A significant percent of women with hyperprolactinemia whom we evaluated had sexual dysfunction. No hormonal changes other than prolactin and no depression was found as a cause of FSD.

OBJECTIVES:The aim of this study was to examine the frequency of Cushing’s syndrome (CS) in obese patients devoid of specific clinical symptoms of Cushing’s syndrome.METHODS:A total of 150 obese patients (129 female, 21 male; mean age 44.41 ± 13.34 yr; mean BMI 35.76 ± 7.13) were included in the study. As a first screening step, we measured 24-h urinary free cortisol (UFC). An overnight 1-mg dexamethasone suppression test was also performed on all patients. Urinary free cortisol levels above 100 μg/24 h were considered to be abnormal. Suppression of serum cortisol <1.8 μg/dL after administration of 1 mg dexamethasone was the cut-off point for normal suppression. The suppression of the serum cortisol levels failed in all of the patients.RESULTS:Measured laboratory values were as follows: ACTH, median level 28 pg/ml, interquartile range (IQR) 14–59 pg/ml; fasting glucose, 100 (91–113) mg/dL; insulin, 15.7 (7.57–24.45) mU/ml; fT4, 1.17 (1.05–1.4) ng/dL; TSH, 1.70 (0.91–2.90) mIU/L; total cholesterol, 209 (170.5–250) mg/dL; LDL-c, 136 (97.7–163) mg/dL; HDL-c, 44 (37.25–50.75) mg/dL; VLDL-c, 24 (17–36) mg/dL; triglycerides, 120.5 (86–165) mg/dL. The median UFC level of the patients was 30 μg/24 h (IQR 16–103). High levels of UFC (>100 μg/24 h) were recorded in 37 patients (24%). Cushing’s syndrome was diagnosed in 14 of the 150 patients (9.33%). Etiologic reasons for Cushing’s syndrome were pituitary microadenoma (9 patients), adrenocortical adenoma (3 patients), and adrenocortical carcinoma (1 patient).CONCLUSION:A significant proportion (9.33%) of patients with simple obesity were found to have Cushing’s syndrome. These findings argue that obese patients should be routinely screened for Cushing’s syndrome.

Abstract. The objective of the present study was to investigate the effects of octreotide long acting release (S-LAR) preparation on GH and IGF-1 serum concentrations and pituitary tumor size in patients with persistent and difficultly controlled acromegaly even after adjuvant irradiation and/or dopamine agonists. Thirty-three patients with active acromegaly (26 female and 7 male, mean age; 43.94 ± 14.01 SD years) were included in this study. Patients were evaluated at baseline and at 6, 12, 30 and 40 months for GH, IGF-1, and GH response to OGTT and biliary ultrasonography. Sella MRI was performed at initial and at 40 months. All patients received 20 mg S-LAR. Afterwards, the dosage was titrated to improve individual GH response and reduction of IGF-1 into normal ranges.

Familial acromegaly without features of multiple endocrine neoplasie type 1 (MEN 1) is an exceptional clinical entity. We report in this article three cases of acromegaly due to pituitary macroadenomas without any other endocrinopathy in a family. A 31-year-old woman (subject A) and her 34-year-old sister (subject B) with elevated basal rolactin (PRL) levels, elevated growth hormone (GH) levels during the oral glucose tolerance test (OGTT) and a pituitary adenoma in Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) were diagnosed as acromegaly. Subject A was treated only with radiotherapy and Lysuride. Subject B underwent transsphenoidal microsurgical extirpation 15 years ago. 11 years later her 24-year-old son (subject C) also presented with typical signs of acromegaly, elevated basal PRL level and elevated GH levels during OGTT. A pituitary macroadenoma was identified by MRI and he also underwent transsphenoidal adenomectomy. Pathology reports confirmed the diagnosis of GH-secreting pituitary adenoma in subject B and C. Immunocytochemistry revealed that tumours of subject B (> 20% of tumour cells) and C (> 50% of tumour cells) were positive for GH. Tumours of subject B (> 10% of tumour cells) and C (> 50% of tumour cells) also exhibited immunoreactivity for PRL. On investigation of histocompatibility antigens, it was observed that the subject A, B, and C shared the same haplotypes [HLA A24(9), HLA B13(6), HLA B35, HLA DQ7(3), HLA DR13(6)] and so it is very possible that investigation of HLA antigens in patients with pituitary tumour, contributes to better identification of its familial nature and frequency. Here we describe an acromegaly family and the distributions of HLA antigens.

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