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Romanian Academy
The Publishing House of the Romanian Academy
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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Case Report
Dumitrache L, Bartos D, Beuran M, Giorghe S, Tarziu C, Badila E
Primary hyperaldosteronism started by hypokalemic coma - case reportActa Endo (Buc) 2009 5(2): 251-258 doi: 10.4183/aeb.2009.251
AbstractPrimary hyperaldosteronism is the cause of approximately 0.05 to 2.2% of all\r\nunselected cases of hypertension. It was first described in 1955 by Conn in conjunction with\r\naldosterone-producing adrenal adenoma, which is the most frequent aetiology, in 65% of\r\ncases. Clinical features are usually non-specific and result from potassium depletion. We\r\nreport here the case of a 54-year-old woman who was admitted to the emergency department\r\ndue to coma (Glasgow score 6). The presence of severe potassium depletion (1.2 mmol/L)\r\nand metabolic alkalosis (PH=7.76, base excess>30 mmol/L) in a hypertensive patient\r\ndetermined the clinicians to search for a secondary cause of hypertension. This was\r\nconfirmed by localizing on computer tomography a right adrenal adenoma of 31-mm\r\ndiameter and on endocrine measurements that showed mineralocorticoid excess (plasma\r\naldosterone=764 pg/mL;N=14-193). Clinical evolution was slowly favourable after\r\nrestoring the electrolyte balance, with increasing of serum K up to 3.05 mmol/L. The patient\r\nbecame asymptomatic in 3 weeks and underwent laparoscopic right adrenalectomy. The\r\npatient had a good postoperatory evolution. Two weeks after laparoscopic right\r\nadrenalectomy, blood pressure normalized after the discontinuation of the antihypertension\r\ntreatment and the aldosterone measurement was normal (102 pg/mL). -
General Endocrinology
Csép K, Gyongyi Dudutz, Marta Vitay, Pascanu I, Banescu C, Koranyi L, Rosivall L
The Relationship Between The PRO12ALA Polymorphism Of The PPAR?2 Gene And The Metabolic Syndrome In A Population Of Central Romania Diagnosed According To The Idf CriteriaActa Endo (Buc) 2008 4(3): 263-271 doi: 10.4183/aeb.2008.263
AbstractThe nuclear receptor coding PPARγ2 (PEROXISOME PROLIFERATORACTIVATED RECEPTOR-GAMMA; *601487) gene influences the lipid and carbohydrate metabolism via multiple pathways and is a candidate for the metabolic syndrome. In this paper we studied the relationship of the CCG (Pro) → GCG (Ala) polymorphism of the gene with the metabolic syndrome diagnosed according to the criteria recommended by the International Diabetes Federation (IDF) in 2005, in a population from central Romania. We have carried out a case-control study on 144 patients and 73 control subjects. Routine biochemical assays have been carried out, fasting insulinemia was measured by ELISA, and insulin sensitivity was assessed by calculating the HOMA and QUICKI indices. Genetic analysis was done by PCR followed by digestion with the restriction enzyme BstU I. The results show that the Pro12 allele had a higher frequency in the group of patients as compared to the healthy controls (76 vs. 65.7%, p<0.05). The risk for developing the metabolic syndrome in the presence of the Pro12 allele in a homozygous combination was found to be low but statistically significant (PP vs. PA + AA: OR = 1.98, CI 95% 1.04 -3.78, p = 0.046). In conclusion, in the local population, the Pro12 allele of the PPARG2 gene seems to contribute to the hereditary predisposition of the metabolic syndrome diagnosed according to the recommendations of the IDF, most likely as part of a polygenic system. Probably the absence of the protective Ala12 allele increases the risk for developing the disease. -
Images in Endocrinology
Niculescu DA, Dumitrascu A, Lica I
Neck tumoral swelling in an endemic iodine deficiency areaActa Endo (Buc) 2010 6(2): 263-263 doi: 10.4183/aeb.2010.263
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Notes & Comments
Kocak MZ, Aktas G, Atak B, Bilgin S, Kurtkulagi O, Duman TT, Ozcil IE
The Association between Vitamin D Levels and Handgrip Strength in Elderly MenActa Endo (Buc) 2020 16(2): 263-266 doi: 10.4183/aeb.2020.263
AbstractContext. Vitamin D is a steroid hormone that acts by binding to the vitamin D receptor (VDR) found in many tissues. According to the long-term mechanism, vitamin D causes the proliferation and differentiation of muscle cells by gene transcription. Objective. We aimed to evaluate the relationship between muscle strength and serum vitamin D levels in elderly men. Design. Cross-sectional study. Subjects and Methods. Male patients over age 50 were included in the study. Study population was divided into 2 groups with handgrip strength according to body mass index, either as subjects with weak or with normal handgrip strength test (HGST). Vitamin D levels and other variables compared between weak and normal groups. Results. Vitamin D level of weak and normal groups were 7.5 (3-19.9) μg/L, and 11.6 (11.6-34.9) μg/L, which means significant reduced vitamin D levels in weakness group (p=0.01). Vitamin D levels were significantly correlated with HGST levels (r:0.362, p=0.001). Vitamin D levels were found to be an independent predictor of weakness according to HGST in logistic regression analysis (OR: 0.453, 95% Cl:0.138-0.769, p=0.05). Conclusions. Low vitamin D level is an independent risk factor for muscle weakness in men aged more than 50 years. Therefore, vitamin D levels should be screened and early replacement should be initiated for the sake of improvement of muscle strength in elderly subjects that vulnerable for frailty. -
Notes & Comments
Voicu V, Medvedovici A, Miron D, Radulescu F
A novel approach on pharmacokinetic/pharmacodynamic correlations of risperidone: understanding its safety and efficacy profilesActa Endo (Buc) 2010 6(2): 265-285 doi: 10.4183/aeb.2010.265
AbstractThe pharmacokinetic characteristics of a compound as well as the immediate consequences of its physicochemical behavior during interactions with biological structures,\r\nrepresent the key issues for its pharmacodynamic profile, starting from the most fundamental global aspects (i.e. central and / or peripheral action) to the most detailed ones (i.e. molecular mechanism of action).\r\nSuccessive metabolic reactions lead to either bioactivation or bioinactivation of themolecular entity. A particular importance is currently assigned to several molecular\r\nphysicochemical descriptors, for instance the polarity degree (mirroring the changes of partition coefficients and of the permeability of biological structures), and emphasizing on distribution and renal excretion rate.\r\nThe active metabolite (9-hydroxy-risperidone) of the atypical antipsychotic agent risperidone has an increased polar character and, consequently, its pharmacokinetic profile is modified compared to the parent drug: especially the penetration through the bood brain barrier and the efflux pump mediated transport were considered. In this context, the kinetic characteristics and their correlation with the pharmacodynamic properties for the two active\r\nentities, as well as the consequences dealing with the antipsychotic efficacy, the safety and efficacy profiles can be anticipated. The present approach critically asseses the available data from literature corroborated with the personal findings over the last years. -
Images in Endocrinology
Radulescu V, Dumitrascu A, Alexandrescu D, Badiu C
Zoster Triggers in Graves OphthalmopathyActa Endo (Buc) 2023 19(2): 267-268 doi: 10.4183/aeb.2023.267
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General Endocrinology
Liu F, Duan JT, Teng X, Peng DQ
The Increased Plasma Levels of Intermedin in Patients with Type 2 Diabetes MellitusActa Endo (Buc) 2022 18(3): 271-277 doi: 10.4183/aeb.2022.271
AbstractContext. Intermedin (IMD) is the member of calcitonin gene-related peptide family, and tightly associated with type 2 diabetes mellitus (T2DM). The change of plasma IMD levels in T2DM is still unknown. Objective. We aimed to investigate the plasma levels of IMD in patients with T2DM. Design. Fortyone patients with T2DM who were hospitalized in the endocrinology department of Civil Aviation General Hospital from January 2012 to June 2015 were enrolled, and 44 volunteers were selected as the control group. Subjects and Methods. Plasma level of IMD was detected by ELISA. Diagnostic value of IMD was analyzed by area under the receiver operating characteristic (ROC) curve (AUC). Results. The plasma level of IMD in T2DM group was higher than that in the healthy control group, whereas smoking or cardiovascular complications did no influence the IMD levels. IMD levels were correlated with BMI, DBP, triglyceride, uric acid, urea nitrogen, fasting and 2 hours postprandial blood glucose, and HbA1C. The greatest value of AUC for IMD was only 58.73%. Conclusions. Although plasma levels of IMD were increased in patients with T2DM, the very low diagnostic value of IMD for T2DM might not be used for the disease diagnosis. -
General Endocrinology
Naumescu S, Georgescu C, Dragatoiu G, Hazi G, Duncea I, Gozariu L
Studies concerning the correlation between leptin and body compositionActa Endo (Buc) 2005 1(3): 271-280 doi: 10.4183/aeb.2005.271
Abstract ReferencesIntroduction: Leptin, which is known to regulate appetite and energy expenditures, may also contribute to mediate the effects of fat mass on the bone.\r\nObjective: The aim of this study was to analyse to what extent leptin and total body composition influence the maintenance of bone mass.\r\nSubjects and methods: We evaluated 34 women divided into two BMI-matched groups based on the ovarian function: 12 premenopausal women, aged 34.08?7.18 years and 22 postmenopausal women aged 61.31?4.51 years, respectively. Total body composition (total fat mass, trunk fat mass and lean mass) and bone mineral density were measured by means of dual-energy X-ray absorptiometry (DXA). Serum leptin concentrations were assessed by ELISA.\r\nResults: The bone mineral content was influenced by both the fat mass (women with normal menstrual cycles r=0.62, p=0.03; postmenopausal women r=0.625, p=0.002) and the trunk fat mass (r=0.597, p=0.004 premenopausal women; r=0.675, p=0.001 postmenopausal women), independently of the ovarian function. Only for the postmenopausal group we could identify a significant correlation between leptin levels and the total body bone mineral density (r=0.479, p=0.024) and the total body bone mineral content (r=0.605, p=0.003), respectively. The serum leptin levels were highly significantly correlated with the total fat mass and the trunk fat mass for both groups. No difference was obtained with regard to the serum leptin levels between pre- and postmenopausal women.\r\nConclusions: Our results suggest the role played by leptin and the fat mass in the maintenance of bone mass.1. Ricci TA, Heymsfield SB, Pierson RN Jr, Stahl T, Chowdhury HA, Shapses SA. Moderate energy restriction increases bone resorption in obese postmenopausal women. Am J Clin. Nutr. 2001; 73(2): 347-352.2. Elefteroiu F, Karsenty G. Bone mass regulation by leptin: a hypothalamic control of bone formation. Pathol Biol. 2004; 52(3): 148-153.3. Jones KB, Mollano AV, Morcuende JA, Cooper RR, Saltzman CL. Bone and brain: a review of neural, hormonal and musculoskeletal connections. Iowa Orthop J. 2004; 24: 123-132.4. Takeda S. Leptin and beta-blockers in bone metabolism. Clin Calcium. 2004; 14(2): 241-247.5. Thomas T. Leptin: a potential mediator for protective effects of fat mass on bone tissue. Joint Bone Spine. 2003; 70(1): 18-21.6. Takeda S, Karsenty G. Central control of bone formation. J Bone Miner Metab. 2001; 19(3): 195- 198.7. Karsenty G. Leptin controls bone formation through a hypothalamic relay. Recent Prog Horm Res. 2001; 56: 401-415.8. Ducy P, Schinke T, Karsenty G. The osteoblast: a sophisticated fibroblast under central surveillance. Science. 2000; 289: 1501-1504.9. Cock TA, Auwerx J. Leptin: cutting the fat off the bone. Lancet. 2003; 362: 1572-1574. [CrossRef]10. Whitfield JF. How to grow bone to treat osteoporosis and mend fractures. Curr Rheumatol Rep. 2003; 5(1): 45-56. [CrossRef]11. Marie P, Debiais F, Cohen Solal M, de Vernejoul MC. New factors controlling bone remodeling. Joint Bone Spine. 2000; 67(3): 150-156.12. Grigorie D, Neacsu E, Marinescu M, Popa O. Circulating osteoprotegerin and leptin levels in postmenopausal women with and without osteoporosis. Rom J Intern Med. 2003; 41(4): 409-415.13. Javaid, Godfrey, Taylor et al. Umbilical cord leptin predicts neonatal bone mass. Calcif Tissue Int. 2005; 76(5): 341-347. [CrossRef]14. Yamauchi M, Sugimoto T, Yamaguchi T. et al. Plasma leptin concentrations are associated with bone mineral density and the presence of vertebral fractures in postmenopausal women. Clin Endocrinol. 2001; 55(3): 341-347.15. Dennison EM, Syddall HE, Fall CH et al. Plasma leptin concentration and change in bone density among elderly men and women: the Hertfordshire cohort Study. Calcif Tissue Int 2004; 74(5): 401- 406.16. Ruhl CE, Everhart JE. Relationship of serum leptin concentrations with bone mineral density in the United States population. J Bone Miner Res. 2002; 17(10): 1896-1903.17. Odabasi E, Ozata M, Turan M. et al. Plasma leptin concentrations in postmenopausal women with osteoporosis. Eur J Endocrinol 2000; 142(2): 170-173.18. Sahin G, Polat G, Baethis S et al. Body composition, body mineral density, and circulating leptin levels in postmenopausal Turkish women. Rheumatol Int. 2003; 23(2): 87-91.19. Hadji P, Bock K, Gotschalk M et al. The influence of serum leptin concentration on bone mass assessed by quantitative ultrasonometry in pre and postmenopausal women. Maturitas. 2003; 44(2): 141-148.20. Shaarawy M, Abassi AF, Hassan H, Salem ME. Relationship between serum leptin concentrations and bone mineral density as well as biochemical markers of bone turnover in women with postmenopausal osteoporosis. Fertil Steril. 2003; 79(4): 919-924.21. Roux C, Arabi A, Porcher R, Garnero P. Serum leptin as a determinant of bone resorption in healthy postmenopausal women. Bone. 2003; 33(5): 847-852.22. Reid IR. Relationships among body mass, its components, and bone. Bone. 2002; 31(5): 547-555. -
Images in Endocrinology
Pop LG, Radulescu M, Toader OD, Suciu ID
Fetal Neuroblastoma. Ultrasound and MRI FindingsActa Endo (Buc) 2019 15(2): 272-273 doi: 10.4183/aeb.2019.272
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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