ACTA ENDOCRINOLOGICA (BUC)

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

in Web of Science Master Journal List

Acta Endocrinologica(Bucharest) is live in PubMed Central

Journal Impact Factor - click here.

Year Volume Issue First page
10.4183/aeb.
Author
Title
Abstract/Title
From through

  • Book Review

    Badiu C

    Neuroendocrine Tumors: Review of Pathology, Molecular and Therapeutic Advances

    Acta Endo (Buc) 2018 14(1): 145-145 doi: 10.4183/aeb.2018.145

  • Book Review

    Badiu C

    Polyendocrine Disorders and Endocrine Neoplastic Syndromes

    Acta Endo (Buc) 2021 17(1): 147-148 doi: 10.4183/aeb.2021.147

  • Book Review

    Badiu C

    Environmental Contaminants and Endocrine Health

    Acta Endo (Buc) 2023 19(1): 147-148 doi: 10.4183/aeb.2023.147

  • General Endocrinology

    Stefanescu AM, Schipor S, Paun D, Dumitrache C, Badiu C

    Plasma versus Salivary Chromogranin A as Selective Markers in Pheochromocytoma Diagnosis

    Acta Endo (Buc) 2011 7(2): 153-161 doi: 10.4183/aeb.2011.153

    Abstract
    Background: Simultaneously determined plasma chromogranin A (CgA) and free metanephrines can substantially enrich laboratory diagnosis of pheochromocytoma (PHEO). CgA-like\r\nimmunoreactivity was discovered in saliva. Salivary CgA (CgA-LIS) could precise PHEO diagnosis in a non-aggressive\r\nmanner for the patient using saliva instead of plasma samples.\r\nSubjects and methods: A group of 10 PHEO patients: 7 women (22 to 72 years ) and 3 men (42 to 59 years) and a control\r\ngroup of 10 subjects were included in this retrospective study. Plasma free metanephrines and CgA were assayed by\r\nElisa kits. Salivary CgA was assayed by an EIA kit. Both analytical and diagnosis performance of the CgA-LIS vs. CgA were compared using Passing& Bablok regression and Receiver Operating Curves (ROC analysis).\r\nResults: In tumor group, mean values for all 4 assayed parameters were significantly increased in comparison with\r\nthe same parameters in normal group as expected: free plasma normetanephrines (NMNp) was: 2773 ? 704.57pg/mL versus 48.51 ? 9.87 pg/mL in controls; free plasma metanephrines (MNp) was: 864.4 ? 330.75 pg/mL versus 19.18 ? 3.69 pg/mL in normals; CgA was: 695.10?235.22 ng/mL versus 74.4?5.37 ng/mL in controls; CgALIS was: 17.62?6.79 pmol/L versus 0.94 ?\r\n0.20 pmol/L in normals. Passing & Bablok regression equation for CgA-LIS versus CgA was: Y=0.0181 + 0.0146X. Cusum test\r\nfor linearity revealed no significant deviation from linearity (P>0.10). A significant correlation between NMNp and CgA-LIS was established in all 20 subjects: r=0.82, P<0.0001. Pairwise comparison of ROC curves for both markers showed no significant difference between areas. Salivary CgA could be successfully used instead of plasma CgA in biochemical diagnosis of pheochromocytoma.\r\nConclusions: We can conclude that salivary CgA could be used as a nonstressfull marker for diagnosis purpose in pheochromocytoma.
  • Images in Endocrinology

    Popa GL, Zurac S., Tanase I., Tomulescu V., Badiu C

    Adrenal Cystic Hemangioma

    Acta Endo (Buc) 2014 10(1): 155-156 doi: 10.4183/aeb.2014.155

  • General Endocrinology

    Poiana C, Stefanescu AM, Caragheorgheopol A, Badiu C, Galoiu S, Coculescu M

    Blood brain barrier by-pass produced by pituitary adenomas for pituitary peptides does not involve leptin

    Acta Endo (Buc) 2005 1(2): 157-166 doi: 10.4183/aeb.2005.157

    Abstract References
    Introduction: The impaired transport of leptin into the brain through a decreased permeability of the blood-brain barrier (BBB) for leptin in obesity represents one of the important mechanisms involved in leptin resistance which is characteristic in human obesity. Some pituitary tumors can increase the blood-cerebrospinal fluid barrier (BCB) permeability for peptides. BCB is a part of BBB.\r\nObjectives: The aim of our study was to search if the by-pass of BCB for pituitary hormones produced by adenomas does influence the transport of leptin into the central nervous system in obese patients.\r\nMaterials and methods: We investigated 20 males with pituitary adenomas: group A (11 patients) had cerebrospinal fluid (CSF) to serum ratio more than one for prolactin (PRL) and in some patients for growth hormone (GH) and follicle stimulating hormone (FSH), suggesting an increased permeability of BCB and a control group C (9 patients), which had CSF/serum ratio less than one for GH, PRL or FSH, suggesting an intact BCB. Both A and C groups contain subgroups of patients with obesity (body mass index, BMI>30 kg/m2) and normal body weight (BMI<25 kg/m2). In these patients we measured the CSF to serum leptin ratio in order to clinically evaluate the leptin transport into the brain. Rapid fluoroimmunoassay method with europium was used. Leptin was assayed by ELISA method.\r\nResults: The patients of group A with pituitary adenomas show a higher level of pituitary peptides, PRL and in some cases GH, FSH in CSF as compared to serum (ratio CSF/serum over 1), both in obese and non-obese. By contrast, in the same patients, there is\r\na low level of CSF leptin as compared to serum leptin (ratio CSF/serum less than 1). In the subgroup of obese patients from group A we found even less ratio of CSF to serum leptin, than in non-obese. There is a well known higher leptin concentration in the plasma of obese patients with pituitary adenomas as compared to non-obese ones (26.4?3.8ng/ml vs 12.4?3.4ng/ml, p<0.05). In the control group C, both pituitary peptides (PRL, or GH, FSH) and leptin showed a ratio CSF/serum less than 1, in all patients.\r\nConclusions: These data show a decrease in hemato-encephalic barrier permeability for leptin in obese patients through a specific mechanism, not influenced by other peptides passing through injuries of BBB produced by pituitary adenomas. It is tempting to suggest that there is a specific by-pass of BCB for pituitary peptides, in some pituitary adenomas.
    1. Wauters M, Considine RV, Van Gaal LF. Human leptin: from an adipocyte hormone to an endocrine mediator. Eur J Endocrinol 2000; 143(3):293-311. [CrossRef]
    2. Rodrigues AM, Radominski RB, Suplicy HL, De Almeida SM, Niclewicz PA, Boguszewski CL. The cerebrospinal fluid/serum leptin ratio during pharmacological therapy for obesity. J Clin Endocrinol Metab 2002; 87(4):1621-1626. [CrossRef]
    3. Chen H, Charlat O, Tartaglia LA, Woolf EA, Weng X, Ellis SJ et al. Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db/db mice. Cell 1996; 84(3):491-495.
    4. Tartaglia LA. The leptin receptor. J Biol Chem 1997; 272(10):6093-6096.
    5. Fei H, Okano HJ, Li C, Lee GH, Zhao C, Darnell R et al. Anatomic localization of alternatively spliced leptin receptors (Ob-R) in mouse brain and other tissues. Proc Natl Acad Sci U S A 1997; 94(13):7001-7005. [CrossRef]
    6. Burguera B, Couce ME, Curran GL, Jensen MD, Lloyd RV, Cleary MP et al. Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats. Diabetes 2000; 49(7):1219-1223. [CrossRef]
    7. 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]
    8. Poiana C, Cucu M, Stefanescu A, Stoian L. Are plasma leptin levels predictive for the bone mineral density in postmenopausal women? Bone 2005; 36(Suppl 2):S341-S342.
    9. Coculescu M, Gheorghiu M, Galoiu S, Trifanescu R, Caragheorgheopol A, Hortopan D et al. Natural and therapeutically-induced evolution of serum and cerebrospinal fluid pituitary hormones in patients with pituitary adenomas. The XIth Symposium of Psychone
    10. Caro JF, Kolaczynski JW, Nyce MR, Ohannesian JP, Opentanova I, Goldman WH et al. Decreased cerebrospinal-fluid/serum leptin ratio in obesity: a possible mechanism for leptin resistance. Lancet 1996; 348(9021):159-161. [CrossRef]
    11. Wong ML, Licinio J, Yildiz BO, Mantzoros CS, Prolo P, Kling M et al. Simultaneous and continuous 24-hour plasma and cerebrospinal fluid leptin measurements: dissociation of concentrations in central and peripheral compartments. J Clin Endocrinol Metab 2 [CrossRef]
    12. Saad MF, Riad-Gabriel MG, Khan A, Sharma A, Michael R, Jinagouda SD et al. Diurnal and ultradian rhythmicity of plasma leptin: effects of gender and adiposity. J Clin Endocrinol Metab 1998; 83(2):453-459. [CrossRef]
    13. Kennedy A, Gettys TW, Watson P, Wallace P, Ganaway E, Pan Q et al. The metabolic significance of leptin in humans: gender-based differences in relationship to adiposity, insulin sensitivity, and energy expenditure. J Clin Endocrinol Metab 1997; 82(4):12 [CrossRef]
    14. 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]
    15. Zlokovic BV, Jovanovic S, Miao W, Samara S, Verma S, Farrell CL. Differential regulation of leptin transport by the choroid plexus and blood-brain barrier and high affinity transport systems for entry into hypothalamus and across the blood-cerebrospinal [CrossRef]
    16. Wiesner G, Vaz M, Collier G, Seals D, Kaye D, Jennings G et al. Leptin is released from the human brain: influence of adiposity and gender. J Clin Endocrinol Metab 1999; 84(7):2270-2274. [CrossRef]
    17. Vidal S, Cohen SM, Horvath E, Kovacs K, Scheithauer BW, Burguera BG et al. Subcellular localization of leptin in non-tumorous and adenomatous human pituitaries: an immuno-ultrastructural study. J Histochem Cytochem 2000; 48(8):1147-1152.
    18. Coculescu M, Poiana C, Pop A, Oprescu M, Constantinovici A, Simionescu N. Altered specificity of the blood cerebrospinal fluid barrier for pituitary hormones in patients with tumoral hypothalamohypophyseal diseases as proved by releasing hormones stimul
  • Endocrine Care

    Iordache N, Copaescu C, Litescu M, Munteanu R, Boru C, Badiu C, Stoica A

    Bariatric surgery evolution in Romania. Results 1 year after a variety of bariatric procedures

    Acta Endo (Buc) 2008 4(2): 161-172 doi: 10.4183/aeb.2008.161

    Abstract
    Obesity is a worldwide public health problem (both in developed and developing countries), the most frequent nutritional disease in the world, with considerable morbiditymortality and high costs for the public healthcare systems. Bariatric surgery has been found to be the only method capable of maintaining proper and long-lasting weight loss for morbid obesity. Laparoscopy is the gold standard for bariatric procedures. We studied a group of 341 patients who underwent different types of laparoscopic bariatric surgical procedures: laparoscopic adjustable gastric banding (LAGB), laparoscopic sleeve gastrectomy (LSG), laparoscopic gastric bypass (LGB) and laparoscopic biliopancreatic diversion (LBPD). They were evaluated preoperative (weight, BMI, comorbidities) and followed-up for 1 year: 238 patients LAGB, 46 LSG, 49 LGB and 8 LBPD. Mortality and conversion rate were nil for all groups. A significant reduction in patients&#8217; weight was shown at 12 months postoperatively. BMI decreased from 45.6 kg/m2 to 37.9 for LAGB, from 54.12 to 40.8 kg/m2 for LGB and from 49.1 to 31.2 kg/m2 for LSG. The excess weight loss for LBPD was 63%. A significant improvement of co-morbidities was noticed; all patients with type 2 diabetes have normal serum glucose levels at 1 year after surgery. Bariatric surgery is safe with a low complication rate and the outcome was similar to literature data. Although we do not benefit of a long time follow-up, the favorable results allow us to state that minimally invasive surgical techniques deserve an important place in the efforts of struggling against obesity and its consequences.
  • Case Report

    Balmes E, Burcea A, Belgun M, Alexandrescu D, Badiu C

    Marine-Lenhart syndrome. Case report and literature review

    Acta Endo (Buc) 2007 3(2): 201-208 doi: 10.4183/aeb.2007.201

    Abstract
    Graves&#8217; disease and toxic nodular goiter both cause thyrotoxicosis by different pathophysiological mechanisms. Rare cases associates both etiologies are undertaken by the diagnosis of Marine-Lenhart syndrome. A woman aged 38, with Graves&#8217; unilateral ophthalmopathy and a solitary, echo-dense thyroid nodule, developed thyrotoxicosis within the following 3 months. The diagnosis was certified by suppressed TSH (0.002 mIU/L), high fT4 (5.6 ng/mL) associated with elevated TRAb (3.5 IU/L), moderately elevated TPOAb (63.1 IU/mL) and ATGl (248 IU/mL). The thyroid radioiodine scan revealed a solitary hot nodule in the left lobe with an elevated radioiodine uptake. Methyl prednisolone was started by oral and pulse therapy, with stabilization of ophthalmopathy within 5 months. After four months with antithyroid drug therapy followed by radioiodine (25 mCi 131I), the thyroid scan revealed diffuse radioiodine uptake. Nine months after radioiodine therapy, the patient was in clinical and biochemical hypothyroidism and substitutive therapy was instituted. A broad literature review suggested that in such rare cases, underlying autoimmune mechanisms might be involved in the development of thyroid nodules with variable function and proliferation activity.
  • Images in Endocrinology

    Badiu C, Alexandrescu D, Miron R, Gavan V

    Astrocytoma exophthalmia

    Acta Endo (Buc) 2008 4(2): 223-223 doi: 10.4183/aeb.2008.223

  • Case Report

    Giulea C, Enciu O, Nadragea M, Badiu C, Miron A

    Pemberton’s Sign and Intense Facial Edema in Superior Vena Cava Syndrome due to Retrosternal Goiter

    Acta Endo (Buc) 2016 12(2): 227-229 doi: 10.4183/aeb.2016.227

    Abstract
    Introduction. Retrosternal goitre enlargement can cause compression of several mediastinal structures, especially the trachea and the superior vena cava. Retrosternal goitre as a cause of superior vena cava syndrome is a rare occurrence. We report the case of a middle aged man that underwent surgery for retrosternal goitre with compression of both innominate veins presenting as superior vena cava syndrome. Case Presentation. A 50 year old man presented with a 2 year history of cyanosis of the upper limbs, head and neck, marked facial edema, plethora, dyspnea on exertion and choking sensation. Pemberton’s sign was present. Computer tomography diagnosed retrosternal goitre at the level of the aortic arch, tracheal compression and important collateral circulation. Endocrine evaluation showed normal thyroid function (fT4 15.8 pmol/L) with low-normal TSH (0.5mU/L), normal calcitonin (<2 pg/mL). The patient underwent successful total thyroidectomy with cervical approach and his symptoms dramatically improved. The facial oedema persisted for the next 3 weeks. Discussion. Less than 3% of superior vena cava syndromes are secondary to a variety of benign causes. Superior vena cava syndrome caused by slow growing retrosternal goitres is very rare and can be asymptomatic for a long period due to venous collateral development. Conclusion. Superior vena cava syndrome secondary to retrosternal goitres, a very rare occurrence, is an indication for total thyroidectomy, with low postoperative morbidity and dramatic resolution of symptoms.