Anargyros Kourtis

Lipid and lipoprotein profile in women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by obesity-related risk factors for cardiovascular disease. The objective of our study was to determine values of key lipid and lipoprotein fractions in PCOS, and their possible relation to insulin resistance. A total of 75 women with PCOS (aged 23.1 +/- 5.1 years, BMI 24.9 +/- 4.7 kg/m(2)), and 56 age- and BMI-matched controls were investigated. In all subjects, basal glucose, cholesterol (total, HDL, and LDL), oxidized LDL (OxLDL), triglycerides, apolipoprotein (apo)A1, apoB, and apoE, nonesterified fatty acids, insulin, testosterone, sex hormone-binding globulin, homeostasis model assessment (HOMA) index, and free androgen index were determined in the follicular phase of the cycle. PCOS patients compared with controls had increased indices of insulin resistance, basal insulin (p < 0.001), and HOMA index (p < 0.001), and worsened insulin resistance-related dyslipidemia with decreased HDL cholesterol (p < 0.01), elevated triglycerides (p = 0.010), and pronounced LDL oxidation (p < 0.001). In conclusion, characteristic dyslipidemia of insulin resistance and unfavorable proatherogenic lipoprotein ratios were present only in women with PCOS and not in controls. Elevated OxLDL and the relation of apoE and nonesterified fatty acids with insulin resistance suggest that women with PCOS are at increased risk for premature atherosclerosis.

The role of estrogen replacement therapy in Alzheimer’s disease

Multiple factors appear to contribute to the expression of Alzheimers disease (AD). About 30% of cases of dementia of the Alzheimers type (DAT) can be attributed to genetic factors. These observations raise the possibility of identifying multiple interventions that may modify the disease process and, therefore, the clinical expression of the dementia. Prominent among factors that may contribute to dementia and, specifically, to dementia of the Alzheimers type is cerebral vascular disease. Estrogen is a potent factor that not only prevents vascular disease but also improves blood flow in diseased vessels, including blood flow in regions of the brain affected by AD. Estrogen also has direct effects on neuronal function that may play an important role not only in the preservation of neurons but in the repair of neurons damaged by the disease process. These effects of estrogen on the CNS suggest that the hormone may be effective not only in the prevention of dementia but also in its treatment. Given the distressingly high prevalence of AD among older women and the exorbitant social and economic costs associated with this disorder, a true risk reduction on the order of one-third to one-half, as suggested by several recent analytical studies, would be of tremendous public health importance.

REVERSIBLE INFERTILITY, PHARMACEUTICAL AND SPONTANEOUS, IN A MALE WITH LATE ONSET CONGENITAL ADRENAL HYPERPLASIA, DUE TO 21-HYDROXYLASE DEFICIENCY

The authors describe a case of a 35-year-old man with 5-year duration infertility. History, clinical examination, and laboratory tests have established the diagnosis of late-onset congenital adrenal hyperplasia, due to 21-hydroxylase deficiency. Treatment with dexamethasone resulted in improvement of sperm quality, and 4 months later a pregnancy was achieved. Two years after the patient fathered his first child, and while he had discontinued dexamethasone treatment, he succeeded at a second pregnancy. The authors conclude that (1) late-onset congenital adrenal hyperplasia presents with significant variation during the patients lifetime; (2) glucocorticoid administration is necessary in infertile men with nonclassic form of 21-hydroxylase deficiency; and (3) in cases of male infertility of unknown origin, the patient must be scrutinized for congenital adrenal hyperplasia, especially the nonclassic form.

Serum vaspin levels in normal pregnancy in comparison with non-pregnant women

OBJECTIVE Pregnancy represents a state of insulin resistance (IR). Vaspin (SERPINA12) is a novel insulin-sensitizing adipokine that might be implicated in endogenous glucose regulation. However, its role in pregnancy and its circulating levels have not been adequately studied. We aimed to evaluate serum vaspin levels in pregnancy and their correlation with known markers of IR. DESIGN A group of 106 women (age 27.9±0.4 years) at the 24-30th week of gestation (pregnancy group) and another 106 age-matched healthy non-pregnant controls (control group) were included in the study. METHODS Serum glucose, insulin, vaspin, adiponectin, and lipid parameters were measured. The quantitative insulin sensitivity check index (QUICKI) was used as an insulin sensitivity index. RESULTS Pregnant women had significantly higher body mass index (BMI), lipids, and serum insulin and lower serum glucose and vaspin levels than controls. Vaspin was positively correlated to adiponectin in both groups (P<0.001 and P<0.004 respectively) but was not correlated to BMI, serum insulin levels, or the QUICKI index in either group. Furthermore, vaspin was negatively correlated to lipid parameters (total cholesterol, triglycerides, and low-density lipoproteins) in the pregnant but not in the non-pregnant women. CONCLUSIONS Vaspin cannot serve as a marker of IR in either pregnant or non-pregnant women, although it is significantly correlated with adiponectin. On the other hand, vaspin might be useful as a surrogate marker of lipid metabolism in pregnancy if confirmed by subsequent studies.

Apelin levels in normal pregnancy

Objective  Apelin is an adipokine secreted from adipose and other tissues with increased expression in obesity, role in glucose metabolism and atherosclerosis, as well as in oxidative stress. Pregnancy is considered a state of hyperlipidemia, oxidative stress and decreased insulin sensitivity. The aim of the present study is to investigate the levels of apelin in human pregnancy and its relation to insulin sensitivity.

Function of the hypothalamic–pituitary–gonadal axis in long-term survivors of hematopoietic stem cell transplantation for hematological diseases

Gonadal dysfunction in adult long-term survivors of hematopoietic stem cell transplantation (HSCT) is an adverse effect of conditioning regimens consisting of chemotherapy and total body irradiation (TBI). The impact of conditioning regimens consisting of chemotherapy alone on the function of the hypothalamic–pituitary–gonadal (HPG) axis was evaluated in a series of 41 female and 31 male patients who had undergone either autologous or allogeneic bone marrow/peripheral blood stem cell transplantation; mean age at transplantation was 32.6 years and mean time interval from transplantation was 1.5 years (range 0.2–9.8 years). Provocative testing of the HPG axis by administration of luteinizing hormone-releasing hormone was included in the first endocrinological evaluation. The follow-up period extended to three consecutive years. Gonadal dysfunction was not reported by any of the patients prior to their underlying illness. Hypergonadotrophic hypogonadism was observed in 97% of female and 19% of male patients. Leydig cell strain (normal testosterone, high luteinizing hormone levels) was evident in 32% and spermatogenesis damage (high follicle-stimulating hormone levels) in 68% of the male population. At the conclusion of the study four women (10%) had regained spontaneous menses and all hypogonadal men had resumed normal testosterone levels. Our results indicate a high incidence of gonadal dysfunction due to target organ failure in HSCT recipients not treated by TBI.

The effect of selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia

This study evaluates, compares, and contrasts the effects of three selective estrogen receptor modulators (SERMs), namely, tamoxifen, toremifene, and raloxifene, on the hypothalamic-pituitary-testicular axis in 284 consecutive subfertile men with idiopathic oligozoospermia using three therapeutic protocols: [1] tamoxifen, 20 mg, once daily (n = 94); [2] toremifene, 60 mg, once daily (n = 99); and [3] raloxifene, 60 mg, once daily (n = 91). The antiestrogenic effects of SERMs at the hypothalamic level result in a statistically significant increase of gonadotropin levels, which is more marked for tamoxifen and toremifene compared with raloxifene.

The influence of tibolone upon serum leptin levels in post-menopausal women

OBJECTIVE To estimate serum leptin levels in post-menopausal women, to relate these to the duration of the post-menopausal period, and to body mass index (BMI), and to assess the influence of tibolone on them. METHODS Fifteen women (age 49-64 years) were included. Three groups were studied; I, those with normal BMI taking tibolone; II, those with a raised BMI taking tibolone, and III, a group with raised BMI not taking tibolone. Blood samples were drawn before and 1, 2, 6, 9 and 12 months after the initiation of tibolone or, in group III, after the start of the study. RESULTS Serum leptin concentrations were high in all women with abnormal BMI. Long-term tibolone administration did not have any significant effect on serum leptin concentrations. There was no correlation between serum leptin levels and the age and the duration of post-menopausal period. There was a high positive correlation between serum leptin levels and BMI values. CONCLUSIONS BMI values affect serum leptin concentrations but long-term tibolone administration does not seem to have any effect on serum leptin levels.

Oxidized low-density lipoprotein and adiponectin levels in pregnancy

Introduction. The aim of the present study was to investigate whether normal pregnancy represents a complex state of oxidative stress, inflammation and insulin resistance. Subjects and methods. One hundred and six pregnant women, between 24th and 28th week of pregnancy (age 27.9 ± 0.4 years) (study group) and one hundred and six age-matched, healthy, non-pregnant women (control group) participated in the study. Serum levels of glucose, insulin, adiponectin, oxidized LDL (oxLDL) and lipid parameters, i.e. total cholesterol (TC), triglycerides (TG), HDL and LDL, were determined. Body mass index (BMI) and QUantitative Insulin sensitivity ChecK Index (QUICKI) were also calculated. Results. Pregnant women presented higher BMI values, insulin and oxLDL serum levels and lower glucose serum levels than controls. Serum levels of lipids (TC, TG, LDL and HDL) were higher in pregnant women. There was a significant positive correlation of oxLDL to adiponectin (p < 0.01) in the study group, but not in the controls, and no other significant correlation with any of the other parameters, in either of groups. Conclusions. Pregnancy is a state of insulin resistance, oxidative stress and pro-atherogenic hyperlipidemia. Adiponectin may, though, have cardioprotective role in pregnant women.

The influence of long-term administration of conjugated estrogens and antiandrogens to serum leptin levels in women with polycystic ovary syndrome

It is well known that a strong exponential relationship exists between leptin levels and body mass index (BMI). The different serum leptin levels, however, that are observed for each BMI value, suggest that other factors, as well, interfere with leptin secretion. This study was designed in order to estimate serum leptin levels in patients with polycystic ovary syndrome (PCOS), before and after long-term treatment with conjugated estrogens and antiandrogens. Sixteen women with PCOS were included in the study. They were divided into two groups: the first group comprised 11 non-obese women (BMI 21.6 ± 0.5 kg/m2), aged 23.5 ± 1.1 years; the second consisted of five obese women (BMI 28.9 ± 1.5 kg/m2), aged 22.8 ± 1.9 years. Blood samples for leptin measurement were drawn before and 2, 4, 6, 9 and 12 months after administration of conjugated estrogens and antiandrogens. Our results showed that obese women exhibited higher serum leptin levels in all blood samples. Moreover, the administration of conjugated estrogens and antiandrogens caused an increase in serum leptin levels in the 2nd, 4th, 6th and 9th month in both groups of women. Finally, leptin concentrations during the 12th month of the treatment returned to basic levels in both groups of women with PCOS. Our results support the view that BMI is the main variable that influences serum leptin levels, and that the effect of conjugated estrogens and antiandrogens on serum leptin concentrations is poor.