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Criteria for Defining Polycystic Ovary Syndrome as a Predominantly Hyperandrogenic Syndrome: An Androgen Excess Society Guideline

Cedars-Sinai Medical Center and The David Geffen School of Medicine at University of California, Los Angeles (R.A.), Los Angeles, California 90048; University of Palermo (E.C.), 90128 Palermo, Italy; Lille University Hospital (D.D.), 59037 Lille, France; University of Athens Medical School (E.D.-K.), GR-157 84 Athens, Greece; Hospital Ramon y Cajal and University of Alcalá (H.F.E.-M.), 28801 Madrid, Spain; Mount Sinai School of Medicine (W.F.), New York, New York 10029; University of Essen (O.E.J.), 45131 Essen, Germany; Pennsylvania State University School of Medicine (R.S.L.), Hershey, Pennsylvania 17033; University of Adelaide (R.J.N.), Woodville, South Australia 5005, Australia; Pfizer Global Research and Development (A.E.T.), Groton, Connecticut 06340; and Children’s Hospital of Pittsburgh (S.F.W.), Pittsburgh, Pennsylvania 15213

Address all correspondence and requests for reprints to: Ricardo Azziz, M.D., M.P.H., M.B.A., Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, 8635 West Third Street, Suite 160 W, Los Angeles, California 90048. E-mail: azzizr{at}cshs.org.

	Abstract

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
Objective: The Androgen Excess Society (AES) charged a task force to review all available data and recommend an evidence-based definition for polycystic ovary syndrome (PCOS), whether already in use or not, to guide clinical diagnosis and future research.

Participants: Participants included expert investigators in the field.

Evidence: Based on a systematic review of the published peer-reviewed medical literature, by querying MEDLINE databases, we tried to identify studies evaluating the epidemiology or phenotypic aspects of PCOS.

Consensus Process: The task force drafted the initial report, following a consensus process via electronic communication, which was then reviewed and critiqued by the AES Board of Directors. No section was finalized until all members were satisfied with the contents and minority opinions noted. Statements that were not supported by peer-reviewed evidence were not included.

Conclusions: Based on the available data, it is the view of the AES Task Force on the Phenotype of PCOS that there should be acceptance of the original 1990 National Institutes of Health criteria with some modifications, taking into consideration the concerns expressed in the proceedings of the 2003 Rotterdam conference. A principal conclusion was that PCOS should be first considered a disorder of androgen excess or hyperandrogenism, although a minority considered the possibility that there may be forms of PCOS without overt evidence of hyperandrogenism but recognized that more data are required before validating this supposition. Finally, the task force recognized, and fully expects, that the definition of this syndrome will evolve over time to incorporate new research findings.

	Introduction

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
THE DISORDER THAT eventually would be known as the polycystic ovary syndrome (PCOS) was initially described by Stein and Leventhal in 1935 (1). There is little disagreement that PCOS should be considered a syndrome, i.e. a collection of signs and features, in which no single test is diagnostic. In essence, the whole (or global assessment) is greater than the sum of the individual features. However, establishing a clear, contemporaneous, and evidence-based definition for this syndrome has important clinical and investigational implications. Nonetheless, the definition of PCOS has continued to generate significant controversy (2, 3, 4).

Clinically, diagnosing a woman as having PCOS implies an increased risk for infertility, dysfunctional bleeding, endometrial carcinoma, obesity, type 2 diabetes mellitus, dyslipidemia, hypertension, and possibly cardiovascular disease (5). Furthermore, it has important familial implications, principally, but not exclusively, for her sisters and daughters (6, 7, 8). Finally, a diagnosis of PCOS may mandate life-long treatments, e.g. the use of insulin sensitizers, and may negatively affect her ability to access health care coverage, principally in capitalistic markets. Consequently, the diagnosis of PCOS should not be assigned lightly, and diagnostic criteria should be based on robust data.

A judicious definition of PCOS is also essential to guide current and future research. The inclusion of patients whose definition, characterization, and selection criteria are unclear continues to plague the PCOS scientific literature. This issue is becoming critical as the field moves to the establishment of larger clinical trials and studies of the molecular biology and genetic nature of the disorder. In addition, definitions not based on clear-cut evidence have the potential effect of discouraging future and needed research into the nature of the disorder, its breadth, and its phenotype. Consequently, a contemporaneous definition based on what is currently known will benefit future investigation in this area.

The Androgen Excess Society (AES) is an international organization dedicated to promoting knowledge, and original clinical and basic research, in every aspect of androgen excess disorders, such as the PCOS, nonclassic adrenal hyperplasia, idiopathic hirsutism, and premature adrenarche. The society was founded in 2000 and currently has more than 200 members principally composed of investigators whose primary focus is the study of androgen excess disorders and PCOS. The Board of Directors of the AES appointed the Task Force on the Phenotype of PCOS and charged it with reviewing all current data concerning the phenotype of PCOS to answer the query: what different component phenotypes (features) constitute PCOS, based on the available published and peer-reviewed data, assuming that long-term morbidity is the anchor? The following summarizes the results of this task force’s year-long investigation.

	Process

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
The Board of Directors of the AES appointed a seven-member task force of experts in the field, intentionally including international investigators. Members of the task force and the board of directors constituted the Writing Committee. No external funding was accepted for this project. The evidence gathered was based on a systematic review of the published peer-reviewed medical literature to identify studies evaluating the epidemiology or phenotypic aspects of PCOS by querying MEDLINE databases. The Medical Subject Headings (MeSH) heading used was polycystic ovary syndrome (C04.182.612.765), with the following limitations: major topic and adolescent (13–18 yr) or adult (19–44 yr) and English and publication date from 1980 to 2005 and core clinical journals and female and humans. A total of 527 articles were initially available for this review, although additional studies (cross-references and those published in 2006) were also considered. Emphasis was placed on those studies that included greater than 100 subjects, although in some areas no studies of this size were available, and the paucity of data was noted. Studies in which epidemiological (e.g. prevalence) data could not be ascertained or calculated or which reported on the same parameter in mostly the same population as a larger study were eliminated from consideration. Unpublished data or personal communications were not included. Although only studies in which the criteria for PCOS were clearly stated were included, we did not define the disorder a priori and rather used each individual investigator’s own definition. In essence, we allowed PCOS to have a variety of definitions to define more clearly common phenotypes or features irrespective of the definition used.

The task force drafted the initial report, following a consensus process via electronic communication, which was then reviewed and critiqued by the AES Board of Directors. No section was finalized until all members were satisfied with the contents and minority opinions noted. Statements that were not supported by peer-reviewed evidence were not included.

	Current Definitions of PCOS

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
Currently two definitions of PCOS are in widespread use. The first arose from the proceedings of an expert conference sponsored in part by the National Institute of Child Health and Human Disease of the U.S. National Institutes of Health (NIH) on April 16–18, 1990. During the meeting, all participants were surveyed regarding their perception of what features formed part of PCOS, and Drs. Zawadski and Dunaif summarized these findings in the meeting proceedings (9). They concluded that the major criteria for PCOS "should include (in order of importance): 1) hyperandrogenism and/or hyperandrogenemia, 2) oligoovulation, (and the) 3) exclusion of other known disorders." This survey identified PCOS as an androgen excess disorder of exclusion, with an ovarian etiology and/or consequences.

Another expert conference was convened in Rotterdam, The Netherlands, May 1–3, 2003, sponsored in part by the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine (10, 11). The meeting proceedings recommended that PCOS be defined when at least two of the following three features were present: 1) oligo- and/or anovulation, 2) clinical and/or biochemical signs of hyperandrogenism, and 3) polycystic ovaries. These criteria also recognize that other androgen excess or related disorders should be excluded before assigning the diagnosis of PCOS. Whether these definitions are consistent with currently available data and whether they are overly narrow or unjustifiably broad were explored by the task force.

	The Essentials of Defining a Syndrome

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
The difficulties and intricacies of defining a syndrome are a challenge that many other organizations have and continue to struggle with (12, 13, 14, 15, 16, 17, 18, 19, 20, 21). A syndrome may be defined by: 1) historical usage in medical practice and/or literature, 2) expert knowledge and consensus processes, or 3) evidence, via analysis of published data.

One evidence-based approach to establishing the limits of a syndrome is to determine whether the various phenotypes defined by the criteria behave in a manner suggestive that they are part of the same disorder. First, all possible phenotypes generated by the definition of a syndrome are catalogued and examined. Second, a feature not included in the definition (i.e. the anchor) is chosen to serve as the common thread (e.g. inheritance pattern, morbidities, a response to intervention). Essentially, for the phenotypes to be part of the same syndrome, they should have a common thread above and beyond the commonality of their definition (which in itself may be arbitrary). For example, if the various phenotypes of PCOS have the same overall morbidity (e.g. insulin resistance and hyperinsulinism), then we could consider these phenotypes to reflect the same overall syndrome. The task force opted for this latter approach in determining what phenotypes (and hence what criteria) reflected PCOS based on current data.

Essentially, the task force considered that PCOS was defined by all those component phenotypes that potentially signaled an increased risk for insulin resistance and the resulting metabolic abnormalities. This is not to say that all individuals with a component phenotype had to demonstrate metabolic abnormalities but that the phenotype as a group should demonstrate an increased prevalence of markers for metabolic dysfunction. A similar approach has been taken when defining the limits of the metabolic syndrome (22).

	The Features of PCOS

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
The task force recognized four key features of PCOS: 1) ovulatory and menstrual dysfunction, 2) hyperandrogenemia, 3) clinical features of hyperandrogenism, and 4) polycystic ovaries. Clinically evident menstrual dysfunction, such as oligoamenorrhea or abnormal uterine bleeding, can be observed in a majority of patients with PCOS.

Ovulatory and menstrual dysfunction

In large series of patients diagnosed with PCOS, approximately 75% have clinically evident menstrual dysfunction (23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37) (Table 1). Current data also suggest that approximately 20% of women with PCOS will present with a history of apparent eumenorrhea (i.e. subclinical oligoanovulation) (23, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39) (Table 1). In clinical practice, the presence of anovulation in clinically hyperandrogenic (i.e. hirsute) eumenorrheic women may be determined by measuring a serum progesterone level sometime during d 20–24 of the cycle. If anovulation is present, it may be prudent to confirm this finding with a repeat study.

Elevated circulating androgen levels are observed in approximately 60–80% of PCOS patients (Table 2) (35, 36, 37, 40, 41, 42). The vast majority of the abnormal values are in the form of free testosterone (T), with the sole measurement of total T adding a limited amount to the diagnosis (36).

The task force noted that the measurement of circulating androgen levels, including free T, was to be used only as an adjuvant for the diagnosis of hyperandrogenic disorders and never as the sole criterion for diagnosis or in lieu of the clinical assessment. This recommendation reflects the fact that between 20 and 40% of women with PCOS will have androgen levels within the normal range (36) and that assays for androgens, particularly total T, tend to be highly variable and inaccurate (45, 46, 47).

Hirsutism, acne, and androgenic alopecia

Clinical features of hyperandrogenism frequently seen in PCOS include hirsutism, acne, and androgenic alopecia. Among women of white, black, southern Asia (Pakistani, Bengali, Gujarati, or Dravidian Indian), Maori, or Pacific Island descent, with PCOS defined by the NIH criteria, approximately 60% are found to be hirsute (Table 2) (24, 25, 26, 29, 30, 31, 32, 35, 36, 37, 40, 41, 42, 48, 49, 50). We note that the degree of facial and body terminal hair growth in women represents a continuum and that a value as low as 3, using the modified Ferriman-Gallwey (mFG) score, may be considered abnormal (51). However, most investigators have used the 95th percentile of controls as the upper normal limit, which corresponds to an mFG score of 6–8 in the white or black populations studied (51, 52).

Acne affects 15–25% of PCOS patients (38, 39, 53), although it is unclear whether the prevalence of acne is significantly increased in these patients over that observed in the general population (54, 55, 56, 57, 58). Finally, androgenic alopecia is a recognized sign of PCOS (39, 40, 59, 60, 61), although the prevalence of this abnormality in PCOS is unclear. In one study of 257 patients undergoing treatment for hyperandrogenic symptoms, only 5% complained of hair loss (39). Further studies are needed to better define the prevalence of acne and androgenic alopecia in PCOS.

Polycystic ovaries

Current data suggest that polycystic ovaries detected by transvaginal ultrasonography may be found in approximately 75% of women with a clinical diagnosis of PCOS (25, 26, 30, 31, 32, 35, 37, 42, 49, 62, 63, 64, 65, 66) (Table 3). However, the task force also recognized that the false-positive rate is relatively high, as evidenced by the high rate of polycystic ovaries in the general population (see above). The task force noted that the diagnosis of polycystic ovaries requires strict criteria (65, 67) and should not be assigned based solely on a polycystic or multicystic appearance of the ovary. The diagnosis of polycystic ovaries has been recently reviewed (68). The most commonly used criteria today are those proposed by Dewailly and colleagues (65) and reaffirmed in the Rotterdam 2003 consensus (10, 11), which indicate that polycystic ovaries can be established when at least one ovary demonstrates an ovarian volume of greater than 10 cm³ (milliliters) or 12 or more follicles measuring 2–9 mm in diameter.

Finally, a number of other features of PCOS have been recognized, including gonadotropic abnormalities, insulin resistance, and obesity. These features have not formed part of any of the recognized definitions to date, and the task force found no evidence to suggest that this should be otherwise.

	PCOS: Exclusion of Other Androgen-Excess and Related Disorders

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
In addition to PCOS, there are a number of other disorders of androgen excess in women, including adrenal hyperplasias (congenital adrenal hyperplasias), the syndromes of severe insulin resistance, and androgen-secreting neoplasms, that have the appearance of androgen excess (e.g. idiopathic hirsutism), or that have not yet been well characterized (e.g. idiopathic hyperandrogenism). There are also a number of other disorders that may result in ovulatory dysfunction, including hyperprolactinemia and thyroid abnormalities. These disorders account for approximately 5–10% of all patients with androgen excess (24, 26, 39, 40, 41, 42, 60, 70, 71, 72, 73, 74, 75, 76) (Table 4) and should be excluded when establishing the diagnosis of PCOS.

A phenotypic approach to defining PCOS: task force recommendations

The task force considered all data published and summarized above, emphasizing larger epidemiological and phenotypic studies, in arriving to its conclusions and recommendations regarding the phenotype of PCOS. These include the following:

PCOS is a hyperandrogenic disorder

The task force concluded that PCOS was above all a disorder of androgen excess in women. As such, with currently available evidence, the diagnosis of PCOS cannot be clearly established without evidence of either clinical or biochemical hyperandrogenism. Whereas the exact measures for these may vary, the task force felt that the single most reliable indices of this feature included hirsutism and free T levels. Nonetheless, the task force recognized that the methods for measuring androgens in the circulation were frequently inaccurate and insensitive and that determination of hirsutism using visual scales was subjective, with significant interobserver variation (78), where cutoff level may be unclear (51). Finally, the task force also noted that whereas many patients with PCOS may have evidence of acne or androgenic alopecia, these features could not be used reliably as clinical signs of hyperandrogenism. The task force also noted that support for this criteria is based on the risk for metabolic morbidity in the disorder, not on whether hyperandrogenism per se is present.

The ovarian morphology should be considered when establishing the diagnosis because polycystic ovaries are found in the majority, although not all, women with PCOS

The task force recognized that approximately 75% of women with PCOS will demonstrate a polycystic ovarian morphology on transvaginal ultrasonography, although they also recognized that the false-positive rate is high, with up to one quarter of unselected reproductive-aged women demonstrating this ovarian morphology. The task force also noted that the diagnosis of polycystic ovaries required the use of clear and strict criteria. Consistent with the recommendation (PCOS is a hyperandrogenic disorder) above, the task force felt strongly that in those women with polycystic ovaries but no evidence of clinical or biochemical hyperandrogenism, the diagnosis of PCOS is less certain, regardless of the presence of concomitant ovulatory dysfunction.

Ovulatory dysfunction is a prominent, but not universal, feature of PCOS

The task force recognized that some patients with PCOS may demonstrate regular ovulation at the time of their evaluation, the so-called ovulatory PCOS (79, 80). However, it was noted that patients with ovulatory PCOS constituted a minority of the PCOS population and had less severe androgenic and metabolic features than anovulatory women with PCOS. It was also recognized that there exist few data regarding the long-term maintenance of ovulation in women with ovulatory PCOS. Nonetheless, the task force recognized that there were persuasive, albeit limited, data to suggest that hyperandrogenic ovulatory women with polycystic ovaries had some degree of metabolic dysfunction and were amenable to the inclusion of this phenotype as a form of PCOS.

Eumenorrhea in the presence of dermatological features suggestive of hyperandrogenism (e.g. hirsutism) could not reliably be used to establish the presence of normal ovulation

A history of regular predictable vaginal bleeding in a patient without clinical signs of hyperandrogenism can be used as strong evidence of normal ovulation. Alternatively, a history of regular menstrual cycles in patients who demonstrate hyperandrogenic features (e.g. hirsutism) could not be relied on as evidence of normal ovulation because up to 40% of these women have oligoanovulation when examined more carefully. In these patients, confirmation of ovulatory function by more objective means is required.

Other well-defined disorders that could result in ovulatory dysfunction, polycystic ovaries, or clinical or biochemical hyperandrogenism had to be excluded

Although the task force recognized that specific androgen excess or other endocrine disorders needed to be excluded when establishing the diagnosis of PCOS, it also recognized the validity of tailoring testing to reflect the prevalence of these disorders in the population being studied.

Recognition of associated abnormalities

The task force noted that the presence of obesity, insulin resistance, and hyperinsulinism and increased LH levels or an LH to FSH ratio, whereas observed in a significant fraction of patients, should not be used as part of the definition of PCOS.

	Minority Report

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
Notwithstanding the above recommendations, the writing committee acknowledged that two of its members considered the possibility that there are forms of PCOS without overt evidence of hyperandrogenism and that may be associated with metabolic abnormalities and morbidity. However, these investigators also recognized, as did the committee as a whole, that more data are required before validating this supposition. For example, a recent study (81) noted that women with oligoanovulation and polycystic ovaries but without evidence of hyperandrogenism (n = 66) had basal insulin levels, the principal metabolic parameter assessed, similar to controls and lower than patients with hyperandrogenemia and oligoanovulation, with (n = 246) or without (n = 27) polycystic ovaries, or those with hyperandrogenemia and polycystic ovaries but without oligoanovulation (n = 67).

	Conclusions

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 
Based on the above review of the available data, it is the view of the AES Task Force on the Phenotype of PCOS that there should be acceptance of the original NIH/National Institute of Child Health and Human Disease criteria of 1990 with some modifications, taking into consideration the opinion expressed in the proceedings of the 2003 Rotterdam conference (Fig. 1). Considering the four features of ovulatory dysfunction, hirsutism, hyperandrogenemia, and polycystic ovaries, the task force identified nine different phenotypes that could be considered as being PCOS with currently available evidence (Table 5).

View larger version (13K): [in this window] [in a new window]   FIG. 1. AES suggested criteria for the diagnosis of PCOS. a Possibly excluding 21-hydroxylase-deficient nonclassic adrenal hyperplasia, androgen-secreting neoplasms, androgenic/anabolic drug use or abuse, Cushing’s syndrome, the syndromes of severe insulin resistance, thyroid dysfunction, and hyperprolactinemia.

However, the task force recognized that clinical features may not be constant even in a single patient and can be modified by changes in body weight and lifestyle choices and age. In addition, the task force also recognized that there may be a number of women who have features suggestive of PCOS but who do not fulfill the criteria; clearly these women and their symptoms should be treated accordingly, regardless of whether a diagnosis of PCOS is established.

A principal conclusion of this report is that PCOS should be first considered a disorder of androgen excess or hyperandrogenism. The absence of clinical or biochemical hyperandrogenism in the untreated state, or in women under the age of 40 yr, makes a diagnosis of PCOS less certain, regardless of the presence of ovulatory or menstrual dysfunction or the presence of polycystic ovaries. Overall, at the present time, in the task force’s assessment, women with oligoamenorrhea and polycystic-appearing ovaries on ultrasonography but no evidence of hyperandrogenism do not have PCOS.

The writing committee also acknowledged that some of its members considered the possibility that there are forms of PCOS without overt evidence of hyperandrogenism but recognized that more data are required before validating this supposition. Alternatively, the diagnosis of PCOS in women who have evidence of hyperandrogenism and polycystic ovaries, in the presence of ovulatory cycles, appears justified based on current data. Finally, whereas the aim of this report was to yield criteria based on currently available data to guide research and clinical diagnosis and future investigations, the task force recognized that the definition of this syndrome will evolve over time to incorporate new research findings.

	Acknowledgments

 
Task Force members included: Ricardo Azziz, M.D., M.P.H., Chair; Enrico Carmina, M.D.; Hector F. Escobar-Morreale, M.D., Ph.D.; Walter Futterweit, M.D.; Onno E. Janssen, M.D.; Richard S. Legro, M.D.; and Selma F. Witchel, M.D. Board of Directors members included: Didier Dewailly, M.D.; Evanthia Diamanti-Kandarakis, M.D.; Robert J. Norman, M.D.; and Ann E. Taylor, M.D.

	Footnotes

 
First Published Online August 29, 2006

Abbreviations: AES, Androgen Excess Society; DHEAS, dehydroepiandrosterone sulfate; IH, idiopathic hirsutism; mFG, modified Ferriman-Gallwey; PCOS, polycystic ovary syndrome; T, testosterone.

Received January 26, 2006.

Accepted August 23, 2006.

	References

Top Abstract Introduction Process Current Definitions of PCOS The Essentials of Defining... The Features of PCOS PCOS: Exclusion of Other... Minority Report Conclusions References

 

1. Stein I, Leventhal M 1935 Amenorrhoea associated with bilateral polycystic ovaries. Am J Obstet Gynecol 29:181–185
2. Balen A, Michelmore K 2002 What is polycystic ovary syndrome? Are national views important? Hum Reprod 17:2219–2227[Abstract/Free Full Text]
3. Azziz R 2006 Controversy in clinical endocrinology: diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature. J Clin Endocrinol Metab 91:781–785[Abstract/Free Full Text]
4. Franks S 2006 Controversy in clinical endocrinology: diagnosis of polycystic ovarian syndrome: in defense of the Rotterdam criteria. J Clin Endocrinol Metab 91:786–789[Abstract/Free Full Text]
5. Azziz R, Marin C, Hoq L, Badamgarav E, Song P 2005 Health care-related economic burden of the polycystic ovary syndrome during the reproductive life span. J Clin Endocrinol Metab 90:4650–4658[Abstract/Free Full Text]
6. Kahsar-Miller MD, Nixon C, Boots LR, Go RC, Azziz R 2001 Prevalence of polycystic ovary syndrome (PCOS) in first-degree relatives of patients with PCOS. Fertil Steril 75:53–58[CrossRef][Medline]
7. Legro RS, Bentley-Lewis R, Driscoll D, Wang SC, Dunaif A 2002 Insulin resistance in the sisters of women with polycystic ovary syndrome: association with hyperandrogenemia rather than menstrual irregularity. J Clin Endocrinol Metab 87:2128–2133[Abstract/Free Full Text]
8. Yildiz BO, Yarali H, Oguz H, Bayraktar M 2003 Glucose intolerance, insulin resistance, and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome. J Clin Endocrinol Metab 88:2031–2036[Abstract/Free Full Text]
9. Zawadski JK, Dunaif A 1992 Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In: Dunaif A, Givens JR, Haseltine FP, Merriam GR, eds. Polycystic ovary syndrome. Boston: Blackwell Scientific Publications; 377–384
10. ESHRE/ASRM 2004 Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 81:19–25[Medline]
11. The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group 2004 Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 19:41–47[Abstract/Free Full Text]
12. Aaron LA, Buchwald D 2001 A review of the evidence for overlap among unexplained clinical conditions. Ann Intern Med 134:868–881[Abstract/Free Full Text]
13. Agency for Healthcare Research and Quality 2001 Defining and managing chronic fatigue syndrome. Summary, Evidence Report/Technology Assessment 42. Rockville, MD (http://www.ahrq.gov/clinic/epcsums/cfssum.htm)
14. Corazziari E 2004 Definition and epidemiology of functional gastrointestinal disorders. Best Pract Res Clin Gastroenterol 18:613–631[CrossRef][Medline]
15. Feng Q, Zhou ZG, Tang WL, Yang XL, Long X 2005 [Comparison of 3 working definitions of metabolic syndrome in male medical examinees]. Zhong Nan Da Xue Xue Bao Yi Xue Ban 30:130–134[Medline]
16. Ford ES, Giles WH 2003 A comparison of the prevalence of the metabolic syndrome using two proposed definitions. Diabetes Care 26:575–581[Abstract/Free Full Text]
17. Hochberg MC 1997 Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 40:1725
18. Linder R, Dinser R, Wagner M, Krueger GR, Hoffmann A 2002 Generation of classification criteria for chronic fatigue syndrome using an artificial neural network and traditional criteria set. In Vivo 16:37–43[Medline]
19. Marchesini G, Forlani G, Cerrelli F, Manini R, Natale S, Baraldi L, Ermini G, Savorani G, Zocchi D, Melchionda N 2004 WHO and ATPIII proposals for the definition of the metabolic syndrome in patients with type 2 diabetes. Diabet Med 21:383–387[CrossRef][Medline]
20. Smith EL, Shmerling RH 1999 The American College of Rheumatology criteria for the classification of systemic lupus erythematosus: strengths, weaknesses, and opportunities for improvement. Lupus 8:586–595[Abstract/Free Full Text]
21. Wiedermann FJ, Mayr A, Schobersberger W, Mutz N 1999 Definition and classification of the antiphospholipid syndrome. J Cardiovasc Surg (Torino) 40:919–920[Medline]
22. Kahn R, Buse J, Ferrannini E, Stern M 2005 The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 28:2289–2304[Abstract/Free Full Text]
23. Goldzieher JW, Axelrod LR 1963 Clinical and biochemical features of polycystic ovarian disease. Fertil Steril 14:631–653[Medline]
24. Ferriman D, Purdie AW 1983 The aetiology of oligomenorrhoea and/or hirsuties: a study of 467 patients. Postgrad Med J 59:17–20[Abstract/Free Full Text]
25. Falsetti L, Eleftheriou G 1996 Hyperinsulinemia in the polycystic ovary syndrome: a clinical, endocrine and echographic study in 240 patients. Gynecol Endocrinol 10:319–326[Medline]
26. Khoury MY, Baracat EC, Pardini DP, Haidar MA, da Motta EL, de Lima GR 1996 Polycystic ovary syndrome: clinical and laboratory evaluation. Sao Paulo Med J 114:1222–1225[Medline]
27. Azziz R, Waggoner WT, Ochoa T, Knochenhauer ES, Boots LR 1998 Idiopathic hirsutism: an uncommon cause of hirsutism in Alabama. Fertil Steril 70:274–278[CrossRef][Medline]
28. Carmina E 1998 Prevalence of idiopathic hirsutism. Eur J Endocrinol 139:421–423[Abstract]
29. Talbott E, Clerici A, Berga SL, Kuller L, Guzick D, Detre K, Daniels T, Engberg RA 1998 Adverse lipid and coronary heart disease risk profiles in young women with polycystic ovary syndrome: results of a case-control study. J Clin Epidemiol 51:415–422[CrossRef][Medline]
30. Alborzi S, Khodaee R, Parsanejad ME 2001 Ovarian size and response to laparoscopic ovarian electro-cauterization in polycystic ovarian disease. Int J Gynaecol Obstet 74:269–274[CrossRef][Medline]
31. Williamson K, Gunn AJ, Johnson N, Milsom SR 2001 The impact of ethnicity on the presentation of polycystic ovarian syndrome. Aust NZ J Obstet Gynaecol 41:202–206[Medline]
32. Amer SA, Li TC, Bygrave C, Sprigg A, Saravelos H, Cooke ID 2002 An evaluation of the inter-observer and intra-observer variability of the ultrasound diagnosis of polycystic ovaries. Hum Reprod 17:1616–1622[Abstract/Free Full Text]
33. Haddad L, Evans JC, Gharani N, Robertson C, Rush K, Wiltshire S, Frayling TM, Wilkin TJ, Demaine A, Millward A, Hattersley AT, Conway G, Cox NJ, Bell GI, Franks S, McCarthy MI 2002 Variation within the type 2 diabetes susceptibility gene calpain-10 and polycystic ovary syndrome. J Clin Endocrinol Metab 87:2606–2610[Abstract/Free Full Text]
34. Glueck CJ, Papanna R, Wang P, Goldenberg N, Sieve-Smith L 2003 Incidence and treatment of metabolic syndrome in newly referred women with confirmed polycystic ovarian syndrome. Metabolism 52:908–915[CrossRef][Medline]
35. Orio Jr F, Matarese G, Di Biase S, Palomba S, Labella D, Sanna V, Savastano S, Zullo F, Colao A, Lombardi G 2003 Exon 6 and 2 peroxisome proliferator-activated receptor-gamma polymorphisms in polycystic ovary syndrome. J Clin Endocrinol Metab 88:5887–5892[Abstract/Free Full Text]
36. Chang WY, Knochenhauer ES, Bartolucci AA, Azziz R 2005 Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups. Fertil Steril 83:1717–1723[CrossRef][Medline]
37. Hahn S, Tan S, Elsenbruch S, Quadbeck B, Herrmann BL, Mann K, Janssen OE 2005 Clinical and biochemical characterization of women with polycystic ovary syndrome in North Rhine-Westphalia. Horm Metab Res 37:438–444[CrossRef][Medline]
38. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO 2004 The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 89:2745–2749[Abstract/Free Full Text]
39. Azziz R, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens KC, Taylor K, Boots LR 2004 Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab 89:453–462[Abstract/Free Full Text]
40. Conway GS, Honour JW, Jacobs HS 1989 Heterogeneity of the polycystic ovary syndrome: clinical, endocrine and ultrasound features in 556 patients. Clin Endocrinol (Oxf) 30:459–470[Medline]
41. Balen AH, Conway GS, Kaltsas G, Techatrasak K, Manning PJ, West C, Jacobs HS 1995 Polycystic ovary syndrome: the spectrum of the disorder in 1741 patients. Hum Reprod 10:2107–2111[Abstract/Free Full Text]
42. Legro RS, Myers ER, Barnhart HX, Carr BR, Carson SA, Diamond MP, Karr BA, Schlaff WD, Coutifaris C, McGovern PG, Cataldo NA, Steinkampf MP, Nestler JE, Gosman G, Giudice LC, Leppert PC The pregnancy in polycystic ovary syndrome (PPCOS) study: baseline characteristics of the randomized cohort including racial effects. Fertil Steril, in press
43. Knochenhauer ES, Key TJ, Kahsar-Miller M, Waggoner W, Boots LR, Azziz R 1998 Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study. J Clin Endocrinol Metab 83:3078–3082[Abstract/Free Full Text]
44. Kumar A, Woods KS, Bartolucci AA, Azziz R 2005 Prevalence of adrenal androgen excess in patients with the polycystic ovary syndrome (PCOS). Clin Endocrinol (Oxf) 62:644–649[CrossRef][Medline]
45. Miller KK, Rosner W, Lee H, Hier J, Sesmilo G, Schoenfeld D, Neubauer G, Klibanski A 2004 Measurement of free testosterone in normal women and women with androgen deficiency: comparison of methods. J Clin Endocrinol Metab 89:525–533[Abstract/Free Full Text]
46. Vermeulen A, Verdonck L, Kaufman JM 1999 A critical evaluation of simple methods for the estimation of free testosterone in serum. J Clin Endocrinol Metab 84:3666–3672[Abstract/Free Full Text]
47. Van Uytfanghe K, Stockl D, Kaufman JM, Fiers T, De Leenheer A, Thienpont LM 2005 Validation of 5 routine assays for serum free testosterone with a candidate reference measurement procedure based on ultrafiltration and isotope dilution-gas chromatography-mass spectrometry. Clin Biochem 38:253–261[CrossRef][Medline]
48. Kiddy DS, Sharp PS, White DM, Scanlon MF, Mason HD, Bray CS, Polson DW, Reed MJ, Franks S 1990 Differences in clinical and endocrine features between obese and non-obese subjects with polycystic ovary syndrome: an analysis of 263 consecutive cases. Clin Endocrinol (Oxf) 32:213–220[Medline]
49. Rajkhowa M, Talbot JA, Jones PW, Pettersson K, Haavisto AM, Huhtaniemi I, Clayton RN 1995 Prevalence of an immunological LH beta-subunit variant in a UK population of healthy women and women with polycystic ovary syndrome. Clin Endocrinol (Oxf) 43:297–303[Medline]
50. Norman RJ, Masters SC, Hague W, Beng C, Pannall P, Wang JX 1995 Metabolic approaches to the subclassification of polycystic ovary syndrome. Fertil Steril 63:329–335[Medline]
51. DeUgarte CM, Woods KS, Bartolucci AA, Azziz R 2006 Degree of facial and body terminal hair growth in unselected black and white women: toward a populational definition of hirsutism. J Clin Endocrinol Metab 91:1345–1350[Abstract/Free Full Text]
52. Ferriman D, Gallwey JD 1961 Clinical assessment of body hair growth in women. J Clin Endocrinol Metab 21:1440–1447[Abstract/Free Full Text]
53. Wijeyaratne CN, Balen AH, Barth JH, Belchetz PE 2002 Clinical manifestations and insulin resistance (IR) in polycystic ovary syndrome (PCOS) among South Asians and Caucasians: is there a difference? Clin Endocrinol (Oxf) 57:343–350[CrossRef][Medline]
54. Cunliffe WJ, Gould DJ 1979 Prevalence of facial acne vulgaris in late adolescence and in adults. Br Med J 1:1109–1110[Abstract/Free Full Text]
55. Dalgard F, Svensson A, Holm JO, Sundby J 2004 Self-reported skin morbidity in Oslo. Associations with sociodemographic factors among adults in a cross-sectional study. Br J Dermatol 151:452–457[CrossRef][Medline]
56. Galobardes B, Davey Smith G, Jefferys M, McCarron P 2005 Has acne increased? Prevalence of acne history among university students between 1948 and 1968. The Glasgow Alumni Cohort Study. Br J Dermatol 152:824–825[CrossRef][Medline]
57. Johnson MT, Roberts J 1978 Skin conditions and related need for medical care among persons 1–74 years. United States, 1971–1974. Vital Health Stat 11:i-v, 1–72
58. Rea JN, Newhouse ML, Halil T 1976 Skin disease in Lambeth. A community study of prevalence and use of medical care. Br J Prev Soc Med 30:107–114[Medline]
59. Futterweit W, Dunaif A, Yeh HC, Kingsley P 1988 The prevalence of hyperandrogenism in 109 consecutive female patients with diffuse alopecia. J Am Acad Dermatol 19:831–836[Medline]
60. O’Driscoll JB, Mamtora H, Higginson J, Pollock A, Kane J, Anderson DC 1994 A prospective study of the prevalence of clear-cut endocrine disorders and polycystic ovaries in 350 patients presenting with hirsutism or androgenic alopecia. Clin Endocrinol (Oxf) 41:231–236[Medline]
61. Cela E, Robertson C, Rush K, Kousta E, White DM, Wilson H, Lyons G, Kingsley P, McCarthy MI, Franks S 2003 Prevalence of polycystic ovaries in women with androgenic alopecia. Eur J Endocrinol 149:439–442[Abstract]
62. Ardaens Y, Robert Y, Lemaitre L, Fossati P, Dewailly D 1991 Polycystic ovarian disease: contribution of vaginal endosonography and reassessment of ultrasonic diagnosis. Fertil Steril 55:1062–1068[Medline]
63. van Santbrink EJ, Hop WC, Fauser BC 1997 Classification of normogonadotropic infertility: polycystic ovaries diagnosed by ultrasound versus endocrine characteristics of polycystic ovary syndrome. Fertil Steril 67:452–458[CrossRef][Medline]
64. Laven JS, Imani B, Eijkemans MJ, de Jong FH, Fauser BC 2001 Absent biologically relevant associations between serum inhibin B concentrations and characteristics of polycystic ovary syndrome in normogonadotrophic anovulatory infertility. Hum Reprod 16:1359–1364[Abstract/Free Full Text]
65. Jonard S, Robert Y, Cortet-Rudelli C, Pigny P, Decanter C, Dewailly D 2003 Ultrasound examination of polycystic ovaries: is it worth counting the follicles? Hum Reprod 18:598–603[Abstract/Free Full Text]
66. Carmina E, Orio F, Palomba S, Longo RA, Lombardi G, Lobo RA 2005 Ovarian size and blood flow in women with polycystic ovary syndrome and their correlations with endocrine parameters. Fertil Steril 84:413–419[CrossRef][Medline]
67. Jonard S, Robert Y, Dewailly D 2005 Revisiting the ovarian volume as a diagnostic criterion for polycystic ovaries. Hum Reprod 20:2893–2898[Abstract/Free Full Text]
68. Balen AH, Laven JS, Tan SL, Dewailly D 2003 Ultrasound assessment of the polycystic ovary: international consensus definitions. Hum Reprod Update 9:505–514[Abstract/Free Full Text]
69. Farquhar CM, Birdsall M, Manning P, Mitchell JM 1994 Transabdominal versus transvaginal ultrasound in the diagnosis of polycystic ovaries in a population of randomly selected women. Ultrasound Obstet Gynecol 4:54–59[CrossRef][Medline]
70. Luciano AA, Chapler FK, Sherman BM 1984 Hyperprolactinemia in polycystic ovary syndrome. Fertil Steril 41:719–725[Medline]
71. Moran C, Tapia MC, Hernandez E, Vazquez G, Garcia-Hernandez E, Bermudez JA 1994 Etiological review of hirsutism in 250 patients. Arch Med Res 25:311–314[Medline]
72. Romaguera J, Moran C, Diaz-Montes TP, Hines GA, Cruz RI, Azziz R 2000 Prevalence of 21-hydroxylase-deficient nonclassic adrenal hyperplasia and insulin resistance among hirsute women from Puerto Rico. Fertil Steril 74:59–62[CrossRef][Medline]
73. Escobar-Morreale HF 2004 Macroprolactinemia in women presenting with hyperandrogenic symptoms: Implications for the management of polycystic ovary syndrome. Fertil Steril 82:1697–1699[CrossRef][Medline]
74. Janssen OE, Mehlmauer N, Hahn S, Offner AH, Gartner R 2004 High prevalence of autoimmune thyroiditis in patients with polycystic ovary syndrome. Eur J Endocrinol 150:363–369[Abstract]
75. Glintborg D, Henriksen JE, Andersen M, Hagen C, Hangaard J, Rasmussen PE, Schousboe K, Hermann AP 2004 Prevalence of endocrine diseases and abnormal glucose tolerance tests in 340 Caucasian premenopausal women with hirsutism as the referral diagnosis. Fertil Steril 82:1570–1579[CrossRef][Medline]
76. Carmina E, Rosato F, Janni A, Rizzo M, Longo RA 2006 Extensive clinical experience: relative prevalence of different androgen excess disorders in 950 women referred because of clinical hyperandrogenism. J Clin Endocrinol Metab 91:2–6[Abstract/Free Full Text]
77. Azziz R, Carmina E, Sawaya ME 2000 Idiopathic hirsutism. Endocr Rev 21:347–362[Abstract/Free Full Text]
78. Wild RA, Vesely S, Beebe L, Whitsett T, Owen W 2005 Ferriman Gallwey self-scoring I: performance assessment in women with polycystic ovary syndrome. J Clin Endocrinol Metab 90:4112–4114[Abstract/Free Full Text]
79. Carmina E, Wong L, Chang L, Paulson RJ, Sauer MV, Stanczyk FZ, Lobo RA 1997 Endocrine abnormalities in ovulatory women with polycystic ovaries on ultrasound. Hum Reprod 12:905–909[Abstract/Free Full Text]
80. Carmina E, Lobo RA 1999 Do hyperandrogenic women with normal menses have polycystic ovary syndrome? Fertil Steril 71:319–322[CrossRef][Medline]
81. Dewailly D, Catteau-Jonard S, Reyss AC, Leroy M, Pigny P 2006 Oligoanovulation with polycystic ovaries but not overt hyperandrogenism. J Clin Endocrinol Metab 91:3922–3927[Abstract/Free Full Text]
82. Robinson S, Kiddy D, Gelding SV, Willis D, Niththyananthan R, Bush A, Johnston DG, Franks S 1993 The relationship of insulin insensitivity to menstrual pattern in women with hyperandrogenism and polycystic ovaries. Clin Endocrinol (Oxf) 39:351–355[Medline]
83. Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA 1992 Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome? Am J Obstet Gynecol 167:1807–1812[Medline]
84. Legro RS, Finegood D, Dunaif A 1998 A fasting glucose to insulin ratio is a useful measure of insulin sensitivity in women with polycystic ovary syndrome. J Clin Endocrinol Metab 83:2694–2698[Abstract/Free Full Text]
85. Legro RS, Kunselman AR, Dodson WC, Dunaif A 1999 Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab 84:165–169[Abstract/Free Full Text]
86. Diamanti-Kandarakis E, Kouli CR, Bergiele AT, Filandra FA, Tsianateli TC, Spina GG, Zapanti ED, Bartzis MI 1999 A survey of the polycystic ovary syndrome in the Greek island of Lesbos: hormonal and metabolic profile. J Clin Endocrinol Metab 84:4006–4011[Abstract/Free Full Text]
87. Ehrmann DA, Barnes RB, Rosenfield RL, Cavaghan MK, Imperial J 1999 Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care 22:141–146[Abstract/Free Full Text]
88. Silfen ME, Denburg MR, Manibo AM, Lobo RA, Jaffe R, Ferin M, Levine LS, Oberfield SE 2003 Early endocrine, metabolic, and sonographic characteristics of polycystic ovary syndrome (PCOS): comparison between nonobese and obese adolescents. J Clin Endocrinol Metab 88:4682–4688[Abstract/Free Full Text]
89. San Millan JL, Corton M, Villuendas G, Sancho J, Peral B, Escobar-Morreale HF 2004 Association of the polycystic ovary syndrome with genomic variants related to insulin resistance, type 2 diabetes mellitus, and obesity. J Clin Endocrinol Metab 89:2640–2646[Abstract/Free Full Text]
90. Gambineri A, Pelusi C, Manicardi E, Vicennati V, Cacciari M, Morselli-Labate AM, Pagotto U, Pasquali R 2004 Glucose intolerance in a large cohort of Mediterranean women with polycystic ovary syndrome: phenotype and associated factors. Diabetes 53:2353–2358[Abstract/Free Full Text]
91. Apridonidze T, Essah PA, Iuorno MJ, Nestler JE 2005 Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab 90:1929–1935[Abstract/Free Full Text]
92. Dokras A, Bochner M, Hollinrake E, Markham S, Vanvoorhis B, Jagasia DH 2005 Screening women with polycystic ovary syndrome for metabolic syndrome. Obstet Gynecol 106:131–137[Medline]
93. Carmina E, Chu MC, Longo RA, Rini GB, Lobo RA 2005 Phenotypic variation in hyperandrogenic women influences the findings of abnormal metabolic and cardiovascular risk parameters. J Clin Endocrinol Metab 90:2545–2549[Abstract/Free Full Text]
94. Ehrmann DA, Liljenquist DR, Kasza K, Azziz R, Legro RS, Ghazzi MN 2006 Prevalence and predictors of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab 91:48–53[Abstract/Free Full Text]
95. Michelmore K, Ong K, Mason S, Bennett S, Perry L, Vessey M, Balen A, Dunger D 2001 Clinical features in women with polycystic ovaries: relationships to insulin sensitivity, insulin gene VNTR and birth weight. Clin Endocrinol (Oxf) 55:439–446[CrossRef][Medline]
96. Legro RS, Chiu P, Kunselman AR, Bentley CM, Dodson WC, Dunaif A 2005 Polycystic ovaries are common in women with hyperandrogenic chronic anovulation but do not predict metabolic or reproductive phenotype. J Clin Endocrinol Metab 90:2571–2579[Abstract/Free Full Text]
97. Norman RJ, Hague WM, Masters SC, Wang XJ 1995 Subjects with polycystic ovaries without hyperandrogenaemia exhibit similar disturbances in insulin and lipid profiles as those with polycystic ovary syndrome. Hum Reprod 10:2258–2261[Abstract/Free Full Text]

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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]

				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]

				C. Roberge, A. C. Carpentier, M.-F. Langlois, J.-P. Baillargeon, J.-L. Ardilouze, P. Maheux, and N. Gallo-Payet Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity Am J Physiol Endocrinol Metab, December 1, 2007; 293(6): E1465 - E1478. [Abstract] [Full Text] [PDF]

				N. Kajaia, H. Binder, R. Dittrich, P. G Oppelt, B. Flor, S. Cupisti, M. W Beckmann, and A. Mueller Low sex hormone-binding globulin as a predictive marker for insulin resistance in women with hyperandrogenic syndrome Eur. J. Endocrinol., October 1, 2007; 157(4): 499 - 507. [Abstract] [Full Text] [PDF]

				P. P. Kayampilly and K. M. J. Menon Follicle-Stimulating Hormone Increases Tuberin Phosphorylation and Mammalian Target of Rapamycin Signaling through an Extracellular Signal-Regulated Kinase-Dependent Pathway in Rat Granulosa Cells Endocrinology, August 1, 2007; 148(8): 3950 - 3957. [Abstract] [Full Text] [PDF]

				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]

				M. Luque-Ramirez, F. Alvarez-Blasco, C. Mendieta-Azcona, J. I. Botella-Carretero, and H. F. Escobar-Morreale Obesity Is the Major Determinant of the Abnormalities in Blood Pressure Found in Young Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., June 1, 2007; 92(6): 2141 - 2148. [Abstract] [Full Text] [PDF]

				A. J. King, N. Bari Olivier, P. S. Mohankumar, J. S. Lee, V. Padmanabhan, and G. D. Fink Hypertension caused by prenatal testosterone excess in female sheep Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1837 - E1841. [Abstract] [Full Text] [PDF]

				E. Codner and H. F. Escobar-Morreale Hyperandrogenism and Polycystic Ovary Syndrome in Women with Type 1 Diabetes Mellitus J. Clin. Endocrinol. Metab., April 1, 2007; 92(4): 1209 - 1216. [Abstract] [Full Text] [PDF]

				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]

				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]

				W. Rosner, R. J. Auchus, R. Azziz, P. M. Sluss, and H. Raff Utility, Limitations, and Pitfalls in Measuring Testosterone: An Endocrine Society Position Statement J. Clin. Endocrinol. Metab., February 1, 2007; 92(2): 405 - 413. [Abstract] [Full Text] [PDF]

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