63 research outputs found

    The investigation of insulin resistance in patients with idiopathic hirsutism

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    Hirsutism, which is characterized by excessive growth of terminal hair in a male pattern, is a common clinical condition in women. It may result from various causes including polycystic ovary syndrome, nonclassic adrenal hyperplasia, adrenal or ovarian tumors, or it may be idiopathic. Idiopathic hirsutism (IH) is considered to be one of the most common forms of hirsutism. Although not universal, insulin resistance and hyperinsulinemia have been demonstrated in women with polycystic ovary syndrome. Because there are not enough data showing whether patients with IH also have insulin resistance, we intended to investigate the presence/ absence of insulin resistance in women with IH. Thirty-two women with IH [ mean age, 24.8 +/- 1.2 yr; body mass index (BMI), 24.6 +/- 0.8 kg/m(2)] and 17 healthy women (mean age, 25.8 +/- 0.6 yr; BMI, 22.5 +/- 0.6 kg/m(2)) were included in the study. Eight of 32 patients with IH had BMI higher than 30 kg/m(2). The presence of insulin resistance was investigated by using basal insulin levels, the oral glucose tolerance test, the iv insulin tolerance test, and the homeostasis model assessment(HOMA) score in both groups. Six (18.7%) patients had impaired glucose tolerance (IGT). Overall, patients with IH had significantly (P< 0.05) higher basal insulin levels (10.5 +/- 1.1 mU/liter vs. 5.7 +/- 0.9 mU/liter) and HOMA scores (2.0 +/- 0.2 vs. 1.1 +/- 0.2) and lower plasma glucose disappearance rate values (5.2 +/- 0.2 vs. 6.0 +/- 0.3) than control subjects. However, patients with IGT were notably more obese than the patients with a normal glucose tolerance test. Analyses after omitting the patients with IGT showed that there was still a significant ( P < 0.05) difference in terms of basal insulin levels and HOMA scores. Six of eight (75%) obese patients with IH showed IGT. These data suggest that IH is associated with insulin resistance and an increased prevalence of IGT in obese patients

    The hypothalamo-pituitary-adrenal axis in chronic fatigue syndrome and fibromyalgia syndrome

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    The hypothalamo-pituitary-adrenal (HPA) axis plays a major role in the regulation of responses to stress. Human stress-related disorders such as chronic fatigue syndrome (CFS), fibromyalgia syndrome (FMS), chronic pelvic pain and posttraumatic stress disorder are characterized by alterations in HPA axis activity. However, the role of the HPA axis alterations in these stress-related disorders is not clear. Most studies have shown that the HPA axis is underactive in the stress-related disorders, but contradictory results have also been reported, which may be due to the patients selected for the study, the methods used for the investigation of the HPA axis, the stage of the syndrome when the tests have been done and the interpretation of the results. There is no structural abnormality in the endocrine organs which comprise the HPA axis, thus it seems that hypocortisolemia found in the patients with stress-related disorder is functional. It may be also an adaptive response of the body to chronic stress. In this review, tests used in the assessment of HPA axis function and the HPA axis alterations found in CFS and FMS are discussed in detail

    The treatment of insulin resistance does not improve adrenal cytochrome P450c17 alpha enzyme dysregulation in polycystic ovary syndrome

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    Objective: To determine whether metformin, when given to non-diabetic women with polycystic ovary syndrome (PCOS), results in a reduction of insulin resistance and hyperinsulinemia while body weight is maintained. Also we aimed to see whether the reduction in insulin levels attenuates the activity of adrenal P450c17 alpha enzyme in patients with PCOS

    Value of Argyrophilic Nucleolar Organizing Region Protein Determinations in Nondiagnostic Fine Needle Aspiration Samples (Due to Insufficient Cell Groups) of Thyroid Nodules

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    OBJECTIVE: To evaluate the diagnostic value of argyrophilic nucleolar organizing regions (AgNORs) in the nondiagnostic fine needle aspiration biopsy (NFNAB) specimens (due to insufficient cell groups) of cases with thyroid nodules

    Endocrine changes in patients with acute organophosphate poisoning

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    In critical illness, several drugs and various stressful conditions modify the functions of neurotransmitters which consequently affect the secretion of pituitary hormones. Although the role of neurotransmitters in the regulation of endocrine system is well known, cholinergic actions have been less investigated. In animals, cholinesterase inhibitors were shown to modify the pituitary-thyroid and pituitary-adrenal axes, and to affect prolactin levels. The aim of the present study was to determine the effect of the organophosphate compounds on endocrine system, particularly pituitary hormones. This prospective study was performed in Medical Intensive Care Unit of Erciyes University Medical School Hospital. Twenty-two consecutive patients (ten males and 12 females aged 28 +/- 8 years) with organophosphate poisoning were included in the study, ACTH (P < 0.002), cortisol (P < 0.0005) and PRL (P < 0.005) levels were significantly higher during poisoning than after resolution of poisoning. FSH levels were significantly lower during poisoning (P < 0.05), Sick euthyroid syndrome was determined in seven patients (31.8%). Two of them had low fT(3) (with normal fT(4) and TSH), two had low fT(3) (with normal fT(3) and TSH) and three had low TSH (with normal fT(3) and fT(4)) levels. Serum levels of these hormones returned to normal values after resolution of poisoning. The present study demonstrated that organophosphate compounds affected PRL, ACTH and cortisol levels, but did not change LH levels, Organophosphate compounds may result in sick euthyroid syndrome, These conditions may be related to the effects of acetylcholine and direct effect of organophosphate compounds

    The value of low dose (1 mu g) ACTH stimulation test in thelpvestiation of non-classic adrenal hyperplasia due to 11 beta-hydroxylase deficieny

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    Non-classic congenital adrenal hyperplasia (NCAH) is a rare cause of hirsutism and it results from a defect in the biosynthetic pathway of cortisol and/or aldosterone. 250 mug ACTH test (SDT) is used in the diagnosis of this disease. Our aim was to investigate the responses of 11-deoxycortisol to 1mug ACTH (LDT) test in women with 'NCAH due to 11-beta hydroxylase (11-beta OH) deficiency and to compare them with the values obtained after SDT in the patients and in the control subjects. Eleven patients with NCAH due to 11-beta OH deficiency and '15 control subjects were involved in the study. The main complaint of the patients with NCAH was hirsutism and the diagnosis was made if the adrenal 11-deoxycortisol response to SDT exceed threefold the 95th percentile of controls. ACTH stimulation tests were carried out consecutively by using 250 mug and 1 mug intravenous ACTH as a bolus injection after an overnight fast, and blood samples were drawn at 0,30 and 60 min. Peak cortisol, 17-hydroxyprogesterone (17-OHP) and DHEAS responses were similar in LOT and SDT while 11-deoxycortisol responses to LDT (15.7 +/- 1.8 nmol/L) were significantly (p < 0.005) lower than the results obtained after SDT (76.3 &PLUSMN; 21.4 nmol/L) in women with 11-&beta; OH deficiency. Peak cortisol and 17-OHP responses to LDT in patients and control subjects were similar. Peak 11-deoxycortisol responses to LDT were significantly (p<0.05) higher in NCAH patients (15.7 +/- 1.8 nmol/L) than in the control subjects (6.5 +/- 0.8 nmol/L). However, in LDT, all patients had peak 11-deoxycortisol level lower than threefold the 95th percentile (25.8 nmol/L) of controls. This study represents the first demonstration that LDT gives similar cortisol but not 11-deoxycortisol responses to SDT in patients with 11-beta OH deficiency. This study also showed that LDT can not replace SDT in every clinical situation

    Investigation of adrenal functions in patients with idiopathic hyperandrogenemia

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    Objective: Some patients with hyperandrogenemia had no identifiable cause, which was named as idiopathic hyperandrogenemia (IHA). The role of the adrenal glands in these patients was investigated
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