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Background: Women with polycystic ovary syndrome (PCOS) have an increased prevalence of insulin resistance (IR) and related disorders. Elevated serum levels of cellular adhesion molecules (CAMs) reflect low-grade chronic inflammation and have been associated with several insulin-resistant states. The objective of this study is to investigate whether soluble inflammatory markers [soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sE-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1) and C-reactive protein (CRP)] are altered in PCOS and to further elucidate the effect of metformin treatment on their levels., Methods: Two young populations were studied [62 women with PCOS and 45 normal women of similar age, BMI and waist-to-hip ratio (WHR)]. Plasma levels of sICAM-1, sVCAM-1, sE-selectin and high-sensitivity CRP (hsCRP) were measured in both groups. Additionally, the effect of metformin on these molecules was investigated in 22 women with PCOS who accepted to metformin protocol (1700 mg daily for a 6-month period)., Results: In the total population studied, plasma levels of hsCRP (mg/l), sICAM-1 (ng/ml) and sE-selectin (ng/ml) were higher in the PCOS group compared with those in controls (hsCRP 1.31 +/- 0.22 versus 0.92 +/- 0.27, P = 0.014, sICAM-1 301.21 +/- 24.80 versus 209.86 +/- 17.05, P = 0.025, sE-selectin 57.37 +/- 4.08 versus 45.67 +/- 4.62, P = 0.045, respectively). sVCAM-1 (ng/ml) did not differ statistically among the two groups (P = 0.896). A significant reduction in hsCRP and sVCAM-1 was achieved after 6 months of metformin administration: PCOS pretreatment hsCRP 1.92 +/- 0.60 versus PCOS post-treatment hsCRP 0.52 +/- 0.26, P = 0.005; PCOS pretreatment sVCAM-1 668.09 +/- 98.38 versus PCOS post-treatment sVCAM-1 365.82 +/- 99.77, P = 0.039., Conclusion: These findings imply the presence of chronic inflammation in women with PCOS. Metformin decreases the levels of plasma inflammatory indices. Further investigation is required to determine whether these findings may prove to be of clinical significance for PCOS patients.

Objective: This study was designed to: [1] measure, for the first time, metastin (kisspeptin) levels in women with polycystic ovary syndrome (PCOS), a condition associated with hypersecretion of LH and hyperandrogenemia; and [2] investigate the possible correlations between metastin and PCOS-related reproductive and metabolic disturbances., Design: Clinical study., Setting: University hospital., Patient(s): Twenty-eight obese and overweight (body mass index [BMI] >25 kg/m2) women with PCOS, 28 normal weight (BMI <25 kg/m2) women with the syndrome, and 13 obese and overweight controls (ovulatory women without clinical or biochemical hyperandrogenemia) were selected., Intervention(s): Blood samples were collected between day 3 and day 6 of a spontaneous bleeding episode in the PCOS groups and a menstrual cycle of the controls, at 9:00 AM, after an overnight fast., Main Outcome Measure(s): Circulating levels of LH, FSH, PRL, T, Delta4-androstenedione (A), DHEAS, 17alpha-OH-P, sex hormone-binding globulin (SHBG), insulin, glucose, and metastin were measured., Result(s): Both normal weight women with PCOS and obese controls were less insulin resistant and had significantly higher metastin levels, compared to obese and overweight women with the syndrome. Plasma kisspeptin levels were negatively correlated with BMI, free androgen index, and indices of insulin resistance., Conclusion(s): These results indicate that metastin is negatively associated with free androgen levels. The PCOS-associated insulin resistance and consequent hyperinsulinemia probably contribute to this effect by [1] stimulating androgen synthesis by the polycystic ovary (PCO) and [2] suppressing SHBG production in the liver.

Objective: Although evidence on elevated creatine phosphokinase (CPK) as a tool for the diagnosis of ectopic pregnancy (EP) is rather conflictive, no previous study on CPK isoenzyme levels and their relative ratio was found in the literature., Study Design: Forty women with EP, 20 with intrauterine (IU) abortive gestation, and 20 regular pregnant women (controls) were studied. Serum total CPK, CPK-MB, and CPK-MM levels were measured at the time of presentation and 24 hours after surgery. Relative operating characteristic (ROC) curves were plotted., Results: Women with EP had significantly higher CPK concentrations and a significantly decreased CPK-MB relative ratio (CPK-MB%), compared with both women with IU abortive pregnancy and controls. The ROC curves demonstrated a significant discriminatory ability of both increased total CPK and decreased CPK-MB% ratio for the diagnosis of EP., Conclusion: Determination of CPK isoenzyme fractions can significantly enhance the diagnostic value of total maternal CPK in the prediction of ectopic pregnancy.

Polycystic ovary syndrome (PCOS) is a complex and heterogeneous disorder characterized by hyperandrogenemia, hyperinsulinemia, insulin resistance, and chronic anovulation. It is the most common endocrine disorder in women of reproductive age with an enigmatic pathophysiologic and molecular basis. The high prevalence of affected individuals and the wide range of phenotypic expression can be explained by the interaction of a number of key genes with environmental factors. Heritability of PCOS has been inferred from studies of the syndrome in various population groups (ethnic groups, twins, and PCOS families). Although evidence of familial segregation and clustering of the disease in first-degree relatives of women diagnosed with PCOS has been presented, no particular pattern of inheritance has emerged. Some of the problems in genetic studies have been the lack of uniform criteria for diagnosis, heterogeneity of phenotypic features, and the fact that the disorder is only expressed clinically in women during their reproductive years. Even within affected families and between sisters with polycystic ovaries, there is heterogeneity in presentation. However, regardless of diagnostic criteria used to identify the propositus and to determine affected status in the kindred, the genetic studies available suggest a strong familial component. Currently, PCOS is considered a polygenic trait that might result from the interaction of susceptible and protective genomic variants and environmental factors, during either prenatal or postnatal life.

Background: Ghrelin is a novel peptide associated with energy balance, obesity, and perhaps gonadal function. The present study was designed in order: (i) to compare plasma ghrelin levels between women with PCOS, women who presented only with hyperandrogenaemia and healthy controls; and (ii) to investigate the relationship between circulating ghrelin and the heterogeneity of clinical and biochemical manifestations of PCOS., Methods: Two hundred and fifty-nine women with PCOS, 25 women who had only hyperandrogenaemia and 46 controls, were studied. Women with PCOS were further divided, based on the presence of chronic anovulation, biochemical hyperandrogenaemia, clinical hyperandrogenism, and polycystic ovary morphology on ultrasound evaluation. In all women, the basal levels of gonadotrophins, androgens, 17-OH-progesterone, sex hormone-binding globulin, glucose, insulin and ghrelin were measured., Results: Women with PCOS had lower ghrelin levels, compared to both women with hyperandrogenaemia and controls; women with hyperandrogenaemia had lower ghrelin levels, compared to controls, but not significantly so. While PCOS-associated hyperandrogenaemia was inversely related to ghrelin levels, anovulation and polycystic ovary morphology were associated with higher concentrations. Ghrelin levels were negatively correlated with 17-OH-progesterone levels., Conclusions: In PCOS, circulating ghrelin and androgens are inversely related and it is possible that this peptide is involved in steroidal synthesis and/or action. It is also likely that different clinical and biochemical manifestations of the syndrome are also associated with different ghrelin concentrations.

Background: Insulin resistance is a prominent feature of polycystic ovary syndrome (PCOS), independent of obesity. It is possible that insulin resistance in PCOS is genetically determined. Adiponectin is a protein that modulates insulin action and is regarded as a possible link between adiposity and insulin resistance. The objective of this study was to examine the role of the adiponectin gene T45G polymorphism, located in exon 2, in PCOS, since this polymorphism has been shown to be associated with obesity and insulin resistance., Subjects and Methods: Two hundred and thirty-two women were studied, and were classified as follows: 132 women with PCOS [62 with body mass index (BMI) > 25 kg/m2 and 70 with BMI < 25 kg/m2] and 100 ovulating women without hyperandrogenemia (controls: 19 with BMI > 25 kg/m2 and 81 with BMI < 25 kg/m2). From all subjects a whole-blood sample was taken and was used for isolation of peripheral blood leukocytes. The adiponectin T45G polymorphism, located in exon 2, was genotyped by amplification of genomic DNA. In all subjects, serum gonadotropin, androgen, 17-OH-progesterone, fasting glucose, insulin and adiponectin levels were measured between the third and sixth day of the menstrual cycle., Results: A statistically significant difference was observed in the frequency of GG and TG genotypes between women with PCOS (40/132; 30.3%) and controls (19/100; 19.0%). In a subgroup of PCOS women with high Delta4-androstenedione levels (Delta4A > 3.11 ng/ml), a statistically significant difference between the frequencies of the genotypes was also noticed compared with the control group, in contrast to the subgroup with relatively low Delta4-androstenedione levels (Delta4A < 3.11 ng/ml). No significant associations were found between this adiponectin polymorphism and BMI, testosterone level, adiponectin levels and glucose-to-insulin ratio., Conclusions: Our study suggests that adiponectin polymorphisms are not causatively involved in the metabolic disturbances of PCOS, but that an interaction between adiponectin and steroid synthesis or action might exist., (Copyright 2004 European Society of Human Reproduction and Embryology)

Design: We examined 16 men who had been subjected to unilateral orchiectomy owing to seminoma and to preventive radiotherapy, in order to investigate the morphologic abnormalities of the spermatozoa (headless and small-round-headedness) that may contribute to infertility., Results: The same morphologic abnormalities of the head and neck found in the semen samples of fertile men were also found in the semen samples of the patients, albeit in higher percentages; the morphologic abnormalities of the tail in the semen samples of the patients were similar to those of the fertile men, both qualitatively and quantitatively., Conclusion: No specifically characteristic morphologic abnormalities of the spermatozoa were detected in men who were subjected to unilateral orchiectomy and to preventive radiotherapy in comparison with fertile men. The percentage rate of morphologic tail abnormalities is not affected by preventive radiotherapy.

Objective: To investigate the frequency of round-headed, or acrosomeless, spermatozoa, determine the percentage and evaluate the possible correlation with other semen parameters., Study Design: Semen specimens from 114 subfertile men aged 24-53 years (mean +/- SD 33.3 +/- 6.3) and from 60 fertile men aged 24-44 years (33.1 +/- 4.2) were studied. Two semen specimens were examined from each individual, with a six- to eight-week interval. Sperm morphology was evaluated from Papanicolaou-stained smears, and the classification of abnormal sperm forms was made according to WHO guidelines., Results: The percentage of round-headed spermatozoa was 2.3% +/- 0.5 in subfertile and 0.5% +/- 0.1 in fertile men. Round-headed spermatozoa existed in semen specimens from 36.8% of subfertile and 25.0% fertile men. Of subfertile men, 14.9% had round-headed spermatozoa at a higher percentage than the highest normal limit found in sperm smears from fertile men., Conclusion: In some subfertile men with a high percentage of round-headed spermatozoa, infertility could be attributed to the cause of this morphologic abnormality. Moreover, morphologic abnormalities in the neck were significantly more frequent in round-headed spermatozoa than in spermatozoa with normal heads.