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Original Studies |
Departments of Endocrinology (M.A., R.M.C., J.S., H.F.E.-M.), Molecular Genetics (J.L.S.M.), and Biochemistry (S.A.), Hospital Ramón y Cajal, Madrid 28034, Spain
Address all correspondence and requests for reprints to: Héctor F. Escobar-Morreale, M.D., Ph.D., Department of Endocrinology, Hospital Ramón y Cajal, Carretera de Colmenar Km. 9,100, 28034 Madrid, Spain.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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At present, the diagnosis of PCOS is usually based on the criteria derived from the 1990 NIH/NICHHD conference (10): 1) menstrual dysfunction, 2) clinical hyperandrogenism (hirsutism, acne, androgenic alopecia) and/or hyperandrogenemia, and 3) exclusion of other related disorders, such as hyperprolactinemia, nonclassic adrenal hyperplasia, or thyroid disease. Using these criteria, Knochenhauer et al. (11) reported a 4.0% prevalence of PCOS in the southeastern U.S., namely, Birmingham, AL. This carefully designed study involved both White and Black women and avoided any significant bias in the selection of the participants. Further, a similar 6.8% prevalence of PCOS has been recently reported in the Greek island of Lesbos (12).
In the present study we estimated the prevalence of PCOS and hirsutism in 154 consecutive Caucasian women from Madrid, Spain, using a design similar to that used by Knochenhauer et al. (11). To avoid any selection of the population, all of the women studied here were consecutive blood donors reporting spontaneously to our hospital for that reason.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The study population consisted in Caucasian female blood donors reporting to the Department of Hematology of the Hospital Ramón y Cajal from May to June 1999. The presence of hirsutism was scored in every woman by a single investigator, using a modification of the Ferriman-Gallwey method (13), quantitating the presence of terminal hairs over nine body areas (i.e. upper lip, chin, chest, upper and lower abdomen, upper and lower back, upper arms, and thighs). The presence or absence of acne and androgenic alopecia was recorded, and weight, height, and waist and hip circumferences were measured.
A history form was completed, including menstrual dating and irregularity, hirsutism and acne, reproductive history, gynecological history, use of medication including oral contraceptive pills, and family history of male pattern premature baldness, carbohydrate intolerance, and arterial hypertension. In women who were receiving hormonal therapy, their menstrual history before treatment and the reason for treatment were recorded. Women with physiological menopause— present or past symptoms of hypoestrogenism such as hot flushes and vaginal dryness, emotional lability, and menstrual abnormalities in a woman older than 45 yr (14)—were excluded from the study. None of the subjects was younger than 18 yr old, which is the minimum legal age for blood donation in Spain. In those women who were found to be suitable blood donors, serum samples were obtained, and were stored at -20 C until assayed. When women were finally not accepted as blood donors because of present anemia or previous history infectious hepatitis, no serum samples were obtained.
The study was approved by the institutional review board of the Hospital Ramón y Cajal, and written informed consent was obtained from all the subjects.
Assays
Serum samples were analyzed for total testosterone (T), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), progesterone (P4), LH, FSH, and estradiol (E2). In women who matched the criteria for PCOS, PRL, TSH, and 17-hydroxyprogesterone (17-OHP) were also measured to exclude hyperprolactinemia, hypothyroidism, and nonclassic 21-hydroxylase deficiency, respectively.
Total T, SHBG, DHEAS, P4, LH, FSH, E2, PRL, and TSH were measured, each hormone in a single assay, using an automated immunochemiluminescence method (Immulite, Diagnostic Products, Los Angeles, CA). 17-OHP was measured by direct RIA using a commercially available kit (ImmuChem, ICN Biomedicals, Inc., Costa Mesa, CA) in a single assay. The mean intraassay coefficients of variation were as follows: 7.4% for T, 6.5% for SHBG, 6.9% for DHEAS, 8.2% for P4, 5.7% for LH, 6.4% for FSH, 9.3% for E2, 6.2% for PRL, 7.1% for TSH, and 9.5% for 17-OHP. The free androgen index (FAI) was calculated using the formula [T (nmol/L) x 100]/SHBG (nmol/L)].
Criteria for the definition of PCOS
As stated above, PCOS was defined by the presence of 1) menstrual dysfunction, 2) clinical hyperandrogenism and/or hyperandrogenemia, and 3) exclusion of other disorders (10). Menstrual dysfunction was considered when the women had oligomenorrhea, defined by more than six cycles with a length of more than 35 days, and/or when the patient had not had any menstrual bleeding for 3 consecutive months during the last year. Clinical hyperandrogenism was defined by the presence of hirsutism, represented by a hirsutism score of 8 or more, persistence of acne during the third decade of life or later, or the presence of androgenic alopecia. No attempts were made to grade the severity of acne or alopecia. Hyperandrogenemia was defined by a circulating T and DHEAS levels and/or FAI higher than the 95th percentile for the women studied here who had no clinical evidence of hyperandrogenism or menstrual disturbances and who were not taking hormonal medication nor had had previous oophorectomy or hysterectomy. Hyperprolactinemia, thyroid dysfunction, and nonclassic 21-hydroxylase deficiency were excluded in all of the women who achieved the other criteria for the diagnosis of PCOS.
Statistical analysis
The results are expressed as the mean ± SD in
the text and tables. One-way ANOVA followed by the least significant
difference test were used to compare the means of the different groups
of women. A 
2 test was used for discontinuous
variables. P < 0.05 was considered significant. A
statistical software package was used to perform the analyses (SPSS for
the Macintosh, version 6.1.1, SPSS, Inc., Chicago,
IL).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Thirty-one women were taking oral contraceptive pills, including those 3 patients being treated for hirsutism and another 3 subjects with a hirsutism score of 8 or more who were taking the pill solely as contraceptive. Seventy-nine women did not have hirsutism, acne, or menstrual disturbances; were not receiving hormonal therapy, and had no history of previous hysterectomy or oophorectomy. These women composed the normal population from which the upper control 95th percentile values for androgens were calculated: T, 2.5 nmol/L; FAI, 3.9; and DHEAS, 11.9 µmol/L.
Of the whole population studied, 30 women (19.5%) had a history consistent with oligomenorrhea, and 13 fulfilled the 2 first criteria (oligomenorrhea and evidence of hyperandrogenism) for the diagnosis of PCOS. However, hyperprolactinemia, defined by serum PRL more than 24 µg/L, was present in 3 of these women (serum PRL levels were 26.8, 50.8, and 80.4 µg/L, respectively), and therefore, the diagnosis of PCOS was sustained in only 10 of the 154 subjects studied (6.5%). In 9 of the 10 patients diagnosed with PCOS, serum samples were available. None of these women had 17-OHP levels above 6.0 nmol/L, which is the cut-off level suggested for maximum sensitivity in the detection of nonclassic adrenal hyperplasia using 17-OHP measurements obtained from nonearly morning samples (15). Further, none of these patients had abnormal serum TSH levels, ruling out thyroid dysfunction.
The clinical characteristics of the 10 patients who met all of the
criteria for the diagnosis of PCOS are described in Table 1
. The diagnosis of PCOS was based on the
presence of oligomenorrhea and hirsutism in 4 of the 10 patients.
Hyperandrogenemia was present in 1 of them, who also presented acne;
another patient was taking oral contraceptive pills, and her normal
androgen levels might represent the effect of such treatment on ovarian
function. In another patient, serum androgen levels were not measured.
The diagnosis of PCOS was solely sustained on the basis of
oligomenorrhea and hyperandrogenemia in 4 patients (1 of these women
had acne, but was 18 yr old) and of oligomenorrhea, acne, and
hyperandrogenemia in 2 patients.
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As stated above, of the 11 patients considered to have hirsutism, 4 were diagnosed as having PCOS, 2 subjects had oligomenorrhea and hyperprolactinemia, and 5 had hirsutism with regular menstrual cycles. Of the latter, hyperandrogenemia was present in only 1 woman, but another 3 were taking oral contraceptive pills, which may have lowered their androgen concentrations.
We then compared the clinical data and serum androgen concentrations of the women diagnosed with PCOS with those of 1) the women with hyperandrogenemia and regular menstrual cycles, 2) the women who presented with idiopathic hirsutism and/or acne but did not have oligomenorrhea or hyperandrogenemia, and 3) the women without clinical hyperandrogenism who had normal serum androgen levels, representing the nonhyperandrogenic group. This group of nonhyperandrogenic women did not completely match the group of women used to define the normal ranges for serum androgens. The latter was selected on a clinical basis before knowing the serum androgen concentrations, and therefore, some of these women actually had increased levels of the androgens measured. These subjects were included in the group of women with hyperandrogenemia and regular menstrual cycles for this analysis. Conversely, some women with nonhyperandrogenic oligomenorrhea, who could not be used to define the normal ranges for serum androgens, were included in the group of nonhyperandrogenic women. Because of the profound effects of oral contraceptives on serum androgen and SHBG levels, women taking these medications were excluded from these comparisons. Also, the three patients in whom PCOS was excluded because of hyperprolactinemia were not included in this analysis.
Women with PCOS and women with hyperandrogenemia and regular cycles
were younger than women with idiopathic hirsutism and/or acne without
oligomenorrhea or hyperandrogenemia and nonhyperandrogenic women (Table 2). The higher hirsutism scores were
found in women with PCOS, but as a group, women with idiopathic
hirsutism and/or acne without oligomenorrhea or hyperandrogenemia had
also higher hirsutism scores than nonhyperandrogenic women (Table 2).
There were no differences among the groups in body mass index, waist to
hip ratios, ages at menarche and pubarche, and number of abortions
(Table 2). On the contrary, women with hyperandrogenemia and regular
cycles had fewer pregnancies and infants born than the
nonhyperandrogenic group or the women with idiopathic hirsutism and/or
acne without oligomenorrhea or hyperandrogenemia (Table 2).
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). Serum T concentrations were
also increased in PCOS patients compared to women with idiopathic
hirsutism and/or acne without oligomenorrhea or hyperandrogenemia and
to nonhyperandrogenic women (Table 2). The FAI and serum DHEAS levels
were increased to a similar extent in women with hyperandrogenemia and
regular cycles and in PCOS patients compared to patients with women
with idiopathic hirsutism and/or acne without oligomenorrhea or
hyperandrogenemia and to nonhyperandrogenic women (Table 2). Women with
PCOS had decreased SHBG levels compared to women with idiopathic
hirsutism and/or acne without oligomenorrhea or hyperandrogenemia and
to nonhyperandrogenic women. There were no differences in serum LH,
FSH, E2, and P4 levels
among the groups (Table 2).
Finally, none of the subjects with hyperandrogenic disorders had a
history of carbohydrate intolerance or hypertension (their blood
pressure measurements were normal at the time of the study), but no
further effort was made to diagnose these disorders. Moreover, no
significant differences were found among the groups of subjects in the
proportion of women with family history of diabetes mellitus, arterial
hypertension, or male pattern premature baldness (Table 2).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Using strict NIH/NICHHD criteria, we found a 6.5% prevalence of PCOS in Caucasian women from Madrid, Spain. However, moderate increases in serum PRL levels are frequently found in women with hyperandrogenism and may also result from the stress of blood sampling and from treatment with oral contraceptives. Without excluding the three patients who were considered as not having PCOS because of mild to moderate hyperprolactinemia, the prevalence of PCOS in our series might have been as high as 8.4%.
Our study share many characteristics with that by Knochenhauer et al. (11), allowing direct comparison between their results and our present findings. Considering that all of the women who entered our present study were Caucasian, the size of the sample we studied was similar to the number of White women included in the study from Knochenhauer et al. (11) and was adequate to estimate the prevalence of PCOS as previously discussed (11). Moreover, both studies were designed to minimize bias of the sample population studied.
We prospectively included consecutive female blood donors attending our hospital during a limited period of time. We believe that blood donors are an especially adequate sample of the population for several reasons: 1) they were usually healthy people, not seeking medical care for any reason at the time of the study; 2) as in Spain blood donation is not rewarded in any way, there is no bias derived from the socio-economic background; 3) blood donors have mixed ethnic origins, representing the population where they live; 4) there is no preselection of blood donors, as they come to the hospital without scheduling; and 5) it is easy to obtain blood samples from them. Finally, as in the study from Knochenhauer et al. (11), we defined the normative data for serum androgens from the group of nonhirsute, nonacneic, eumenorrheic women of the study population who were not taking hormonal preparations. On the contrary, as occurred to Knochenhauer et al. (11) in their study, we were not able to control precisely for the time of the day of serum sampling or for the day of the menstrual cycle. However, as elegantly discussed by Knochenhauer et al. (11), none of these factors has been demonstrated to have a significant impact on the clinical value of circulating androgens.
Madrid is representative of the population of Spain, as its present population was conformed during the last 50 yr by immigrants from all areas of the country. All of the women studied here were Caucasian, although it should be noted that the population from Spain has important Jewish and Arabic influences dating back to the Middle Ages, as occurs with most Mediterranean countries.
Minor differences in the design of the study may explain the slightly higher prevalence of PCOS found in Spain (6.5%) compared to White women from Alabama (4.7%). We defined clinical hyperandrogenism by the presence of hirsutism and/or acne, whereas Knochenhauer et al. (11) only considered hirsutism for the diagnosis of PCOS. Although in none of our PCOS patients did the diagnosis rely solely on acne and oligomenorrhea, in the study by Knochenhauer et al. (11), the inclusion of acne as a sign of hyperandrogenism would have increased the prevalence of PCOS in White women to 5.4%. Further, we used less stringent criteria for the definition of oligomenorrhea, which might be responsible for the 1% increase in the prevalence of PCOS in Spain compared to Alabama.
However, we found higher prevalences of hirsutism, as defined by a hirsutism score of 8 or more, and acne in Spanish women (7.1% and 12.3%, respectively) compared to White women from Alabama (2.8% and 5.2%, respectively) (11), suggesting that hyperandrogenic disorders might be more prevalent in Spain. As reviewed by Knochenhauer et al. (11), older studies have reported excess "hairiness" in 5–15% of consecutive Caucasian women (16, 17, 18, 19, 20), and Ferriman and Gallwey (21) found that only 5% of the general population had a hirsutism score of 6 or greater in the original study. The prevalence of hirsutism in our series does not appear to be exaggerated with respect to these previous studies.
As stated above, Diamanti-Kandarakis et al. (12) recently found a 6.8% prevalence of PCOS in the Greek island of Lesbos. However, this study, which in addition to evaluating the prevalence of PCOS was designed to evaluate hormonal and metabolic abnormalities and family history of metabolic disorders in these patients, presented significant methodological differences compared to our present study and that by Knochenhauer et al. (11). First, instead of studying unselected women, the sample of the female population of Lesbos was recruited after a large scale informational campaign offering free medical examination by an endocrinologist (12). Second, the definition of PCOS used by Diamanti-Kandarakis et al. (12) included only women with oligomenorrhea and hyperandrogenemia. If women with clinical hyperandrogenism, normal androgen levels, and oligomenorrhea were also considered to have PCOS, as in our present study and that by Knochenhauer et al. (11), the prevalence would have been 10.4% (12). Moreover, as free T was the only androgen measured, the prevalence of PCOS in Lesbos would have been even higher if other serum androgens were measured.
In addition to women with PCOS, Diamanti-Kandarakis et al. (12) found a 29% prevalence of idiopathic hirsutism in women from Lesbos, an exaggerated figure in view of the prevalences in Madrid, Alabama (11), and elsewhere (16, 17, 18, 19, 20). Taken together with the statement of the authors that their recruitment of patients was not fully randomized (12), these high prevalences of PCOS and hirsutism in Lesbos suggest a selection bias in the studied population.
In our present study, women with PCOS and women with hyperandrogenemia and regular cycles were significantly younger than women with idiopathic hirsutism and/or acne without oligomenorrhea or hyperandrogenemia and than women without evidence of hyperandrogenic disorders. The older woman diagnosed with PCOS was 34 yr old in our series and 29 yr old in that by Knochenhauer et al. (11). Further, a recent study reported that the finding of polycystic ovaries by sonography is also much more common in unselected women 35 yr old or younger (21.6% prevalence) than in women older than 36 yr (7.8% prevalence) (6). In agreement, our previous results in a different series of hirsute patients showed that for a similar severity of hyperandrogenic symptoms, younger patients had higher androgen levels of ovarian and/or adrenal origin than older women (22).
These findings may be derived from the well known decline of adrenal androgens with age (23), but might also indicate that age, possibly reflecting the influence of growth factors on adrenal and ovarian function, modulates the clinical and biochemical expression of hyperandrogenism. Definite proof of this point will require studies specifically designed to address this question. Finally, we did not found any influence of obesity or abdominal distribution of fat on the hyperandrogenic disorders studied here.
In conclusion, we found a 6.5% prevalence of PCOS, as defined by the criteria derived from the NIH/NICHHD-sponsored conference in 1990, in a minimally biased population of Caucasian women from Spain. PCOS and hirsutism are common endocrine disorders in women, especially at younger ages.
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Acknowledgments |
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Footnotes |
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Received September 8, 1999.
Revised January 13, 2000.
Revised March 16, 2000.
Accepted March 19, 2000.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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. Fertil Steril. 62:521–530.[Medline]
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J.-P. Baillargeon, J. E. Nestler, R. E. Ostlund, T. Apridonidze, and E. Diamanti-Kandarakis Greek hyperinsulinemic women, with or without polycystic ovary syndrome, display altered inositols metabolism Hum. Reprod., June 1, 2008; 23(6): 1439 - 1446. [Abstract] [Full Text] [PDF]
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S. Franks, J. Stark, and K. Hardy Follicle dynamics and anovulation in polycystic ovary syndrome Hum. Reprod. Update, May 22, 2008; (2008) dmn015v1. [Abstract] [Full Text] [PDF]
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R. Azziz Polycystic Ovary Syndrome Is a Family Affair J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1579 - 1581. [Full Text] [PDF]
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S. E. Recabarren, R. Smith, R. Rios, M. Maliqueo, B. Echiburu, E. Codner, F. Cassorla, P. Rojas, and T. Sir-Petermann Metabolic Profile in Sons of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1820 - 1826. [Abstract] [Full Text] [PDF]
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M. Mohlig, M. O Weickert, E. Ghadamgahi, A. M Arafat, J. Spranger, A. F H Pfeiffer, and C. Schofl Retinol-binding protein 4 is associated with insulin resistance, but appears unsuited for metabolic screening in women with polycystic ovary syndrome. Eur. J. Endocrinol., April 1, 2008; 158(4): 517 - 523. [Abstract] [Full Text] [PDF]
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M. Corton, J. I. Botella-Carretero, J. A. Lopez, E. Camafeita, J. L. San Millan, H. F. Escobar-Morreale, and B. Peral Proteomic analysis of human omental adipose tissue in the polycystic ovary syndrome using two-dimensional difference gel electrophoresis and mass spectrometry Hum. Reprod., March 1, 2008; 23(3): 651 - 661. [Abstract] [Full Text] [PDF]
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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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H. F. Escobar-Morreale, R. Sanchon, and J. L. San Millan A Prospective Study of the Prevalence of Nonclassical Congenital Adrenal Hyperplasia among Women Presenting with Hyperandrogenic Symptoms and Signs J. Clin. Endocrinol. Metab., February 1, 2008; 93(2): 527 - 533. [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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J. Calaf, E. Lopez, A. Millet, J. Alcaniz, A. Fortuny, O. Vidal, J. Callejo, F. Escobar-Jimenez, E. Torres, J. J. Espinos, et al. Long-Term Efficacy and Tolerability of Flutamide Combined with Oral Contraception in Moderate to Severe Hirsutism: A 12-Month, Double-Blind, Parallel Clinical Trial J. Clin. Endocrinol. Metab., September 1, 2007; 92(9): 3446 - 3452. [Abstract] [Full Text] [PDF]
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 M. Luque-Ramirez, F. Alvarez-Blasco, J. I. Botella-Carretero, R. Sanchon, J. L. San Millan, and H. F. Escobar-Morreale Increased Body Iron Stores of Obese Women With Polycystic Ovary Syndrome Are a Consequence of Insulin Resistance and Hyperinsulinism and Are Not a Result of Reduced Menstrual Losses Diabetes Care, September 1, 2007; 30(9): 2309 - 2313. [Abstract] [Full Text] [PDF]
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M. Mohlig, M. O Weickert, E. Ghadamgadai, A. Machlitt, B. Pfuller, A. M Arafat, A. F H Pfeiffer, and C. Schofl Adipocyte fatty acid-binding protein is associated with markers of obesity, but is an unlikely link between obesity, insulin resistance, and hyperandrogenism in polycystic ovary syndrome women Eur. J. Endocrinol., August 1, 2007; 157(2): 195 - 200. [Abstract] [Full Text] [PDF]
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M. Luque-Ramirez, F. Alvarez-Blasco, J. I. Botella-Carretero, E. Martinez-Bermejo, M. A. Lasuncion, and H. F. Escobar-Morreale Comparison of Ethinyl-Estradiol Plus Cyproterone Acetate Versus Metformin Effects on Classic Metabolic Cardiovascular Risk Factors in Women with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2453 - 2461. [Abstract] [Full Text] [PDF]
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T. Sir-Petermann, B. Echiburu, M M. Maliqueo, N. Crisosto, F. Sanchez, C. Hitschfeld, M. Carcamo, P. Amigo, and F. Perez-Bravo Serum adiponectin and lipid concentrations in pregnant women with polycystic ovary syndrome Hum. Reprod., July 1, 2007; 22(7): 1830 - 1836. [Abstract] [Full Text] [PDF]
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M. 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]
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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]
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K.-M. Seow, C.-C. Juan, Y.-P. Hsu, J.-L. Hwang, L.-W. Huang, and L.-T. Ho Amelioration of insulin resistance in women with PCOS via reduced insulin receptor substrate-1 Ser312 phosphorylation following laparoscopic ovarian electrocautery Hum. Reprod., April 1, 2007; 22(4): 1003 - 1010. [Abstract] [Full Text] [PDF]
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 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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B. Banaszewska, L. Pawelczyk, R. Z. Spaczynski, J. Dziura, and A. J. Duleba Effects of Simvastatin and Oral Contraceptive Agent on Polycystic Ovary Syndrome: Prospective, Randomized, Crossover Trial J. Clin. Endocrinol. Metab., February 1, 2007; 92(2): 456 - 461. [Abstract] [Full Text] [PDF]
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S.A. Amer, S. Laird, W.L. Ledger, and T.C. Li Effect of laparoscopic ovarian diathermy on circulating inhibin B in women with anovulatory polycystic ovary syndrome Hum. Reprod., February 1, 2007; 22(2): 389 - 394. [Abstract] [Full Text] [PDF]
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C. Hughes, M. Elgasim, R. Layfield, and W. Atiomo Genomic and post-genomic approaches to polycystic ovary syndrome--progress so far: Mini Review Hum. Reprod., November 1, 2006; 21(11): 2766 - 2775. [Abstract] [Full Text] [PDF]
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 F. Alvarez-Blasco, J. I. Botella-Carretero, J. L. San Millan, and H. F. Escobar-Morreale Prevalence and characteristics of the polycystic ovary syndrome in overweight and obese women. Arch Intern Med, October 23, 2006; 166(19): 2081 - 2086. [Abstract] [Full Text] [PDF]
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E. Elia, V. Sander, C.G. Luchetti, M.E. Solano, G. Di Girolamo, C. Gonzalez, and A.B. Motta The mechanisms involved in the action of metformin in regulating ovarian function in hyperandrogenized mice Mol. Hum. Reprod., August 1, 2006; 12(8): 475 - 481. [Abstract] [Full Text] [PDF]
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 M. M. Kushnir, A. L. Rockwood, W. L. Roberts, E. G. Pattison, W. E. Owen, A. M. Bunker, and A. W. Meikle Development and Performance Evaluation of a Tandem Mass Spectrometry Assay for 4 Adrenal Steroids Clin. Chem., August 1, 2006; 52(8): 1559 - 1567. [Abstract] [Full Text] [PDF]
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 M. J. Himelein and S. S. Thatcher Depression and Body Image among Women with Polycystic Ovary Syndrome J Health Psychol, July 1, 2006; 11(4): 613 - 625. [Abstract] [PDF]
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S.K. Blank, C.R. McCartney, and J.C. Marshall The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome Hum. Reprod. Update, July 1, 2006; 12(4): 351 - 361. [Abstract] [Full Text] [PDF]
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S. Hahn, S. Benson, S. Elsenbruch, K. Pleger, S. Tan, K. Mann, M. Schedlowski, W. B. van Halteren, R. Kimmig, and O. E. Janssen Metformin treatment of polycystic ovary syndrome improves health-related quality-of-life, emotional distress and sexuality Hum. Reprod., July 1, 2006; 21(7): 1925 - 1934. [Abstract] [Full Text] [PDF]
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E. Codner, N. Soto, P. Lopez, L. Trejo, A. Avila, F. C. Eyzaguirre, G. Iniguez, and F. Cassorla Diagnostic Criteria for Polycystic Ovary Syndrome and Ovarian Morphology in Women with Type 1 Diabetes Mellitus J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2250 - 2256. [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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L. Ibanez and F. de Zegher Low-dose flutamide-metformin therapy for hyperinsulinemic hyperandrogenism in non-obese adolescents and women Hum. Reprod. Update, May 1, 2006; 12(3): 243 - 252. [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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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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A. Gonzalez, M.E. Saez, M.J. Aragon, J.J. Galan, P. Vettori, L. Molina, C. Rubio, L.M. Real, A. Ruiz, and R. Ramirez-Lorca Specific haplotypes of the CALPAIN-5 gene are associated with polycystic ovary syndrome Hum. Reprod., April 1, 2006; 21(4): 943 - 951. [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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V. Sander, C. G. Luchetti, M. E. Solano, E. Elia, G. Di Girolamo, C. Gonzalez, and A. B. Motta Role of the N, N'-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone. Reproduction, March 1, 2006; 131(3): 591 - 602. [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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S. Hahn, U. Haselhorst, B. Quadbeck, S. Tan, R. Kimmig, K. Mann, and O. E Janssen Decreased soluble leptin receptor levels in women with polycystic ovary syndrome Eur. J. Endocrinol., February 1, 2006; 154(2): 287 - 294. [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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L. Ibanez, C. Valls, and F. de Zegher Discontinuous low-dose flutamide-metformin plus an oral or a transdermal contraceptive in patients with hyperinsulinaemic hyperandrogenism: normalizing effects on CRP, TNF-{alpha} and the neutrophil/lymphocyte ratio Hum. Reprod., February 1, 2006; 21(2): 451 - 456. [Abstract] [Full Text] [PDF]
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H. F. Escobar-Morreale, J. I. Botella-Carretero, F. Alvarez-Blasco, J. Sancho, and J. L. San Millan The Polycystic Ovary Syndrome Associated with Morbid Obesity May Resolve after Weight Loss Induced by Bariatric Surgery J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6364 - 6369. [Abstract] [Full Text] [PDF]
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R. Zhou, I. M. Bird, D. A. Dumesic, and D. H. Abbott Adrenal Hyperandrogenism Is Induced by Fetal Androgen Excess in a Rhesus Monkey Model of Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6630 - 6637. [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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G. Villuendas, J. I. Botella-Carretero, B. Roldan, J. Sancho, H. F. Escobar-Morreale, and J. L. S. Millan Polymorphisms in the insulin receptor substrate-1 (IRS-1) gene and the insulin receptor substrate-2 (IRS-2) gene influence glucose homeostasis and body mass index in women with polycystic ovary syndrome and non-hyperandrogenic controls Hum. Reprod., November 1, 2005; 20(11): 3184 - 3191. [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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L. Ibanez, A. M. Jaramillo, A. Ferrer, and F. de Zegher High neutrophil count in girls and women with hyperinsulinaemic hyperandrogenism: normalization with metformin and flutamide overcomes the aggravation by oral contraception Hum. Reprod., September 1, 2005; 20(9): 2457 - 2462. [Abstract] [Full Text] [PDF]
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S. Sam, R. S. Legro, R. Bentley-Lewis, and A. Dunaif Dyslipidemia and Metabolic Syndrome in the Sisters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4797 - 4802. [Abstract] [Full Text] [PDF]
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R. Azziz, C. Marin, L. Hoq, E. Badamgarav, and P. Song Health Care-Related Economic Burden of the Polycystic Ovary Syndrome during the Reproductive Life Span J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4650 - 4658. [Abstract] [Full Text] [PDF]
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D.H. Abbott, D.K. Barnett, C.M. Bruns, and D.A. Dumesic Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome? Hum. Reprod. Update, July 1, 2005; 11(4): 357 - 374. [Abstract] [Full Text] [PDF]
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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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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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