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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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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
Noorafshan A, Ebrahimi S, Esmaeilzadeh E, Arabzadeh H, Bahmani-Jahromi M, S A
Effects of Arnebia Euchroma Extract on Streptozotocin Induced Diabetes in Rats: A Stereological StudyActa Endo (Buc) 2017 13(3): 272-277 doi: 10.4183/aeb.2017.272
AbstractBackground. Diabetes mellitus (DM) is considered as an important health confounder in our world, which necessitates its better management by new methods. In this study, we have evaluated the effects of oral Arnebia Euchroma (AE) extract on different stereological parameters of the pancreas as well as blood glucose in Streptozotocin (STZ)-induced diabetes in rats. Methods. We divided 48 Wistar rats into 4 groups: C1 including normal rats, C2 not-treated diabetic rats, E1 with diabetic rats receiving 100 mg/kg AE extract orally, and E2 including diabetic rats treated with 300 mg/kg AE extract. Stereological study was done and the levels of blood glucose were also estimated and compared between experimental and control groups. Results. There were significant differences in volumes of pancreatic islets, β cell populations, blood glucose levels in AE treated groups compared with nottreated diabetic group. Conclusion. Although AE did not completely prevent or heal the pancreatic damage, its oral administration showed promising effects on maintaining the population of beta cells, the main insulin secreting cells, after STZ-induced injury and also lowered blood glucose levels compared to the not-treated diabetic group. -
Images in Endocrinology
Gheorghisan-Galateanu AA
The Fascinating World of Electron Microscopy: Ultrastructural Morphology of Adrenal Chromaffin CellsActa Endo (Buc) 2018 14(2): 272-273 doi: 10.4183/aeb.2018.272
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Endocrine Care
Aminorroaya A, Amini M, Hovsepian S
Prevalence of hyperthyroidism in Isfahan-Iran, in the ear 2006, fifteen years after universal salt iodization: a community based studyActa Endo (Buc) 2008 4(3): 273-285 doi: 10.4183/aeb.2008.273
AbstractThe objective of this study was to investigate the prevalence of hyperthyroidism in Isfahan, a centrally located city in Iran, fifteen years after universal salt iodization. In a cross-sectional study, 2523 Isfahani adult people (aged >20 years, 1275 men and 1248 women) were selected by multistage cluster sampling method. TSH was measured in all (n=2523) and urinary iodine concentration (UIC) in one fourth of participants. Those with low TSH <0.3 mIU/L were recalled and re-tested (n=115). Low TSH with normal FT4I and T3 at the second measurement was considered as subclinical and low TSH with high FT4I or T3 as overt hyperthyroidism. TPOAb, TgAb and UIC were measured in hyperthyroid patients and controls. The prevalence of hyperthyroidism was 1.8 % (n=46): overt-0.8% (n=21) and subclinical hyperthyroidism 1.0% (n=25). Hyperthyroidism was observed in 2.6% of women (n=32) and 1.1% of men (n=14) (OR= 2.4, CI 95%: 1.3-4.5, P=0.006). Iodine deficiency and excess were observed in 21.4% and 18.7% of all population, being 38% and 33% in hyperthyroid patients, respectively (P>0.05). Thyroid function had no statistically significant correlation with iodine intake status. Nobody had UIC more than 100 µg/dl. The prevalence of positive TPOAb and/ or TgAb was 54.5% and 29.2% in hyperthyroid and euthyroid people, respectively (OR= 2.9, CI 95%: 1.2-7, P=0.01). Conclusions:The rate of hyperthyroidism in our region was similar to iodine sufficient areas. Its development is not a direct effect of iodine intake. Antithyroid autoimmunity may have a role. -
Case Report
Chentli F, Belahcene S, Rezzoug M, Fedala NS, Belhimer F
McCune Albright Syndrome with a Somatolactotroph Pituitary Adenoma Causing Gigantism: Econography and Literature ReviewActa Endo (Buc) 2011 7(2): 273-282 doi: 10.4183/aeb.2011.273
AbstractMcCune Albright syndrome (MAS) is a rare disease due to a sporadic mutation in Gs protein inducing polyostotic fibrous\r\ndysplasia, pigmented skin patches and hyper functioning endocrinopathies. We aimed to report its association with a hot thyroid nodule and gigantism.\r\nCase report. A man aged 37, with a history of pigmented skin lesions and lameness was referred for acromegaly. He was giant (height = 1.94 m/ target stature = 1.68 m), and had ?caf? au lait? spots. Biological analyses argued for pituitary mixed secretion (random growth hormone = 22 ng/ mL, N<5; prolactin = 27 ng/mL, N<10). Brain CT scan showed a pituitary process of 11x10 mm. Thyroid radioiodine scan revealed a hot nodule. Bone x-ray demonstrated large osteolytic lesions in the right femur and pelvis. He was operated on for endocrine tumours. The thyroid nodule\r\nwas benign and immunohistochemistry pituitary was positive for GH, prolactin and α subunit.\r\nConclusion. Somatolactotrop adenoma causing gigantism associated with MAS is exceptional. It should be known, diagnosed, and treated early to avoid bone deformations\r\nand malignant transformation of osseous lesions under GH and/or IGF1 excess. One should also know that radiotherapy for the pituitary process is contraindicated, because of higher risk of sarcomatous transformation. -
Case Report
Capraru OM, Pascanu I, Marginean OC
Suprasellar Germinoma with Chronic Hypernatremia, Adipsic Diabetes Insipidus and Hypopityuitarism. Case ReportActa Endo (Buc) 2014 10(2): 273-282 doi: 10.4183/aeb.2014.273
AbstractIntracranial germ cell tumors (GCT) are rare brain tumors that typically arise in the pineal or suprasellar regions. Germinomas are highly radiosensitive among pediatric CNS tumors. Suprasellar GCTs most commonly present with hypothalamic/ pituitary dysfunctions. We report a case of an 18 year old boy with particularly long term evolution from the onset of symptoms to the positive diagnosis of suprasellar germinoma. At 9 years he was diagnosed with idiopathic central diabetes insipidus and started DDAVP therapy. In the subsequent years he presented delay in longitudinal growth and delayed pubertal development. At 16 years he was referred to our institute with relatively good general condition despite an extremely severe hypernatremia of 186 mEq/L, serum osmolality of 405 mOsm/kg and impaired thirst sensation. He developed sinus thrombosis as a consequence of hyperosmolality and presented intermittent rises of temperature, but no septic episodes. During a long term follow neuroimaging eventually revealed a thickening of the pituitary stalk, mimicking as an infiltrative lesion. Finally, two supracentimetric tumor nodules were shown on contrast enhanced MRI in the suprasellar region and at the floor of the left lateral ventricle. Stereotactic biopsy concluded a pure germinoma, and craniospinal irradiation was performed. At present he has an infracentimetric suprasellar tumor remnant, reperfused sinus veins, optochiasmatic syndrome sequelae. He benefits from L-Thyroxin and testosterone replacement, and maintains hydro-electrolytic balance on DDAVP and controlled oral fluid intake. -
Editorial
Copaescu C
Metabolic SurgeryActa Endo (Buc) 2013 9(2): 273-278 doi: 10.4183/aeb.2013.273
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Case Report
Cucu CI, Giurcaneanu C, Mihai MM, Voiculescu VM, Beiu C, Martin S, Negoita S, Popa LG , Miron A
Hidradenitis Suppurativa in PostmenopauseActa Endo (Buc) 2021 17(2): 274-277 doi: 10.4183/aeb.2021.274
AbstractBackground. Hidradenitis suppurativa (HS) is a chronic, debilitating disease with a profound impact on the quality of life of patients. Objectives. To describe a rare case of HS with postmenopausal onset, to review the literature data regarding late onset HS and to discuss the current knowledge on the role of endocrine abnormalities in the development of HS. Case report. We report the case of a 68-year-old patient in whom HS occurred 10 years after menopause. She was referred to our clinic for the presence of an open fistula on the left groin, fibrotic scars and visible alteration of the vulvar anatomy due to numerous surgical interventions. The patient shared features of the metabolic syndrome (obesity, arterial hypertension, dyslipidemia, aortic atherosclerosis), but showed no signs of virilism and no hormonal abnormality. HS was controlled using antiseptics, topical retinoids and antibiotics. Conclusions. This case is of particular interest given the late onset of HS, long time after menopause. The development of HS requires a complex interaction between genetic predisposing factors, endocrine dysregulation, metabolic alterations, bacterial overgrowth and an aberrant inflammatory response. Evidence points to an important role of sex-hormones in the emergence and progression of the disease, but the underlying mechanisms are still unclear. A better understanding of HS pathogenesis is needed to elucidate the precise way in which endocrine factors influence the disease onset and course. This would guide the way to novel therapies and a better control of this challenging disease. -
Actualities in medicine
Constantin AM, Baicus C
Estradiol in Systemic Lupus ErythematosusActa Endo (Buc) 2023 19(2): 274-276 doi: 10.4183/aeb.2023.274
AbstractSystemic Lupus Erythematosus (SLE) is a chronic autoimmune polymorphous disease that primarily affects women of reproductive age. This gender disparity has suggested the importance of investigating the role of reproductive hormones in the pathogenesis of the disease. Estradiol, the most potent form of estrogen, plays a key role in shaping the immune system including the production of lymphocytes, the peripheral differentiation of regulatory T cells (T-regs), antibody production, and the complement and interferon systems, and has been studied in the pathogenesis of systemic lupus erythematosus (SLE). It operates by binding to estrogen receptors (ERs) α and β, initiating cellular responses including alterations in gene expression. Regulatory T cells are instrumental in preserving immunological self-tolerance and moderating immune responses. Estradiol’s serum levels correlate with the expansion of CD4+CD25+ and FoxP3+ in healthy females. However, this response is reduced in lupus patients. Estradiol also interacts with microRNAs (miRNAs) in gene regulation. Hsa-miR-10b-5p, a miRNA targeting SRSF1, is overexpressed in SLE patients and its levels increase with exposure to estrogens. Other miRNAs also show correlation with plasma Estradiol levels. The precise role of Estradiol in the pathogenesis of SLE remains complex and multifaceted and is a topic for further research.