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From the Clinical Research Centers |
Departments of Obstetrics and Gynecology (R.S.L., W.C.D.) and Health Evaluation Sciences (A.R.K.), Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033; and the Division of Women’s Health, Departments of Medicine and Obstetrics and Gynecology, Brigham and Women’s Hospital (A.D.), Boston, Massachusetts 02115
Address all correspondence and requests for reprints to: Andrea Dunaif, M.D., Division of Women’s Health, PBB-5, 75 Francis Street, Brigham and Women’s Hospital, Boston, Massachusetts 02115. E-mail: adunaif{at}bics.bwh.harvard.edu
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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2 = 7.0;
P = 0.01; odds ratio = 2.76; 95% confidence
interval = 1.23–6.57). Variables most associated with
postchallenge glucose levels were fasting glucose levels
(P < 0.0001), PCOS status (P =
0.002), waist/hip ratio (P = 0.01), and body mass
index (P = 0.021). The American Diabetes
Association criteria applied to fasting glucose significantly
underdiagnosed diabetes compared to the WHO criteria (3.2%
vs. 7.5%; 2 = 4.7; P
= 0.046; odds ratio = 2.48; 95% confidence interval =
1.01–6.69). We conclude that 1) PCOS women are at significantly
increased risk for IGT and type 2 diabetes mellitus at all weights and
at a young age; 2) these prevalence rates are similar in 2 different
populations of PCOS women, suggesting that PCOS may be a more important
risk factor than ethnicity or race for glucose intolerance in young
women; and 3) the American Diabetes Association diabetes diagnostic
criteria failed to detect a significant number of PCOS women with
diabetes by postchallenge glucose values. |
Introduction |
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It was first reported in 1980 (5) and subsequently confirmed (6, 7, 8, 9, 10) that PCOS women were hyperinsulinemic, suggesting the presence of insulin resistance. We showed that PCOS women have profound insulin resistance independent of obesity (11), that is secondary to a unique, apparently genetic, disorder of insulin action (12, 13, 14, 15, 16). Insulin resistance is now recognized as a major risk factor for the development of type 2 diabetes mellitus (17, 18, 19). Pancreatic ß-cell dysfunction is a second important risk factor (19), an abnormality that is also found in PCOS (20, 21, 22). PCOS women would thus be predicted to be at an increased risk for type 2 diabetes mellitus.
We began to prospectively assess glucose tolerance in PCOS women in 1983 as part of our research studies on insulin action in the disorder. We were the first to report in a series of 46 PCOS women (23) that there appeared to be an increased risk for impaired glucose tolerance (IGT) and type 2 diabetes mellitus in obese PCOS women. However, we did not compare the prevalence of glucose intolerance to that in a control group in that study (23). The metabolic abnormalities occurred at an early age (18–36 yr) (23).
To assess the prevalence of glucose intolerance and to determine parameters associated with increased risk, we examined our entire clinical experience in 254 PCOS women studied prospectively at 2 centers, Mt. Sinai School of Medicine (New York, NY) and Pennsylvania State University College of Medicine (Hershey, PA). We also evaluated the utility of the new American Diabetes Association (ADA) diabetes diagnostic criteria based on fasting glucose values (24) for detecting this disorder in PCOS women. We report here for the first time that not only is the prevalence of IGT and undiagnosed diabetes significantly increased in PCOS compared to control women, but also that a substantial number of nonobese PCOS women have these disorders.
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Subjects and Methods |
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We prospectively studied 254 PCOS women, aged 14–44 yr, and 80 control women, aged 18–40 yr, from 1983–1998. One hundred and ten PCOS women were studied at the Mt. Sinai School of Medicine (Mt. Sinai) between 1983 and 1991. One hundred and forty-four PCOS women and all control women were studied at the Pennsylvania State University College of Medicine (Penn State) in Hershey, PA from 1992 to 1998. The studies were approved by the institutional review boards of Mt. Sinai and Penn State, and the subjects gave written informed consent.
All women were in good health and, for at least 1 month before study, were not taking any medication (except for oral contraceptive agents that were stopped for 3 months before study) known to affect sex hormone or carbohydrate metabolism. The diagnosis of PCOS was made by the presence of chronic anovulation in association with elevated circulating androgen levels (1, 15, 23). Nonclassical adrenal 21-hydroxylase deficiency, hyperprolactinemia, and androgen-secreting tumors were excluded by appropriate tests before the diagnosis of PCOS was made (1, 23). No PCOS patient had diagnosed diabetes mellitus. The control women had menses every 27–32 days and were not hirsute. To control for conditions altering insulin action, control women did not engage in regular aerobic exercise, nor did they have a history of hypertension, a personal history of diabetes, or a first degree relative with diabetes (25, 26, 27).
PCOS women were recruited from the practices of the authors, attending physicians at the medical centers, and advertisements. Control women were recruited through advertisements. Ethnicity was recorded for 108 Mt. Sinai women: 51 were non-Hispanic white, 6 were Asian Indian, 39 were Caribbean-Hispanic, and 12 were African-American. The ethnicity of the PCOS women at Penn State was 138 non-Hispanic white, 3 Caribbean-Hispanic, and 3 African-American. The ethnicity of the control women was 70 non-Hispanic white, 7 Caribbean-Hispanic, and 3 African-American. A history of diabetes in first degree relatives was recorded for 28 Mt. Sinai PCOS women and all Penn State subjects.
Protocol
An oral glucose tolerance test was performed between 0800–1000 h after a 3-day 300-g carbohydrate diet and an overnight fast of 10–14 h. A waist/hip girth ratio was determined as previously reported (12) on 63 Mt. Sinai PCOS women, 127 Penn State PCOS women, and 75 control women. Eighty women at Mt. Sinai (all subjects before 1988) were administered a 40 g/m2 body surface area oral glucose challenge (23). Thirty subjects at Mt. Sinai and all subjects at Penn State were administered a 75-g oral glucose challenge. Blood was obtained for glucose determinations at 0 and 2 h. Insulin levels were also determined in these samples, but are not reported here because the RIA used has been changed several times over the years. An additional blood sample was obtained at 0 h for testosterone (T), nonsex hormone-binding globulin-bound testosterone (uT), and dehydroepiandrosterone sulfate (DHEAS) levels in all Penn State subjects. Some of the oral glucose tolerance test data have been reported as part of our previous studies of insulin action in PCOS (11, 14, 22, 23, 28, 29). Data for 123 Penn State PCOS women have not been previously reported. This is the first report of the cumulative prevalence of glucose intolerance in our population of PCOS women since 1987 (23).
Assays
Plasma glucose levels were determined by the glucose oxidase technique (22, 23, 29). Levels of T, uT, and DHEAS were determined as previously reported (29).
Data analysis
Glucose tolerance was assessed by WHO criteria (30). Categorical
data were analyzed using 2, odds ratio (OR), and exact
95% confidence intervals (CI). Continuous data were compared between
PCOS and control groups using unpaired t tests and are
reported as the mean ± 1 SD. P 
0.05 was considered statistically significant.
Among all PCOS women, no differences in 2-h glucose values according
oral glucose challenge [40 g/m2 vs. 75 g;
132 ± 42 vs. 138 ± 44 mg/ml, respectively
(P = 0.32); 7.3 ± 2.3 vs. 7.7 ±
2.4 mmol/L] were found. Thus, PCOS women from the two study sites were
combined to examine diabetes diagnostic categories based on
postchallenge glucose levels using WHO criteria (30) compared to those
determined according to the 1997 ADA criteria based on fasting glucose
values [normal fasting glucose, <110 mg/dL (<6.1 mmol/L); impaired
fasting glucose, 110–125 mg/dL (6.1–6.9 mmol/L); diabetes 
126 mg/dL
(7.0 mmol/L)] (24).
A multiple regression analysis was preformed to determine which
variables predicted postchallenge glucose values (31). To control for
the potential confounding effects of a family history of diabetes and
ethnicity, we included only Penn State non-Hispanic white control and
PCOS women without a first degree relative with diabetes in this
analysis. The candidate predictive variables were status (PCOS
vs. control), age, body mass index (BMI), waist/hip ratio,
and fasting glucose values. Androgen values were not considered as
candidate predictive variables, because they were used to make the
diagnosis of PCOS. The criterion for a predictive variable to remain in
the model was P 0.15. All analyses were performed
using the SAS statistical software package (SAS Institute, Inc., Cary, NC) or Epi Info version 6 (Centers for Disease
Control and Prevention, Atlanta, GA).
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Results |
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The clinical and biochemical characteristics of the subjects are
summarized in Table 1
. Seventy-eight
percent of PCOS women were overweight (BMI, 25 kg/m2),
and 73% were obese (BMI, 27 kg/m2). Overall, 38.6% (98
of 254) of the PCOS women had either IGT (31.1%) or diabetes (7.5%)
by WHO criteria (Fig. 1). The prevalence
was 30.0% IGT and 7.3% diabetes in the urban, ethnically diverse
population of Mt. Sinai and 31.9% IGT and 7.6% diabetes in the rural,
predominantly non-Hispanic white population of Penn State. There was no
significant difference in the overall prevalence of glucose intolerance
according to study site (2 = 0.14; P =
0.71) despite the fact that there were significantly more nonobese PCOS
women (BMI, 27 kg/m2) at Mt. Sinai than at Penn State
(2 = 25.2; P < 0.001; Table 2). The Mt. Sinai population did contain
substantially more members of high risk ethnic/racial groups
(Caribbean-Hispanic, 36% Mt. Sinai vs. 2% Penn State;
African-American, 11% Mt. Sinai vs. 2% Penn State). There
was no difference in prevalence by oral glucose load (data not shown).
Fourteen percent of the control women had IGT, and none had diabetes.
In the combined population of nonobese PCOS women (BMI, <27
kg/m2), 10.3% had IGT, and 1.5% had diabetes (Table 2). The youngest PCOS woman in the study (14 yr old) had IGT (Table 3). Although IGT and diabetes were
detected in nonobese and/or young PCOS women, the prevalence of both
significantly increased with BMI (by stratified Cochran-Armitage trend
test, P < 0.0001; Table 2) and with age (by stratified
Cochran-Armitage trend test, P < 0.002; Table 3) while
controlling for the site where the PCOS woman was studied.
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We examined the prevalence of glucose intolerance in non-Hispanic
white Penn State PCOS women without a first degree relative with
diabetes (n = 100) compared to that in non-Hispanic white control
women (n = 70) to adjust for confounding effects of ethnicity and
family history of diabetes. These PCOS women were significantly younger
than control women (27 ± 6 vs. 30 ± 6 yr old,
respectively; P = 0.001), with no significant
difference in BMI (35.6 ± 8.4 vs. 33.2 ± 8.9
kg/m2, respectively; P = 0.08). They
had a significantly higher prevalence of glucose intolerance (30.0%
IGT; 4.0% diabetes) compared to control women (15.7% IGT; 0%
diabetes; 2 = 7.0; P = 0.01; OR =
2.76; 95% CI = 1.23–6.57). To assess the impact of a family
history of diabetes, we compared the prevalence of glucose intolerance
in non-Hispanic white PCOS women from Penn State and found that it was
borderline significantly higher in PCOS women with a first degree
relative with diabetes (52.6% first degree relative with diabetes
vs. 34% no first degree relative with diabetes;
2 = 4.0; P = 0.053; OR = 2.44;
95% CI = 0.94–4.94).
Predictors of glucose intolerance
Of the 170 non-Hispanic white women without a first degree
relative with diabetes mellitus, 154 (88 PCOS women and 66 controls)
had complete data for all candidate variables and were analyzed via the
multiple regression model. There were no significant interactions of
status (PCOS vs. control) with the other variables. The
variables remaining in the final model were fasting glucose
(P < 0.0001), PCOS status (P = 0.002),
waist/hip ratio (P = 0.01), BMI (P =
0.02), and age (P = 0.14; Table 4). The model accounted for 50%
(r2) of the total variation. The impact of these variables
on postchallenge glucose values in PCOS is summarized in Table 4.
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The majority of PCOS women with glucose intolerance had normal
fasting glucose levels by ADA criteria (Fig. 2). Using the ADA criteria, 3.2% of PCOS
women would be classified as having diabetes, whereas 7.5% would be
classified as having diabetes by WHO criteria, a difference of 4.3%.
Thus, 11 of 19 (58%) PCOS women with diabetes diagnosed by WHO
criteria would have been missed using ADA criteria. No PCOS women had
diabetes by fasting glucose values who did not have it by postchallenge
glucose. The WHO criteria diagnosed significantly more diabetes in PCOS
women than the ADA criteria (2 = 4.7; P
= 0.046; OR = 2.48; 95% CI = 1.01–6.69). According to the
ADA criteria, 4.7% of PCOS women had impaired fasting glucose, whereas
31.1% had IGT by postchallenge glucose values.
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Discussion |
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The prevalence rates of IGT and diabetes were well above those reported among U.S. Hispanic and African-American women of similar age (34) and did not differ in the two groups of PCOS women studied, one an urban, ethnically mixed group and one a rural, ethnically homogeneous group. A preliminary report by Ehrmann and colleagues (35) found similar prevalence rates in an ethnically mixed PCOS population from the Chicago area. These observations suggest that PCOS is a more important risk factor for glucose intolerance in young women than race or ethnicity (34, 36), although we were unable to test this hypothesis statistically.
The ADA has recently recommended that fasting glucose criteria be used for the diagnosis of diabetes in asymptomatic individuals (24). Fasting glucose levels were poor predictors, however, of diabetes in PCOS, and few women with IGT had impaired fasting glucose values. Using ADA criteria, only 3.2% of PCOS women would have been classified as having diabetes, whereas 7.5% had diabetes by WHO criteria, a difference of 4.3%. In the Third National Health and Nutrition Survey (37), the difference between the criteria in an older cohort was -2.0% with ADA criteria. In the insulin-resistant San Antonio Heart Study population, the ADA criteria missed 27.3% of diabetes detected by postchallenge glucose values (38), whereas in our PCOS population the ADA criteria missed 58% of diabetes.
It is not possible at this juncture to recommend that PCOS women undergo formal glucose tolerance testing, because individuals who do not fulfill the ADA fasting glucose criteria for diabetes are at low risk for microvascular disease (24), and the benefit of treating IGT remains to be proven (39). Nevertheless, it is important to recognize that PCOS women are at high risk for type 2 diabetes and for cardiovascular disease because of their increased prevalence of glucose intolerance (33, 35, 39, 40, 41).
It has been suggested that a family history of diabetes worsens insulin secretion and glucose tolerance in PCOS (21). Consistent with this hypothesis, we showed that a first degree relative with diabetes was associated with an increased risk of glucose intolerance in PCOS women. However, the prevalence of glucose intolerance in PCOS, even in those women without a first degree relative with diabetes, was still much greater than that reported in the general U.S. population (32, 34, 36) and was significantly higher than that in control women. The factors associated with glucose intolerance in PCOS, age, BMI, waist/hip ratios, and family history of diabetes, were identical to those in other populations (17, 27, 32, 36). This suggests that the pathogenesis of type 2 diabetes is similar in all of these groups. An underlying genetic defect conferring insulin resistance and perhaps ß-cell dysfunction interacts with environmental factors worsening insulin resistance (17, 18, 19, 36, 42). ß-Cell function worsens, and glucose intolerance supervenes (18, 19, 36, 42).
Only women with the endocrine syndrome of hyperandrogenism and chronic anovulation appear to be insulin resistant and, accordingly, at high risk for glucose intolerance (15, 23, 43). Ovulatory women with the polycystic ovary morphology are not insulin resistant (43). The inclusion of both ovulatory and anovulatory women may explain the failure of a previous large study of glucose tolerance in hyperandrogenic women to detect glucose intolerance using the National Diabetes Data Group criteria (44). Differences in ethnicity and in the prevalence of obesity among PCOS populations may also have contributed to these discrepant findings (32, 34, 45).
In summary, PCOS women have significantly increased prevalence rates of IGT and undiagnosed diabetes, well above the prevalence in women in the general U.S. population of this age, including racial and ethnic minorities (32, 34). The prevalence rates of glucose intolerance are similar in ethnically diverse populations of PCOS women. Although obesity and age substantially increase risk, IGT and diabetes can occur in young, nonobese PCOS women. Fasting glucose levels are poor predictors of diabetes in PCOS women.
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Footnotes |
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Received July 15, 1998.
Revised October 8, 1998.
Accepted October 9, 1998.
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References |
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M. Luque-Ramirez, C. Mendieta-Azcona, F. Alvarez-Blasco, and H. F. Escobar-Morreale Androgen excess is associated with the increased carotid intima-media thickness observed in young women with polycystic ovary syndrome Hum. Reprod., December 1, 2007; 22(12): 3197 - 3203. [Abstract] [Full Text] [PDF]
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M. Urbanek, S. Sam, R. S. Legro, and A. Dunaif Identification of a Polycystic Ovary Syndrome Susceptibility Variant in Fibrillin-3 and Association with a Metabolic Phenotype J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4191 - 4198. [Abstract] [Full Text] [PDF]
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B. Trolle, A. Flyvbjerg, U. Kesmodel, and F.F. Lauszus Efficacy of metformin in obese and non-obese women with polycystic ovary syndrome: a randomized, double-blinded, placebo-controlled cross-over trial Hum. Reprod., November 1, 2007; 22(11): 2967 - 2973. [Abstract] [Full Text] [PDF]
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 P. Velasquez-Mieyer, C. P. Neira, R. Nieto, and P. A. Cowan Review: Obesity and cardiometabolic syndrome in children Therapeutic Advances in Cardiovascular Disease, October 1, 2007; 1(1): 61 - 81. [Abstract] [PDF]
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R. L. Barbieri Clomiphene Versus Metformin for Ovulation Induction in Polycystic Ovary Syndrome: The Winner Is .... J. Clin. Endocrinol. Metab., September 1, 2007; 92(9): 3399 - 3401. [Full Text] [PDF]
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S. Hahn, M. Backhaus, M. Broecker-Preuss, S. Tan, T. Dietz, R. Kimmig, M. Schmidt, K. Mann, and O. E Janssen Retinol-binding protein 4 levels are elevated in polycystic ovary syndrome women with obesity and impaired glucose metabolism Eur. J. Endocrinol., August 1, 2007; 157(2): 201 - 207. [Abstract] [Full Text] [PDF]
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S. Palomba, A. Falbo, T. Russo, F. Manguso, A. Tolino, F. Zullo, P. De Feo, and F. Orio Jr. Insulin Sensitivity after Metformin Suspension in Normal-Weight Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2007; 92(8): 3128 - 3135. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden Gut Hormones, Obesity, Polycystic Ovarian Syndrome, Malignancy, and Lipodystrophy Syndromes Diabetes Care, July 1, 2007; 30(7): 1934 - 1939. [Full Text] [PDF]
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M. Luque-Ramirez, F. Alvarez-Blasco, J. I. Botella-Carretero, E. Martinez-Bermejo, M. A. Lasuncion, and H. F. Escobar-Morreale Comparison of Ethinyl-Estradiol Plus Cyproterone Acetate Versus Metformin Effects on Classic Metabolic Cardiovascular Risk Factors in Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2453 - 2461. [Abstract] [Full Text] [PDF]
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N. Crisosto, E. Codner, M. Maliqueo, B. Echiburu, F. Sanchez, F. Cassorla, and T. Sir-Petermann Anti-Mullerian Hormone Levels in Peripubertal Daughters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2739 - 2743. [Abstract] [Full Text] [PDF]
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T. Sir-Petermann, B. Echiburu, M M. Maliqueo, N. Crisosto, F. Sanchez, C. Hitschfeld, M. Carcamo, P. Amigo, and F. Perez-Bravo Serum adiponectin and lipid concentrations in pregnant women with polycystic ovary syndrome Hum. Reprod., July 1, 2007; 22(7): 1830 - 1836. [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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K.-M. Seow, C.-C. Juan, Y.-P. Hsu, J.-L. Hwang, L.-W. Huang, and L.-T. Ho Amelioration of insulin resistance in women with PCOS via reduced insulin receptor substrate-1 Ser312 phosphorylation following laparoscopic ovarian electrocautery Hum. Reprod., April 1, 2007; 22(4): 1003 - 1010. [Abstract] [Full Text] [PDF]
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K.-M. Seow, C.-C. Juan, L.-T. Ho, Y.-P. Hsu, Y.-H. Lin, L.-W. Huang, and J.-L. Hwang Adipocyte resistin mRNA levels are down-regulated by laparoscopic ovarian electrocautery in both obese and lean women with polycystic ovary syndrome Hum. Reprod., April 1, 2007; 22(4): 1100 - 1106. [Abstract] [Full Text] [PDF]
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 C. Gagnon and J.-P. Baillargeon Suitability of recommended limits for fasting glucose tests in women with polycystic ovary syndrome Can. Med. Assoc. J., March 27, 2007; 176(7): 933 - 938. [Abstract] [Full Text] [PDF]
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D. C.W. Lau Screening for diabetes in women with polycystic ovary syndrome Can. Med. Assoc. J., March 27, 2007; 176(7): 951 - 952. [Full Text] [PDF]
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 C. Vollmert, S. Hahn, C. Lamina, C. Huth, M. Kolz, A. Schopfer-Wendels, K. Mann, F. Bongardt, J. C. Mueller, F. Kronenberg, et al. Calpain-10 variants and haplotypes are associated with polycystic ovary syndrome in Caucasians Am J Physiol Endocrinol Metab, March 1, 2007; 292(3): E836 - E844. [Abstract] [Full Text] [PDF]
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 R. S. Legro A 27-Year-Old Woman With a Diagnosis of Polycystic Ovary Syndrome JAMA, February 7, 2007; 297(5): 509 - 519. [Abstract] [Full Text] [PDF]
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R. Azziz, E. Carmina, D. Dewailly, E. Diamanti-Kandarakis, H. F. Escobar-Morreale, W. Futterweit, O. E. Janssen, R. S. Legro, R. J. Norman, A. E. Taylor, et al. Criteria for Defining Polycystic Ovary Syndrome as a Predominantly Hyperandrogenic Syndrome: An Androgen Excess Society Guideline J. Clin. Endocrinol. Metab., November 1, 2006; 91(11): 4237 - 4245. [Abstract] [Full Text] [PDF]
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J. C. Lo, S. L. Feigenbaum, G. J. Escobar, J. Yang, Y. M. Crites, and A. Ferrara Increased Prevalence of Gestational Diabetes Mellitus Among Women With Diagnosed Polycystic Ovary Syndrome: A population-based study Diabetes Care, August 1, 2006; 29(8): 1915 - 1917. [Full Text] [PDF]
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X. Chen, D. Yang, L. Li, S. Feng, and L. Wang Abnormal glucose tolerance in Chinese women with polycystic ovary syndrome Hum. Reprod., August 1, 2006; 21(8): 2027 - 2032. [Abstract] [Full Text] [PDF]
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 L. J Moran, M. Noakes, P. M Clifton, G. A Wittert, G. Williams, and R. J Norman Short-term meal replacements followed by dietary macronutrient restriction enhance weight loss in polycystic ovary syndrome Am. J. Clinical Nutrition, July 1, 2006; 84(1): 77 - 87. [Abstract] [Full Text] [PDF]
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S.K. Blank, C.R. McCartney, and J.C. Marshall The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome Hum. Reprod. Update, July 1, 2006; 12(4): 351 - 361. [Abstract] [Full Text] [PDF]
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R. Pasquali and A. Gambineri Insulin-sensitizing agents in polycystic ovary syndrome. Eur. J. Endocrinol., June 1, 2006; 154(6): 763 - 775. [Abstract] [Full Text] [PDF]
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A. Gambineri, V. Vicennati, S. Genghini, F. Tomassoni, U. Pagotto, R. Pasquali, and B. R. Walker Genetic Variation in 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Predicts Adrenal Hyperandrogenism among Lean Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2295 - 2302. [Abstract] [Full Text] [PDF]
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 S. Sam, R. S. Legro, P. A. Essah, T. Apridonidze, and A. Dunaif Evidence for metabolic and reproductive phenotypes in mothers of women with polycystic ovary syndrome PNAS, May 2, 2006; 103(18): 7030 - 7035. [Abstract] [Full Text] [PDF]
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T. L. Setji, N. D. Holland, L. L. Sanders, K. C. Pereira, A. M. Diehl, and A. J. Brown Nonalcoholic Steatohepatitis and Nonalcoholic Fatty Liver Disease in Young Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1741 - 1747. [Abstract] [Full Text] [PDF]
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G. Paradisi, A. Biaggi, R. Savone, F. Ianniello, C. Tomei, L. Caforio, and A. Caruso Cardiovascular Risk Factors in Healthy Women with Previous Gestational Hypertension J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1233 - 1238. [Abstract] [Full Text] [PDF]
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J. C. Lo, S. L. Feigenbaum, J. Yang, A. R. Pressman, J. V. Selby, and A. S. Go Epidemiology and Adverse Cardiovascular Risk Profile of Diagnosed Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1357 - 1363. [Abstract] [Full Text] [PDF]
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N. I. Leibel, E. E. Baumann, M. Kocherginsky, and R. L. Rosenfield Relationship of Adolescent Polycystic Ovary Syndrome to Parental Metabolic Syndrome J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1275 - 1283. [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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R. Azziz Diagnosis of Polycystic Ovarian Syndrome: The Rotterdam Criteria Are Premature J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 781 - 785. [Abstract] [Full Text] [PDF]
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A. Corbould, H. Zhao, S. Mirzoeva, F. Aird, and A. Dunaif Enhanced Mitogenic Signaling in Skeletal Muscle of Women With Polycystic Ovary Syndrome Diabetes, March 1, 2006; 55(3): 751 - 759. [Abstract] [Full Text] [PDF]
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T. Bridger, S. MacDonald, F. Baltzer, and C. Rodd Randomized Placebo-Controlled Trial of Metformin for Adolescents With Polycystic Ovary Syndrome Arch Pediatr Adolesc Med, March 1, 2006; 160(3): 241 - 246. [Abstract] [Full Text] [PDF]
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M. Mohlig, J. Spranger, M. Ristow, A. F H Pfeiffer, T. Schill, H. W Schlosser, L. Moltz, G. Brabant, and C. Schofl Predictors of abnormal glucose metabolism in women with polycystic ovary syndrome Eur. J. Endocrinol., February 1, 2006; 154(2): 295 - 301. [Abstract] [Full Text] [PDF]
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A. D. Coviello, R. S. Legro, and A. Dunaif Adolescent Girls with Polycystic Ovary Syndrome Have an Increased Risk of the Metabolic Syndrome Associated with Increasing Androgen Levels Independent of Obesity and Insulin Resistance J. Clin. Endocrinol. Metab., February 1, 2006; 91(2): 492 - 497. [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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D. A. Ehrmann, D. R. Liljenquist, K. Kasza, R. Azziz, R. S. Legro, M. N. Ghazzi, and for the PCOS/Troglitazone Study Group Prevalence and Predictors of the Metabolic Syndrome in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 48 - 53. [Abstract] [Full Text] [PDF]
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N. A. Cataldo, F. Abbasi, T. L. McLaughlin, M. Basina, P. Y. Fechner, L. C. Giudice, and G. M. Reaven Metabolic and ovarian effects of rosiglitazone treatment for 12 weeks in insulin-resistant women with polycystic ovary syndrome Hum. Reprod., January 1, 2006; 21(1): 109 - 120. [Abstract] [Full Text] [PDF]
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M. Urbanek, A. Woodroffe, K. G. Ewens, E. Diamanti-Kandarakis, R. S. Legro, J. F. Strauss III, A. Dunaif, and R. S. Spielman Candidate Gene Region for Polycystic Ovary Syndrome on Chromosome 19p13.2 J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6623 - 6629. [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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E. Diamanti-Kandarakis and C. Piperi Genetics of polycystic ovary syndrome: searching for the way out of the labyrinth Hum. Reprod. Update, November 1, 2005; 11(6): 631 - 643. [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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 P. Velasquez-Mieyer, S. Perez-Faustinelli, and P. A. Cowan Identifying Children at Risk for Obesity, Type 2 Diabetes, and Cardiovascular Disease Diabetes Spectr, October 1, 2005; 18(4): 213 - 220. [Abstract] [Full Text] [PDF]
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R. K. Danish and B. B. West Rapid Progression From Pre-diabetes to Severely Ill Diabetes While Under "Expert Care": Suggestions for Improved Screening for Disease Progression Diabetes Spectr, October 1, 2005; 18(4): 229 - 239. [Abstract] [Full Text] [PDF]
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I.A.A. Penna, P.R.B. Canella, R.M. Reis, M.F. Silva de Sa, and R.A. Ferriani Acarbose in obese patients with polycystic ovarian syndrome: a double-blind, randomized, placebo-controlled study Hum. Reprod., September 1, 2005; 20(9): 2396 - 2401. [Abstract] [Full Text] [PDF]
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M. Yilmaz, N. Bukan, R. Ersoy, A. Karakoc, I. Yetkin, G. Ayvaz, N. Cakir, and M. Arslan Glucose intolerance, insulin resistance and cardiovascular risk factors in first degree relatives of women with polycystic ovary syndrome Hum. Reprod., September 1, 2005; 20(9): 2414 - 2420. [Abstract] [Full Text] [PDF]
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 N. A Christy, A. S Franks, and L B. Cross Spironolactone for Hirsutism in Polycystic Ovary Syndrome Ann. Pharmacother., September 1, 2005; 39(9): 1517 - 1521. [Abstract] [Full Text] [PDF]
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I. Munir, H.-W. Yen, T. Baruth, R. Tarkowski, R. Azziz, D. A. Magoffin, and A. J. Jakimiuk Resistin Stimulation of 17{alpha}-Hydroxylase Activity in Ovarian Theca Cells in Vitro: Relevance to Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4852 - 4857. [Abstract] [Full Text] [PDF]
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S. Sam, R. S. Legro, R. Bentley-Lewis, and A. Dunaif Dyslipidemia and Metabolic Syndrome in the Sisters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4797 - 4802. [Abstract] [Full Text] [PDF]
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R. Azziz, C. Marin, L. Hoq, E. Badamgarav, and P. Song Health Care-Related Economic Burden of the Polycystic Ovary Syndrome during the Reproductive Life Span J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4650 - 4658. [Abstract] [Full Text] [PDF]
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D.H. Abbott, D.K. Barnett, C.M. Bruns, and D.A. Dumesic Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome? Hum. Reprod. Update, July 1, 2005; 11(4): 357 - 374. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden Second World Congress on the Insulin Resistance Syndrome: Mediators, pediatric insulin resistance, the polycystic ovary syndrome, and malignancy Diabetes Care, July 1, 2005; 28(7): 1821 - 1830. [Full Text] [PDF]
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