COMPARISON OF FINASTERIDE, METFORMIN, AND FINASTERIDE PLUS METFORMIN IN PCOS.

The effects of finasteride on insulin resistance and of metformin on hyperandrogenism in patients with polycystic ovary syndrome (PCOS) are not clear. This study therefore compared the effects of finasteride, metformin, and finasteride plus metformin treatments on hormone levels, insulin resistance, and hirsutism score in women with PCOS. Fifty-two patients with PCOS were randomly assigned to receive finasteride 5 mg/day, metformin 1700 mg/day or finasteride plus metformin for 12 months. Body mass index (BMI), Ferriman Gallway score (FGS), serum concentrations of estradiol, sex hormone-binding globulin, free testosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and homeostasis model assessment of insulin resistance (HOMA-IR) index and areas under the curve (AUC) for insulin and glucose were evaluated before and after 12 months of treatment. Reductions in FGS, free testosterone, DHEAS, androstenedione, HOMA-IR, AUC-insulin, and AUC-glucose were significant within each group, whereas BMI and estradiol were not. Comparisons of changes in parameters in the 3 groups did not clearly show the superiority of any treatment modality. The treatment with finasteride alone significantly reduced both androgen levels and parameters of insulin resistance. In addition, metformin alone was effective, and not inferior to finasteride, in the treatment of hyperandrogenism.

Increased micronucleus, nucleoplasmic bridge, nuclear bud frequency and oxidative DNA damage associated with prolactin levels and pituitary adenoma diameters in patients with prolactinoma.

Prolactinoma is the most common pituitary tumor. Most pituitary tumors are benign, but they often are clinically significant. We investigated cytokinesis-block micronucleus cytome (CBMN cyt) assay parameters and oxidative DNA damage in patients with prolactinoma to assess the relations among age, prolactin level, pituitary adenoma diameter and 8-hydroxy-2'-deoxyguanosine (8-OHdG) level in patients with prolactinoma. We investigated 27 patients diagnosed with prolactinoma and 20 age- and sex-matched healthy controls. We measured CBMN cyt parameters and plasma 8-OHdG levels in peripheral blood lymphocytes of patients with prolactinoma and controls. The frequencies of micronucleus (MN), nucleoplasmic bridge, nuclear bud, apoptotic and necrotic cells, and plasma 8-OHdG levels in patients with prolactinoma were significantly greater than controls. MN frequency was correlated positively with age, prolactin levels and pituitary adenoma diameters in patients with prolactinoma. The increased chromosomal and oxidative DNA damage, and the positive correlation between MN frequency, prolactin levels and pituitary adenoma diameters may be associated with increased risk of cancer in patients with prolactinoma, because increased MN frequency is a predictor of cancer risk.

GENETIC DISORDERS OF PITUITARY DEVELOPMENT IN PATIENTS WITH SHEEHAN'S SYNDROME.

INTRODUCTION: Genetic disorders associated with the development of the pituitary gland and cranial bones may cause a genetic tendency toward Sheehan's syndrome (SS). Our aim in this study was to investigate expression disorders in the genes responsible for the development of the pituitary gland and cranial bones in patients with SS. MATERIALS AND METHODS: Forty-four patients who were previously diagnosed with SS and 43 healthy women were compared in terms of the mean expression values of genes including the prophet of PIT-1 (PROP1), HESX homeobox 1 (HESX1), POU class 1 homeobox 1 (POU1F1), LIM homeobox 3 (LHX3), LHX4, glioma-associated oncogene homolog 2 (GLI2), orthodenticle homeobox 2 (OTX2), SIX homeobox 3 (SIX3), SIX6, T-box transcription factor 19 (TBX19), transducin-like enhancer protein 1 (TLE1), TLE3, distal-less homeobox 2 (DLX2), DLX5, MSH homeobox 2 (MSX2), and paired box 3 (PAX3). RESULTS: The mean expression values of the HESX1, TLE1, TLE3, and MSX2 genes were significantly different in the SS group from the healthy control group, while the mean expression values of the remaining genes were similar. CONCLUSION: The present study concludes that abnormal expressions of HESX1, TLE1, TLE3, and MSX2 genes may cause a genetic predisposition to the development of SS.

Evaluation of long-term pituitary functions in patients with severe ventricular arrhythmia: a pilot study.

INTRODUCTION: Traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), stroke and cerebrovascular disease (CVD) are identified as risk factors for hypopituitarism. Pituitary dysfunction after TBI, SAH, and CVD may present in the acute phase or later in the course of the event. Chronic hypopituitarism, particularly growth hormone (GH) deficiency is related to the increased cardiovascular morbidity and mortality. In patients with serious ventricular arrhythmias, who need cardiopulmonary resuscitation, brain tissue is exposed to short-term severe ischemia and hypoxia. However, there are no data in the literature regarding pituitary dysfunction after ventricular arrhythmias. PATIENTS AND METHODS: Forty-four patients with ventricular arrhythmias [ventricular tachycardia (VT), ventricular fibrillation (VF)] (mean age, 55.6 ± 1.8 years; 37 men, 7 women) were included in the study. The patients were evaluated after mean period of 21.2 ± 0.8 months from VT-VF. Basal hormone levels, including serum free triiodothyronine (fT3), free thyroxine (fT4), TSH, ACTH, prolactin, FSH, LH, total testosterone, estradiol, IGF-1, and cortisol levels were measured in all patients. To assess (GH)-insulin like growth factor-1 (IGF-1) axis, glucagon stimulation test was performed and 1 µg ACTH stimulation test was used for assessing hypothalamic-pituitary-adrenal (HPA) axis. RESULTS: The frequencies of GH, gonadotropin and TSH deficiency were 27.2, 9.0, 2.2%, respectively. Mean IGF-1 levels were lower in GH deficiency group, but it was not statistically significant. CONCLUSION: The present preliminary study showed that ventricular arrhythmias may result in hypopituitarism, particularly in growth hormone deficiency. Unrecognized hypopituitarism may be responsible for some of the cardiovascular problems at least in some patients.