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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
Mogos IC, Niculescu DA, Dusceac R, Poiana C
The Independent Effects of Type 2 Diabetes Mellitus and Chronic Kidney Disease on Bone Turnover MarkersActa Endo (Buc) 2024 20(1): 27-32 doi: 10.4183/aeb.2024.27
AbstractBackground. Chronic kidney disease (CKD) and type 2 diabetes mellitus (T2DM) are associated with disturbed mineral homeostasis and serum bone biomarkers. The interplay between T2DM and CKD on serum bone turnover markers (BTM) is unclear. Our aim was to describe the BTM in patients with T2DM, CKD or both. Methods. In this observational, single-centre, prospective study, we included 320 patients over 40 years, divided into four groups: T2DM and normal kidney function (n=142), T2DM and CKD (n=36), CKD and normal glucose metabolism (n=29) and healthy controls (n=113). We excluded patients treated for osteoporosis and with secondary osteoporosis. Patients were compared by age, levels of glycated hemoglobin, PTH, alkaline phosphatase, osteocalcin (OC), CTx and 25 OH vitamin D. Results. Univariate analysis showed that GFR correlated significantly with PTH (r=0.37), OC (r=0.43) and CTX (r=0.45) in the diabetes group but only with PTH (r=0.34) in the non-T2DM group. Multivariate analysis showed that GFR remained significantly correlated with the same bone markers even after adjustment for age, sex or 25(OH)D levels. Diabetics seem to have lower levels of alkaline phosphatase (68±22.1 U/L) and CTX (0.37±0.24 ng/mL) than those without diabetes (76.7±29.6. U/L and 0.5±0.19 ng/mL, respectively). There was no correlation between BTM and glycated hemoglobin. Conclusions. Bone turnover markers correlate with GFR, particularly in patients with T2DM. However, alkaline phosphatase is lower in T2DM than in non-T2DM. -
Endocrine Care
Dobre R, Niculescu DA, Cirstoiu C, Popescu G, Poiana C
Osteoporotic Hip Fracture Incidence Rates in the Main Urban Area of RomaniaActa Endo (Buc) 2021 17(1): 60-67 doi: 10.4183/aeb.2021.60
AbstractContext. Estimation of osteoporotic hip fracture incidence and Romanian FRAX model were based on nationally reported hospital ICD 10 coding admissions of all hip fractures (without a validation process). Objective. We aimed to calculate, based on individual hospital charts analysis, the incidence of osteoporotic hip fracture in the main urban area of Romania and compare it with data reported to the National Institute of Public Health (NIPH). Design. We retrospectively analyzed the charts of all patients (>40 years old) admitted for hip fracture in a 12-month period in hospitals with an Orthopedic Department in Bucharest and surrounding Ilfov County (11.8% of Romania population). Subjects and Methods. All ICD 10 fracture and event/fall codes were validated against the charts. We calculated the age and sex adjusted incidence of osteoporotic hip fracture and used the national reported hip fracture data base for comparison. Results. There were 2203 hip fractures of which 1997 (90.65%) were fragility fractures. The crude incidence of low-energy hip fractures was 171/100,000 (225/100,000 in women, 103/100,000 in men). The incidence rose with age to a maximum rate of 1902/100,000 in women >85 years. The NIPH-reported incidence of hip fracture was 181/100,000 for the region of interest and 176/100,000 at the national level. Conclusion. The incidence of osteoporotic hip fracture was lower than the incidence based on hip fractures reported codes in the national database, but the incidence of fragility fractures calculated by our group was higher than the incidence reported in previous national studies. Nationwide studies are warranted. -
Editorial
Poiana C, Niculescu DA, Gharib H
The First Regional International AACE Chapters’ MeetingActa Endo (Buc) 2016 12(1): 63-64 doi: 10.4183/aeb.2016.63
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Case Report
Poiana C, Carsote M, Popescu A, Hortopan D, Stanescu B, Ioachim D
Primary hyperparathyroidism associated with cerebral meningiomas - three cases reportActa Endo (Buc) 2007 3(1): 81-92 doi: 10.4183/aeb.2007.81
AbstractMeningiomas are the most common benign tumors of the brain, accounting for about 15 to 20% of all primary brain tumors. They are more common in females than in males and are most likely found in the sixth and seventh decades. Meningiomas arise from leptomeninges. Even the hyperostosis of the overlying skull occurs in 15-20% of cases and most of them have the tendency to calcify. The biological one can find hypercalcemia in a patient with cerebral meningioma, only if it associates other diseases like hyperparathyroidism. Between January 2000 and December 2006, in the Department of Pituitary and Neuroendocrine Pathology of the “C.I.Parhon” Institute of Endocrinology, Bucharest there have been admitted 29 patients with primary hyperparathyroidism, 7 males and 22 females. From the 22 women with primary hyperparathyroidism, 3 cases presented multiple endocrine neoplasia type I and 19 sporadic primary hyperparathyroidism. In the same period of time we found in 3 of these cases the association between sporadic primary hyperparathyroidism and cerebral meningiomas. We present the cases of three female patients of 56, 55, respectively 58 years old, diagnosed with primary hyperparathyroidism during the follow-up for nontoxic goiter. Two of them were known with cerebral meningiomas, unsuccessfully surgically approached, while the third one was newly diagnosed with meningioma, based on neuroimaging. There are a couple of studies regarding the association between cerebral meningiomas and the multiple endocrine neoplasia type 1 (MEN 1), but we found in the literature only three cases of both cerebral meningioma and sporadic primary hyperparathyroidism. Clinicians should be aware of the possible association between cerebral meningiomas and primary hyperparathyroidism. -
Clinical review/Extensive clinical experience
Poiana C, Capatina C, Streinu Cercel A, Sandulescu O, Cercel AS
Hypovitaminosis D in Hiv-Infected PatientsActa Endo (Buc) 2019 15(1): 102-106 doi: 10.4183/aeb.2019.102
AbstractIntroduction. Vitamin D (VD) deficiency is highly prevalent worldwide. Aim. To assess the prevalence of hypovitaminosis D in HIV-positive Romanian patients compared to controls. Methods. Serum 25OHD concentration was measured in HIV-infected patients and a control sample, matched by age, sex and menopausal status. The 25OHD status was defined as: deficiency < 20 ng/mL (severe deficiency <10 ng/mL), insufficiency 20-30 ng/mL, normal >30 ng/mL. Results. We evaluated 118 HIV-positive patients (72 males, 46 females), aged 36.9±12.2 years. 98.14% of them were on complex antiviral regimens. The B/C hepatitis coinfection rate was 9.3%. The control sample consisted of 119 subjects, (74 males, 45 women). The median and interquartile range for serum 25OHD concentration in patients was 17.6 (9.7, 26.9) ng/mL and 23.7 (18.4, 27.5) ng/mL in controls (p=0.001). Only 15.96% of HIV-positive cases and 12.71% of controls had normal VD status. The percentage of cases with severe VD deficiency was significantly higher in HIV positive cases (23.52%) compared to HIV-negative controls (4.2%, p=0.001). Conclusions. Hypovitaminosis D was identified in 84.04% of HIV-infected patients, but the serum 25OHD concentration was not associated with specific HIV-related factors in our sample. Clinical guidelines regarding VD status determination and supplementation in HIV patients are needed. -
Images in Endocrinology
Niculescu D, Dumitrascu A, Neamtu D, Poiana C
Indolent Papillary Thyroid Carcinoma: 18 Years Evolution of Untreated Pulmonary MetastasesActa Endo (Buc) 2015 11(1): 114-114 doi: 10.4183/aeb.2015.114
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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 leptinActa Endo (Buc) 2005 1(2): 157-166 doi: 10.4183/aeb.2005.157
Abstract ReferencesIntroduction: 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 Psychone10. 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 -
General Endocrinology
Cocolos AM, Vladoiu S, Caragheorgheopol A, Ghemigian AM, Ioachim D, Poiana C
Vitamin D Level and its Relationship aith Cancer Stage in Patients with Differentiated Thyroid CarcinomaActa Endo (Buc) 2022 18(2): 168-173 doi: 10.4183/aeb.2022.168
AbstractBackground. Differentiated thyroid carcinoma (DTC) has witnessed an increase in incidence and although it is considered to have a slow grow potential and a 90% 10- year survival rate, local or distant metastases can be observed in 20%. It is essential to recognize other factors associated with malignancy and poor prognosis. Vitamin D and its deficiency has proven useful as a prognostic biomarker for many types of cancer, including thyroid cancer. Aim. Evaluate the relationship between vitamin D status in DTC and benign thyroid disorders patients and correlation between vitamin D and histopathological findings in DTC group. Methods. Study included 170 patients with confirmed DTC and 200 with benign thyroid pathology. Evaluation included 25-hydroxy vitamin D [25(OH)D], ultrasound and histopathologic features. Results. In DTC patients, mean value of vitamin D was significantly lower (17.86 ng/mL ± 9.31 DS versus 20.26 ng/mL ± 9.31 DS, p=0.029). Statistical analysis confirmed a negative correlation between vitamin D levels and tumor size (T) according to TNM classification (r=-0.176, p=0.02). Conclusions. Vitamin D level was significantly lower in the DTC group and 25(OH)D levels may be correlated with histopathology features like tumor size and aggressiveness according to TNM classification. -
Endocrine Care
Dusceac R, Niculescu DA, Ismail G, Poiana C
Radius Age-Adjusted Bone Mineral Density is Correlated with Parathyroid Hormone Serum Levels in Patients with End-Stage Renal DiseaseActa Endo (Buc) 2015 11(2): 175-179 doi: 10.4183/aeb.2015.175
AbstractRenal osteodystrophy and low bone mass are frequently found in patients with end-stage renal disease (ESRD). Our aim was to identify the independent predictors of age - and sex-adjusted bone mineral density (BMD), measured at different traditional sites, in patients with ESRD treated by hemodialysis (HD) or peritoneal dialysis (PD). Patients and Methods. We consecutively assessed 23 patients with ESRD (17 on HD and 6 on PD). Patients treated with 1,25 dihydroxyvitamin D, vitamin D derivates (paricalcitol) or calcimimetics were excluded. Serum parathormone and 25OH vitamin D were measured in all patients. In HD patients all biochemical measurements were done in the day between dialysis sesions. BMD was assessed at following sites: femoral neck, total proximal femur, 1/3 radius, ultradistal (UD) radius and total radius. Radial BMD was assessed in the forearm without arteriovenous fistula. BMD Z-score provided by the manufacturer was used. Results. In patiens undergoing PD the femoral neck BMD Z-score was significantly higher than in HD patients (difference -0.77 DS, 95% CI for difference -1.48 to -0.06). PTH correlated significantly with BMD Z-score at the 1/3 (r=-0.664, p<0.001) and total (r=-0.583, p=0.002) radius levels. Total proximal femur and UD radius BMD Z-scores did not correlate with any of the proposed variables. Years of dialysis, 25OH vitamin D and body mass index did not correlate with BMD Z-score at any site. Conclusion. In patients with ESRD PTH correlates strongly with BMD Z-score at cortical sites. PD seems to be less harmful to BMD than HD. -
Case Report
Coculescu M, Poiana N, Raducanu-Lichiardopol C, Ionescu M
Gonadoblastoma in a patient with 46XY gonadal dysgenesisActa Endo (Buc) 2006 2(2): 227-238 doi: 10.4183/aeb.2006.227
AbstractWe present a 18 year old phenotypic female patient who presented for primary amenorrhea. Pelvic ultrasound revealed a hypoplastic uterus and CT scan showed a hypoplastic right gonad and a left gonadal tumor with extrapelvic location. Karyotype was 46XY. Hormonal assessment indicated hypergonadotropic hypogonadism: FSH was 39.69 mUI/ml, estradiol was 28.07 pg/ml, testosterone was 0.17 ng/ml. DHEA level was high – 21 ng/ml. Gonadectomy was performed at 15 years and histologic examination diagnosed left gonadoblastoma and right teratoma in a dysgenetic gonad. The patient had a good postoperatory evolution. Menses were induced with estrogenic and then estroprogestogenic treatment. Plastic breast surgery was performed at 18 years. Establishing the genotypic sex in patients with primary amenorrhea represents a crucial step knowing that intersex disorders bearing Y chromosomal material have a high risk for gonadoblastoma and germ cell tumors.