|Year : 2017 | Volume
| Issue : 2 | Page : 66-72
The role of anti-mullerian hormone as an indicator of reproductive health in women with obesity and concomitant polycystic ovary syndrome
Moharram A Abdel Hay1, Seham A El-Berri1, Tarek E Sleem2, Mohammed I Mohammed1, Salwa T Nour El-Deen3
1 Department of Obstetrics and Gynecology, Benha Faculty of Medicine. Benha University, Benha, Egypt
2 Department of Clinical Pathology, Mansoura Faculty of Medicine, Mansoura University, Mansoura, Egypt
3 Ministry of Health and Populations, Egypt
|Date of Submission||24-Jan-2017|
|Date of Acceptance||16-Mar-2017|
|Date of Web Publication||20-Nov-2017|
Salwa T Nour El-Deen
Source of Support: None, Conflict of Interest: None
Background Obesity has harmful effects on the female reproductive system. Anti-Mullerian hormone (AMH) is considered to reflect the extent of follicular growth and the reservoir of ovarian function. The relation between AMH and obesity was not fully investigated in polycystic ovary syndrome (PCOS).
Aim The aim of this study was to evaluate the relation between AMH and antral follicular count (AFC) and BMI in patients with PCOS, and the relation between AMH, AFC, and site.
Patients and methods The study included 200 patients with the diagnosis of PCOS. The patients included in the study were divided into four equal groups according to BMI: group A included individuals with average body weight; group B included individuals with BMI between 25 and 30 (overweight); group C included individuals with BMI between 30 and 35 (mild obesity); and group D included individuals with BMI greater than 35 (morbid obesity). The female participants were subjected to full history taking, clinical examination, evaluation of serum levels of AMH, and transvaginal ultrasound.
Results There was a significant decrease in parity with increased BMI. AMH ranged from 0.30 to 17.22 ng/dl, and there was a significant increase in AMH with increased BMI. There was a positive correlation between BMI, waist–hip ratio, and ovarian volume and AMH, whereas there was a significant inverse correlation between parity and AMH. Moreover, there was a significant positive correlation between AFC and age, BMI, waist–hip ratio, mean ovarian volume, and AMH, whereas there was a significant negative correlation between AFC and parity. There was a significant increase in AMH in female patients with acne when compared with female patients without acne. In addition, female patients with acne showed a significant increase in AFC when compared with cases without acne.
Conclusion The level of AMH was positively correlated with both BMI and AFC. These results reflect that body weight can play a role in the pathogenesis of polycystic ovary.
Keywords: anti-mullerian, obesity, polycystic ovary
|How to cite this article:|
Abdel Hay MA, El-Berri SA, Sleem TE, Mohammed MI, Nour El-Deen ST. The role of anti-mullerian hormone as an indicator of reproductive health in women with obesity and concomitant polycystic ovary syndrome. Benha Med J 2017;34:66-72
|How to cite this URL:|
Abdel Hay MA, El-Berri SA, Sleem TE, Mohammed MI, Nour El-Deen ST. The role of anti-mullerian hormone as an indicator of reproductive health in women with obesity and concomitant polycystic ovary syndrome. Benha Med J [serial online] 2017 [cited 2018 Sep 18];34:66-72. Available from: http://www.bmfj.eg.net/text.asp?2017/34/2/66/218820
| Introduction|| |
Polycystic ovary syndrome (PCOS) is the most common endocrine derangement, affecting up to 6–10% of reproductive age women. It is characterized by menstrual irregularity, androgen excess, polycystic ovaries (PCOs), and disturbances in glucose metabolism . Insulin resistance is pathophysiologically implicated in reproductive and metabolic abnormalities in PCOS . Dyslipidemia is a common aberration in PCOS. The atherogenic lipid profile including low-density lipoprotein cholesterol and triglycerides and decreased high-density lipoprotein cholesterol levels is associated with PCOS .
According to the Rotterdam 2003 consensus , PCOS has been characterized by at least two out of the following three criteria: oligo-ovulation or anovulation, clinical or biochemical hyperandrogenism, and PCOs on ultrasound (US). More recently, serum anti-Mullerian hormone (AMH) has emerged as a novel marker for ovarian function. AMH, also termed Mullerian-inhibiting substance, is a member of the transforming growth factor-β superfamily of glycoprotein . AMH has been found to play an important role in excessive early follicular growth. It also plays a key role in preventing the selection of one follicle from the increased pool and its further maturation to a dominant follicle (follicle arrest) , by inhibiting the initial recruitment of primordial follicles  and promoting follicular arrest . A high serum AMH level is correlated with an excessive antral follicle count (AFC). However, it is uncertain whether serum AMH levels can predict the phenotypes of PCOS and metabolic disturbances . Several studies have reported abundant evidence that obesity has a significant adverse effect on pregnancy in women seeking to become pregnant by natural means . Increased BMI has been associated with reduced fertility, and an increased risk for miscarriage compared with normal-weight women . During pregnancy, overweight and obesity are associated with an increased risk for adverse maternal and infant health outcomes. Attention to weight loss before conception might improve fertility, and maternal and infant health outcomes of pregnancy. Once pregnancy is achieved in a woman with a high BMI, there is a substantially increased risk for miscarriage and pregnancy complications. The etiology of poor fertility outcomes in overweight women has been investigated, seeking to determine whether these outcomes are due to an ovarian or endometrial effect . In addition to impairing spontaneous conception, high BMI might impair the probability of achieving pregnancy with assisted reproductive technology. There is a high prevalence of obese women in the infertile population, and numerous studies have highlighted the link between obesity and infertility. Obesity contributes to anovulation and menstrual irregularities, reduced conception rate, and a reduced response to fertility treatment. Markers of ovarian reserve, including baseline follicle stimulating hormone, estradiol, inhibin B, AFC, ovarian volume, and, recently, AMH, have been used to counsel patients as regards their reproductive outcomes .
Exploring the relationship between AMH and obesity might clarify the association between obesity and infertility, especially in terms of ovarian response. The evaluation of the level of AMH has clinical value in predicting the success of in-vitro fertilization. Various studies have evaluated the association between AMH and BMI, but reported contradictory results overall. However, some of the studies in the literature have reported a significant inverse correlation between AMH levels and BMI , whereas others found no relationship between AMH and BMI .
| Aim|| |
The aim of this study was to evaluate the relation between AMH, antrafollicular count, and BMI and evaluate the relation between AMH and AFC and site in patients with PCOS.
| Patients and methods|| |
This study was designed as a prospective comparative study and was conducted in Sherbin General Hospital, during the period from 1 June 2014 to 30 June 2016. The study was approved by the institutional Research Ethical Committee. It included 200 patients with the diagnosis of PCOS according to Rotterdam 2003 criteria. These criteria included the following: clinical hyperandrogenism (HA) (Ferriman–Gallwey Score ≥8) or biochemical HA (elevated total/free testosterone); oligomenorrhea (<6–9 menses per year) or oligo-ovulation; and PCOs on US (≥12 antral follicles in one ovary or ovarian volume ≥10 cm3). For the diagnosis of PCOS, the patient must fulfill at least two of the previous criteria. The patients were divided into four groups according to BMI: group A, which included 50 women with average body weight (BMI<25); group B, which included 50 women with BMI between 25 and 30 (overweight); group C, which included 50 women with BMI between 30 and 35 (mild obesity); and group D, which included 50 women with BMI greater than 35 (morbid obesity).
(a) Women in their reproductive age (18–35 years), (b) women diagnosed with PCOS according to Roterdam 2003 criteria, and (c) those who provided informed consent for participation in the study after full explanation of the study aim and methodology were included in the study.
Women who fulfilled the following criteria were excluded from the study: (a) pregnancy and (b) breastfeeding.
All patients included in the present study were subjected to the following: (a) careful history taking, (b) thorough clinical examination (general, abdominal, and pelvic examination), (c) pelvic US for PCO criteria at ovaries (12 or more follicles measuring 2–9 mm and/or an increased ovarian volume of >10 cm3); and (d) laboratory investigations, including serum AMH and testosterone.
Determination of anti-Mullerian hormone
AMH was determined using enzyme-linked immunosorbent assay kit procured from Kamiya Biomedical Company (Tukwila, Washington, USA).
Transvaginal US: it was performed using Sonoscape S11 (SS-11BW) (2014; Sonoscape Shenzhen, China). It was performed at the early follicular phase (day 1–3). An US probe is placed inside the vagina, which allows the physician to examine the reproductive organs and look for abnormalities. The thickness of the endometrium can be measured. ‘The revised Rotterdam criteria now define PCO as the presence of 12 or more small (2–9 mm) follicles in each ovary’. Once the ovary was located, the probe was rotated to find out the longest diameter of the ovary and was stored as one frame on a dual screen. Thereafter, the probe was rotated 90°, to obtain the true transverse axis of the ovary. The largest longitudinal, transverse, and anteroposterior diameter of the ovary in centimeters was recorded and ovarian volume was calculated using the formula L×H×W×0.523, where L stands for length, H for height, and W for weight. The number and site of antral follicles were counted in the longest section of the ovary, and, for better results, it was counted in the whole ovary by taking a two-dimensional sweep across the whole ovary. This method is very feasible and reliable when the number of follicles is much more as in PCO.
The collected data were coded, organized, tabulated, and statistically analyzed using statistical package of the social sciences, version 16 (SPSS; SPSS Inc., Chicago, Illinois, USA), running on IBM compatible computer. Qualitative data were represented as a relative frequency and percent distribution and for comparison between groups; the χ2-test or the Mann–Whitney test was used. Quantitative data were represented as mean and SD, minimum and maximum. For comparison between two mean, the unpaired Student t-test was used, whereas for comparison between more than two mean the one-way analysis of variance F-test was used. For interpretation of results, P value less than 0.05 was considered significant.
| Results|| |
In the present work, there was no significant difference between studied groups with regard to the right, left, or mean ovarian volume. In addition, 146 (73.0%) cases of 200 cases had follicles mainly in the periphery of the ovary, whereas 54 (27.0%) cases had mixed (present in both peripheral and central areas) follicles. There was no significant difference between studied groups ([Table 2]). There was a significant increase in AMH with increased BMI (i.e. it was significantly higher in group D when compared with other groups and in group C when compared with groups B and A). In addition, AFC ranged from 11 to 36 and AFC was significantly increased with an increase in BMI (i.e. group D had the higher count, followed by groups C, B, and A, respectively; the mean values were 25.44±4.84, 21.18±4.34, 19.04±5.32, and 17.08±4.62, respectively) ([Table 1]).
|Table 1 Comparison between studied groups as regards ultrasound findings, anti-Mullerian hormone levels, and antral follicular count|
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|Table 2 Correlation between anti-Mullerian hormone and other studied parameters|
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In the present study, there was no significant correlation between age and AMH, whereas there was a positive correlation between BMI, waist–hip ratio, and ovarian volume and AMH. There was a significant inverse correlation between parity and AMH. In addition, there was a significant positive correlation between AFC and age, BMI, waist–hip ratio, mean ovarian volume, and AMH, whereas there was a significant negative correlation between AFC and parity ([Table 2]).
In the present work, there was no relation between AMH and HA, hirsutism, and follicle distribution. However, there was a statistically significant increase in AMH in women with acne when compared with women without acne (7.46±2.50 vs. 6.59±2.06, respectively). In addition, there was no relation between AFC and HA, hirsutism, or follicle distribution. However, patients with acne showed a significant increase in AFC when compared with cases without acne (21.91±5.30 vs. 20.17±5.78, respectively) ([Table 3]).
|Table 3 Relation between biochemical hyperandrogenism and clinical data and anti-Mullerian hormone regardless of BMI|
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| Discussion|| |
PCOS frequently manifests during adolescence and is primarily characterized by ovulatory dysfunction and HA. The cause of PCOS is unknown, but considerable evidence suggests that PCOS results from a complex combination of traits that often become apparent at the onset of puberty . Diagnosis of PCOS has life-long implications, with increased risk for infertility, metabolic syndrome, type 2 diabetes mellitus, and, possibly, cardiovascular disease . Metabolic features of insulin resistance are common in adolescents with PCOS, and obesity is of major importance to PCOS-associated insulin resistance. AMH, also known as Mullerian-inhibiting substance, is a dimeric glycoprotein that belongs to the transforming growth factor-β superfamily . AMH has primarily been studied in terms of its regulatory role in male sex differentiation. It is produced by the Sertoli cells More Details in the fetal testis and induces regression of Mullerian ducts. In women, AMH is produced after birth by granulosa cells in preantral and small antral follicles . In general, the production rate of AMH is considered to reflect the extent of follicular growth in ovaries and the reservoir of ovarian function in women . In women with PCOS, circulating AMH is 2–3-fold higher than that in healthy women of reproductive age, possibly because of increased follicular mass. Circulating AMH is significantly higher in adolescent patients with PCOS than in unaffected adolescent girls; this is in accordance with corresponding values observed in adult women with and without PCOS . To date, no data are available on the potential association between plasma AMH and body weight in pregnant patients with PCOS.
Different researchers have described a high prevalence of obesity with infertility and PCOS ,. These studies reflect the importance of evaluation of obese women with PCOS and explain why we chose this category of patients to conduct the present study. After fulfilling the inclusion criteria, the included participants were subjected to full history taking, clinical examination, evaluation of serum levels of AMH, and transvaginal US.
In the present study, right ovarian volume ranged from 10.80 to 15.20 with a mean of 11.94±0.77 cm3, whereas left ovarian volume ranged from 11 to 15.90 with a mean of 12.24±0.78 cm3. Finally, the mean ovarian volume ranged from 10.90 to 15.30 with a mean of 12.09±0.76 cm3, and there was no significant difference between studied groups as regards ovarian volume. These results are in agreement with those of Balen et al. , who reported that increased ovarian volume is a characteristic feature of PCOS.
In the present work, 146 (73.0%) cases of 200 cases had follicles mainly in the periphery of the ovary, whereas 54 (27.0%) cases had mixed follicles. There was no significant difference between studied groups. These results are comparable to those reported by Guraya  who found that, the peripheral distribution of ovarian follicles in 89 (82.8%).
In the present series, AMH ranged from 0.30 to 17.22 ng/dl and there was a significant increase in AMH with increased BMI (i.e. it was significantly higher in group D when compared with other groups and in group C when compared with groups B and A). These results are in agreement with the results obtained by Freeman et al. , Gracia et al. , and Chen et al. , who found differences in plasma AMH between normal-weight and overweight–obese adolescent patients with or without PCOS. In addition, Piouka et al.  and Siow et al.  have found increased serum AMH levels in women with PCOS. However, these results are contradictory to the results obtained by Cengiz et al. , who did not find any significant difference between obese and nonobese adolescents with PCOS as regards AMH levels. This contradiction may be attributed to the different age groups between the two studies, as we included cases in their reproductive period and they included adolescent cases (≥18 years of age). In addition, Legro et al.  reported that there was a significant decrease in AMH with increased severity of obesity. This contradiction may be attributed to the fact that they investigated morbidly obese women alone in comparison with nonobese PCOS patients. Furthermore, other investigators reported that obesity has been shown to decrease serum AMH levels, whereas normal-weight women with PCOS had significantly higher serum AMH levels compared with overweight and obese ,.
To explain the mechanism of ovulatory changes in PCOS, it had been reported that ovulatory disorders in women with the PCO syndrome are caused by the following: (a) an increased early follicular growth, resulting in a larger than normal reserve of selectable follicles; and (b) defective selection of one follicle from this increased pool, leading to follicular arrest . As AMH has been shown not only to inhibit the initial follicle recruitment  but also to cause follicular arrest , and AMH levels are increased in the syndrome, it has been proposed that its involvement in PCOS-associated ANOV lies only in the second mechanism . Nevertheless, other data support an additional PCOS-associated defect in the early production of AMH by the granulosa cells of growing follicles, indicating a possible involvement of decreased AMH in the disordered early follicle development observed in anovulatory women with the syndrome . It has also been reported that the excess AMH production by PCO is a result of the increased small follicle number per se . However, as indicated by the present results, the increased number of follicles 2–9 mm in diameter, demonstrated as PCO sonographic morphology, is not the only determinant of serum AMH.
In the present study, there was no significant correlation between age and AMH. However, there was a positive correlation between BMI, waist–hip ratio, and ovarian volume and AMH, and there was a significant inverse correlation between parity and AMH. These results are in disagreement with the results reported by Skalba et al. , who found no significant correlation between BMI and serum AMH in obese PCOS patients. However, there was a significant correlation between BMI and AMH in normal-weight PCOS and non-PCOS groups. Unfortunately, we did not examine each group separately as all groups in the present study had PCOS. Skalba et al.  added that their results suggest only a weak impact of the body weight on plasma AMH levels in young women in reproductive age. These results are contradictory to the results of the present study, which showed a moderate impact of the body weight on plasma AMH levels in women in reproductive age.
In the present study, AFC ranged from 11 to 36 with a mean of 20.68±5.68. AFC was significantly increased with an increase in BMI (i.e. group D had the higher count, followed by groups C, B, and A, respectively; mean values were 25.44±4.84, 21.18±4.34, 19.04±5.32, and 17.08±4.62, respectively). These results are contradictory to those reported by Legro et al. , who reported that an increase in obesity is associated with lower AFC. This contradiction may be attributed to different inclusion criteria and different methods used in estimation of AFC.
In the present study, there was a significant positive correlation between AFC and age, BMI, waist–hip ratio, mean ovarian volume, and AMH, whereas there was a significant negative correlation between AFC and parity. These results are in agreement with a previous work, which reported a direct and significant correlation between follicle number and serum AMH levels , suggesting that the increased AMH levels in PCOS are the results of the increased number of early antral follicles . However, other reports demonstrated that the increase in AMH concentration is largely due to the increase in the production of AMH by each follicle and not just a consequence of an increase in follicle number . The AMH may constitute a marker for ovarian aging as it correlates with the number of early antral follicles, which might in turn represent the size of the resting pool of follicles ; therefore, if the level of AMH is being reduced, ovarian reserve may be compromised. In addition, Elmashad  reported there was a significant positive correlation between plasma AMH levels and both ovarian volume and the antral follicle number in PCOS, which was not surprising as ovarian volume is a reflection of the number of small antral follicles present in PCOS, which are the only source of AMH. There was also a positive correlation between AMH and clinical hyperandorgenism in PCOS. These findings are consistent with that of the present study and with the results of previous studies ,,. Finally, Begawy et al.  reported a significant positive correlation between AMH and number of follicles less than 10 mm in the whole group of patients and in each group separately, which is in line with the finding that serum AMH levels reflect the number of small antral follicles demonstrated in several studies.
| Conclusion|| |
Results of the present study revealed that patients with PCOS had higher levels of AMH that positively correlated with both BMI and AFC. These results reflect that body weight can play a role in the pathogenesis of PCOS.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Dumesic DA, Richards JS. Ontogeny of the ovary in polycystic ovary syndrome. Fertil Steril 2013; 100:23–38.
Diamanti-Kandarakis E, Kandarakis SA, Chrousos GP. Patho-physiology and types of dyslipidemia in PCOS. Trends Endocrinol Metab 2007; 18:280–285.
Nardo LG, Christodoulou D, Laing I. Anti-Mullerian hormone levels and antral follicle count in women enrolled in in vitro fertilization cycles: relationship to lifestyle factors and reproductive history. Gynecol Endocrinol 2007; 23:486–493.
Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group. Consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2003; 19:41–47.
Parahuleva N, Pehlivanov B, Orbecova M, Deneva T, Uchikova E. Serum levels of anti-muller hormone in women with polycystic ovary syndrome and healthy women of reproductive age. Akush Ginekol (Sofiia) 2013; 52(Suppl 1):16–23.
Jonard S, Dewailly D. The follicular excess in polycystic ovaries, due to intra-ovarian hyperandrogenism, may be the main culprit for the follicular arrest. Hum Reprod Update 2004; 10:107–117.
Durlinger A, Visser J, Themmen A. Regulation of ovarian function: the role of AMH. Reproduction 2002; 124:601–609.
La Marca A, Volpe A. The Anti-Mullerian hormone and ovarian cancer. Hum Reprod Update 2007; 13:265–273.
Hwang IM, Sung NY, Cha SH. Can high serum anti-Müllerian hormone levels predict the phenotypes of polycystic ovary syndrome (PCOS) and metabolic disturbances in PCOS patients? Clin Exp Reprod Med 2013; 40:135–140.
Erel CT, Senturk LM. The impact of body mass index on assisted reproduction. Curr Opin Obstet Gynecol 2009; 21:228–235.
Usta T, Oral E. Is the measurement of anti-Müllerian hormone essential? Curr Opin Obstet Gynecol 2012; 24:151–157.
Norman RJ, Chura LR, Robker RL. Effects of obesity on assisted reproductive technology outcomes. Fertil Steril 2008; 89:1611–1612.
Georgopoulos NA, Saltamavros AD, Decavalas G. Serum AMH, FSH, and LH levels in PCOS. Fertil Steril 2010; 93:e13.
Park AS, Lawson MA, Chuan SS, Chang RJ. Serum anti-Mullerian hormone concentrations are elevated in oligomenorrheic girls without evidence of hyperandrogenism. J Clin Endocrinol Metab 2010; 95:1786–1792.
Cengiz H, Ekin M, Yildiz S. Comparison of serum anti-Müllerian hormone levels in normal weight and overweight-obese adolescent patients with polycystic ovary syndrome. Eur J Obstet Gynecol Reprod Biol 2014; 180:46–50
Fauser BC, Bouchard P. Uncertainty remains in women with PCOS regarding the increased incidence of cardiovascular disease later in life, despite the indisputable presence of multiple cardiovascular risk factors at a young age. J Clin Endocrinol Metab 2011; 96:3675–3677.
Josso N, Picard JY, Rey R, di Clemente N. Testicular anti-Müllerian hormone: history, genetics, regulation and clinical applications. Pediatr Endocrinol Rev 2006; 3:347–358.
Weenen C, Laven JS, von Bergh AR, Themmen AP. Anti-Mullerian hormone expression pattern in the human ovary: potential implications for initial and cyclic follicle recruitment. Mol Hum Reprod 2004; 10:77–83.
Visser JA, de Jong FH, Laven JS, Themmen AP. Anti-Mullerian hormone: a new marker for ovarian function. Reproduction 2006; 131:1–9.
Siow Y, Kives S, Hertweck P, Perlman S, Fallat M. Serum Mullerian-inhibiting substance levels in adolescent girls with normal menstrual cycles or with polycystic ovary syndrome. Fertil Steril 2005; 84:938–944.
Haq F, Aftab O, Rizvi J. Clinical, biochemical and ultrasonographic features of infertile women with polycystic ovarian syndrome. J Coll Physicians Surg Pak 2007; 17:76–80.
Barber TM, Golding SJ, Alvey C, Wass JA. Global adiposity rather than abnormal regional fat distribution characterizes women with polycystic ovary syndrome. J Clin Endocrinol Metab 2008; 93:999–1004.
Balen AH, Laven JS, Tan SL, Dewailly D. Ultrasound assessment of the polycystic ovary: international consensus definitions. Hum Reprod Update 2003; 9:505–514.
Guraya SS. Prevalence and ultrasound features of polycystic ovaries in young unmarried Saudi females. J Microsc Ultrastruct 2013; 1:30–34.
Freeman EW, Gracia CR, Strauss JF 3rd. Association of anti-mullerian hormone levels with obesity in late reproductive-age women. Fertil Steril 2007; 87:101–106.
Gracia CR, Freeman EW, Sammel MD, Lin H, Deborah N. The relationship between obesity and race on inhibin B during the menopause transition. Menopause 2005; 12:559–566.
Chen MJ, Yang WS, Yang YS, Ho HN. The relationship between anti-Mullerian hormone, androgen and insulin resistance on the number of antral follicles in women with polycystic ovary syndrome. Hum Reprod 2008; 23:952–957.
Piouka A, Farmakiotis D, Gerou S. Anti-Mullerian hormone levels reflect severity of PCOS but are negatively influenced by obesity: relationship with increased luteinizing hormone levels. Am J Physiol Endocrinol Metab 2009; 296:E238–E243.
Legro RS, Brzyski RG, Diamond MP. The pregnancy in polycystic ovary syndrome II study: baseline characteristics and effects of obesity from a multicenter randomized clinical trial. Fertil Steril 2014; 101:258–269.e8.
Panidis D, Farmakiotis D, Rousso D, Kourtis A. Obesity, weight loss, and the polycystic ovary syndrome: effect of treatment with diet and orlistat for 24 weeks on insulin resistance and androgen levels. Fertil Steril 2008; 89:899–906.
Panidis D, Katsikis I, Karkanaki A. Serum anti-Mullerian hormone (AMH) levels are differentially modulated by both serum gonadotropins and not only by serum follicle stimulating hormone (FSH) levels. Med Hypotheses 2011; 77:649–653.
Durlinger AL, Gruijters MJ, Grootegoed JA. Anti-Mullerian hormone attenuates the effects of FSH on follicle development in the mouse ovary. Endocrinology 2001; 142:4891–4899.
Stubbs SA, Hardy K, Da Silva-Buttkus P, Stark J, Webber LJ, Flanagan AM et al.
Anti-mullerian hormone protein expression is reduced during the initial stages of follicle development in human polycystic ovaries. J Clin Endocrinol Metab 2005; 90:5536–5543.
Skalba P, Cygal A, Madej P, Olszanecka-Glinianowicz M. Is the plasma anti-Mullerian hormone (AMH) level associated with body weight and metabolic, and hormonal disturbances in women with and without polycystic ovary syndrome? Eur J Obstet Gynecol Reprod Biol 2011; 158:254–259.
Laven JE, Mulders AM, Visser J. Anti-Mullerian hormone serum concentrations in normoovulatory and anovulatory women of reproductive age. J Clin Endocrinol Metab 2004; 89:318–323.
Pigny P, Jonard S, Robert Y. Serum anti-Mullerian hormone as a surrogate for antral follicle count for definition of the polycystic ovary syndrome. J Clin Endocrinol Metab 2006; 91:941–945.
Catteau-Jonard S, Pigny P, Dewailly D. Changes in serum AMH level during low-dose recombinant follicular stimulating hormone therapy for anovulation in polycystic ovary syndrome. J Clin Endocrinol Metab 2007; 92:4138–4143.
Elmashad AI. Impact of laparoscopic ovarian drilling on anti-Mullerian hormone levels and ovarian stromal blood flow using three-dimensional power Doppler in women with anovulatory polycystic ovary syndrome. Fertil Steril 2011; 95:2342–2346.
Pigny P, Merlen E, Robert Y, Cortet-Rudelli C. Elevated serum level of anti-Mullerian hormone in patients with polycystic ovary syndrome: relationship to the ovarian follicle excess and to the follicular arrest. J Clin Endocrinol Metab 2003; 88:5957–5962.
Begawy AF, El-Mazny AN, Abou-Salem NA, El-Taweel NE. Anti-Mullerian hormone in polycystic ovary syndrome and normo-ovulatory women: correlation with clinical, hormonal and ultrasonographic parameters. Middle East Fertil Soc J 2010; 15:253–258
[Table 1], [Table 2], [Table 3]