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ACTA ENDOCRINOLOGICA (BUC)
The International Journal of Romanian Society of Endocrinology / Registered in 1938in Web of Science Master Journal List
Acta Endocrinologica(Bucharest) is live in PubMed Central
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General Endocrinology
Arslan S, Kiragi D, Kadayifcilar S, Samur G
Increased Dietary Intake and Serum Levels of Advanced Glycation End Products (Ages) are Associated With Diabetic Macular EdemaActa Endo (Buc) 2022 18(3): 278-287 doi: 10.4183/aeb.2022.278
AbstractAim. Diabetic macular oedema (DME) can develop at all stages of diabetic retinopathy, causing visual impairment and blindness. Modern diets are high in advanced glycation end products (dAGEs), derived from processing methods, exerting a pivotal role in promoting diabetic retinopathy risk. In present study, we investigate the relationship between dietary and serum levels of AGEs and DME in type 2 diabetic subjects. Methods. This case-control study was conducted between July 2018 and February 2019 on 50 case subjects with DME and 40 healthy controls without DM without DME. The sociodemographic characteristics, nutritional status, and anthropometric measurements were evaluated. The advanced glycation end products (AGEs) and receptor for AGEs (sRAGE) levels in serum were analysed. Results. The AGEs levels of the DME group were higher than in the control group (p <0.05). sRAGE levels were higher in the DME group, but not statistically significant (p >0.05). The dietary intake of AGEs was higher in the DME group (p <0.05). It was found that an increase in neck circumference increased the risk of DME (p <0.001). Conclusion. A positive correlation was found between DME and AGEs, dAGE, neck circumference, and waist circumference. For the validity of these results, studies, including controlled nutrition interventions, are needed. -
Letter to the Editor
Panaitescu AM
Resuming Adequate Screening for Gestational Diabetes Mellitus During the Ongoing Covid-19 PandemicActa Endo (Buc) 2021 17(2): 278-279 doi: 10.4183/aeb.2021.278
AbstractThe novel coronavirus disease 2019 (COVID-19) pandemic has had a profound impact on antenatal care, forcing authorities to consider some medical services unessential in the pursuit of avoiding the valid risk of patient contamination. The oral glucose tolerance test (OGTT) has been in some cases overlooked for screening in pregnancy, with potential detrimental consequences in terms of not diagnosing and treating gestational diabetes mellitus (GDM). The number of tests has dropped by 35% in 2020 in our hospital. We make a plea for resuming OGTT at 24-28 weeks gestation at least for women considered at high risk. -
General Endocrinology
Bonakdaran S, Khorasani ZM, Jafarzadeh F
Increased Serum Level of FGF21 in Gestational Diabetes MellitusActa Endo (Buc) 2017 13(3): 278-281 doi: 10.4183/aeb.2017.278
AbstractObjective. Gestational diabetes mellitus (GDM) is a common endocrine complication in pregnancy. There are few risk factors that clearly correlate with GDM. Fibroblast growth factor 21 (FGF21) is a metabolic hormone that can regulate glucose metabolism. It has been recognized that serum levels of FGF21 are significantly increased in diabetes and insulin resistance states. The objective of this study was to determine the serum FGF21 levels in women with GDM compared with non-GDM women and its correlation with insulin resistance. Methods. Thirty GDM patients and 60 healthy pregnant controls that matched for maternal and gestational age were selected. Women with previous history of GDM, hypertension, polycystic ovary syndrome, renal or liver failure and drug consumption with effects on glucose or insulin levels were excluded. FGF21 was determined and correlated with biochemical parameters of glucose metabolism and insulin resistance. Results. FGF21 concentration was significantly higher in GDM (264.5±196.2 ng/L) as compared with control groups (59.1±36.5ng/L). Correlation of FGF21 with insulin resistance was not significant. A cut-off 82.07 ng/L of FGF21 had sensitivity of 100% and specificity of 85% for prediction of GDM. Conclusion. FGF21 is increased in GDM and it is independent of insulin resistance. We suggest that FGF21 resistance could be directly involved in pathophysiology of GDM. -
Case Report
Ghervan CM, Sufana C., Filip A., Silaghi A., Valea A., Ghervan L., Muntean V
McCune-Albright Syndrome – The Difficult Therapeutic Strategy in the Context of Multiple Tissue Damage: Fibrous Dysplasia, Acromegaly and Cushing SyndromeActa Endo (Buc) 2013 9(2): 279-288 doi: 10.4183/aeb.2013.279
AbstractIntroduction. McCune-Albright syndrome (MAS) is a noninherited, genetic condition defined by the clinical triad: polyostotic fibrous dysplasia (FD), café-aulait skin spots and different hyper functioning endocrinopathies. Case presentation. The patient, a 39-year-old female previously diagnosed with MAS, presented with severe, left-sided skeletal pain and accentuated asymmetrical facial features. Although there were no clinical signs (except type II diabetes) the hormonal dosages revealed GH hypersecretion and ACTH-independent hypercortisolism. The modified bone anatomy rendered the surgical adenomectomy impossible, whereas radiotherapy was not an option due to the increased risk of sarcomatous transformation of FD; therefore somatostatin analogues were used. Cushing syndrome was cured by left adrenalectomy. For the facial dysmorphism, surgical cure was proposed. CT revealed a pituitary microadenoma, severe craniofacial hyperostosis and left-side macronodular adrenal hyperplasia. Conclusion. We report the case of an adult female with MAS associating both acromegaly and Cushing syndrome, the MAS-Cushing syndrome association having been identified only in children up to present. The setting of a therapeutic strategy in these cases is difficult determined by the multiple concomitant tissue damage and by the limited number of therapeutic options available, not only for acromegaly, but also for pain management and the cure of bone deformities. -
Actualities in medicine
Niculescu DA
European Thyroid Association (ETA) Guidelines for Central HypothyroidismActa Endo (Buc) 2018 14(2): 280-281 doi: 10.4183/aeb.2018.280
Abstract- -
Images in Endocrinology
Dobrescu R, Stanescu B, Ioachim D, Badiu C
What is Hidden in a Cystic Lesion after Extensive Surgery for Medullary Thyroid Carcinoma?Acta Endo (Buc) 2021 17(2): 280-281 doi: 10.4183/aeb.2021.280
Abstract- -
General Endocrinology
Xu F, Chen R, Ma C, Tang L, Wan W, You F, Chen L, Li J, Chen Z, Liang F
Electroacupuncture Improves Insulin Sensitivity in High-Fat Diet-Induced Insulin Resistant Rats by Activating SIRT1 and GLUT4 in Quadriceps FemorisActa Endo (Buc) 2020 16(3): 280-287 doi: 10.4183/aeb.2020.280
AbstractObjectives. To assess the effects of electroacupuncture (EA) at the Zusanli (ST36), Guanyuan (CV4), Zhongwan (CV12), and Fenglong (ST40) acupoints on sirtuin 1 (SIRT1) and glucose transporter type 4 (GLUT4) expression in high-fat diet (HFD)-induced insulin-resistant (IR) rats. Methods. Wistar rats were divided into normal control (NC), HFD, and HFD+EA groups. NC rats were fed a standard chow diet and did not receive EA. After being fed an HFD for eight weeks, rats in the HFD+EA group received EA at 2 Hz five times a week for eight weeks. Rats in the HFD group did not receive EA. Results. In HFD-induced IR rats, EA inhibited body weight increase and water intake, which were observed in HFD rats. EA had no effect on fasting blood glucose and postprandial blood sugar levels. Intraperitoneal insulin tolerance testing revealed that EA enhanced insulin sensitivity in HFD-induced IR rats. Compared with NC rats, SIRT1 and GLUT4 were downregulated in the quadriceps femoris of HFD-fed rats but were increased after eight weeks of EA stimulation. Conclusions. EA enhanced HFD-induced insulin resistance by activating SIRT1 and GLUT4 in the quadriceps femoris. These results provide powerful evidence supporting the beneficial effects of EA on HFD-induced insulin resistance. -
General Endocrinology
Genes D, Pekkolay Z, Simsek M, Saracoglu H, Turgut M, Tekes S, Tuzcu AK
Comparison of C-Peptide Levels in Monogenic Forms of Diabetes with other Types of Diabetes: a Single-Center StudyActa Endo (Buc) 2023 19(3): 281-285 doi: 10.4183/aeb.2023.281
AbstractObjective. This study aimed to evaluate the utility of C-peptide levels in the differentiation of monogenic forms of diabetes from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in clinical practice. Subjects and Methods. A total of 104 patients aged >16 who visited the Dicle University’s Faculty of Medicine between April 2011 and December 2020 and were diagnosed with monogenic diabetes by genetic analysis or with T1DM and T2DM were randomly selected for retrospective evaluation. The C-peptide levels of these patients at the time of diagnosis of diabetes were compared. Results. Of the 104 patients, 24 (23%) were diagnosed with maturity-onset diabetes of the young (MODY), 40 (38.5%) with T1DM, and 40 (38.5%) with T2DM. Median C-peptide levels (ng/mL) (interquartile range) were 1.78 (1.24–2.88) in MODY group, 0.86 (0.34– 1.22) in T1DM group, and 2.38 (1.58–4.27) in T2DM group. Conclusions. There was a difference in C-peptide levels between MODY and T1DM groups but not between MODY and T2DM groups. As per clinical evaluations, although C-peptide levels of patients with MODY are similar to those of patients with T2DM patients, the possibility of C-peptide levels being similar to those required for T1DM diagnosis should also be considered. -
Endocrine Care
Gheorghiu ML, Gussi I, Lutescu I, Galoiu S, Hortopan D, Caragheorgheopol A, Coculescu M
Mantaining physiological levels of serum prolactin in prolactinomas treated with dopamine agonists throughout pregnancy prevents tumor growthActa Endo (Buc) 2005 1(3): 281-298 doi: 10.4183/aeb.2005.281
Abstract ReferencesIntroduction: Prolactinomas may grow during pregnancy. Dopamine agonists (DA) prevent tumor growth, but usually suppress prolactin (PRL) both in mother and fetus. Possible long-term consequences on fetal development remain unknown.\r\nAim: to assess whether DA treatment throughout pregnancy in a dosage able to maintain physiological gestational serum levels of prolactin (PRL) still prevents prolactinoma growth.\r\nPatients and methods: We evaluated 68 pregnancies in 49 women with prolactinoma (PRM) and 46 pregnancies in healthy women as controls. Thirty-three pregnancies were recorded in 27 women treated throughout pregnancy with bromocriptine (BRC) (n = 25) or cabergoline (CAB) (n = 2) divided in 2 groups: group A (22 pregnancies in 18 patients) had suppressed serum PRL (below the 5th percentile of the control group Z during the last trimester); group B (11 pregnancies in 10 patients) had physiological serum PRL levels. Other 26 pregnancies in 21 patients were incompletely evaluated and included only in the pregnancy outcome and cure rate analysis. Treated patients were compared with the control group Y 8 women with PRM who discontinued DA after pregnancy induction (9 pregnancies) and a control group Z of 46 healthy pregnant women, randomly selected from two departments of Obstetrics. Patients with multiple pregnancies were recorded in each corresponding study group.\r\nResults: In the control group Y, tumor size showed an increase in 2 (intrasellar macroPRM) out of 8 cases (25%). DA treatment throughout gestation in 27 women with PRM prevented the growth in all cases and induced a shrinkage of more than 30% of tumor mass in 8/14 macroPRM (57.1%), i.e., in 4/7 (57.1%) of macroPRM with physiological serum PRL levels during pregnancy, and in 5/8 (62.5%) of macroPRM with suppressed PRL levels (p = NS) (1 patient had pregnancies in both groups). Low dose DA (BRC 2.5 ? 5 mg/day or CAB 0.5 mg/week) maintains physiological PRL levels in 6/12 (50%) macroPRM, but suppressed PRL in 80% of microPRM. Cure was recorded in 6/49 (12.2%) of patients. Two patients with PRM-induced neuroophthalmic syndrome were successfully treated with DA throughout 1 and respectively 3 pregnancies.\r\nConclusions: Some women with prolactinomas showed a tumour size increase if they were not treated with dopamine agonists throughout pregnancy. Maintaining physiological serum PRL levels during pregnancy (frequently with low doses of DA) prevented tumor growth, avoiding a PRL suppression that may have subtle influence on long-term foetal development.1. Sobrinho LG, Nunes MC, Santos MA, Mauricio JC. Radiological evidence for regression of prolactinoma after treatment with bromocriptine. Lancet 1978; 2(8083):257-258. [CrossRef]2. McGregor AM, Scanlon MF, Hall R, Hall K. Effects of bromocriptine on pituitary tumour size. Br Med J 1979; 2(6192):700-703. [CrossRef]3. Colao A, Annunziato L, Lombardi G. Treatment of prolactinomas. Ann Med 1998; 30(5):452-459. [CrossRef]4. Coculescu M, Simionescu N, Oprescu M, Alessandrescu D. Bromocriptine treatment of pituitary adenomas. Evaluation of withdrawal effect. Endocrinologie 1983; 21(3):157-168.5. Schlechte JA. Clinical practice. Prolactinoma. N Engl J Med 2003; 349(21):2035-2041. [CrossRef]6. Passos VQ, Souza JJ, Musolino NR, Bronstein MD. Long-term follow-up of prolactinomas: normoprolactinemia after bromocriptine withdrawal. J Clin Endocrinol Metab 2002; 87(8):3578-3582. [CrossRef]7. Coculescu M, Anghel R, Badiu C, Caragheorgheopol A, Hortopan D, Dumitrascu A et al. Additional effects of radiotherapy to dopamine agonists in the treatment of macroprolactinomas. Acta Endocrinologica (Buc) 2005; 1(1):43-60. [CrossRef]8. Colao A, Di Sarno A, Cappabianca P, Di Somma C, Pivonello R, Lombardi G. Withdrawal of longterm cabergoline therapy for tumoral and nontumoral hyperprolactinemia. N Engl J Med 2003; 349(21):2023-2033. [CrossRef]9. Robert E, Musatti L, Piscitelli G, Ferrari CI. Pregnancy outcome after treatment with the ergot derivative, cabergoline. Reprod Toxicol 1996; 10(4):333-337. [CrossRef]10. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]11. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]12. Alessandrescu D, Coculescu M, Oprescu M, Brotea G, Zagrean L, Petrenciuc O. Pregnancy induced and maintained under 2-Br-alfa-ergocryptin in a patient with evolutive prolactinoma (in Romanian). Obstetrica si Ginecologia 1981; 29:209-215.13. Briggs GG, Freeman RK, Yaffe SJ. Bromocriptine. Drugs in pregnancy and lactation. Philadelphia: Lippincott Williams & Wilkins, 2002: 143-145.14. Kletzky OA, Rossman F, Bertolli SI, Platt LD, Mishell DR, Jr. Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy. Am J Obstet Gynecol 1985; 151(7):878-884.15. Ben Jonathan N, Hnasko R. Dopamine as a prolactin (PRL) inhibitor. Endocr Rev 2001; 22(6):724-763. [CrossRef]16. Bigazzi M, Ronga R, Lancranjan I, Ferraro S, Branconi F, Buzzoni P et al. A pregnancy in an acromegalic woman during bromocriptine treatment: effects on growth hormone and prolactin in the maternal, fetal, and amniotic compartments. J Clin Endocrinol Me [CrossRef]17. Handwerger S, Freemark M. Role of placental lactogen and prolactin in human pregnancy. Adv Exp Med Biol 1987; 219:399-420.18. American College of Obstetricians and Gynecologists CoTB. Early pregnancy loss. ACOG Technical Bulletin 212. 1995.19. Elster AD, Sanders TG, Vines FS, Chen MY. Size and shape of the pituitary gland during pregnancy and post partum: measurement with MR imaging. Radiology 1991; 181(2):531-535.20. Gonzalez JG, Elizondo G, Saldivar D, Nanez H, Todd LE, Villarreal JZ. Pituitary gland growth during normal pregnancy: an in vivo study using magnetic resonance imaging. Am J Med 1988; 85(2):217-220. [CrossRef]21. Scheithauer BW, Sano T, Kovacs KT, Young WF, Jr., Ryan N, Randall RV. The pituitary gland in pregnancy: a clinicopathologic and immunohistochemical study of 69 cases. Mayo Clin Proc 1990; 65(4):461-474.22. Kupersmith MJ, Rosenberg C, Kleinberg D. Visual loss in pregnant women with pituitary adenomas. Ann Intern Med 1994; 121(7):473-477.23. Molitch ME. Pregnancy and the hyperprolactinemic woman. N Engl J Med 1985; 312(21):1364-1370. [CrossRef]24. Crosignani P, Ferrari C, Mattei AM. Visual field defects and reduced visual acuity during pregnancy in two patients with prolactinoma: rapid regression of symptoms under bromocriptine. Case reports. Br J Obstet Gynaecol 1984; 91(8):821-823.25. Konopka P, Raymond JP, Merceron RE, Seneze J. Continuous administration of bromocriptine in the prevention of neurological complications in pregnant women with prolactinomas. Am J Obstet Gynecol 1983; 146(8):935-938.26. Coculescu M, Hudita D, Gussi I, Gheorghiu M, Hortopan D, Caragheorgheopol A. Tumor size changes in prolactinomas treated with minimum bromocriptine throughout gestation . Gynecological Endocrinology 2000; 14(suppl 2):50.27. Canales ES, Garcia IC, Ruiz JE, Zarate A. Bromocriptine as prophylactic therapy in prolactinoma during pregnancy. Fertil Steril 1981; 36(4):524-526.28. Shanis BS, Check JH. Relative resistance of a macroprolactinoma to bromocriptine therapy during pregnancy. Gynecol Endocrinol 1996; 10(2):91-94. [CrossRef]29. Liu C, Tyrrell JB. Successful treatment of a large macroprolactinoma with cabergoline during pregnancy. Pituitary 2001; 4(3):179-185. [CrossRef]30. de Turris P, Venuti L, Zuppa AA. [Long-term treatment with cabergoline in pregnancy and neonatal outcome: report of a clinical case]. Pediatr Med Chir 2003; 25(3):178-180.31. Verhelst J, Abs R, Maiter D, van den BA, Vandeweghe M, Velkeniers B et al. Cabergoline in the treatment of hyperprolactinemia: a study in 455 patients. J Clin Endocrinol Metab 1999; 84(7):2518-2522. [CrossRef]32. Cannavo S, Curto L, Squadrito S, Almoto B, Vieni A, Trimarchi F. Cabergoline: a first-choice treatment in patients with previously untreated prolactin-secreting pituitary adenoma. J Endocrinol Invest 1999; 22(5):354-359.33. Ciccarelli E, Grottoli S, Razzore P, Gaia D, Bertagna A, Cirillo S et al. Long-term treatment with cabergoline, a new long-lasting ergoline derivate, in idiopathic or tumorous hyperprolactinaemia and outcome of drug-induced pregnancy. J Endocrinol Inves34. Jones J, Bashir T, Olney J, Wheatley T. Cabergoline treatment for a large macroprolactinoma throughout pregnancy. J Obstet Gynaecol 1997; 17(4):375-376.35. Divers WA, Jr., Yen SS. Prolactin-producing microadenomas in pregnancy. Obstet Gynecol 1983; 62(4):425-429.36. Luthman M, Bremme K, Eneroth P, Werner S. Women with prolactin-producing pituitary adenoma show decreased serum placental lactogen during pregnancy. Gynecol Obstet Invest 1993; 35(2):80-85. [CrossRef]37. Kubota T, Nagae M, Yaoi Y, Kumasaka T, Saito M. Prolactin-releasing system in maternal, fetal, and amniotic compartments during labor. Obstet Gynecol 1986; 68(1):80-85.38. Yuen BH, Moon YS, Shin DH. Inhibition of human chorionic gonadotropin production by prolactin from term human trophoblast. Am J Obstet Gynecol 1986; 154(2):336-340.39. Leav I, Merk FB, Lee KF, Loda M, Mandoki M, McNeal JE et al. Prolactin receptor expression in the developing human prostate and in hyperplastic, dysplastic, and neoplastic lesions. Am J Pathol 1999; 154(3):863-870. [CrossRef]40. Gussi I, Gheorghiu M, Lutescu I, Hortopan D, Caragheorgheopol A, Hudita D et al. Maintaining physiological profile of prolactin throughout pregnancy in women with prolactinomas on dopamine agonists. Rom J Endocrinol Metab 2002; 1(suppl 4):23.41. Molitch ME. Pituitary tumors and pregnancy. Growth Horm IGF Res 2003; 13 Suppl A:S38-S44.42. Ahmed M, al Dossary E, Woodhouse NJ. Macroprolactinomas with suprasellar extension: effect of bromocriptine withdrawal during one or more pregnancies. Fertil Steril 1992; 58(3):492-497.43. Daya S, Shewchuk AB, Bryceland N. The effect of multiparity on intrasellar prolactinomas. Am J Obstet Gynecol 1984; 148(5):512-515.44. Fujimoto M, Yoshino E, Mizukawa N, Hirakawa K. Spontaneous reduction in size of prolactinproducing adenoma after delivery. Case report. J Neurosurg 1985; 63(6):973-974. [CrossRef]45. Hammond CB, Haney AF, Land MR, van der Merwe JV, Ory SJ, Wiebe RH. The outcome of pregnancy in patients with treated and untreated prolactin-secreting pituitary tumors. Am J Obstet Gynecol 1983; 147(2):148-157.46. Yamada M, Miyake A, Koike K, Ikegami H, Aono T, Tanizawa O. Spontaneous pregnancy after a pregnancy induced by treatment in hyperprolactinemic women. Eur J Obstet Gynecol Reprod Biol 1990; 35(2-3):125-129. [CrossRef]47. Bergh T, Nillius SJ, Larsson SG, Wide L. Effects of bromocriptine-induced pregnancy on prolactin-secreting pituitary tumours. Acta Endocrinol (Copenh) 1981; 98(3):333-338. -
General Endocrinology
Capusa C, Chirculescu B, Vladu I, Viasu L, Lipan M, Mota E, , Mircescu G
The Prevalence of Biochemical Abnormalities of Chronic Kidney Disease. Mineral and Bone Disorders in Untreated Non-dialysis Patients – A Multicenter StudyActa Endo (Buc) 2016 12(3): 282-290 doi: 10.4183/aeb.2016.282
AbstractBackground. There are scarce data about prevalence of mineral metabolism (MM) disorders in Romanian predialysis patients, so we assessed their occurrence and relationships in mild to severe chronic kidney disease (CKD). Methods. One hundred fifteen non-dialysis CKD (eGFR 31, 95% CI 29-35mL/min) and 33 matched non-CKD subjects entered this multicentric, cross-sectional study. Serum 25-hydroxyvitamin D (25OHD), intact parathyroid hormone (iPTH), phosphate (PO4), total calcium (tCa) and alkaline phosphatase (AP) were measured, along with demographic and past medical history data. Results. Hypovitaminosis D was equally prevalent in Controls and CKD (91% vs. 96% had 25OHD<30ng/mL). Increasing proportions of hyperparathyroidism (33% - stage 2 to 100% - stage 5; p<0.001) and hyperphosphatemia (2% - stage 3 to 38% - stage 5; p<0.001) were found. Hypocalcemia was more prevalent in stage 5 (25% vs. 6% in stage 4, none in stage 3 and Controls, p<0.001). Mineral metabolism parameters correlated with eGFR. In addition, iPTH was directly associated with PO4, AP, and urinary albumin-tocreatinine ratio (ACR), but inversely with tCa and 25OHD, while negative correlation of 25OHD with age, AP, ACR, and C-reactive protein emerged. In multiple regression, eGFR was the only predictor of iPTH (Beta -0.68, 95%CI -1.35 to -0.90, R2 0.46, p<0.001), whereas age and ACR were the determinants of 25OHD (a model which explained 14% of its variation). Conclusions. Hypovitaminosis D was very common irrespective of CKD presence and severity, and it seems worsened by older age and higher albuminuria. Hyperparathyroidism preceded hyperphosphatemia and hypocalcemia, and it seems mostly dependent on kidney function decline