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

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  • General Endocrinology

    Armasu I, Preda C, Ianole V, Mocanu V, Hristov I, Andriescu EC, Cretu-Silivestru I, Vasiliu, Dascalu CG, Lupascu CD, Crumpei I, Serban DN, Serban IL , Ciobanu Apostol DG

    Insights on Aromatase Immunohistochemistry: Variations between Intrinsic Molecular Subtypes of Breast Cancers

    Acta Endo (Buc) 2020 16(1): 22-29 doi: 10.4183/aeb.2020.22

    Context. Aromatase is a key enzyme in local estrogen production by androgen conversion, especially in women post-menopause. There have been controversies concerning aromatase localization in breast carcinomas and its association with current histopathological variables. Material and Methods. Using polyclonal antibody immunohistochemistry we assessed (by intensity and percentage scores) the immunolocalization of aromatase in 70 tissue samples, and described particularities within the molecular subtypes of breast cancer. Results. Aromatase was found in all tissue compartments: tumor (95.7%), stroma (58.6%) and adipose tissue (94.3%). Aromatase expression in tumor cells correlated inversely with tumor grading (p=-0.361, p=0.027), and positively with estrogen receptor status (ER, p=0.143, p<0.001). Dividing the study group by intrinsic subtypes, a strongly inversely association between tumor aromatase and grading (p=-0.486, p<0.001), and between stromal aromatase and Ki67-index (p=-0.448, p=0.048) was observed in luminal A breast cancer. Tumor aromatase and ER percentage scores had stronger correlations in luminal B HER2 negative (p=0.632, p=0.002), and positive (p=0.324, p=0.026) tumors. In contrast, in triple negative tumors, a positive association stromal aromatase and Ki67 index (p=- 0.359, p=0.007) was observed. Conclusion. Local aromatase was linked to better tumor differentiation and proliferation in luminal breast subtypes, and not in triple negative cases, suggesting a potential prognostic role of aromatase in breast carcinomas.
  • Case Series

    Das D

    Growth Hormone Dynamics among Children with Mixed Gonadal Dysgenesis (45,X/46,XY)

    Acta Endo (Buc) 2021 17(1): 117-123 doi: 10.4183/aeb.2021.117

    Context. Learn the growth hormone dynamics and discuss the issues of growth hormone therapy in subjects with 45,X/46XY. Objective. To study the growth hormone dynamics in children with 45,X/46,XY karyotyping and mixed gonadal dysgenesis (MGD). Design. Descriptive clinical study. Participants. Five subjects with karyotype 45,X / 46,XY with or without genital ambiguity and somatic features of SHOX haploinsufficiency. Interventions. Growth hormone dynamic study and gonadectomy. Main outcome. IGF-1, peak GH levels, Turner’s stigmata and histology of gonadal tissue. Results. Five cases of MGD with both male and female phenotype were studies. IGF-1 levels and GH levels showed both features of growth hormone deficiency and growth hormone insensitivity. One study subject has gonadal germ cell tumour (dysgerminoma). We discuss here the issues regarding the GH therapy in MGD subjects. Conclusion. Growth deceleration in MGD subjects is partly due to defective growth hormone secretion and partly due to growth hormone insensitivity. MGD subjects are at high risk for occurrence of gonadal tumours. Gonadectomy or biopsy of underlying dysgenetic gonads is essential prior GH therapy. Close surveillance for second neoplasm is to be considered in subjects with history of gonadal tumors prior starting GH for short stature.
  • General Endocrinology

    Ladasiu Ciolacu FC, Ardelean A, Turcus V, Mândrutiu I, Belengeanu AD, Bechet D, Frentescu L, Mihali CV, Benga G

    A Simple, Sensitive and Highly Accurate Procedure for Plasma Phenylalanine Determination by HPLC

    Acta Endo (Buc) 2015 11(2): 143-146 doi: 10.4183/aeb.2015.143

    Phenylketonuria (PKU) is the most frequent inherited amino acid metabolic disorder, and it may also be treated by dietary means. The determination of phenylalanine (Phe) levels in the blood plasma is important not only in early diagnostic, but also in monitoring the treatment of PKU. Purpose. The aim of our work was to develop a simple, sensitive and highly accurate procedure to determine the plasma concentration of Phe. Procedure. The measurement of plasma Phe concentration involves two steps: a) separation of plasma (from the blood taken on heparin), isolation and preparation of a concentrated solution of amino acids (by ion-exchange column chromatography on Dowex-50X8 and evaporation of the eluate in vacuum at 40˚C), and b) determination of Phe concentration in the solution of amino acids by HPLC. This analysis was performed using a Dionex Ultimate 3000 instrument equipped with a Ultimate 3000 diode array detector (DAD). The values of Phe concentration in the plasma of several patients were calculated using a calibration curve made with standards of Phe (dilutions of a stock solution of 50 mg/ dL). The measurements in duplicate (plasma Phe) or a greater number of samples from the same concentration of standards of Phe showed extremely small sample to sample differences. Concentrations as low as 0.2 mg/dL could be determined. Conclusion. The whole procedure presented here is relatively simple, rather inexpensive, however very sensitive and highly accurate. Consequently, it is very adequate for confirming the diagnosis of PKU in patients with neonatal hyperphenylalaninemia, as well as for monitoring the plasma concentration of Phe in patients with PKU.
  • Endocrine Care

    Zahan AE, Watt T, Pascanu I, Rasmussen AK, Hegedüs L, Bonnema SJ, Feldt-Rasmussen U, Bjorner JB, Nadasan V, Boila A, Merlan I, Borda A

    The Romanian Version of the Thyroid-Related Patient-Reported Outcomes Thypro and Thypro-39. Translation and Assessment of Reliability and Crosscultural Validity

    Acta Endo (Buc) 2018 14(2): 192-200 doi: 10.4183/aeb.2018.192

    Background. ThyPRO is a recently developed thyroid-specific quality of life (QoL) questionnaire applicable to patients with benign thyroid disorders(BTD). The aim of the present study was to translate ThyPRO and ThyPRO-39 into Romanian, and to evaluate reliability and cross-cultural validity. Methods. Standard methodology for translation and linguistic validation of patient-reported outcomes (PRO) was applied. The questionnaire was completed by 130 patients with benign thyroid diseases seen at Department of Endocrinology in the Emergency County Hospital, Tîrgu Mureș, Romania, between October 2015 and March 2016. Internal reliability of the Romanian version of the ThyPRO (ThyPROro) scales was assessed for multi-item scales using Cronbach’s alpha coefficient. An efficient method for testing cross-cultural validity is analysis of differential item functioning (DIF). Uniform DIF between the Romanian and the original Danish sample was investigated using ordinal logistic regression. The translation process proceeded without difficulties, and any disagreements were revised by one of the developers and the language coordinator. Results. Internal reliability for ThyPRO was satisfactory. Cronbach`s alpha coefficients for the 13 scales ranged from 0.78 to 0.93 for the ThyPROro and 0.78 to 0.87 for the ThyPROro-39. In the 85-item ThyPRO, nine instances of DIF were found. Most were minor, explaining <3% of the variation in scale score, but DIF in positively worded items were larger, with explained variance (R2’s) around 10-15%. Conclusion. The ThyPROro questionnaire is ready for assessment of health-related quality of life in Romanian patients with benign thyroid diseases.
  • Case Report

    Dyrmishi B, Olldashi T, Rista E, Fureraj T, Ylli D, Ylli A

    Severe Hypokalemia Induced Rhabdomyolysis by Primary Hyperaldosteronism Coexistent with Recurrent Bilateral Renal Calculi

    Acta Endo (Buc) 2017 13(2): 228-231 doi: 10.4183/aeb.2017.228

    Primary Hyperaldosteronism is one of the causes of secondary hypertension. Primary Hyperaldosteronism is characterised by an increase in the production of aldosterone and the inhibition of the secretion of renin. We described here a case with rhabdomyolysis and severe hypokalemia as a cause of primary hyperaldosteronism. The creatine kinase, aldosterone were very high. Cortisol values and midnight salivary cortisol values were within normal range. The patient had been under treatment for high blood pressure for more than six years, with ARBs and calcium channel blockers. During this time the potassium values measured frequently every year were below normal range, but primary hyperaldosteronism was not suspected.
  • Clinical review/Extensive clinical experience

    Soldat-Stankovic V, Popovic Pejicic S, Stankovic S, Jovanic J, Bjekic-Macut J, Livadas S, Ognjanovic S, Mastorakos G, Micic D, Macut D

    The Effect of Myoinositol and Metformin on Cardiovascular Risk Factors in Women with Polycystic Ovary Syndrome: a Randomized Controlled Trial

    Acta Endo (Buc) 2021 17(2): 241-247 doi: 10.4183/aeb.2021.241

    Context. Cardiovascular risk is increased in women with polycystic ovary syndrome (PCOS). Do insulin sensitizing agents such as metformin (MET) and myoinositol (MI) ameliorate biomarkers of cardiovascular risk? Objective. To compare the effects of MET and MI on blood pressure, lipid profile and high sensitive C-reactive protein (hs-CRP) in women with PCOS in respect to their body mass index (BMI). Design. Open label, parallel randomized, single center study. Subjects and Methods. Sixty six women with PCOS (33 normal-weight and 33 overweight/obese) were randomized to either MI (4 g/day) or MET (1500 mg/day) for a period of 6 months. Serum concentration of hormones, lipid profile, oxidized LDL (ox-LDL), hs-CRP, blood pressure measurement and clinical assessment of BMI, waist circumference (WC) and Ferriman Gallwey score (FG score) were performed before and after treatment. Results. Thirty patients in each group completed the trial. Compared with MET, MI significantly decreased diastolic blood pressure (DBP) (p=0.036) and significantly increased serum hs-CRP (p=0.043). No differences between groups in total cholesterol (TC), HDL-cholesterol, LDLcholesterol, ox-LDL and triglycerides were reported after 6 months. Treatment with MI reduced BMI (p=0.037), WC (p=0.005), DBP (p=0.021) and TC (p=0.008). During MET treatment a significant decrease in BMI (p=0.005), WC (p=0.004), FG score (p=0.001), testosterone (p=0.013) and free androgen index (FAI) (p=0.006) was observed. Conclusions. Our study showed an advantage of MI in reduction of DBP and TC thus predicting favorable metabolic and cardiovascular outcomes in PCOS women. MET more effectively decrease indices of hyperandrogenism.
  • Endocrine Care

    Lopez-Sandoval J, Sanchez-Enriquez, Rivera-Leon EA, Bastidas-Ramirez BE, Garcia-Garcia MR, Gonzalez-Hita ME

    Cardiovascular Risk Factors in Adolescents: Role of Insulin Resistance and Obesity

    Acta Endo (Buc) 2018 14(3): 330-337 doi: 10.4183/aeb.2018.330

    ntroduction. Childhood obesity is a public health problem characterized by early insulin resistance (IR), inflammation, and oxidative stress. The presence of an uninterrupted low-grade inflammatory state impairs metabolic and cardiovascular health. The population is particularly susceptible to develop metabolic disorders related to increased body fat. Methods. Eighty-three adolescents were recruited and grouped according to HOMA-IR and BMI in either with or without IR and obese or normal-weight respectively. Anthropometric, biochemical, immunological and hormonal variables were determined. Transverse Analytical Study. Results. Obesity, dyslipidemia, IL-6, and C-reactive protein were significantly higher in the IR group than in the non-IR group. Obese adolescents showed increased insulin levels, HOMA-IR, inflammatory markers, and triglycerides; while having lower HDL-C, and adiponectin when compared to normal-weight adolescents. As expected, obesity-related anthropometric markers positively correlated with IR and inflammatory markers while negatively correlated with adiponectin levels. Conclusions. Early IR, subclinical inflammation, dyslipidemia, and hypoadiponectinemia characterize obesity in adolescents. These factors may increase the risk of future coronary heart disease (CHD) and diabetes mellitus development (DM) in early adulthood.
  • General Endocrinology

    Dasgupta R, Paramita Ray P, Maity A, Pradhan D, Sarkar S, Maiti BR

    Dual Action of Arecoline on Adrenal Function and Glucose-Glycogen Homeostasis in Metabolic Stress in Mice

    Acta Endo (Buc) 2017 13(4): 400-409 doi: 10.4183/aeb.2017.400

    Background. People chew betel nut (Areca catechu) for physical work and stress reduction, but it contains arecoline, which has both therapeutic value and untoward effects on endocrine and gonadal functions. Objective. Aim of the present study is to investigate its role on adrenal with its target in metabolic stress in mice. Materials and methods. Mice were deprived of water / food, each for 5 days / treated with arecoline (10 mg / kg body wt daily for 5 days) / arecoline after water or food deprivation, for 5 days each. Results. Water or food-deprivation caused adrenocortical hyperactivity, evident from abundance of enlarged mitochondria and smooth endoplasmic reticulum (SER) with elevation of corticosterone level (C: 68.31 ± 2.30, WD: 159.31 ± 4.10 / FD: 194.12 ± 3.40 μg/ mL). Arecoline treatment alone or in water deprivation (C: 68.31 ± 2.30, AR: 144.50 ± 4.33, AR+WD: 194.42 ± 3.35 μg/ mL) / food deprivation (AR + FD: 180.89 ± 4.51 μg/ mL) stress also stimulated adrenocortical activity as recorded in metabolic stress. In contrast, adrenomedullary activity was not altered following water/ food deprivation. Arecoline treatment alone or in metabolic stress suppressed adrenomedullary activity by showing depletion of chromaffin granules (E/NE?), epinephrine (E) and norepinephrine (NE) concentrations. Both the stress decreased blood glucose and liver glycogen levels. Arecoline treatment decreased blood glucose level, with a rise in liver glycogen level, but elevated blood glucose level in water deprivation unlike in starvation. Conclusion. Arecoline alone or in metabolic stress involves adrenal and probably other endocrine glands (pancreas, posterior pituitary and rennin-angiotensin system) to maintain homeostasis in metabolic stress in mice.
  • General Endocrinology

    Comandasu DE, Mohora M, Vîrgolici B, Mehedintu C, Berceanu C, Cîrstoiu M, Bratila E

    Maternal-Fetal Metabolism Disorders Induced by Maternal Obesity in an Animal Model

    Acta Endo (Buc) 2016 12(4): 407-412 doi: 10.4183/aeb.2016.407

    Context. Adipokines secreted by fat cells are vital to the control of energy metabolism, communicating the nutrient status with the tissues responsible for controlling both energy intake and expenditure and insulin sensitivity. Objective. We aimed to prove in an experimental animal study that maternal obesity has long term adverse fetal metabolic consequences, which pass on even to the next generation of descendants. Design. The effects of maternal obesity have been studied on animal model using 50 obese female Wistar rats, in which we induced obesity by high-calorie high-fat diet administered by gavage. Subjects and Methods. Obese rat females were sacrificed at gestation term and we analyzed the secretion of adipokines from maternal venous blood: leptin and adiponectin, placental, pancreatic, liver and brain homogenates lipid peroxidation levels estimated by: MDA (malonyl-dialdehyde), total thiols and GSH – as antioxidant factors and routine biochemistry. Results. Low levels of adiponectin and increased levels of leptin positively correlated with the value of placental and fetal tissue lipid peroxidation (from the liver, pancreas and brain) measured by elevated MDA and total thiols and low levels of GSH. The lipid peroxidation in the organs examined generated consistent results, showing high levels of peroxidation expressed through high values of MDA in the groups with Omega 6 supplements respectively no supplementation, and low levels of antioxidants expressed through glutathione and thiols. Conclusions. Endocrine secretion of adipokines from the adipocytes and the recruited macrophages of obese mothers is positively correlated with placental and tissue lipid peroxidation level and routine biochemical parameters.
  • General Endocrinology

    Dasgupta R, Pradhan D, Sengupta SC, Nag T, Maiti BR

    Ultrastructural and hormonal modulations of adrenal gland with alterations of glycemic and liver glycogen profiles following arecoline administration in albino mice

    Acta Endo (Buc) 2010 6(4): 413-430 doi: 10.4183/aeb.2010.413

    Background. Arecoline, a plant alkaloid of betel nut, is consumed by millions of people, for increased capacity of work. It causes immunosuppression, hepatotoxicity, and disturbance in antioxidant production, but it stimulates HPA axis and induces thyroid dysfunction.\r\nAim. To investigate the role of arecoline on adrenal activity, glycemia and glycogen profile in mice.\r\nMaterials and methods. Arecoline was injected intraperitoneally at a dose of 10 mg/kg body wt for 20-60 min for acute administration. In chronic administration the same dose was used daily for 15 days. Corticosterone, epinephrine, norepinephrine, blood glucose and liver glycogen profiles were measured after 20, 40 and 60 min, in acute administration and after 15 days in chronic administration.\r\nResults. Arecoline in acute administration increased corticosterone, norepinephrine and epinephrine levels and induced hyperglycemia with depletions of liver glycogen. But\r\nchronic arecoline administration with the same dose for 15 days caused ultrastructural degenerations of adrenal cortex and medulla with the elevation of corticosterone, and\r\ndepletions of norepinephrine and epinephrine levels. Arecoline also caused hypoglycemia and elevated liver glycogen. Atropine (arecoline receptor antagonist) prevented arecoline action on adrenal activity or blood glucose ? liver glycogen interaction.\r\nConclusion. The findings indicate that arecoline initially stimulates adrenal activity, but subsequently inhibits it with alterations of glycemic and glycogen profiles. Arecoline action is mediated by arecoline receptor in mice. Arecoline may have immunological action via adrenal hormonal suppression in mice.