| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Division of Reproductive Medicine (J.S.E.L., A.G.M.G.J.M., B.C.J.M.F.), Department of Obstetrics and Gynecology, Erasmus Medical Center, Rotterdam, The Netherlands; and Section of Endocrinology (J.A.V., A.P.T., F.H.D.J.), Department of Internal Medicine, Erasmus Medical Center Rotterdam, Rotterdam, The Netherlands
Address all correspondence and requests for reprints to: J. S. E. Laven, M.D., Ph.D., Division of Reproductive Medicine, Department of Obstetrics and Gynecology, Erasmus Medical Center, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. E-mail: j.laven{at}erasmusmc.nl.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Serum AMH concentrations are significantly (P < 0.001) elevated in WHO 2 patients [median, 7.6 µg/liter (range, 0.1–40.0)], compared with controls [median, 2.1 µg/liter (0.1–7.4)]. In 106 patients presenting with polycystic ovaries (PCOs) (
12 follicles/ovary measuring 2–9 mm and/or an ovarian volume > 10 ml), AMH levels were elevated [9.3 µg/liter (1.8–40.0)], compared with 22 patients without PCOs [6.4 µg/liter (0.1–22.1)] (P < 0.0001). In WHO 2 patients, AMH concentrations correlated with features characteristic for polycystic ovary syndrome such as LH concentrations (r = 0.331; P = 0.0001), testosterone levels (r = 0.477, P = 0.0001), mean ovarian volume (r = 0.421; P = 0.0001), and the number of ovarian follicles (r = 0.308; P = 0.0001). AMH levels correlated well with age in WHO 2 patients (r = -0.248; P = 0.002) as well as in controls (r = -0.465; P = 0.005). However, the relative decline in AMH with age is less pronounced in WHO 2 patients. In a subset of patients no significant correlation was found between AMH serum concentrations and the FSH response dose, the duration of stimulation, and the total number of ampoules of FSH used.
In conclusion, serum AMH concentrations are elevated in WHO 2 women, especially in those patients exhibiting PCOs. Because AMH concentrations correlated well with other clinical, endocrine, and ultrasound markers associated with polycystic ovary syndrome, AMH may be used as a marker for the extent of the disease. A less pronounced AMH decrease over time in these women may suggest retarded ovarian aging. The latter hypothesis, however, should be confirmed by longitudinal studies.
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Female AMH null mice were reported to be fertile and produced normal-sized litters (5). However, ovaries of AMH null mice as well as female mice heterozygous for the AMH null mutation contained less primordial follicles and more growing follicles, compared with their wild-type littermates (6). In addition, AMH was able to inhibit the initiation of primordial follicle growth in cultured neonatal mouse ovaries (6) and stimulate growth of rat preantral follicles (7). Hence, AMH appears to regulate early follicle development directly. Furthermore, the absence of AMH has been shown to enhance FSH-induced follicle growth in female mice (8).
Recently serum AMH levels have been shown to decrease over time in young normoovulatory women, whereas other markers associated with ovarian aging did not change during this time interval (9). Although AMH concentrations did correlate with age and FSH, AMH serum levels were most strongly associated with the number of antral follicles. Therefore, AMH might represent a sensitive marker for ovarian aging (10). Indeed, it has been shown that poor response during in vitro fertilization, indicative of a diminished ovarian reserve (11), is associated with reduced baseline serum AMH concentrations (12, 13).
Chronic anovulation constitutes a major (20–25%) proportion of infertile couples (14, 15). According to the World Health Organization (WHO), approximately 80% of patients suffering from chronic anovulation present with serum FSH levels within the normal range along with normal endogenous estrogen activity. These women are classified as having normogonadotropic normoestrogenic anovulatory infertility, more commonly referred to as WHO class 2 (16). Because etiologic factors underlying this condition may vary from one patient to another, WHO 2 anovulatory women including those with polycystic ovary syndrome (PCOS) constitute a notoriously heterogeneous population (17). In WHO 2 patients, the number of small antral follicles is generally increased due to disturbed dominant follicle selection (18). Because AMH is predominantly expressed by small follicles in mice (4) as well as in the human (19), AMH serum concentrations may be increased in patients with polycystic ovaries (PCOs). Indeed, in PCOS patients exhibiting the classical features of the syndrome, AMH levels were found to be elevated, compared with normal controls (20). The current study was designed to evaluate AMH as a clinically relevant marker for the extent of ovarian dysfunction in WHO 2 anovulatory women, with or without PCOs.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
The local Medical Ethics Review Committee approved this study, and informed consent was obtained from all participants. Included in the present study were 128 patients attending our fertility clinic between 1994 and 1999 with the following: 1) infertility; 2) oligomenorrhea (interval between periods >35 d) or amenorrhea (absence of vaginal bleeding for at least 6 months); 3) serum FSH concentrations within normal limits (1–10 IU/liter) (21); 4) positive withdrawal bleeding after progestogen administration in case of amenorrhea; and 5) age between 19 and 41 yr. Standardized initial screening [clinical investigation, transvaginal ultrasound, and fasting blood withdrawal] was performed on a random day between 0900 and 1100 h, irrespective of the interval between blood sampling and the preceding bleeding, as previously described (22). A subgroup of these patients was diagnosed with PCOS due to hyperandrogenemia and an increased follicle number and/or ovarian volume. Hyperandrogenemia was defined as an elevated (>4.5) free androgen index (testosterone x 100/ SHBG). Similarly, an increased follicle number was defined as 12 follicles or more per ovary measuring 2–9 mm, and the ovarian volume was considered to be increased above 10 ml (15).
For sonographic imaging, we used a 6.5 MHz vaginal transducer (model EUB-415, Hitachi Medical Corp., Tokyo, Japan). The ovaries were localized and scanned as described previously (23). Ovarian volume, stroma echogenicity (arbitrarily scored from 1 to 3 per ovary), and the mean follicle number were assessed as described earlier (15). Women exhibiting PCOs had either an increased ovarian volume (>10 ml) or an increased number of follicles (12 follicles measuring 2–9 mm in at least one ovary).
The control group consisted of 41 healthy volunteers selected by advertisement and paid for participation as previously published (21). Inclusion criteria were a regular menstrual cycle (26–30 d), age of 20–36 yr, normal body mass index (18–25 kg/m2), and no previous use of medication or oral contraceptives during at least 3 months before the study. Transvaginal ultrasound and blood sampling was performed during the early follicular phase (cycle d 3, 4, or 5).
Ovulation induction treatment
In a subgroup of WHO 2 women (those who failed to ovulate or conceive after clomiphene citrate treatment), gonadotropin treatment was commenced within 3–5 d after initiation of a spontaneous or progestogen-induced withdrawal bleeding. Patients received daily sc injections of recombinant FSH (Gonal-F, Ares-Serono, Geneva, Switzerland). During all first cycles, a low-dose step-up protocol was used with a starting dose of FSH of one ampoule (75 IU) per day. The daily dose was increased by 
ampoule if ovarian response (at least one follicle of at least 10 mm) was absent after 14 d. Thereafter the dose was increased by ampoule every 7 d if required. The FSH response dose was defined as the dose at which an ovarian response was observed (24). In case a sufficient ovarian response was observed, the dose was kept constant until administration of 5000 IU human chorionic gonadotropin (Profasi, Ares-Serono).
Hormone assays
Blood samples were obtained by venepuncture and processed within 2 h after withdrawal. Serum was stored at -20 C and assayed for AMH, LH, FSH, androstenedione (AD), testosterone (T), SHBG, inhibin B, and estradiol (E2). Serum AMH levels were assessed using an ultrasensitive immunoenzymometric assay (Immunotech-Coulter, Marseilles, France), as described elsewhere (9). The limit of detection (defined as blank +3 SD of the blank) amounted to 0.05 µg/liter. For quality control, samples of pooled serum with high and low levels of AMH were assayed in all separate assays. Intra- and interassay coefficients of variation were less then 5% and 8%, respectively.
Serum levels of LH, FSH, and SHBG were measured using luminescence-based immunoassays (Immulite, Diagnostic Products Corp., Los Angeles, CA), whereas serum E2, T, and AD levels were measured using coated-tube RIAs provided by the same supplier. Intra- and interassay coefficients of variation were less than 5% and 15% for LH, less than 3% and 8% for FSH, less than 8% and 11% for AD, less than 3% and 5% for T, less than 5% and 7% for E2, and less than 4% and 5% for SHBG, respectively.
Dimeric inhibin B levels were assessed using an immunoenzymometric assay obtained from Serotec (Oxford, UK), as described previously (21). The detection limit of the assay, defined as the amount of inhibin equivalent with the signal of the blank +3 SDs of this signal, was 3.4 ng/liter. Intra- and interassay coefficients of variation for inhibin B were less than 9% and 15%, respectively.
Data analysis
Statistical analysis was performed using a commercially available software package (SPSS, SPSS Inc., Chicago, IL). Data were analyzed for normal distribution. Data are presented as the mean ± SD if distributed normally or otherwise as the median and range. To determine differences between groups, Mann-Whitney U or Kruskal-Wallis tests were used if data were not normally distributed. In case data were normally distributed, Student’s t test or ANOVA was used. Correlations were expressed as Spearman’s correlation coefficients. Regression statistics were applied to assess the differences in decline of parameters in time. P 
0.05 was considered to be statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
. Briefly, patients were comparable with control subjects as far as age was concerned. Endocrine parameters in control subjects were all well within the normal range for regularly cycling women. Similarly ultrasound scans revealed normal follicle counts in both ovaries in these volunteers.
|
AMH levels were significantly (P < 0.001) different between controls (median 2.1 µg/liter; range, 0.1–7.1 µg/liter) and WHO 2 patients (median 7.6 µg/liter; range 0.1–40.0 µg/liter). When WHO 2 women were categorized into those with and without PCOs (12 follicles measuring between 2 and 9 mm and/or ovarian volume >10 ml), AMH levels were significantly higher (9.3 µg/liter; range 1.8–40.0 µg/liter) in PCO patients, compared with non-PCO (6.4 µg/liter; range 0.1–22.1 µg/liter; P < 0.001) and controls (2.1 µg/liter; range 0.1–7.1 µg/liter; P < 0.001) (Fig. 1).
|
).
|
).
|
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
On histological examination it has been shown that PCOs exhibit the same number of primordial follicles, whereas the number of developing and subsequent atretic follicles was doubled, compared with normoovulatory controls (25). Despite the increased number of developing follicles, inhibin B serum levels (a marker for small developing follicles) were normal in WHO 2 patients, suggesting an increased number of atretic follicles (26). It appears that follicle development is arrested in PCOS at the stage in which dominant follicle selection occurs under normal conditions (27, 28, 29, 30). Follicle maturation arrest during later stages of development may lead to a build up of many immature follicles, which in itself could explain increased AMH levels. Hence, it might be anticipated that the increased number of follicles, which are generally present in PCOs, are the source of increased AMH production (20).
Because AMH constitutes a marker for the number of small follicles, its correlation with ovarian volume and the number of follicles present in the ovary, is not surprising. PCOs as observed during ultrasound constitute a sensitive marker for the extent of ovarian dysfunction in anovulatory women as well as for ovulation induction outcome (31, 32). Although AMH serum levels were the highest in anovulatory patients with prominent PCOs, women without PCOs also exhibited elevated levels. In the female, AMH is solely synthesized by granulosa cells of preantral and small antral follicles (4). Apparently, smaller follicles, which are not readily detected on ultrasound, do significantly contribute to serum AMH levels. Therefore, AMH might even constitute a more sensitive marker of ovarian dysfunction in WHO 2 patients than PCO on ultrasound. Indeed, AMH serum levels correlated well with other parameters indicative for the extent of ovarian dysfunction such as elevated LH and T concentrations.
Unfortunately, AMH serum concentrations were not significantly correlated with outcome parameters of ovulation induction using gonadotropins in those women who previously failed clomiphene citrate ovulation induction. Similarly, pregnancy rates and miscarriage rates were similar in patients with moderately and severely elevated AMH serum levels. Hence, elevated AMH serum levels are not associated with adverse treatment outcome, indicating a limited predictive power of AMH levels in these patients. It seems therefore that the clinical relevance of AMH serum concentrations is limited in women in whom clomiphene citrate ovulation induction previously failed.
In PCOS patients, aromatase activity may be decreased because follicles from PCOs do not produce large amounts of E2. It has been shown that follicular fluid has a potent inhibitory effect on E2 production in PCOS (33, 34). This follicular fluid-derived inhibitor decreases aromatase activity by suppressing the P450 aromatase mRNA expression in follicles of PCOS patients (35). Because AMH serum concentrations do correlate with serum levels of T, AD, and SHBG and only weakly with E2 concentrations, it might be speculated that AMH might constitute this follicular fluid-derived inhibitory factor. Indeed, exogenous AMH did inhibit the biosynthesis of aromatase in cultured rat granulosa cells (36). Moreover, in PCOS women an inverse relationship between E2 and AMH serum levels has been previously established (20).
A surprising finding constitutes the difference in relative decline in AMH serum levels with increasing age between normal controls and WHO 2 patients, suggesting that the latter group might reach menopause later in life. Because AMH levels correlate with the number of early antral follicles, which might in turn represent the size of the resting pool of follicles, AMH may constitute a marker for ovarian aging (9, 13). Hence, increased intraovarian AMH production in PCOs may slow down the process of primordial follicle recruitment and thus retard depletion of the primordial follicle pool. Although it has been reported that cycle irregularities and hormonal profiles improve with increasing age (37, 38, 39), data regarding the age of menopause in these women are lacking. However, menopausal age in these women is difficult to establish because most of them will regulate their cycles up to advanced age using oral contraceptive pills. Whether AMH can be used as a reliable marker in PCOS should be further substantiated. Moreover, the challenging concept of retarded ovarian aging in PCOS needs further confirmation by properly designed longitudinal follow-up studies.
In conclusion, serum AMH concentrations are elevated in WHO 2 women, which appears to be related to the increased number of small preantral and early antral follicles, especially in those patients exhibiting PCOs. Because AMH concentrations correlated well with other clinical, endocrine, and ultrasound parameters indicative of ovarian dysfunction in these patients, AMH may constitute a novel marker for the extent of the disease. Elevated AMH serum levels in WHO 2 and especially PCOS patients might indicate an increased ovarian reserve.
|
Footnotes |
|---|
Abbreviations: AD, Androstenedione; AMH, anti-Müllerian hormone; E2, estradiol; PCO, polycystic ovary; PCOS, PCO syndrome; T, testosterone.
Received May 28, 2003.
Accepted October 14, 2003.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
 |
|
 |
|
  R. Homburg Androgen circle of polycystic ovary syndrome Hum. Reprod., July 1, 2009; 24(7): 1548 - 1555. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.M. Carlsen, E. Vanky, and R. Fleming Anti-Mullerian hormone concentrations in androgen-suppressed women with polycystic ovary syndrome Hum. Reprod., July 1, 2009; 24(7): 1732 - 1738. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. La Marca, F.J. Broekmans, A. Volpe, B.C. Fauser, N.S. Macklon, and on behalf of the ESHRE Special Interest Group for Anti-Mullerian hormone (AMH): what do we still need to know? Hum. Reprod., June 11, 2009; (2009) dep210v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Diamanti-Kandarakis, A. Piouka, S. Livadas, C. Piperi, I. Katsikis, A. G Papavassiliou, and D. Panidis Anti-mullerian hormone is associated with advanced glycosylated end products in lean women with polycystic ovary syndrome Eur. J. Endocrinol., May 1, 2009; 160(5): 847 - 853. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R.L. Thomson, J.D. Buckley, L.J. Moran, M. Noakes, P.M. Clifton, R.J. Norman, and G.D. Brinkworth The effect of weight loss on anti-Mullerian hormone levels in overweight and obese women with polycystic ovary syndrome and reproductive impairment Hum. Reprod., April 20, 2009; (2009) dep101v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. H. Knauff, M. J. C. Eijkemans, C. B. Lambalk, M. J. ten Kate-Booij, A. Hoek, C. C. M. Beerendonk, J. S. E. Laven, A. J. Goverde, F. J. M. Broekmans, A. P. N. Themmen, et al. Anti-Mullerian Hormone, Inhibin B, and Antral Follicle Count in Young Women with Ovarian Failure J. Clin. Endocrinol. Metab., March 1, 2009; 94(3): 786 - 792. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Kevenaar, A. P.N. Themmen, A. J. van Kerkwijk, O. Valkenburg, A. G. Uitterlinden, F. H. de Jong, J. S.E. Laven, and J. A. Visser Variants in the ACVR1 gene are associated with AMH levels in women with polycystic ovary syndrome Hum. Reprod., January 1, 2009; 24(1): 241 - 249. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Rico, S. Fabre, C. Medigue, N. d. Clemente, F. Clement, M. Bontoux, J.-L. Touze, M. Dupont, E. Briant, B. Remy, et al. Anti-Mullerian Hormone Is an Endocrine Marker of Ovarian Gonadotropin-Responsive Follicles and Can Help to Predict Superovulatory Responses in the Cow Biol Reprod, January 1, 2009; 80(1): 50 - 59. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Catteau-Jonard, S. P. Jamin, A. Leclerc, J. Gonzales, D. Dewailly, and N. di Clemente Anti-Mullerian Hormone, Its Receptor, FSH Receptor, and Androgen Receptor Genes Are Overexpressed by Granulosa Cells from Stimulated Follicles in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., November 1, 2008; 93(11): 4456 - 4461. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Das, D.J. Gillott, E. Saridogan, and O. Djahanbakhch Anti-Mullerian hormone is increased in follicular fluid from unstimulated ovaries in women with polycystic ovary syndrome Hum. Reprod., September 1, 2008; 23(9): 2122 - 2126. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A I Qureshi, S S Nussey, G Bano, P Musonda, S A Whitehead, and H D Mason Testosterone selectively increases primary follicles in ovarian cortex grafted onto embryonic chick membranes: relevance to polycystic ovaries Reproduction, August 1, 2008; 136(2): 187 - 194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
M. E. Kevenaar, J. S. E. Laven, S. L. Fong, A. G. Uitterlinden, F. H. de Jong, A. P. N. Themmen, and J. A. Visser A Functional Anti-Mullerian Hormone Gene Polymorphism Is Associated with Follicle Number and Androgen Levels in Polycystic Ovary Syndrome Patients J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1310 - 1316. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Codner, G. Iniguez, C. Villarroel, P. Lopez, N. Soto, T. Sir-Petermann, F. Cassorla, and R. A. Rey Hormonal Profile in Women with Polycystic Ovarian Syndrome with or without Type 1 Diabetes Mellitus J. Clin. Endocrinol. Metab., December 1, 2007; 92(12): 4742 - 4746. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Arbo, D.V. Vetori, M.F. Jimenez, F.M. Freitas, N. Lemos, and J.S. Cunha-Filho Serum anti-mullerian hormone levels and follicular cohort characteristics after pituitary suppression in the late luteal phase with oral contraceptive pills Hum. Reprod., December 1, 2007; 22(12): 3192 - 3196. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Catteau-Jonard, P. Pigny, A.-C. Reyss, C. Decanter, E. Poncelet, and D. Dewailly Changes in Serum Anti-Mullerian Hormone Level during Low-Dose Recombinant Follicular-Stimulating Hormone Therapy for Anovulation in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4138 - 4143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. van Beek, M. M. van den Heuvel-Eibrink, J. S. E. Laven, F. H. de Jong, A. P. N. Themmen, F. G. Hakvoort-Cammel, C. van den Bos, H. van den Berg, R. Pieters, and S. M. P. F. de Muinck Keizer-Schrama Anti-Mullerian Hormone Is a Sensitive Serum Marker for Gonadal Function in Women Treated for Hodgkin's Lymphoma during Childhood J. Clin. Endocrinol. Metab., October 1, 2007; 92(10): 3869 - 3874. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Nelson, R. W. Yates, and R. Fleming Serum anti-Mullerian hormone and FSH: prediction of live birth and extremes of response in stimulated cycles implications for individualization of therapy Hum. Reprod., September 1, 2007; 22(9): 2414 - 2421. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Crisosto, E. Codner, M. Maliqueo, B. Echiburu, F. Sanchez, F. Cassorla, and T. Sir-Petermann Anti-Mullerian Hormone Levels in Peripubertal Daughters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2739 - 2743. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Kevenaar, A. P.N. Themmen, J. S.E. Laven, B. Sonntag, S. L. Fong, A. G. Uitterlinden, F. H. de Jong, H. A.P. Pols, M. Simoni, and J. A. Visser Anti-Mullerian hormone and anti-Mullerian hormone type II receptor polymorphisms are associated with follicular phase estradiol levels in normo-ovulatory women Hum. Reprod., June 1, 2007; 22(6): 1547 - 1554. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Dewailly, S. Catteau-Jonard, A.-C. Reyss, C. Maunoury-Lefebvre, E. Poncelet, and P. Pigny The excess in 2-5 mm follicles seen at ovarian ultrasonography is tightly associated to the follicular arrest of the polycystic ovary syndrome Hum. Reprod., June 1, 2007; 22(6): 1562 - 1566. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. S. Wachs, M. S. Coffler, P. J. Malcom, and R. J. Chang Serum Anti-Mullerian Hormone Concentrations Are Not Altered by Acute Administration of Follicle Stimulating Hormone in Polycystic Ovary Syndrome and Normal Women J. Clin. Endocrinol. Metab., May 1, 2007; 92(5): 1871 - 1874. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Visser, A. L. L. Durlinger, I. J. J. Peters, E. R. van den Heuvel, U. M. Rose, P. Kramer, F. H. de Jong, and A. P. N. Themmen Increased Oocyte Degeneration and Follicular Atresia during the Estrous Cycle in Anti-Mullerian Hormone Null Mice Endocrinology, May 1, 2007; 148(5): 2301 - 2308. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Pellatt, L. Hanna, M. Brincat, R. Galea, H. Brain, S. Whitehead, and H. Mason Granulosa Cell Production of Anti-Mullerian Hormone Is Increased in Polycystic Ovaries J. Clin. Endocrinol. Metab., January 1, 2007; 92(1): 240 - 245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Meduri, N. Massin, J. Guibourdenche, A. Bachelot, O. Fiori, F. Kuttenn, M. Misrahi, and P. Touraine Serum anti-Mullerian hormone expression in women with premature ovarian failure Hum. Reprod., January 1, 2007; 22(1): 117 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Maheshwari, P. Fowler, and S. Bhattacharya Assessment of ovarian reserve--should we perform tests of ovarian reserve routinely? Hum. Reprod., November 1, 2006; 21(11): 2729 - 2735. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Al-Qahtani and N. P. Groome Anti-Mullerian Hormone: Cinderella Finds New Admirers. J. Clin. Endocrinol. Metab., October 1, 2006; 91(10): 3760 - 3762. [Full Text] [PDF]
|
|
|
|
|
|
C. Y. Andersen and A. G. Byskov Estradiol and Regulation of Anti-Mullerian Hormone, Inhibin-A, and Inhibin-B Secretion: Analysis of Small Antral and Preovulatory Human Follicles' Fluid J. Clin. Endocrinol. Metab., October 1, 2006; 91(10): 4064 - 4069. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Sir-Petermann, E. Codner, M. Maliqueo, B. Echiburu, C. Hitschfeld, N. Crisosto, F. Perez-Bravo, S. E. Recabarren, and F. Cassorla Increased Anti-Mullerian Hormone Serum Concentrations in Prepubertal Daughters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2006; 91(8): 3105 - 3109. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Fleming, N. Deshpande, I. Traynor, and R.W.S. Yates Dynamics of FSH-induced follicular growth in subfertile women: relationship with age, insulin resistance, oocyte yield and anti-Mullerian hormone Hum. Reprod., June 1, 2006; 21(6): 1436 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Pigny, S. Jonard, Y. Robert, and D. Dewailly Serum Anti-Mullerian Hormone as a Surrogate for Antral Follicle Count for Definition of the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 941 - 945. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A Visser, F. H de Jong, J. S E Laven, and A. P N Themmen Anti-Mullerian hormone: a new marker for ovarian function Reproduction, January 1, 2006; 131(1): 1 - 9. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
S. A. Stubbs, K. Hardy, P. Da Silva-Buttkus, J. Stark, L. J. Webber, A. M. Flanagan, A. P. N. Themmen, J. A. Visser, N. P. Groome, and S. Franks Anti-Mullerian Hormone Protein Expression Is Reduced during the Initial Stages of Follicle Development in Human Polycystic Ovaries J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5536 - 5543. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Eldar-Geva, E. J. Margalioth, M. Gal, A. Ben-Chetrit, N. Algur, E. Zylber-Haran, B. Brooks, M. Huerta, and I. M. Spitz Serum anti-Mullerian hormone levels during controlled ovarian hyperstimulation in women with polycystic ovaries with and without hyperandrogenism Hum. Reprod., July 1, 2005; 20(7): 1814 - 1819. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Piltonen, L. Morin-Papunen, R. Koivunen, A. Perheentupa, A. Ruokonen, and J. S. Tapanainen Serum anti-Mullerian hormone levels remain high until late reproductive age and decrease during metformin therapy in women with polycystic ovary syndrome Hum. Reprod., July 1, 2005; 20(7): 1820 - 1826. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. La Marca, S. Giulini, R. Orvieto, V. De Leo, and A. Volpe Anti-Mullerian hormone concentrations in maternal serum during pregnancy Hum. Reprod., June 1, 2005; 20(6): 1569 - 1572. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Lutchman Singh, M. Davies, and R. Chatterjee Fertility in female cancer survivors: pathophysiology, preservation and the role of ovarian reserve testing Hum. Reprod. Update, January 1, 2005; 11(1): 69 - 89. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Oppelt, P.L. Strissel, A. Kellermann, S. Seeber, A. Humeny, M.W. Beckmann, and R. Strick DNA sequence variations of the entire anti-Mullerian hormone (AMH) gene promoter and AMH protein expression in patients with the Mayer-Rokitanski-Kuster-Hauser syndrome Hum. Reprod., January 1, 2005; 20(1): 149 - 157. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Jansen, J. S. E. Laven, H. B. R. Dommerholt, J. Polman, C. van Rijt, C. van den Hurk, J. Westland, S. Mosselman, and B. C. J. M. Fauser Abnormal Gene Expression Profiles in Human Ovaries from Polycystic Ovary Syndrome Patients Mol. Endocrinol., December 1, 2004; 18(12): 3050 - 3063. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Nikolaou and C. Gilling-Smith Early ovarian ageing: are women with polycystic ovaries protected? Hum. Reprod., October 1, 2004; 19(10): 2175 - 2179. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. G.M.G.J. Mulders, J. S.E. Laven, M. J.C. Eijkemans, F. H. de Jong, A. P.N. Themmen, and B. C.J.M. Fauser Changes in anti-Mullerian hormone serum concentrations over time suggest delayed ovarian ageing in normogonadotrophic anovulatory infertility Hum. Reprod., September 1, 2004; 19(9): 2036 - 2042. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Jonard and D. Dewailly The follicular excess in polycystic ovaries, due to intra-ovarian hyperandrogenism, may be the main culprit for the follicular arrest Hum. Reprod. Update, March 1, 2004; 10(2): 107 - 117. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
