Text] [PDF]
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 D. M. Selva, V. Hirsch-Reinshagen, B. Burgess, S. Zhou, J. Chan, S. McIsaac, M. R. Hayden, G. L. Hammond, A. W. Vogl, and C. L. Wellington The ATP-binding cassette transporter 1 mediates lipid efflux from Sertoli cells and influences male fertility J. Lipid Res., June 1, 2004; 45(6): 1040 - 1050. [Abstract] [Full Text] [PDF]
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S. Taponen, H. Martikainen, M.-R. Jarvelin, U. Sovio, J. Laitinen, A. Pouta, A.-L. Hartikainen, M. I. McCarthy, S. Franks, M. Paldanius, et al. Metabolic Cardiovascular Disease Risk Factors in Women with Self-Reported Symptoms of Oligomenorrhea and/or Hirsutism: Northern Finland Birth Cohort 1966 Study J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 2114 - 2118. [Abstract] [Full Text] [PDF]
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N. Boulman, Y. Levy, R. Leiba, S. Shachar, R. Linn, O. Zinder, and Z. Blumenfeld Increased C-Reactive Protein Levels in the Polycystic Ovary Syndrome: A Marker of Cardiovascular Disease J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 2160 - 2165. [Abstract] [Full Text] [PDF]
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 D. J. Salmi, H. C. Zisser, and L. Jovanovic Screening for and Treatment of Polycystic Ovary Syndrome in Teenagers Experimental Biology and Medicine, May 1, 2004; 229(5): 369 - 377. [Abstract] [Full Text] [PDF]
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 J. F. Reckelhoff and L. A. Fortepiani Novel Mechanisms Responsible for Postmenopausal Hypertension Hypertension, May 1, 2004; 43(5): 918 - 923. [Abstract] [Full Text] [PDF]
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 M. T. Sheehan Polycystic Ovarian Syndrome: Diagnosis and Management Clin. Med. Res., February 1, 2004; 2(1): 13 - 27. [Abstract] [Full Text] [PDF]
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R. S. Legro, R. Azziz, D. Ehrmann, A. G. Fereshetian, M. O'Keefe, and M. N. Ghazzi Minimal Response of Circulating Lipids in Women with Polycystic Ovary Syndrome to Improvement in Insulin Sensitivity with Troglitazone J. Clin. Endocrinol. Metab., November 1, 2003; 88(11): 5137 - 5144. [Abstract] [Full Text] [PDF]
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 V. De Leo, A. la Marca, and F. Petraglia Insulin-Lowering Agents in the Management of Polycystic Ovary Syndrome Endocr. Rev., October 1, 2003; 24(5): 633 - 667. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden The Endocrine Society Meeting: Topics in Insulin Sensitivity and Hypertension Diabetes Care, September 1, 2003; 26(9): 2679 - 2688. [Full Text] [PDF]
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R. S. Legro Polycystic Ovary Syndrome and Cardiovascular Disease: A Premature Association? Endocr. Rev., June 1, 2003; 24(3): 302 - 312. [Abstract] [Full Text] [PDF]
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E. Diamanti-Kandarakis, J.-P. Baillargeon, M. J. Iuorno, D. J. Jakubowicz, and J. E. Nestler A Modern Medical Quandary: Polycystic Ovary Syndrome, Insulin Resistance, and Oral Contraceptive Pills J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 1927 - 1932. [Full Text] [PDF]
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F. C. W. Wu and A. von Eckardstein Androgens and Coronary Artery Disease Endocr. Rev., April 1, 2003; 24(2): 183 - 217. [Abstract] [Full Text] [PDF]
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M. Schachter, A. Raziel, S. Friedler, D. Strassburger, O. Bern, and R. Ron-El Insulin resistance in patients with polycystic ovary syndrome is associated with elevated plasma homocysteine Hum. Reprod., April 1, 2003; 18(4): 721 - 727. [Abstract] [Full Text] [PDF]
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F. Orio Jr., S. Palomba, S. Di Biase, A. Colao, L. Tauchmanova, S. Savastano, D. Labella, T. Russo, F. Zullo, and G. Lombardi Homocysteine Levels and C677T Polymorphism of Methylenetetrahydrofolate Reductase in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., February 1, 2003; 88(2): 673 - 679. [Abstract] [Full Text] [PDF]
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L. A. Stadtmauer, B. C. Wong, and S. Oehninger Should patients with polycystic ovary syndrome be treated with metformin?: Benefits of insulin sensitizing drugs in polycystic ovary syndrome--beyond ovulation induction Hum. Reprod., December 1, 2002; 17(12): 3016 - 3026. [Abstract] [Full Text] [PDF]
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E. Seli and A. J. Duleba Should patients with polycystic ovarian syndrome be treated with metformin? Hum. Reprod., September 1, 2002; 17(9): 2230 - 2236. [Abstract] [Full Text] [PDF]
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B. O. Yildiz, I. C. Haznedaroglu, S. Kirazli, and M. Bayraktar Global Fibrinolytic Capacity Is Decreased in Polycystic Ovary Syndrome, Suggesting a Prothrombotic State J. Clin. Endocrinol. Metab., August 1, 2002; 87(8): 3871 - 3875. [Abstract] [Full Text] [PDF]
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J. E. Nestler Should patients with polycystic ovarian syndrome be treated with metformin?: An enthusiastic endorsement Hum. Reprod., August 1, 2002; 17(8): 1950 - 1953. [Abstract] [Full Text] [PDF]
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 K. Lakhani, A. M. Seifalian, and P. Hardiman Impaired Carotid Viscoelastic Properties in Women With Polycystic Ovaries Circulation, July 2, 2002; 106(1): 81 - 85. [Abstract] [Full Text] [PDF]
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K. Elter, G. Imir, and F. Durmusoglu Clinical, endocrine and metabolic effects of metformin added to ethinyl estradiol-cyproterone acetate in non-obese women with polycystic ovarian syndrome: a randomized controlled study Hum. Reprod., July 1, 2002; 17(7): 1729 - 1737. [Abstract] [Full Text] [PDF]
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C. G. Solomon, F. B. Hu, A. Dunaif, J. E. Rich-Edwards, M. J. Stampfer, W. C. Willett, F. E. Speizer, and J. E. Manson Menstrual Cycle Irregularity and Risk for Future Cardiovascular Disease J. Clin. Endocrinol. Metab., May 1, 2002; 87(5): 2013 - 2017. [Abstract] [Full Text] [PDF]
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C. J. G. Kelly, A. Speirs, G. W. Gould, J. R. Petrie, H. Lyall, and J. M. C. Connell Altered Vascular Function in Young Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., February 1, 2002; 87(2): 742 - 746. [Abstract] [Full Text] [PDF]
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E. Diamanti-Kandarakis, G. Spina, C. Kouli, and I. Migdalis Increased Endothelin-1 Levels in Women with Polycystic Ovary Syndrome and the Beneficial Effect of Metformin Therapy J. Clin. Endocrinol. Metab., October 1, 2001; 86(10): 4666 - 4673. [Abstract] [Full Text] [PDF]
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 Y. Liu, J. Ding, T. L. Bush, J. C. Longenecker, F. J. Nieto, S. H. Golden, and M. Szklo Relative Androgen Excess and Increased Cardiovascular Risk after Menopause: A Hypothesized Relation Am. J. Epidemiol., September 15, 2001; 154(6): 489 - 494. [Abstract] [Full Text] [PDF]
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J. F. Reckelhoff Gender Differences in the Regulation of Blood Pressure Hypertension, May 1, 2001; 37(5): 1199 - 1208. [Abstract] [Full Text] [PDF]
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G. Paradisi, H. O. Steinberg, A. Hempfling, J. Cronin, G. Hook, M. K. Shepard, and A. D. Baron Polycystic Ovary Syndrome Is Associated With Endothelial Dysfunction Circulation, March 13, 2001; 103(10): 1410 - 1415. [Abstract] [Full Text] [PDF]
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M.W. Elting, T.J.M. Korsen, P.D. Bezemer, and J. Schoemaker Prevalence of diabetes mellitus, hypertension and cardiac complaints in a follow-up study of a Dutch PCOS population Hum. Reprod., March 1, 2001; 16(3): 556 - 560. [Abstract] [Full Text] [PDF]
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S. A. Arslanian, V. D. Lewy, and K. Danadian Glucose Intolerance in Obese Adolescents with Polycystic Ovary Syndrome: Roles of Insulin Resistance and {beta}-Cell Dysfunction and Risk of Cardiovascular Disease J. Clin. Endocrinol. Metab., January 1, 2001; 86(1): 66 - 71. [Abstract] [Full Text]
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 E. O. Talbott, D. S. Guzick, K. Sutton-Tyrrell, K. P. McHugh-Pemu, J. V. Zborowski, K. E. Remsberg, and L. H. Kuller Evidence for Association Between Polycystic Ovary Syndrome and Premature Carotid Atherosclerosis in Middle-Aged Women Arterioscler Thromb Vasc Biol, November 1, 2000; 20(11): 2414 - 2421. [Abstract] [Full Text] [PDF]
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K. J. Mather, S. Verma, B. Corenblum, and T. J. Anderson Normal Endothelial Function Despite Insulin Resistance in Healthy Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., May 1, 2000; 85(5): 1851 - 1856. [Abstract] [Full Text]
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D. Cibula, R. Cifkova, M. Fanta, R. Poledne, J. Zivny, and J. Skibova Increased risk of non-insulin dependent diabetes mellitus, arterial hypertension and coronary artery disease in perimenopausal women with a history of the polycystic ovary syndrome Hum. Reprod., April 1, 2000; 15(4): 785 - 789. [Abstract] [Full Text] [PDF]
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P. L. Chang, S. R. Lindheim, C. Lowre, M. Ferin, F. Gonzalez, L. Berglund, E. Carmina, M. V. Sauer, and R. A. Lobo Normal Ovulatory Women with Polycystic Ovaries Have Hyperandrogenic Pituitary-Ovarian Responses To Gonadotropin-Releasing Hormone-Agonist Testing J. Clin. Endocrinol. Metab., March 1, 2000; 85(3): 995 - 1000. [Abstract] [Full Text]
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 P. A. Lotufo, C. U. Chae, U. A. Ajani, C. H. Hennekens, and J. E. Manson Male Pattern Baldness and Coronary Heart Disease: The Physicians' Health Study Arch Intern Med, January 24, 2000; 160(2): 165 - 171. [Abstract] [Full Text] [PDF]
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M. W. Elting, T. J.M. Korsen, L. T.M. Rekers-Mombarg, and J. Schoemaker Women with polycystic ovary syndrome gain regular menstrual cycles when ageing Hum. Reprod., January 1, 2000; 15(1): 24 - 28. [Abstract] [Full Text] [PDF]
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E. Carmina and R. A. Lobo Polycystic Ovary Syndrome (PCOS): Arguably the Most Common Endocrinopathy Is Associated with Significant Morbidity in Women J. Clin. Endocrinol. Metab., June 1, 1999; 84(6): 1897 - 1899. [Full Text]
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E. Diamanti-Kandarakis, A. Mitrakou, S. Raptis, G. Tolis, and A. J. Duleba The Effect of a Pure Antiandrogen Receptor Blocker, Flutamide, on the Lipid Profile in the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 1998; 83(8): 2699 - 2705. [Abstract] [Full Text]
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J. Holte, G. Gennarelli, L. Wide, H. Lithell, and C. Berne High Prevalence of Polycystic Ovaries and Associated Clinical, Endocrine, and Metabolic Features in Women with Previous Gestational Diabetes Mellitus J. Clin. Endocrinol. Metab., April 1, 1998; 83(4): 1143 - 1150. [Abstract] [Full Text]
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T. L. Daniels and S. L. Berga Resistance of Gonadotropin Releasing Hormone Drive to Sex Steroid-Induced Suppression in Hyperandrogenic Anovulation J. Clin. Endocrinol. Metab., December 1, 1997; 82(12): 4179 - 4183. [Abstract] [Full Text] [PDF]
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M. Rajkhowa, R. H. Neary, P. Kumpatla, F. L. Game, P. W. Jones, M. S. Obhrai, and R. N. Clayton Altered Composition of High Density Lipoproteins in Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., October 1, 1997; 82(10): 3389 - 3394. [Abstract] [Full Text] [PDF]
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S. M. Herman, J. T.C. Robinson, R. J. McCredie, M. R. Adams, M. J. Boyer, and D. S. Celermajer Androgen Deprivation Is Associated With Enhanced Endothelium-Dependent Dilatation in Adult Men Arterioscler Thromb Vasc Biol, October 1, 1997; 17(10): 2004 - 2009. [Abstract] [Full Text]
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D. A. Ehrmann, D. J. Schneider, B. E. Sobel, M. K. Cavaghan, J. Imperial, R. L. Rosenfield, and K. S. Polonsky Troglitazone Improves Defects in Insulin Action, Insulin Secretion, Ovarian Steroidogenesis, and Fibrinolysis in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 1997; 82(7): 2108 - 2116. [Abstract] [Full Text] [PDF]
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G. B. Phillips, B. H. Pinkernell, and T.-Y. Jing Relationship Between Serum Sex Hormones and Coronary Artery Disease in Postmenopausal Women Arterioscler Thromb Vasc Biol, April 1, 1997; 17(4): 695 - 701. [Abstract] [Full Text]
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