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Original Studies |
Departments of Obstetrics and Gynecology (E.S.K., W.W., L.R.B., R.A.), Occupational Health (T.J.K.), Genetics (M.M.-K.), and Medicine (R.A.), University of Alabama, Birmingham, Alabama 35233
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Abstract |
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5) or
acne and were receiving no hormonal therapy; n = 98]. Considering
all 369 women studied, White and Black women had similar mean ages
(29.4 ± 7.1 and 31.1 ± 7.8 yr, respectively), although
White women had a lesser body mass than Black women (24.9 ± 6.1
vs. 29.2 ± 8.1 kg/m2, respectively;
P < 0.001). Of these 7.6%, 4.6%, and 1.9%
demonstrated a F-G score of 6 or more, 8 or 10, respectively, and there
was no significant racial difference, with hirsutism prevalences of
8.0%, 2.8%, and 1.6% in Whites, and 7.1%, 6.1%, and 2.1% in
Blacks, respectively. Of the 277 women consenting to a history and
hormonal evaluation, 4.0% had PCOS as defined, 4.7% (6 of 129) of
Whites and 3.4% (5 of 148) of Blacks. In conclusion, in our consecutive population of unselected women the prevalence of hirsutism varied from 2–8% depending on the chosen cut-off F-G score, with no significant difference between White and Black women. Using an F-G score of 6 or more as indicative of hirsutism, 3.4% of Blacks and 4.7% of Whites had PCOS as defined. These data suggest that PCOS may be one of most common reproductive endocrinological disorders of women.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The prevalence of PCOS, like that of any other complex multifactorial disorder, greatly depends on which criteria are used to define it. Most past studies have defined PCOS using a limited number of features, particularly morphological evidence of polycystic ovaries. When the presence of PCOS is defined solely by the finding of polycystic ovaries at either surgery or sonography, between 1–20% of unselected women have been reported to be affected (10, 11, 12, 13). However, this marker is relatively nonspecific, because up to 25% of patients with this ovarian morphology on sonography are asymptomatic (14). In addition, not all patients with hyperandrogenic oligoovulation demonstrate polycystic- appearing ovaries (13, 14, 15, 16).
A more comprehensive definition of PCOS arose from a conference on the disorder in April 1990, sponsored by the NIH/NICHHD. Although a clear-cut consensus was never reached, the majority of participants believed that PCOS should be defined by 1) ovulatory dysfunction, 2) clinical evidence of hyperandrogenism (hirsutism, acne, androgenic alopecia) and/or hyperandrogenemia, and 3) exclusion of related disorders, such as hyperprolactinemia, thyroid disorders, and nonclassic adrenal hyperplasia (NCAH) (17). No indication of how to define ovulatory dysfunction, hirsutism, or hyperandrogenemia was given. It is this definition of PCOS that is used in this report.
In addition to limiting the criteria for the disorder, most reports examining the prevalence of PCOS have also used populations of women seeking medical care (10, 11, 12, 13), albeit for reasons unrelated to hyperandrogenic complaints, a potential bias. Furthermore, no study has been made of non-White populations, particularly Black women. Because of the potentially significant public health impact of PCOS, we undertook the following prospective study of 369 consecutive women (195 Black and 174 White), evaluated during the time of a mandated preemployment physical, to assess the prevalence of the disorder and the extent of hirsutism.
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Subjects and Methods |
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All prospective employees to the University of Alabama at Birmingham (UAB) from resident staff to environmental workers undergo an entrance physical that includes a brief history and physical and blood sampling by the Division of Occupational Health and Safety of the Department of Family Medicine. It should be noted that UAB is the single largest employer in the city of Birmingham and the third largest employer in the state of Alabama. Consecutive females aged 18–45 yr who were being evaluated for employment to UAB were asked to participate. The study was approved by the institutional review board of UAB.
Two occupational health nurses were trained to score the degree of hirsutism using a previously described modified Ferriman-Gallwey (F-G) method, quantitating the presence of terminal hairs over nine body areas (i.e. upper lip, chin, chest, upper and lower abdomen, thighs, upper and lower back, and upper arms) (18). All women seen by these nurses for their employment physical had the extent of hirsutism scored. They also recorded the presence of acne, although no specific scoring system was applied. Informed consent was provided, and if the subject agreed, an additional standardized history form was completed, with emphasis on menstrual dating and regularity, hirsutism and acne, gynecological history, medications, and family history. In those women who consented, a 30-cc sample of blood was obtained in plain-top tubes for subsequent hormonal analysis. Serum was stored at -70 C until assayed.
To maximize uniformity all subjects with an F-G score above 3 according to the occupational health nurses were recalled, and hirsutism was rescored by one of the investigators (E.S.K.). To minimize treatment bias we included all women regardless of hormonal therapy or prior hysterectomy or oophorectomy. This was particularly important, as PCOS may predispose to the use of hormonal therapy and/or to surgical hysterectomy or castration. In these women, we determined menstrual history before their hormonal/surgical therapy and the reason for treatment. Circulating androgen levels were not obtained in either oophorectomized women or those receiving hormonal treatment.
Defining the presence of PCOS
As noted above, the presence of PCOS in these unselected women
was defined by the presence of 1) ovulatory dysfunction, 2) clinical
hyperandrogenism (i.e. hirsutism) and/or hyperandrogenemia,
and 3) the exclusion of other known disorders, as previously reported
(17). Specifically, these individual criterion were defined as follows.
1) Clinical hyperandrogenism was diagnosed by the presence of hirsutism
(i.e. F-G score 
6; see above). 2) Hyperandrogenemia was
defined as a total and/or free testosterone (T), androstenedione (A4),
and/or dehydroepiandrosterone sulfate (DHEAS) level above the upper
95th percentile of those race-matched women from the study population
who were normal, i.e. those with regular menstrual cycles
(26–34 days in length), who were nonhirsute (i.e. F-G score
of 0–5), had no evidence of acne, and were taking no hormonal therapy.
3) Ovulatory dysfunction was surmised by a history of eight or fewer
menstrual cycles in a year. 4) All subjects who after initial
examination (and reexamination) and hormonal analysis potentially had
PCOS (i.e. oligomenorrhea with hirsutism or acne, and/or
hyperandrogenemia) had their serum samples further assayed for
circulating PRL, TSH, and 17-hydroxyprogesterone (17-HP) levels to
exclude hyperprolactinemia, thyroid dysfunction, and
21-hydroxylase-deficient NCAH, respectively.
All women who had an elevated screening 17-HP level (i.e. >6.36 nmol/L) underwent an acute ACTH stimulation test to exclude 21-hydroxylase-deficient NCAH, as previously described (19). As the level of 17-HP, which is used to screen for NCAH (19), is increased in the luteal phase of the menstrual cycle, a serum progesterone (P4) level was also measured in all serum samples. If the P4 level was 12.72 nmol/L or less, the subject was considered to be in the follicular phase. If the P4 level was above 12.72 nmol/L, the subject was considered to have been in the luteal phase of the menstrual cycle, and any values of 17-HP above 6.36 nmol/L were disregarded. In this event, the patient was recalled, and the test was repeated in the follicular phase of a subsequent cycle. The diagnosis of PCOS was also excluded in women with persistent elevations of PRL (i.e. >29 µg/L) or abnormal TSH values (>5 mIU/L or <1 mIU/L). Finally, Cushing’s syndrome and androgenic tumors were excluded by appropriate testing if suspected clinically, as previously described (20).
All study subjects with abnormal findings were notified of the results of their evaluations, and those individuals with abnormal physical, historical, or biochemical findings were encouraged to undergo further investigation and/or therapy.
Hormonal analysis
Excluding those samples from women who either did not consent, were oophorectomized, or were receiving hormonal treatment, serum samples were analyzed for total and free T, sex hormone-binding globulin (SHBG), DHEAS, A4, and P4. Selected individuals (see above) also underwent measurements of PRL, TSH, and 17-HP. Samples were batched at regular intervals for analysis to minimize the impact of interassay variability while providing study subjects with timely information.
Total T was measured by an in-house RIA method after serum extraction, as previously described (21, 22). SHBG activity was measured by diffusion equilibrium dialysis, using Sephadex G-25 and [3H]T as the ligand, and free T was calculated, as previously described (23). DHEAS, P4, A4, PRL, TSH, and 17-HP were measured by direct RIA, using commercially available kits (DHEAS and P4 from Diagnostic Products Corp., Los Angeles, CA; A4 from Diagnostics Systems Laboratories, Webster, TX; and TSH and PRL from Nichols Institute Diagnostics, San Juan Capistrano, CA). The intra- and interassay variances for 17-HP and A4 (19) and for total T (21, 22) have been previously reported. The intra- and interassay coefficients of variances for the DHEAS assay were 3.2% and 1.6%, and 2.6% and 6.0% for low and high levels, respectively; for SHBG, they were 7.8% and 4.1%, and 5.1% and 6.8%, respectively; for TSH, they were 12.0% and 1.9%, and 13.0% and 5.7%, respectively; and for PRL, they were 6.4% and 6.45, and 13.4% and 5.0%, respectively.
Sample size, power calculations, and statistical analysis
The primary objective of this investigation was to generate an
estimate of the prevalence of PCOS separately for White and Black women
in the Birmingham area. Published reports indicated that the prevalence
in the general population ranged from 1–20%, with an average of
5–10% (10, 11, 12, 13). We further assumed that the overall prevalence of
PCOS was similar in White and Black women. Consequently, we selected a
sample size sufficient to generate a relatively narrow confidence
interval around the point estimate. With a sample size of 150 in each
racial group, the size of a two-sided 95% confidence interval ranged
from 1.6–8.4%, assuming a prevalence of 5%, and from 5.2–14.8% for
a prevalence of 10%. P < 0.05 was considered
significant. A statistical software package was used to perform
Student’s t test on the continuous data, a Mann-Whitney
test (nonparametric comparison) was used for discrete data, and a
2 test was used for the discontinuous variables
(Kiwkstat-Winks 4.21 Basic, TexasSoft, Cedar Hill, TX). Power analysis
was performed using PASS software (Jerry Hintze, Kayville, UT).
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Results |
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There was no significant racial difference in the prevalence of excess hair growth, with 8.0%, 2.8%, and 1.7% of White women and 7.1%, 6.1%, and 2.1% of Black women affected, respectively. Overall, the distribution of F-G scores did not demonstrate a significant difference between Black and White patients. There was also no difference in the incidence acne between White and Black women (5.2% vs. 4.1%, respectively).
Of the remaining 45 women with an F-G score above 3, 33 were able to be reexamined (73%). Reasons why subjects were not reexamined included refusal to participate in the study (n = 2), refusal to return for exam (n = 5), moving out of the area (n = 1), and inability to contact (n = 4), as not all subjects undergoing the preemployment physical were actually hired or remained at the university. Of the 33 women reexamined, only 1 had a change in her original F-G score by more than 5 points, from a score of 20 down to 8. In the vast majority of women reexamined by the investigator (28 of 33, or 85%) the F-G scores did not change by more than 2 points compared to the research nurse’s assessment. None of those changes affected the subsequent diagnosis of PCOS in these patients.
Of the total of 369 women screened, 24.9% (45 White and 47 Black) refused to participate beyond the initial exam. Most of the women refusing to participate did not want to complete the questionnaire. The 92 women who refused to participate did not differ in racial composition (24.1% Black vs. 25.8% White) or mean BMI (27.8 ± 8.0 vs. 26.9 ± 7.4 kg/m2, respectively) from those agreeing to enter the study, although they did differ in mean age (32.5 ± 7.8 vs. 29.6 ± 7.3 yr, respectively; P < 0.001) and mean initial F-G score (0.52 ± 1.02 vs. 1.64 ± 2.88, respectively; P < 0.001), from those 277 women consenting to the full study. It should be noted that of the 45 women with F-G scores above 3, only 2 (4.4%) refused to participate in the full study. The 2 women who did not agree to participate had F-G scores of 4 each, as initially screened by the research nurse.
The racial composition of the 277 subjects agreeing to participate
further in the study was divided almost equally between Black (n =
148) and White (n = 129) women (P > 0.05). Of
these, 198 (118 Black and 80 White) were taking no hormonal therapy,
and their sera were assayed as noted above. Seventy-nine women (28.5%;
30 Black and 49 White) were receiving estrogen/progestin therapy, of
whom 56 (24 Black and 32 White) were taking an oral contraceptive pill
solely for the purpose of birth control. Ninety-eight women (45 White
and 53 Black) were nonhirsute (i.e. F-G score 5),
nonacneic, eumenorrheic (regular cycles at <35-day intervals), and
taking no hormonal therapy. These women then composed the normal
population from which the upper control limits of the androgen values
were drawn. As there was no statistical (or clinically apparent)
difference in mean androgen values between Black and White women, their
hormonal data were pooled to establish the upper control 95th
percentile values of androgens, as follows: total T, 2.94 nmol/L; free
T, 0.026 nmol/L; DHEAS, 6.64 mol/L; and A4, 8.73 nmol/L.
Of the 277 (75.1%) women who consented to further evaluation, 35
(11.9%) had a history consistent with oligoovulation, with no
significant difference between Black and White women (12.2%
vs. 13.2%, respectively). Overall, of the 277 women studied
by history and exam, 11 (4.0%) had PCOS as previously defined, with no
significant difference between the races (6 of 129 or 4.7% of Whites,
and 5 of 148 or 3.4% of Blacks). In total, 8 of the 11 subjects with
PCOS had hyperandrogenemia (subjects 1–8 in Table 1
); 3 of the women were diagnosed with
PCOS solely based on their F-G score and history of oligomenorrhea
(subjects 9–11 in Table 1), as the androgen levels in subject 9 were
normal, and serum androgen levels were not determined in subjects 10
and 11, as they were concurrently receiving oral contraceptive
pills.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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We have tried to minimize selection bias in the inclusion of subjects in this study. All subjects were undergoing a mandated preemployment physical exam, which includes all medical, nursing, clerical, and support staff seeking employment to UAB. Furthermore, racial and socio-economic bias is minimized, as UAB is the single largest employer in the city of Birmingham. However, our study was biased toward underestimating the prevalence of PCOS, as clinical hyperandrogenism was defined only by the presence of hirsutism, circulating androgen levels could not be determined in women already receiving hormonal therapy, and ovulatory function was estimated from menstrual history. For example, acne and androgenetic alopecia may also be peripheral signs of hyperandrogenism. As the optimum system for acne scoring remains highly disputed (27), we elected to simply record its presence, without a grade, in our subjects. In our population, three women (two Black and one White) had evidence of acne, and their consideration would have increased the overall incidence of PCOS to 5.1%.
In our population, 25% of subjects were receiving either oral
contraceptive pills or a progestin only contraceptive; two thirds of
these were taking these for contraceptive purposes. Of the 79 women
receiving hormonal therapy, 2 were categorized as having PCOS according
to F-G score and menstrual history alone. Of the remaining 77 subjects
receiving hormonal therapy, 10 had a history of irregular menses but no
hirsutism. If we assume that 50% of these treated patients with
menstrual irregularity (i.e. 5) actually had PCOS without
hirsutism (i.e. hyperandrogenemia and oligoovulation), then
the overall prevalence of PCOS would be increased to 5.4%. Finally, in
an unrelated study we noted that up to 40% of hirsute women who
claiming to have regular menses actually have oligoovulation when
evaluated more closely (28). Applying this finding to our current study
population, we note that 28 subjects had hirsutism (i.e. F-G
score 6), and all participated in the study. Of these, 3 were
categorized as PCOS based on menstrual history. Hence, if we assumed
that 40% of the remaining subjects (i.e. 25) claiming to
have regular menses actually had ovulatory dysfunction (and therefore
PCOS), then the overall prevalence of PCOS would have increased to
7.6%.
Based on these assumptions, our overall population of patients with PCOS could have been as high as 29 of the 277 subjects fully studied, i.e. including those women with oligomenorrhea and acne, and those fractions of subjects with either oligomenorrhea during hormonal therapy or hirsutism and regular menstrual cycles, assumed to have PCOS. This would yield an overall maximum prevalence for the disorder of 10.5%. Alternatively, we may have overestimated the prevalence of PCOS by not being able to consider those women who refused to participate further in the study, i.e. complete a thorough gynecological history form and provide serum samples. It is possible that these women may have been, as a population, less affected than those participating, resulting in their lesser interest in the study. If all the women who refused participation were assumed to not be affected, then the overall prevalence of PCOS could have been as low as 3.0% (11 of 369).
It should be noted that it was not possible to adequately control for the time of the day of serum sampling because exams are performed between 0800–1600 h, nor for the day of the menstrual cycle. Nonetheless, although total T and A4 measured by RIA increase slightly in the late follicular and luteal phase in normal premenopausal women, these values generally remain within normal limits (29, 30, 31). In addition, total T does not have significant diurnal variation, at least in postmenopausal women (32). Although some investigators have noted that A4 levels follow the adrenocortical circadian cycle (32), we were unable to demonstrate a significant difference in mean A4 levels obtained between 0700–0900 h and 1500–1700 h in five healthy control women sampled every 5 min (33). DHEAS does not vary with menstrual cycle (29) and, at least in men, varies little diurnally (34). Finally, SHBG, used to determine the concentration of free T, does not demonstrate a consistent alteration with the menstrual cycle (23, 35) or the circadian rhythm (36). Overall, neither the time of exam nor the day of the menstrual cycle appears to have a significant impact on the clinical value of circulating androgens.
In addition to determining the prevalence of PCOS, this study also allowed us to crudely establish the overall incidence of hirsutism. Various investigators have noted that excess "hairiness" occurs in 5–15% of consecutive Caucasian women (29, 37, 38, 39, 40). In the present study of 369 consecutive unselected women, the prevalence of hirsutism varied from 2–8%, depending on the chosen cut-off F-G score, with no significant difference between White and Black women. We chose an F-G score of 6 or more as indicating the presence of significant hirsutism. In the original study by Ferriman and Gallwey (41), a score of 6 or greater was observed in only 5% of the general population. Furthermore, Lorenzo (42) studied 300 unselected female medical patients, using a modification of the F-G score with lesser areas assessed, and did not observe a score over 5 among them.
In conclusion, we have observed that in an unselected minimally biased population of consecutive women, the overall prevalence of PCOS appears to be approximately 4.6%, although it could be as low as 3.5% and as high as 11.2%, using the NIH/NICHHD 1990 criteria. There appeared to be no significant difference in prevalence between White and Black women. Our data support the concept that PCOS is one of most common reproductive endocrinological disorders of women.
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Footnotes |
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1 This was supported in part by Grant RO1-HD-29364, an administrative
supplement to Grant RO1-HD-29364, from the NIH (to R.A.). 
Received February 17, 1998.
Revised May 19, 1998.
Accepted May 29, 1998.
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A. Mueller, L. J. Gooren, S. Naton-Schotz, S. Cupisti, M. W. Beckmann, and R. Dittrich Prevalence of Polycystic Ovary Syndrome and Hyperandrogenemia in Female-to-Male Transsexuals J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1408 - 1411. [Abstract] [Full Text] [PDF]
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B. A. Swiglo, M. Cosma, D. N. Flynn, D. M. Kurtz, M. L. LaBella, R. J. Mullan, P. J. Erwin, and V. M. Montori Antiandrogens for the Treatment of Hirsutism: A Systematic Review and Metaanalyses of Randomized Controlled Trials J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1153 - 1160. [Abstract] [Full Text] [PDF]
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A. Z. Steiner, L. Chang, Q. Ji, M. Ookhtens, A. Stolz, R. J. Paulson, and F. Z. Stanczyk 3{alpha}-Hydroxysteroid Dehydrogenase Type III Deficiency: A Novel Mechanism for Hirsutism J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1298 - 1303. [Abstract] [Full Text] [PDF]
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S. Palomba, F. Giallauria, A. Falbo, T. Russo, R. Oppedisano, A. Tolino, A. Colao, C. Vigorito, F. Zullo, and F. Orio Structured exercise training programme versus hypocaloric hyperproteic diet in obese polycystic ovary syndrome patients with anovulatory infertility: a 24-week pilot study Hum. Reprod., March 1, 2008; 23(3): 642 - 650. [Abstract] [Full Text] [PDF]
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S. Franks, A. Layton, and A. Glasier Cyproterone acetate/ethinyl estradiol for acne and hirsutism: time to revise prescribing policy Hum. Reprod., February 1, 2008; 23(2): 231 - 232. [Abstract] [Full Text] [PDF]
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 J. E. Nestler Metformin for the Treatment of the Polycystic Ovary Syndrome N. Engl. J. Med., January 3, 2008; 358(1): 47 - 54. [Full Text] [PDF]
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B. O. Yildiz, E. S. Knochenhauer, and R. Azziz Impact of Obesity on the Risk for Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2008; 93(1): 162 - 168. [Abstract] [Full Text] [PDF]
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K. E. S. Salley, E. P. Wickham, K. I. Cheang, P. A. Essah, N. W. Karjane, and J. E. Nestler POSITION STATEMENT: Glucose Intolerance in Polycystic Ovary Syndrome A Position Statement of the Androgen Excess Society J. Clin. Endocrinol. Metab., December 1, 2007; 92(12): 4546 - 4556. [Abstract] [Full Text] [PDF]
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E. Moll, F. van der Veen, and M. van Wely The role of metformin in polycystic ovary syndrome: a systematic review Hum. Reprod. Update, November 1, 2007; 13(6): 527 - 537. [Abstract] [Full Text] [PDF]
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O. Celik, I. Sahin, N. Celik, S. Hascalik, L. Keskin, H. Ozcan, A. Uckan, and F. Kosar Diagnostic potential of serum N-terminal pro-B-type brain natriuretic peptide level in detection of cardiac wall stress in women with polycystic ovary syndrome: a cross-sectional comparison study Hum. Reprod., November 1, 2007; 22(11): 2992 - 2998. [Abstract] [Full Text] [PDF]
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X. Ma, L. Fan, Y. Meng, Z. Hou, Y.-D. Mao, W. Wang, W. Ding, and J.-Y. Liu Proteomic analysis of human ovaries from normal and polycystic ovarian syndrome Mol. Hum. Reprod., August 1, 2007; 13(8): 527 - 535. [Abstract] [Full Text] [PDF]
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 S. D. Pedersen, S. Brar, P. Faris, and B. Corenblum Polycystic ovary syndrome: Validated questionnaire for use in diagnosis Can Fam Physician, June 1, 2007; 53(6): 1041 - 1047. [Abstract] [Full Text] [PDF]
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M. F. Costello, B. Shrestha, J. Eden, N. P. Johnson, and P. Sjoblom Metformin versus oral contraceptive pill in polycystic ovary syndrome: a Cochrane review Hum. Reprod., May 1, 2007; 22(5): 1200 - 1209. [Abstract] [Full Text] [PDF]
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 H. C. Zisser Polycystic Ovary Syndrome and Pregnancy: Is Metformin the Magic Bullet? Diabetes Spectr, April 1, 2007; 20(2): 85 - 89. [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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R. L. Rosenfield Identifying Children at Risk for Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., March 1, 2007; 92(3): 787 - 796. [Abstract] [Full Text] [PDF]
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R. Wu, S. Fujii, N.K. Ryan, K.H. Van der Hoek, M.J. Jasper, I. Sini, S.A. Robertson, R.L. Robker, and R.J. Norman Ovarian leukocyte distribution and cytokine/chemokine mRNA expression in follicular fluid cells in women with polycystic ovary syndrome Hum. Reprod., February 1, 2007; 22(2): 527 - 535. [Abstract] [Full Text] [PDF]
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M. C Amato, A. Galluzzo, S. Merlino, A. Mattina, P. Richiusa, A. Criscimanna, and C. Giordano Lower insulin sensitivity differentiates hirsute from non-hirsute Sicilian women with polycystic ovary syndrome Eur. J. Endocrinol., December 1, 2006; 155(6): 859 - 865. [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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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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D. Macut, S. Damjanovic, D. Panidis, N. Spanos, B. Glisic, M. Petakov, D. Rousso, A. Kourtis, J. Bjekic, and N. Milic Oxidised low-density lipoprotein concentration - early marker of an altered lipid metabolism in young women with PCOS. Eur. J. Endocrinol., July 1, 2006; 155(1): 131 - 136. [Abstract] [Full Text] [PDF]
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J. M. Vink, S. Sadrzadeh, C. B. Lambalk, and D. I. Boomsma Heritability of Polycystic Ovary Syndrome in a Dutch Twin-Family Study J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2100 - 2104. [Abstract] [Full Text] [PDF]
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M. F. Costello, M. Chapman, and U. Conway A systematic review and meta-analysis of randomized controlled trials on metformin co-administration during gonadotrophin ovulation induction or IVF in women with polycystic ovary syndrome Hum. Reprod., June 1, 2006; 21(6): 1387 - 1399. [Abstract] [Full Text] [PDF]
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D. J. Handelsman The Rationale for Banning Human Chorionic Gonadotropin and Estrogen Blockers in Sport J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1646 - 1653. [Abstract] [Full Text] [PDF]
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C. R. McCartney, K. A. Prendergast, S. Chhabra, C. A. Eagleson, R. Yoo, R. J. Chang, C. M. Foster, and J. C. Marshall The Association of Obesity and Hyperandrogenemia during the Pubertal Transition in Girls: Obesity as a Potential Factor in the Genesis of Postpubertal Hyperandrogenism J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1714 - 1722. [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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N. Xita and A. Tsatsoulis Fetal Programming of Polycystic Ovary Syndrome by Androgen Excess: Evidence from Experimental, Clinical, and Genetic Association Studies J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1660 - 1666. [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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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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C. M. DeUgarte, K. S. Woods, A. A. Bartolucci, and R. Azziz Degree of Facial and Body Terminal Hair Growth in Unselected Black and White Women: Toward a Populational Definition of Hirsutism J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1345 - 1350. [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. Elsenbruch, S. Benson, S. Hahn, S. Tan, K. Mann, K. Pleger, R. Kimmig, and O. E. Janssen Determinants of emotional distress in women with polycystic ovary syndrome Hum. Reprod., April 1, 2006; 21(4): 1092 - 1099. [Abstract] [Full Text] [PDF]
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 F Gonzalez, N S Rote, J Minium, and J P Kirwan In vitro evidence that hyperglycemia stimulates tumor necrosis factor-{alpha} release in obese women with polycystic ovary syndrome. J. Endocrinol., March 1, 2006; 188(3): 521 - 529. [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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E. Carmina, F. Rosato, A. Janni, M. Rizzo, and R. A. Longo Relative Prevalence of Different Androgen Excess Disorders in 950 Women Referred because of Clinical Hyperandrogenism J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 2 - 6. [Abstract] [Full Text] [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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P. Dursun, E. Demirtas, A. Bayrak, and H. Yarali Decreased serum paraoxonase 1 (PON1) activity: an additional risk factor for atherosclerotic heart disease in patients with PCOS? Hum. Reprod., January 1, 2006; 21(1): 104 - 108. [Abstract] [Full Text] [PDF]
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R. L. Rosenfield Hirsutism N. Engl. J. Med., December 15, 2005; 353(24): 2578 - 2588. [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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 S. E. Recabarren, V. Padmanabhan, E. Codner, A. Lobos, C. Duran, M. Vidal, D. L. Foster, and T. Sir-Petermann Postnatal developmental consequences of altered insulin sensitivity in female sheep treated prenatally with testosterone Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E801 - E806. [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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C. K. Welt, A. E. Taylor, J. Fox, G. M. Messerlian, J. M. Adams, and A. L. Schneyer Follicular Arrest in Polycystic Ovary Syndrome Is Associated with Deficient Inhibin A and B Biosynthesis J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5582 - 5587. [Abstract] [Full Text] [PDF]
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F. Gonzalez, J. Minium, N. S. Rote, and J. P. Kirwan Hyperglycemia Alters Tumor Necrosis Factor-{alpha} Release from Mononuclear Cells in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5336 - 5342. [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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 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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J. K. Wickenheisser, V. L. Nelson-DeGrave, K. L. Hendricks, R. S. Legro, J. F. Strauss III, and J. M. McAllister Retinoids and Retinol Differentially Regulate Steroid Biosynthesis in Ovarian Theca Cells Isolated from Normal Cycling Women and Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4858 - 4865. [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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T. Sir-Petermann, C. Hitchsfeld, M. Maliqueo, E. Codner, B. Echiburu, R. Gazitua, S. Recabarren, and F. Cassorla Birth weight in offspring of mothers with polycystic ovarian syndrome Hum. Reprod., August 1, 2005; 20(8): 2122 - 2126. [Abstract] [Full Text] [PDF]
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M.A. Checa, A. Requena, C. Salvador, R. Tur, J. Callejo, J.J. Espinos, F. Fabregues, J. Herrero, and (Reproductive Endocrinology Interest Group of the Insulin-sensitizing agents: use in pregnancy and as therapy in polycystic ovary syndrome Hum. Reprod. Update, July 1, 2005; 11(4): 375 - 390. [Abstract] [Full Text] [PDF]
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M. van Wely, N. Bayram, F. van der Veen, and P. M.M. Bossuyt Predicting ongoing pregnancy following ovulation induction with recombinant FSH in women with polycystic ovary syndrome Hum. Reprod., July 1, 2005; 20(7): 1827 - 1832. [Abstract] [Full Text] [PDF]
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G. Gennarelli, V. Rovei, R. F. Novi, J. Holte, F. Bongioanni, A. Revelli, G. Pacini, P. Cavallo-Perin, and M. Massobrio Preserved Insulin Sensitivity and {beta}-Cell Activity, but Decreased Glucose Effectiveness in Normal-Weight Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3381 - 3386. [Abstract] [Full Text] [PDF]
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E. V. Bokal, H. M. Vrtovec, I. V. Klun, and I. Verdenik Prolonged HCG action affects angiogenic substances and improves follicular maturation, oocyte quality and fertilization competence in patients with polycystic ovarian syndrome Hum. Reprod., June 1, 2005; 20(6): 1562 - 1568. [Abstract] [Full Text] [PDF]
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E. B. Kilicdag, T. Bagis, E. Tarim, E. Aslan, S. Erkanli, E. Simsek, B. Haydardedeoglu, and E. Kuscu Administration of B-group vitamins reduces circulating homocysteine in polycystic ovarian syndrome patients treated with metformin: a randomized trial Hum. Reprod., June 1, 2005; 20(6): 1521 - 1528. [Abstract] [Full Text] [PDF]
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