ACTA ENDOCRINOLOGICA (BUC)

The International Journal of Romanian Society of Endocrinology / Registered in 1938

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Year Volume Issue First page
10.4183/aeb.
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  • Case Report

    Tastekin E, Can N, Ayturk S, Celik M, Ustun F, Guldiken S, Sezer A, Celik H, Koten M

    Clinically Undetectable Occult Thyroid Papillary Carcinoma Presenting with Cervical Lymph Node Metastasis

    Acta Endo (Buc) 2016 12(1): 72-76 doi: 10.4183/aeb.2016.72

    Abstract
    Background. Occult papillary thyroid carcinoma presented as isolated cervical lymphadenopathy without clinical and radiologic findings has been rarely reported. Case report. A 47 years old female patient admitted to otorhinolaryngology clinic with 4X3 cm sized cervical mass. Physical examination of the patient was noted as a nontender, firm, mobile lymph node at right lateral cervical region. There was no inflammatory or infection disease in the history of patients anamnesis and no abnormal value on laboratory tests. Ultrasound screening of the neck detected a lymph node with suspicious features for malignancy. Head and neck examination was normal and there is no evidence of a tumoral mass or nodule in the thyroid gland. Whole body scan of MRI showed no pathologic sign both in the neck and body. Excisional biopsy was performed and revealed a carcinoma with papillary morphology. Immunohistochemical staining features of the tumor confirmed a papillary carcinoma derived from the thyroid gland. Second look USG of the neck and thyroid was performed but it revealed no tumoral mass. The patient underwent total thyroidectomy with right functional and central lymph node dissection. Histological examination of the thyroid gland showed multicentric 2 mm sized, three foci of papillary carcinoma located in bilateral thyroid lobes and metastatic lymph nodes in the right side of the neck. Conclusion. A metastatic cervical lymph node can be evidence of a clinically undetected occult papillary thyroid carcinoma. Specific immunohistochemistry staining of specimen may lead to appropriate surgery and progression of carcinoma may be hindered by application of additional RAI therapy.
  • Endocrine Care

    Dong Q, Liu X, Wang F, Xu Y, Liang C, Du W, Gao G

    Dynamic Changes of TRAb and TPOAb after Radioiodine Therapy in Graves’ Disease

    Acta Endo (Buc) 2017 13(1): 72-76 doi: 10.4183/aeb.2017.72

    Abstract
    Context. To analyze the dynamic changes of serum thyrotrophin receptor antibody (TRAb) and thyroid peroxidase antibody (TPOAb) in Graves’ disease (GD) patients before and after radioactive iodine (RAI) treatment and to investigate if TRAb and TPOAb play a role in the occurrence of early hypothyroidism after 131I therapy for Graves’ hyperthyroidism. Subjects and Methods. A total of 240 patients newly diagnosed with GD were selected to study. A clinical and laboratory assessment was performed before and at 3, 6, and 12 months after 131I therapy. Chemiluminescent immunoassays were used to detect serum free triiodothyronine (FT3), free thyroxine (FT4), sensitive thyroid-stimulating hormone (TSH) and TPOAb concentration. Radio-receptor assay was used to measure serum TRAb concentration. According to the early onset of hypothyroidism in a year after RAI therapy, patients were divided into early hypothyroidism group (group A) and non-early hypothyroidism group (group B). Results. In both groups, serum TRAb and TPOAb increased at 3 months, reached the highest level at 6 months and returned to the baseline at 12 months after RAI therapy. TRAb showed a significant difference between the two groups at 6 months (P<0.01). Serum TPOAb in group A was higher than that in group B before and at 3, 6, 12 months after RAI therapy (P<0.05). Conclusions. Serum TRAb and TPOAb are closely related to the occurrence of the early hypothyroidism, and play an important role in judging prognosis after 131I treatment in Graves’ disease.
  • Endocrine Care

    Livadariu R, Timofte D, Trifan A, Danila R, Ionescu L, Sîngeap AM, Ciobanu D

    Vitamin D Deficiency, A Noninvasive Marker of Steatohepatitis in Patients with Obesity and Biopsy Proven Nonalcoholic Fatty Liver Disease

    Acta Endo (Buc) 2018 14(1): 76-84 doi: 10.4183/aeb.2018.76

    Abstract
    Context. Nonalcoholic fatty liver disease (NAFLD) includes simple steatosis, steatohepatitis (NASH) which can evolve with progressive fibrosis, cirrhosis and hepatocellular carcinoma. As liver biopsy cannot be used as a screening method, noninvasive markers are needed. Objective. The aim of this study was to test if there is a significant association between vitamin D deficit and the severity of NAFLD. Design. The patients were divided into two groups (vitamin D insufficiency/deficiency) and statistical analyses were performed on the correlation of clinical and biochemical characteristics with histopathological hepatic changes. Subjects and methods. We prospectively studied 64 obese patients referred for bariatric surgery between 2014 and 2016 to our Surgical Unit. Anthropometric, clinical measurements, general and specific biological balance were noted. NAFLD diagnosis and activity score (NAS) were evaluated on liver biopsies. Results. Increased serum fibrinogen was correlated with NASH (p=0.005) and higher NAS grade. T2DM was positively correlated with liver fibrosis (p=0.002). 84.37% of the patients had vitamin D deficit and 15.62% were vitamin D insufficient. Lobular inflammation correlated with vitamin D deficit (p=0.040). Fibrosis (p=0.050) and steatohepatitis (p=0.032) were independent predictors of low vitamin D concentration. Conclusions. Vitamin D status in conjunction with other parameters - such as T2DM - or serum biomarkers – namely fibrinogen level and PCR level - may point out the aggressive forms of NAFLD and the need for liver biopsy for appropriate management.
  • Editorial

    Coman L, Paunesc H, Catana R, Coman LI, Voiculescu S, Coman OA

    Alzheimer’s Disease – Estrogens and Selective Estrogen Receptor Modulators, Friends or Foes?

    Acta Endo (Buc) 2017 13(1): 77-83 doi: 10.4183/aeb.2017.77

    Abstract
    Alzheimer’s disease(AD) is the leading cause of dementia and is characterized by the presence of extensive plaque deposition and neurofibrillary pathology. The aim of the present study was to make an update regarding the influence of estrogens and SERMs on inflammation and on the resolution of inflammation, respectively, focusing on these most important features implicated in the pathophysiology of AD. Several hypothesised mechanisms of action of estrogens and SERM are exposed and also some relevant clinical studies on this subject are analysed. The analyzed studies have a high heterogeneity of preparations used, of administration routes, of the female population included and of the periods of time from the appearance/ induction of menopause to the therapeutic intervention and also of follow-up periods of patients and of the means of evaluating their cognitive decline. One can say that all the ways of pharmacological influence on the membrane or intracellular signalling system associated to estrogens that may have clinical importance in the prevention and possibly in the treatment of AD have not been exhausted. Estrogens with selective ERα or G protein-coupled estrogen receptors (GPER1 or GqMER) effects could be used to influence the resolution of inflammation process, with positive effects on AD evolution.
  • Clinical review/Extensive clinical experience

    Cvasciuc IT, Gull S, Oprean R, Lim KH, Eatock F

    Changing Pattern of Pheochromocytoma and Paraganglioma in a Stable UK Population

    Acta Endo (Buc) 2020 16(1): 78-85 doi: 10.4183/aeb.2020.78

    Abstract
    Context. Pheochromocytomas and paragangliomas (PCC/PGLs) are diagnosed variously with increasing incidence and changing clinical and pathology pattern. Objective. The aim was to further characterize PCC/PGLs in a stable population. Methods. A retrospective, single institution study analysed adrenalectomies for PCC/PGLs between January 2010 - January 2019. Demographics, symptoms, blood pressure, preoperative hormones, imaging, histology, hospital stay, complications and three subgroups [based on the modality of diagnosis - incidentaloma group (IG), genetic group (GG) and symptomatic group (SG)] were noted. Results. 86 patients included IG 51 (59.3%), GG 10 (11.62%) and SG 25 patients (29.06%). Incidence was 5.30 cases/1 million population. 33.34% of the IG had a delayed diagnosis with a mean interval of 22.95 months (4- 120 months). Females presented more often with paroxysmal symptoms (PS) (p=0.011). Patients with PS and classic symptoms were younger (p=0.0087, p=0.0004) and those with PS required more inotropes postoperatively (p=0.014). SG had higher preoperative hormone levels (p=0.0048), larger tumors (p=0.0169) and more likely females. GG are younger compared with those from the IG (p=0.0001) or SG (p= 0.178). Conclusion. Majority of patients had an incidental and delayed diagnosis. If symptomatic, patients are more likely to be young females with higher hormone levels and larger tumors.
  • Endocrine Care

    Elian VI, Serafinceanu C

    WEIGHT LOSS IN YOUNG OBESE SUBJECTS IMPROVES LIPIDS AND ADIPOKINES LEVELS AND REDUCES ARTERIAL STIFFNESS

    Acta Endo (Buc) 2013 9(1): 79-86 doi: 10.4183/aeb.2013.79

    Abstract
    Background The cardiovascular risk in obese patients is very high and is the main cause of mortality and morbidity. While many studies have focused on obese patients who already developed cardiovascular pathologies few tried to address the prevention of atherosclerosis in healthy young adults. Objectives In the present study we assessed the effect of weight loss on atherosclerosis risk factors and on vascular stiffness. While no important clinical events were expected our goal was to show that weight loss in obese patients will lower the vascular risk. Subjects and methods 159 obese patients with no cardiovascular pathology were assigned, for 6 months, to either weight loss program or a weight maintenance recommendation. The intensive care group subjects participated to weekly visits consisting of counseling on hypocaloric diets and physical exercise programs. We have measured BMI, lipid profile, adipokines levels, glycemia as well as markers of arterial stiffness (CAVI, BP, ABI). Results At the study endpoint, we found a clinically and statistically significant (p<0.001) difference between the lipid and the adipokines profiles, and, in univariate analysis, this difference correlates with weight loss: for total cholesterolemia decrease r= 0.63, LDL decrease r= 0.65, HDL increase r= -0.48, adiponectin increase r= -0.59, leptin decrease r=0.6 and also with abdominal circumference decrease. We also found correlation between vascular stiffness parameters (CAVI, diastolic blood pressure) and the adipose tissue loss (r = 0,71; p < 0,001 for CAVI and r = 0,4; p = 0,001 for DBP). Conclusions : We found that using a moderate hypocaloric diet and encouraging physical exercise, even after a short period of time, subjects can lose weight, mainly by losing fat mass. The weight loss improved the lipid and adipokines levels and had reduced vascular stiffness
  • Endocrine Care

    Niculescu DA, Botusan I, Rasanu C, Radian S, Filip O, Coculescu M

    Central sleep apnea in acromegaly versus obesity

    Acta Endo (Buc) 2005 1(1): 79-88 doi: 10.4183/aeb.2005.79

    Abstract References
    INTRODUCTION: Sleep apnea syndrome is a common manifestation of acromegaly. Although the obstructive type of apnea was thought to be predominant there are some reports suggesting that central apneic episodes show a high rate and are related to abnormalities of central respiratory control.\r\nAIM: The present study determines the presence and severity of central sleep apnea syndrome in patients with acromegaly compared with obese subjects.\r\nMATERIALS AND METHODS: 35 consecutive acromegalic patients (min GH (growth hormone) during oral glucose tolerance test (OGTT) 6.6 ng/ml) and 19 obese subjects (BMI=44 kg/m2) were polisomnographically recorded between 10 p.m and 6 a.m. Sleep and respiratory disturbances were manually staged according to standard criteria.\r\nRESULTS: The prevalence of sleep apnea syndrome in acromegaly group was 45.7% (16 out of 35 patients). The median of minimum GH level during OGTT was 8.3 ng/ml in apnea group and 5.16 ng/ml in nonapneic group (p>0.05). In acromegaly group with severe sleep apnea syndrome central apnea rate was greater than 10% in 6 out of 7 subjects with REM sleep and in 7 out of 10 with NREM sleep whereas in obesity group this percent was present in 6 out of 18 (REM sleep), respectively 7 out of 19 (NREM sleep).\r\nCONCLUSIONS: The study confirms the high prevalence of sleep apnea in acromegaly. GH serum level is not an indicator for the presence and severity of sleep apnea. Although the total time of central apnea per hour of sleep did not differ between the two groups, the percent (rate) of central apnea was significantly greater in acromegaly group.
    1. Laroche C, Festal G, Poenaru S, Caquet R, Lemaigre D, Auperin A. [A case of periodic respiration in a patient with acromegaly]. Ann Med Interne (Paris) 1976; 127(5):381-385.
    2. Roxburgh F, Collis A. Notes on a case of acromegaly. Br Med J 1886; 2:63-65.
    3. Grunstein RR, Ho KY, Sullivan CE. Sleep apnea in acromegaly. Ann Intern Med 1991; 115(7): 527-532.
    4. Pelttari L, Polo O, Rauhala E, Vuoriluoto J, Aitasalo K, Hyyppa MT et al. Nocturnal breathing abnormalities in acromegaly after adenomectomy. Clin Endocrinol (Oxf) 1995; 43(2):175-182. [CrossRef]
    5. Rosenow F, Reuter S, Deuss U, Szelies B, Hilgers RD, Winkelmann W et al. Sleep apnoea in treated acromegaly: relative frequency and predisposing factors. Clin Endocrinol (Oxf) 1996; 45(5):563-569. [CrossRef]
    6. Colao A, Ferone D, Marzullo P, Lombardi G. Systemic complications of acromegaly: epidemiology, pathogenesis, and management. Endocr Rev 2004; 25(1):102-152. [CrossRef]
    7. Grunstein RR, Ho KY, Berthon-Jones M, Stewart D, Sullivan CE. Central sleep apnea is associated with increased ventilatory response to carbon dioxide and hypersecretion of growth hormone in patients with acromegaly. Am J Respir Crit Care Med 1994; 150(2
    8. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques, and Scoring System for Sleep Stages of Human Subjects. Washington, DC: National Institutes of Health, 1968.
    9. American Academy of Sleep Medicine. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999; 22(5):6
    10. Kryger M. Monitoring Respiratory and Cardiac Function. In: Kryger M, Roth T, Dement W, editors. Principles and Practice of Sleep Medicine. Philadelphia: W.B. Saunders, 2000: 1217-1230.
    11. Dostalova S, Sonka K, Smahel Z, Weiss V, Marek J, Horinek D. Craniofacial abnormalities and their relevance for sleep apnoea syndrome aetiopathogenesis in acromegaly. Eur J Endocrinol 2001; 144(5):491-497. [CrossRef]
    12. Hochban W, Brandenburg U. Morphology of the viscerocranium in obstructive sleep apnoea syndrome?cephalometric evaluation of 400 patients. J Craniomaxillofac Surg 1994; 22(4):205-213. [CrossRef]
    13. Hochban W, Ehlenz K, Conradt R, Brandenburg U. Obstructive sleep apnoea in acromegaly: the role of craniofacial changes. Eur Respir J 1999; 14(1):196-202. [CrossRef]
    14. Herrmann BL, Wessendorf TE, Ajaj W, Kahlke S, Teschler H, Mann K. Effects of octreotide on sleep apnoea and tongue volume (magnetic resonance imaging) in patients with acromegaly. Eur J Endocrinol 2004; 151(3):309-315. [CrossRef]
    15. Isono S, Saeki N, Tanaka A, Nishino T. Collapsibility of passive pharynx in patients with acromegaly. Am J Respir Crit Care Med 1999; 160(1):64-68.
    16. Weiss V, Sonka K, Pretl M, Dostalova S, Klozar J, Rambousek P et al. Prevalence of the sleep apnea syndrome in acromegaly population. J Endocrinol Invest 2000; 23(8):515-519.
    17. Cadieux RJ, Kales A, Santen RJ, Bixler EO, Gordon R. Endoscopic findings in sleep apnea associated with acromegaly. J Clin Endocrinol Metab 1982; 55(1):18-22. [CrossRef]
    18. Lindgren AC, Hellstrom LG, Ritzen EM, Milerad J. Growth hormone treatment increases CO(2) response, ventilation and central inspiratory drive in children with Prader-Willi syndrome. Eur J Pediatr 1999; 158(11):936-940. [CrossRef]
    19. Grunstein RR, Ho KY, Berthon-Jones M, Stewart D, Sullivan CE. Central sleep apnea is associated with increased ventilatory response to carbon dioxide and hypersecretion of growth hormone in patients with acromegaly. Am J Respir Crit Care Med 1994; 150(2
    20. Llona I, Ampuero E, Eugenin JL. Somatostatin inhibition of fictive respiration is modulated by pH. Brain Res 2004; 1026(1):136-142. [CrossRef]
    21. Chen ZB, Engberg G, Hedner T, Hedner J. Antagonistic effects of somatostatin and substance P on respiratory regulation in the rat ventrolateral medulla oblongata. Brain Res 1991; 556(1):13-21. [CrossRef]
    22. Pedersen ME, Dorrington KL, Robbins PA. Effects of somatostatin on the control of breathing in humans. J Physiol 1999; 521 Pt 1:289-297. [CrossRef]
    23. Lopata M, Freilich RA, Onal E, Pearle J, Lourenco RV. Ventilatory control and the obesity hypoventilation syndrome. Am Rev Respir Dis 1979; 119(2 Pt 2):165-168.
    24. Zwillich CW, Sutton FD, Pierson DJ, Greagh EM, Weil JV. Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome. Am J Med 1975; 59(3):343-348. [CrossRef]
    25. Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996; 334(5):292-295. [CrossRef]
    26. Schwartz MW, Peskind E, Raskind M, Boyko EJ, Porte D, Jr. Cerebrospinal fluid leptin levels: relationship to plasma levels and to adiposity in humans. Nat Med 1996; 2(5):589-593. [CrossRef]
    27. Fruhbeck G, Jebb SA, Prentice AM. Leptin: physiology and pathophysiology. Clin Physiol 1998; 18(5):399-419. [CrossRef]
    28. Lundberg JM, Pernow J, Fried G, Anggard A. Neuropeptide Y and noradrenaline mechanisms in relation to reserpine induced impairment of sympathetic neurotransmission in the cat spleen. Acta Physiol Scand 1987; 131(1):1-10. [CrossRef]
    29. Mann K, Benkert O, R?schke J. Effects of corticotropin-releasing hormone on respiratory parameters during sleep in normal men. Exp Clin Endocrinol 1994; 103:233-240. [CrossRef]
    30. O?donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR et al. Leptin prevents respiratory depression in obesity. Am J Respir Crit Care Med 1999; 159(5 Pt 1):1477-1484.
    31. Shimura R, Tatsumi K, Nakamura A, Kasahara Y, Tanabe N, Takiguchi Y et al. Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome. Chest 2005; 127(2):543-549. [CrossRef]
    32. Tatemoto K. Neuropeptide Y: complete amino acid sequence of the brain peptide. Proc Natl Acad Sci USA 1982; 79(18):5485-5489. [CrossRef]
    33. Clark JT, Karla PS, Crowley WR, Karla SP. Neuropeptide Y and human pancreatic polypeptide stimulate feeding behavior in rats. Endocrinology 1984; 115:427-429. [CrossRef]
    34. Stanley BG, Kyrkouli SE, Lampert S, Leibowitz SF. Neuropeptide Y chronically injected into the hypothalamus: a powerful neurochemical inducer of hyperphagia and obesity. Peptides 1986; 7(6):1189-1192. [CrossRef]
    35. Thorsell A, Heilig M. Diverse functions of neuropeptide Y revealed using genetically modified animals. Neuropeptides 2002; 36(2-3):182-193. [CrossRef]
    36. Nam SY, Kratzsch J, Kim KW, Kim KR, Lim SK, Marcus C. Cerebrospinal fluid and plasma concentrations of leptin, NPY, and alpha-MSH in obese women and their relationship to negative energy balance. J Clin Endocrinol Metab 2001; 86(10):4849-4853. [CrossRef]
    37. Harfstrand A. Brain neuropeptide Y mechanisms. Basic aspects and involvement in cardiovascular and neuroendocrine regulation. Acta Physiol Scand Suppl 1987; 565:1-83.
    38. Morton KD, McCloskey MJ, Potter EK. Cardiorespiratory responses to intracerebroventricular injection of neuropeptide Y in anaesthetised dogs. Regul Pept 1999; 81(1-3):81-88. [CrossRef]
  • Editorial

    Macut D, Opalic M, Popovic B, Ognjanovic S, Bjekic-Macut J, Livadas S, Petrovic T, Hrncic D, Stanojlovic O, Vojnovic Milutinovic D, Micic D , Mastorakos G

    The Effects of Endocrine Disruptors on Female Gonadal Axis: an Update

    Acta Endo (Buc) 2023 19(1): 81-86 doi: 10.4183/aeb.2023.81

    Abstract
    Endocrine disruptors (EDs) are considered to have an impact on the function of reproductive axis at different levels as well on reproductive organs in both sexes. Complexity of female reproductive system influenced with various stressors including EDs lead to morphological and functional alterations. This is resulting in modulation of neuroendocrine regulation with consequent developmental irregularities and derangements, causative infertility, endometriosis as well as premature ovarian insufficiency or polycystic ovary syndrome. A number of experimental clues was obtained on female animal models using various EDs such as synthetic estrogens and phytoestrogens, neurotransmitters, pesticides or various chemicals. These substances lead towards consequent derangement of the neuroendocrine control of reproduction from early phases of reproductive development towards different phases of adult reproductive period. This text will address some novel insights into the effects of EDs on neuroendocrine regulation of gonadal axis, effects on ovaries as well on endometrium during implantation period.
  • Endocrine Care

    Hashemi SB, Sarbolouki S., Djalali M., Dorosty A., Djazayery S.A., Eshraghian M.R., Ebadi A., Sharif M.R., Nikoueinejad H

    Adiponectin and Glycemic Profiles in Type 2 Diabetes Patients on Eicosapentaenoic Acid with or without Vitamin E

    Acta Endo (Buc) 2014 10(1): 84-96 doi: 10.4183/aeb.2014.84

    Abstract
    Background. Secreting different adipocytokines, adipose tissue plays an important role in health and disease. Upon omega-3 consumption, changes in the secretion of adipose tissue and its effects on glycemic profile are a controversial subject at the present time. Objectives. We evaluated the effects of eicosapentaenoic acid (EPA) alone and in combination with vitamin E on adiponectin and serum glycemic indices in type II Diabetes patients. Design. This double-blind clinical trial divided all patients randomly into four balanced permuted blocks of EPA, Vitamin E, EPA and vitamin E and placebo (Corn oil). Subjects and Methods. 127 patients with type II diabetes living in Kashan in 2008, 35-50 years old, and 25≤BMI ≤30 were enrolled. ELISA, Glucose Oxidase, spectrophotometry, and Radioimmunoassay methods were used for measurement of serum adiponectin, Fasting Blood Glucose (FBG), HbA1C, and Insulin, respectively. Results. Serum adiponectin increased significantly after EPA consumption in EPA and EPA+E groups. Moreover, FBG, HbA1c, serum insulin and Homeostasis Model HOMA-IR decreased significantly after EPA consumption in the two previously mentioned groups. Conclusions. This study showed that EPA supplementation affects the secretion of adipose tissue, improves the FBS as well as HbA1c values and significantly decreases fasting serum insulin and insulin resistance.
  • Clinical review/Extensive clinical experience

    Diri H, Bayram F, Simsek Y, Caliskan Z, Kocer D

    Comparison of Finasteride, Metformin, and Finasteride Plus Metformin in PCOS

    Acta Endo (Buc) 2017 13(1): 84-89 doi: 10.4183/aeb.2017.84

    Abstract
    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, AUCinsulin, 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.