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OBJECTIVE: The aim of the study was to analyse the relationship between nutritional status, selected adipokines and plasma anti-Müllerian hormone (AMH) levels in women with polycystic ovary syndrome (PCOS). STUDY DESIGN PATIENTS AND MEASUREMENTS: A prospective, cross-sectional study, involving 87 PCOS (48 obese) women and 67 non-PCOS women (36 obese). Anthropometric parameters were measured, and body composition was determined by the bioimpedance method. Fasting serum glucose, androgens, FSH, LH, SHBG, insulin, AMH, apelin-36, adiponectin, leptin and omentin-1 were measured. RESULTS: Plasma AMH levels were significantly higher in PCOS compared to the non-PCOS group (7.8 ± 4.3 ng/ml vs 44 ± 2.4 ng/ml; P < 0.001). Furthermore, AMH levels were higher in both PCOS and non-PCOS normal weight than in obese subgroups (8.9 ± 4.4 ng/ml vs 7.0 ± 4.0 ng/ml; P < 0.05 and 5.1 ± 2.4 ng/ml vs 3.9 ± 2.3 ng/ml; P < 0.05). There were negative correlations between AMH levels and anthropometric parameters (body mass, BMI, fat mass and percentage, as well as waist circumference) and plasma omentin-1 concentrations (R = -0.28, P < 0.001; R = -0.30, P < 0.001; R = -0.36, P < 0.001; R = -0.34, P < 0.001; R = -0.23, P < 0.01; and R = -0.20, P < 0.05, respectively) in all study groups. In multiple regression analysis, circulating AMH level variability was explained by omentin-1 levels and anthropometric parameters (excluding waist circumference). CONCLUSIONS: In this observational study, nutritional status appears to be the main factor influencing circulating AMH levels independent of PCOS. The observed AMH association with omentin-1 levels suggests that this adipokine may be a link between hormonal dysfunction of adipose tissue related to obesity and decreased AMH secretion.

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OBJECTIVE: It is suggested that disturbed adipokines release plays a role in PCOS pathogenesis. The aim of this study was to assess plasma levels of omentin and adiponectin as well as the omentin to adiponectin ratio, as markers of adipose tissue dysfunction in relation to hormonal or metabolic changes in PCOS. STUDY DESIGN, PATIENTS AND MEASUREMENTS: A cross-sectional study involved 87 PCOS (48 obese) and 72 non-PCOS women (41 obese). Anthropometric parameters and body composition were determined, and serum glucose, hormones, omentin-1 and adiponectin levels were measured. RESULTS: The adiponectin level was similar in PCOS and non-PCOS groups, but, in both, was significantly lower in obese compared with normal weight subgroups, while the omentin-1 level was significantly lower in the PCOS compared with the non-PCOS group, and not related to body mass. The adiponectin to omentin-1 ratio (AOR) was significantly higher in the PCOS than non-PCOS group. Moreover, AOR was significantly higher in the normal weight than in obese subgroups in both PCOS and non-PCOS groups. Multiple regression analyses revealed that AOR variability is explained by oestradiol level and all anthropometric parameters as well as FAI, but not LH to FSH and HOMA-IR values. CONCLUSIONS: Our results suggest secondary to insulin resistance and hyperandrogenism impairment of hormonal stroma adipose tissue function in PCOS, independent of nutritional status. Contrarily, the adipocyte hormonal dysfunction is primarily dependent on excessive fat accumulation. It seems that the AOR may be useful in the assessment of adipose tissue dysfunction not only in PCOS.

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OBJECTIVES: To examine liver mitochondrial function in women using combined oral contraceptives (COCs) containing ethinylestradiol. METHODS: A breath test after oral administration of 1 mg/kg (13)C-alpha-ketoisocaproic acid ((13)C-KICA) and 20 mg/kg L-leucine was performed twice: (i) in 15 women on day 14, 15, 16, 17 or 18 of COC intake, and between day 1 and 5 of the withdrawal bleeding; and (ii) in 15 regularly menstruating females not taking hormonal contraceptives: during the luteal phase, between the 18th and the 22nd day of the cycle, and again between day 1 and 5 of the menstruation. RESULTS: In women on COCs the maximum (13)C elimination in breath air (Dmax) was higher (26.8 ± 1.6%/h) than during withdrawal bleeding (23.5 ± 1.2%/h; p = 0.012). The time to reach the Dmax was similar on the two study days: 33.3 ± 2.4 min during the phase of pill intake vs. 37.0 ± 2.5 min during the pill-free interval. The one-hour cumulative breath (13)C elimination was greater after two weeks of COC intake than during the withdrawal bleeding: 17.49 ± 1.03% vs. 15.32 ± 0.85% (p = 0.024). In the control group no menstrual cycle phase-dependent fluctuations in the results of the (13)C-KICA breath test were observed. CONCLUSION: The metabolism of (13)C-alpha-ketoisocaproic acid augments during the intake of COCs containing ethinylestradiol, reflecting enhanced liver mitochondrial metabolic activity.

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INTRODUCTION: Anti-Müllerian hormone (AMH) has been suggested as a predictor of ovarian response to ovulation induction and controlled ovarian hyperstimulation. MATERIAL AND METHODS: Twenty-six women, wishing to become pregnant and who showed resistance to clomiphene citrate, were included in the study. All women received recombinant follicle-stimulating hormone (recFSH). RESULTS: In the group of good responders, luteinising hormone (LH) and oestradiol levels were lower than in the group of non-responders. Free testosterone levels, free androgen index, and insulin resistance were higher in the group of non-responders. In the group of good responders, AMH levels decreased on successive days of ovarian stimulation and a greater slope of AMH levels was observed in patients with a higher number of increasing follicles. PCOS patients have low FSH and high AMH levels. It could be suggested that the serum AMH decrease preceded growth of many follicles, which is a consequence of the FSH stimulation. In anovulatory PCOS women, gently increasing the serum FSH level reduces the AMH excess, thus relieving the inhibition from the latter on aromatase expression by selectable follicles and allowing the emergence of growing follicles. Patients with severe hyperandrogenism, insulin resistance and high level of LH do not respond to stimulation. CONCLUSIONS: The decrease of AMH levels in PCOS women after one week of ovarian stimulation is a practical, valuable indicator which could predict the patients with a high risk of ovarian hyperstimulation. Anovulating PCOS patients with severe hyperandrogenism, insulin resistance and hyperinsulinaemia should not be qualified for recFSH ovarian stimulation.

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OBJECTIVES: To check whether currently used combined oral contraceptives (COCs) containing ethinylestradiol (EE) affect the liver microsomal metabolism. METHODS: (13)C-methacetin breath test ((13)C-MBT) - a sensitive non-invasive probe of cytochrome P-450 1A2 activity - was performed in 15 women on day 14, 15, 16, 17 or 18 of intake of their COC (containing EE), and between day 1 and 5 during the withdrawal bleeding, as well as in nine women not using hormonal contraception during the luteal phase of their cycle (between the 17th and the 23rd day), and between day 1 and 5 during menstruation. RESULTS: The maximum breath (13)C elimination was significantly lower during the phase of intake of contraceptive pills than during withdrawal bleeding: 31.5 ± 2.2 %/h vs. 38.2 ± 1.9 %/h (p = 0.0045), whereas the time to reach it was similar on the two study days: 21.2 ± 1.2 min vs. 21.0 ± 1.1 min. Between the 27th and the 180th min of observation the cumulative breath (13)C elimination was statistically significantly lower during intake of the pill than during withdrawal bleeding. No significant menstrual cycle phase-dependent fluctuations in the results of the (13)C- methacetin breath test were observed in the control group. CONCLUSION: COCs containing EE markedly inhibit hepatic microsomal function. This phenomenon must be taken into consideration when interpreting results of (13)C-MBT.

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A combination of the congenital abnormalities, Müllerian duct aplasia, renal aplasia, and cervicothoracic somite dysplasia, is defined as the MURCS association. Various genetic defects have been described in the MURCS association so far, yet the unambiguous molecular basis of these disorders has not been established. We report the case of an 18-year-old woman who presented with primary amenorrhea, right kidney, Arnold-Chiari malformation, and Klippel-Feil syndrome. In addition, the patient showed the following unusual features: right ovarian and Skenes gland agenesis, cubitus valgus with hyperextension and decreased range of motion at elbows, and facial changes. Moreover, the performed DNA analysis showed interstitial duplication in chromosome 5 (5q35.1). In the duplicated region, there are genes whose function is not well known. It is thought that they have an influence on the early stages of development and their joining in the later period can lead to neoplastic disorders, especially leukemias.

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OBJECTIVE: The aim of the study was to analyse relationships between plasma apelin-36 and apelin-12 levels, nutritional status, insulin resistance and hormonal disturbances, as well as plasma adiponectin, leptin and resistin concentrations in PCOS women. STUDY DESIGN PATIENTS AND MEASUREMENTS: A cross-sectional study involving 87 PCOS (48 obese) and 67 non-PCOS women (36 obese). Anthropometric parameters and body composition were determined. Serum glucose, androgens, FSH, LH, SHBG, insulin, apelin-36, apelin-12, adiponectin, leptin and resistin were measured in the fasting state. RESULTS: Plasma apelin-36 and apelin-12 levels were significantly higher in normal weight women than in the obese women with PCOS (3·1 ± 2·2 vs 1·2 ± 0·7 µg/l, P < 0·001; 2·9 ± 2·4 vs 0·5 ± 0·7 µg/l; P < 0·001 respectively). Both plasma apelin-36 and -12 levels correlated positively with adiponectin levels, and inversely with leptin or resistin levels. There was a negative correlation between plasma apelin-36, apelin-12 and serum LH levels. In addition, an inverse correlation between apelin-12 level and LH to FSH ratio was found. In multiple regression analysis 9% of LH variability was explained by apelin-12 levels (ß = -0·14; P < 0·001). CONCLUSIONS: Nutritional status seems to have different effects on apelin release, particularly, its active isoform, in women with PCOS compared with women without PCOS. This may be partially caused by changes in leptin and resistin secretion and may enhance pituitary-ovarian axis disturbances. The association between both isoforms of apelin and insulin resistance seems to be bidirectional.

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Anovulatory cycles and endometriosis are the main causes of female infertility. The most frequently anovulatory cycles are related to polycystic ovary syndrome (PCOS) commonly associated with obesity and hormonal disturbances in the course of obesity. Recently published studies revealed that infertility affects about one in six couples during their lifetime and is more frequent in obese. Obesity is also associated with male infertility related to erectile dysfunction, hormonal disturbances and lower semen quality. Any of these above mentioned disorder is the important risk factor of psychological disturbances and poor quality of life among women and men in the reproductive age. On the other hand the mood disorders may exacerbate the hormonal disturbances and worsen the effectiveness of infertility management. Infertility, its therapy with accompanying psychological disturbances may also significantly affect the partners relationships. The review summarize the results described in the current literature on the association between obesity and infertility and psychological disturbances as well as their impact on quality of life and sexual functioning in women and men. Moreover, the impact of infertility and psychological disturbances on partners relationships is discussed.

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OBJECTIVE: To analyze potential interactions of visfatin and retinol-binding protein 4 (RBP4) levels with body mass, metabolic, and hormonal status in normal weight and obese women with PCOS. STUDY DESIGN: Body composition was determined by bioimpedance in 83 women (44 obese) diagnosed with PCOS and in 67 women (36 obese) without PCOS. In addition, serum glucose, lipids, androgens, FSH, LH, SHBG, insulin, visfatin, and RBP4 were measured in a fasting state and the free androgen index (FAI) was calculated, as was insulin resistance using the HOMA-IR assessment. RESULTS: Plasma RBP4 levels were significantly higher in women of normal weight compared to obese subjects when both were diagnosed with PCOS (14.1 ± 4.6 vs.10.9 ± 4.5 ng/mL, p<0.001); while in non-PCOS subjects the opposite was found (10.8 ± 4.5 vs. 18.4 ± 11.6 ng/mL, p<0.01; respectively). Plasma visfatin levels were similar in PCOS and non-PCOS subjects. In non-PCOS subjects, positive correlations between RBP4 level and anthropometric parameters were observed. In PCOS, RBP4 levels inversely correlated with serum insulin levels and HOMA-IR values. No correlation was found between plasma visfatin levels and anthropometric parameters in all study groups. Similarly, no correlation was found in PCOS and non-PCOS subgroups. Additionally, there was an inverse correlation between RBP4 and LH concentrations and LH/FSH ratio in all study subjects. CONCLUSIONS: Plasma visfatin level is not a useful biomarker of insulin resistance and hyperandrogenism. RBP4 level reflects visceral body fat content in non-PCOS women. Decreasing RBP4 release along with increasing insulin resistance and hormonal disturbances may be a compensatory mechanism preventing deterioration in obese PCOS.

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This article presents the role of the hypothalamus in reproduction, the definition of hypogonadotropic hypogonadism (HH), and the causes of acquired and syndromic HH and idiopathic HH (IHH). The authors present a short review of major causes of acquired HH, but most of the causes of IHH will not be discussed because they do not fall within the scope of the article. More attention is devoted to idiopathic HH, especially the genetic basis of IHH. Also presented in the article are clinical criteria of CHARGE syndrome. Later, the article discusses the clinical presentation, establishing the diagnosis, and management of IHH. The article ends with a brief overview of nutritional hypothalamic dysfunction and athletic amenorrhea.

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Anti-Müllerian hormone (AMH) belongs to a family of growth and differentiation factors beta (TGF-beta). In male fetuses AMH induces regression of Müller's ducts whereas in female ones this hormone plays an important role during adolescence and reproductive period. AMH participates in regulation of folliculogenesis by inhibiting the recruitment of prenatal and antral follicles. The aim of the present study was to summarize the current knowledge of the role of AMH in menstrual and fertility disturbances in obese women and those with polycystic ovary syndrome.

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BACKGROUND: Non-standard hypertrophy of the adrenal cortex is a rare endocrinopathy causing the incidence of hyperandrogenism among women of procreative age. The primary objective of this paper is the specification of the clinical picture and modifications of the concentration of pituitary, ovarian and adrenal hormones in the blood of female patients with the syndrome of non-standard hypertrophy of the adrenal cortex (NPKN). MATERIAL AND METHODS: In the Gynaecological Endocrinology Clinic of the Silesian Medical University in Katowice, Poland, 2,353 female patients were hospitalised between 1 January 2003 and 30 June 2009 with symptoms of hyperandrogenism. Of these, 55 were selected for the study. Eventually, 25 female patients with diagnosed NPKN, and 30 randomly selected patients with the polycystic ovarian disease polycystic ovary syndrome (PCOS) were enrolled in the study. RESULTS: Of the 2,353 female patients hospitalised in the Gynaecological Endocrinology Clinic with symptoms of hyperandrogenism between 1 January 2003 and 30 June 2009, NPKN was found in 1.2% of them. Patients with NPKN displayed a strong hirsutism, which was significantly more intense than in the comparative group. Insulin resistance was found more frequently in the group of female patients with PCOS (67%) compared to the group with NPKN (40%). Polycystic ovarian disease was more frequently observed in the group of patients with PCOS (93%), compared to the group with NPKN (72%). The average concentration of androstendione in the blood serum in the group of patients with NPKN amounted to 7.60 ng/ml (SD = 3.57) and was significantly higher than in the group of patients with PCOS where it was 3.46 ng/ml (SD = 1.53). The average concentration of free testosterone in the blood serum in the group of patients with NPKN amounted to 7.30 pg/ml (SD = 4.13) and was significantly higher than in the group of patients with PCOS, where it was 2.90 pg/ml (SD =1.43 ). The average concentration of DHEAS in the blood serum in the group of patients with NPKN accounted for 403.23 µg/dl (SD = 192.59), and in the group with PCOS it was 257.39 µg/dl (SD = 63.67). This concentration was statistically significantly higher in the group with NPKN than in the group with PCOS. The average concentration of estradiole in the blood serum in the group with NPKN amounted to 111.98 pg/ml (SD = 113.68), while in the group with PCOS it was 62.39 pg/ml (SD = 31.18). The difference of concentrations between the groups NPKN and PCOS was statistically significant. We found a positive correlation between the 17-OHP concentration after 60 minutes of the ACTH test and the severity of hirsutism in the group of patients with NPKN (r = 0.77896). In addition, we found a correlation between the free testosterone and the 17-OHP concentration after 60 minutes of the ACTH test in the group of patients with NPKN (r = 0.48149). A positive correlation was also reported between the symptom of hypertrophy of the clitoris and the 17-OHP concentration after 60 minutes of the ACTH stimulation test in the group of patients with NPKN (r = 0.77221). In the comparative group of patients with PCOS, there was no correlation between the free testosterone and 17-OHP concentration after 60 minutes of the ACTH test (r = 0.3059). There was also no correlation between the severity of hirsutism and the concentration of 17-OHP concentration analysed after 60 minutes of the ACTH test. In all female patients from the PCOS group, there was a correct size of clitoris. CONCLUSIONS: Analysing the clinical picture of the examined population of patients with NPKN enabled us to specify symptoms of disease which were significant for diagnosis, and which helped differentiate NPKN from other endocrinopathies involving hyperandrogenism, including in particular PCOS. Taking everything into consideration, non-standard hypertrophy of the adrenal cortex is a rare cause of hyperandrogenism in women of procreative age. Intense hirsutism and features of virilisation presenting as hypertrophy of the clitoris predominate in the clinical picture of non-standard hypertrophy of the adrenal cortex. The laboratory confirmation of diagnosis of NPKN constitutes the analysis of the 17-OHP level in blood in the ACTH stimulation test. The analyses of free testosterone and its unbound fraction, androstendione and estradiole, help differentiate NPKN from polycystic ovarian disease.

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OBJECTIVE: The aim of the study was to analyze interrelation between AMH levels and body weight, metabolic, and hormonal status in normal and overweight weight women with and without polycystic ovary syndrome (PCOS). STUDY DESIGN: Eighty-seven women (54 normal weight and 33 overweight) diagnosed with PCOS and 50 apparently healthy women - Non-PCOS (28 normal weight and 22 overweight) were enrolled. The body weight and height were measured and BMI was calculated. In addition to serum glucose, lipids, androgens, FSH, LH, SHBG and insulin, AMH were assessed in fasting state and free androgens index (FAI) was calculated. The insulin resistance was assessed based on the homeostasis model of assessment-insulin resistance (HOMA-IR). RESULTS: Plasma AMH levels were similar in normal weight and overweight PCOS groups (9.6±3.5 vs. 11.2±4.5ng/mL, respectively), and as expected markedly higher than in both Non-PCOS groups (2.5±0.8 and 2.3±0.7ng/mL, respectively). There were no correlations between BMI and AMH levels in all study groups. A significant positive correlation between HOMA-IR, free testosterone concentrations or FAI and AMH levels were found (R=0.31, p<0.001; R=0.91, p<0.001 and R=0.62, p<0.001, respectively). Moreover, there was positive correlation between total or LDL cholesterol and AMH levels (R=0.22, p<0.05 and R=0.31, p<0.05, respectively) and a negative one between HDL cholesterol and AMH levels (R=-0.17, p<0.05) in all study subjects. CONCLUSIONS: The plasma AMH level is associated with insulin resistance but not with BMI per se. Increased circulating AMH level seems to reflect the disturbances of gonadotrophins release in PCOS. It seems that AMH level may be used not only as new surrogate marker of ovarian hyperandrogenism in PCOS but also as a potential new cardiovascular risk factor.

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OBJECTIVES: It seems that adipokines participate in disturbances of the function of the hypothalamus-pituitary-ovary axis. The aim of the study was to assess the relationship between plasma adiponectin and resistin levels and insulin resistance and markers of hyperandrogenism in lean and obese PCOS women. STUDY DESIGN: Forty-one women with PCOS (22 lean and 19 obese) and 16 healthy lean women were enrolled. Body mass and height were measured and body mass index was calculated. In addition to serum glucose, lipids, androgens and insulin, adiponectin and resistin concentration were assessed in the fasting state. The insulin resistance was calculated based on the HOMA-IR. RESULTS: Similar serum resistin concentrations were found in both PCOS subgroups and controls. The obese PCOS subgroup was characterized by the lowest serum adiponectin level (10.8 ± 8.3, compared with 21.0 ± 15.1 in the normal weight PCOS subgroup and 26.7 ± 12.5 µg/ml in controls). There were no correlations between resistin and adiponectin levels and HOMA-IR values and serum androgen concentrations. Significant positive correlations between adiponectin to resistin ratio and plasma FSH (r = 0.49; p = 0.001) and LH (r = 0.45; p = 0.003) concentrations, and a negative correlation with free androgen index (r = -0.34; p = 0.03) in PCOS group were found. CONCLUSIONS: Obese but not normal weight PCOS women have lower adiponectin levels whereas resistin concentration did not differ in normal weight and obese PCOS compared to control subjects. We hypothesize that changes of the relative proportion of adiponectin to resistin, but not circulating adiponectin and resistin levels themselves, may play a role in hormonal disturbances but not in insulin resistance in PCOS.

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A case of POF in a 31-year-old woman with karyotype 47,XXX. The aim of the study was to discuss a case of POF in a 31-year-old patient with polysomy 47,XXX. The described karyotype is not usually associated with this characteristic physical phenotype. In some rare cases, menstrual disorders, sterility, secondary amenorrhoea, premature menopause, and low intelligence are found. Our observations revealed the necessity for cytogenetic examination in all women at reproductive age with symptoms of premature ovarian failure. According to the data found in literature, patients with POF and karyotype disorders belong to the risk group of premature death, mostly for cardiological reasons. Raising patient awareness about the risk may have a positive effect on quality of life and regularity of check-ups.

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The main biological role of the anti-Mullerian hormone (AMH) is to induce the involution of the Muller ducts in embryos during differentiation of masculine gender. In case of women, AMH is produced in granular cells of primary, preantral and antral follicles. The expression of AMH initiates at the moment of the follicle recruitment and it lasts until the stage of an antral follicle. The level of this hormone decreases with age and in postmenopausal period is undetectable in blood. Therefore, AMH could be a useful marker of ovarian reserve. Multiple investigations have revealed higher AMH levels in the blood of PCOS patients. It is believed to be the consequence of the increased amount of small antral follicles. AMH is considered to have an essential role in folliculogenesis. It inhibits the process of recruitment of primordial follicles and modifies the growth of preantral and antral follicles by diminishing the sensitivity of follicles for FSH stimulation. The paper is a review of the present knowledge of the structure and activity of AMH. AR gene and protein. Participation of AMH in folliculogenesis and changes of AMH levels depending on structure and age of the ovary have also been discussed. Recent findings concerning the possibility of using AMH to assess ovarian reserve and efficiency of the stimulation of ovulation in infertile women have been presented. It is believed that increased knowledge concerning AMH might improve the diagnosis and treatment of infertility caused by lack of ovulation.

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