Biomedical subjects
Publications and source records attributed to A I Kourtis.
Adenomyosis is characterized as ectopic endometrial tissues within the myometrium in the uterus. The etiology and pathogenetic mechanism(s) responsible for adenomyosis are poorly understood. Definite diagnosis is made on hysterectomy specimens, although attempts are made at securing preoperative diagnosis by magnetic resonance imaging and myometrial biopsies. Definite treatment of symptomatic women is hysterectomy.
Polycystic ovary syndrome (PCOS) is a syndrome involving defects in primary cellular control mechanisms that result in the expression of chronic anovulation and hyperandrogenism. In this syndrome the relation between the various parameters is of particular interest. These relations constitute the cornerstone of the pathogenesis of PCOS. The fact that the pathogenesis of the PCOS has not yet been clarified, despite the plethora of relative information, may be the result of a general way of thinking in the interpretation of several scientific data, and especially those that refer to biochemical phenomena. The use of the various models of the theory of chaos, that permits a concrete approach for the interpretation of data, may constitute an optional procedure for the future understanding of the association of different parameters and their disturbances in the pathogenesis of PCOS.
Multiple factors appear to contribute to the expression of Alzheimer's disease (AD). About 30% of cases of dementia of the Alzheimer's 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 Alzheimer's 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.
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.
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.
In this study, the evaluation of the total number of morphological anomalies per 100 sperm was more reliable, as far as potential fertility is concerned than the concentration of sperm per milliliter, the percentage of motile sperm, and the percentage of sperm with normal or abnormal morphology. This parameter allows for discrimination between subfertile and fertile semen and therefore can help in the selection of men who require assisted reproduction techniques.
OBJECTIVE: The ratio of androgens to estrogens in patients with polycystic ovarian syndrome (PCOS) and controls was evaluated in order to investigate whether hyperinsulinemia might induce hyperandrogenemia by decreasing androgen catabolism. STUDY DESIGN: Forty women were divided into four groups according to the presence of PCOS, insulin resistance, and normal or abnormal body mass index (BMI); each group consisted of 10 women. Group I comprised patients with PCOS, insulin resistance, and abnormal BMI. Group II consisted of patients with PCOS, without insulin resistance, and with normal BMI. Group III consisted of healthy women (controls) with abnormal BMI. Group IV consisted of healthy women with normal BMI. RESULTS: We found that: (1) the mean fasting insulin levels of groups II, III, and IV were significantly lower than those of group I (P < .001); (2) serum testosterone levels were significantly lower in groups III and IV than in group I and II; (3) there were no significant differences in serum estradiol and estrone levels between women of all groups; (4) women of groups III and IV had significantly lower ratios of testosterone to estradiol at time 0 compared to patients of groups I and II. CONCLUSION: Our results support the view that since hyperinsulinemia induces hyperandrogenism, the increase of androgens should not be attributed to the decrease of androgen catabolism.