George Kourounis

Basal metabolic rate is decreased in women with polycystic ovary syndrome and biochemical hyperandrogenemia and is associated with insulin resistance.

OBJECTIVE To evaluate basal metabolic rate (BMR) in women with PCOS and to determine its association with insulin resistance (IR). DESIGN Prospective assessment of BMR in women with PCOS. SETTING Outpatient clinic of the Division of Reproductive Endocrinology. PATIENT(S) The study included 91 Greek women with PCOS and biochemical hyperandrogenemia, with mean age 24.03 +/- 0.55 years and mean body mass index (BMI) 26.67 +/- 0.69 kg/m(2), and 48 matched regularly menstruating women, with mean age 26.33 +/- 0.93 years and mean BMI 23.35 +/- 0.85 kg/m(2), as control subjects. INTERVENTION(S) Assessment of BMR by indirect calorimetry, IR by HOMA and QUICKI indices, fasting insulin, and fasting glucose/insulin ratio. MAIN OUTCOME MEASURE(S) Reduced BMR in PCOS with or without IR. RESULT(S) Adjusted BMR was 1,868 +/- 41 kcal/day in the control group, 1,445.57 +/- 76 in all PCOS women, 1,590 +/- 130 in PCOS women without IR and 1,116 +/- 106 in PCOS women with IR. Adjusted BMR showed a statistically significant difference between women with PCOS and control subjects, with lowest values in the group of PCOS women with IR, even after adjusting all groups for age and BMI. CONCLUSION(S) Women with PCOS, particularly those with IR, present a significantly decreased BMR.

Estrogen receptor polymorphisms in tamoxifen-treated women with breast cancer

In postmenopausal women with estrogen receptor (ER)-positive breast cancer, long-term tamoxifen administration has proved beneficial after surgical treatment and subsequent chemotherapy. One of the major adverse effects of tamoxifen is the development of endometrial pathology (polyps, endometrial hyperplasia and endometrial cancer). PvuII and XbaI polymorphisms of the estrogen receptor-α gene (ERα) and RsaI and AluI polymorphisms of the estrogen receptor-β gene (ERβ) have been associated with breast cancer. Thus the present study aimed to identify whether ER gene polymorphisms are associated with breast cancer stage or endometrial responsiveness to long-term tamoxifen treatment in 87 postmenopausal, tamoxifen-treated women with ER-positive breast cancer. The mean age of the patients was 58.7 ± 4.7 years and the mean duration of tamoxifen treatment was 3.9 ± 1.1 years. At diagnosis, the stage of breast cancer was determined as follows: 29 women (32%) at Stage I, 49 (58%) at Stage II and 9 (10%) at Stage III. The frequency distributions of the estrogen receptor polymorphisms in all women with breast cancer were not different from those predicted by the Hardy-Weinberg equilibrium hypothesis (p > 0.10). None of the ER polymorphisms studied was linked to either the presence of endometrial pathology or the stage of breast cancer.

The Shift in the “Paradigm” of the Pharmacology of Hypertension

Until recently elevated blood pressure was considered as a hemodynamic entity representing an increase in workload for the heart and the arterial tree. Control of hypertension meant hemodynamic unloading, through inhibition of vasoconstrictor pathways, principally renin-angiotensin system and sympathetic system. In recent years however a new pharmacological approach has evolved as a result of (i) the dissociation of endothelial dysfunction and vascular pathology from increased blood pressure; (ii) the recognition that endothelial dysfunction regards not only the vascular reactivity, but also promotes atherosclerosis and thrombosis; and (iii) an improved understanding of the complexity of local-tissue renin angiotensin system and of the vasodilatory and cytoprotective role of natriuretic peptides. This has led to a reconsideration of existing medicines in terms of specification on endothelial function, more rationalized application of drugs and search for new compounds targeting both vasodilatory and anti-proliferative pathways. Examples include beta1-adrenergic antagonists, such as Nebivolol and Carvedilol, and vasopeptidase inhibitors, such as Omapatrilat, that inhibit simultaneously the angiotensin converting enzyme and neutral endopeptidase. Furthermore the identification of genetic polymorphisms in the effectors involved in the pathophysiology of hypertension or in the response to anti-hypertensive drugs, such as the p22phox subunit of NADPH oxidase, alpha-adducin or adrenergic receptors, has promoted the prospective of both better understanding of hypertension and individualized strategies for its treatment.

α2β adrenoreceptor 301–303 deletion polymorphism in polycystic ovary syndrome

Abstractα2β adrenoreceptor 301–303 deletion polymorphism does not influence basal metabolic rate, insulin resistance or weight gain in Greek women with polycystic ovary syndrome.

Long-term follow-up of combined pituitary hormone deficiency in two siblings with a Prophet of Pit-1 gene mutation.

Combined pituitary hormone deficiency (CPHD) is a rare disorder resulting from an impaired pituitary function due to different causes, characterized by impaired secretion of growth hormone (GH) and one or more of the other anterior pituitary hormones. To date, 16 distinct human Prophet of Pit-1 (Prop1) gene mutations have been identified in patients with CPHD, inducing a phenotype involving GH, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin and thyroid-stimulating hormone (TSH), and rarely adrenocorticotropic hormone, deficiency. Herein we present two siblings of different sexes from a family with parental consanguinity presenting the 301–302delAG mutation in the Prop1 gene. The female presented failure of growth from the age of 6 years and was treated for 10 years with GH, ending in a final height (standard deviation score) of −0.28. TSH deficiency was manifested after the initiation of GH and was treated with thyroxine while puberty was initiated with conjugated estrogens. The male presented TSH deficiency since childhood, treated with thyroxine, and growth failure at the age of 14 years, treated for a period of 2 years with GH. Puberty was initiated with increasing doses of testosterone, while human chorionic gonadotropin was added in order to achieve increased testicular volume. In conclusion, these two siblings of different sexes with CPHD carrying the 301–302delAG mutation in the Prop1 gene presented a variable phenotype characterized by GH, TSH, LH and FSH deficiency.

Texture Analysis for Classification of Endometrial Tissue in Gray Scale Transvaginal Ultrasonography

Computer-aided classification of benign and malignant endometrial tissue, as depicted in 2D gray scale transvaginal ultrasonography (TVS), was attempted by computing texture-based features. 65 TVS endometrial images were collected (15 malignant, 50 benign) and processed with a wavelet based enhancement technique. Two regions of interest (ROIs) were identified (endometrium, endometrium margin) on each processed image. Thirty-two textural features were extracted from each ROI employing first and second order statistics texture analysis algorithms. Textural feature-based models were generated for differentiating benign from malignant endometrial tissue employing stepwise logistic regression analysis. Models’ performance was evaluated by means of receiver operating characteristics (ROC) analysis. The best benign versus malignant classification was obtained from the model combining three textural features from endometrium and four textural features from endometrium margin, with corresponding area under ROC curve (Az) 0.956.