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
From through

  • Case Report

    Badiu C, Capatana C, Cristofor D, Mircescu G, Coculescu M

    Apparent mineralocorticoid excess in a case of lung paraneoplastic Cushing syndrome

    Acta Endo (Buc) 2005 1(1): 97-107 doi: 10.4183/aeb.2005.97

    Abstract References
    Severe hypokalemia is a life threatening event, which triggers a number of therapeutic and diagnostic attitudes. In this paper we present a case of 63 years old man, who presented with progressive lassitude, edema, weight loss. The mild hypertension and hyperglycaemia were treated with spironolactone and diet. Initial evaluation showed severe hypokalemia (1.7 mmol/l), hepatomegalia, hyperplasic/nodular adrenal masses; in addition, he has developed a right middle lobe pneumonia which improved with antibiotics. Referred for the suspicion of hyperaldosteronism, aldosterone values were normal (9.3-9.5 ?g/dl), but ACTH was high (725 pg/ml) and did not suppress (710.8 pg/ml) to high dose DXM, as well as cortisol: basal values 27.78 ug/dl, high dose DXM 35.06 ug/dl, showing an ACTH dependent Cushing syndrome despite lack of suggestive clinical signs. Tumor markers suggested a neuroendocrine neoplasia: carcinoembryonic antigen=101 ng/ml (normal values=0.52-6.3 ng/ml), CA 19-9= 155 ng/ml (N < 33 ng/ml). Further radiological evaluation showed a 3 cm right lobe lung tumour. Despite high potassium supplements and spironolactone, the hypokalemia remained around 3.2 mmol/l, characteristic for an apparent mineralocorticoid excess. Because of aggressive evolution of the lung tumour, he died three months after the initial admission into the hospital. Pathology report showed a lung carcinoma. ACTH immunostaining of the lung tumour was positive and revealed a paraneoplastic secretion.
    1. Martinez Maldonado Manuel. Approach to the patient with hypokalemia. In: Humes H.David, editor. Kelley?s Textbook of Internal Medicine. Lippincott Williams & Wilkins, 2000.
    2. Beuschlein F, Hammer GD. Ectopic pro-opiomelanocortin syndrome. Endocrinol Metab Clin North Am 2002; 31(1):191-234. [CrossRef]
    3. Schrier W Robert. The patient with hypokalemia or hyperkalemia. Manual of nephrology. Lippincott Williams& Wilkins, 2000.
    4. Davison M.Alex. Hypo-hyperkalemia. Oxford Textbook of Clinical Nephrology. Oxford University Press, 2003.
    5. Walker BR, Campbell JC, Fraser R, Stewart PM, Edwards CR. Mineralocorticoid excess and inhibition of 11 beta-hydroxysteroid dehydrogenase in patients with ectopic ACTH syndrome. Clin Endocrinol (Oxf) 1992; 37(6):483-492. [CrossRef]
    6. Campusano C, Arteaga E, Fardella C, Cardenas I, Martinez P. [Cushing syndrome by ectopic ACTH secretion: analysis of the physiopathologic mechanism of hypokalemia. Report of two cases]. Rev Med Chil 1999; 127(3):332-336.
    7. Torpy DJ, Mullen N, Ilias I, Nieman LK. Association of hypertension and hypokalemia with Cushing?s syndrome caused by ectopic ACTH secretion: a series of 58 cases. Ann N Y Acad Sci 2002; 970:134-144. [CrossRef]
    8. Torpy DJ, Mullen N, Ilias I, Nieman LK. Association of hypertension and hypokalemia with Cushing?s syndrome caused by ectopic ACTH secretion: a series of 58 cases. Ann N Y Acad Sci 2002; 970:134-144. [CrossRef]
    9. Newell-Price J, Trainer P, Besser M, Grossman A. The diagnosis and differential diagnosis of Cushing?s syndrome and pseudo-Cushing?s states. Endocr Rev 1998; 19(5):647-672. [CrossRef]
    10. Howlett TA, Drury PL, Perry L, Doniach I, Rees LH, Besser GM. Diagnosis and management of ACTH-dependent Cushing?s syndrome: comparison of the features in ectopic and pituitary ACTH production. Clin Endocrinol (Oxf) 1986; 24(6):699-713. [CrossRef]
    11. Schiller JH, Jones JC. Paraneoplastic syndromes associated with lung cancer. Curr Opin Oncol 1993; 5(2):335-342. [CrossRef]
    12. Crapo L. Cushing?s syndrome: a review of diagnostic tests. Metabolism 1979; 28(9):955-977. [CrossRef]
    13. White A, Clark AJ, Stewart MF. The synthesis of ACTH and related peptides by tumours. Baillieres Clin Endocrinol Metab 1990; 4(1):1-27. [CrossRef]
    14. Wajchenberg BL, Mendonca B, Liberman B, Adelaide M, Pereira A, Kirschner MA. Ectopic ACTH syndrome. J Steroid Biochem Mol Biol 1995; 53(1-6):139-151.
    15. Kraus J, Buchfelder M, Hollt V. Regulatory elements of the human proopiomelanocortin gene promoter. DNA Cell Biol 1993; 12(6):527-536. [CrossRef]
    16. Stewart PM, Gibson S, Crosby SR, Penn R, Holder R, Ferry D et al. ACTH precursors characterize the ectopic ACTH syndrome. Clin Endocrinol (Oxf) 1994; 40(2):199-204. [CrossRef]
    17. Wajchenberg BL, Mendonca B, Liberman B, Adelaide M, Pereira A, Kirschner MA. Ectopic ACTH syndrome. J Steroid Biochem Mol Biol 1995; 53(1-6):139-151.
    18. Kocijancic I, Vidmar K, Zwitter M, Snoj M. The significance of adrenal metastases from lung carcinoma. Eur J Surg Oncol 2003; 29(1):87-88. [CrossRef]
    19. Usalan C, Emri S. Membranoproliferative glomerulonephritis associated with small cell lung carcinoma. Int Urol Nephrol 1998; 30(2):209-213. [CrossRef]
    20. Norris SH. Paraneoplastic glomerulopathies. Semin Nephrol 1993; 13(3):258-272.
    21. Terzolo M, Reimondo G, Ali A, Bovio S, Daffara F, Paccotti P et al. Ectopic ACTH syndrome: molecular bases and clinical heterogeneity. Ann Oncol 2001; 12 Suppl 2:S83-S87. [CrossRef]
    22. Shepherd FA, Laskey J, Evans WK, Goss PE, Johansen E, Khamsi F. Cushing?s syndrome associated with ectopic corticotropin production and small-cell lung cancer. J Clin Oncol 1992; 10(1):21-27.
    23. Abeloff MD, Trump DL, Baylin SB. Ectopic adrenocorticotrophic (ACTH) syndrome and small cell carcinoma of the lung-assessment of clinical implications in patients on combination chemotherapy. Cancer 1981; 48(5):1082-1087. [CrossRef]
    24. Pastore V, Santini M, Vicidomini G, D?Aniello G, Fiorello A, Parascandolo V. [Role of the surgeon in the treatment of small cell lung carcinoma]. Minerva Endocrinol 2001; 26(4):263-267.
  • Clinical review/Extensive clinical experience

    Badiu C

    Endocrine Management in Prader-Willi Syndrome

    Acta Endo (Buc) 2012 8(1): 99-106 doi: 10.4183/aeb.2012.99

    Prader Willi syndrome (PWS) is a genetic disorder (15q11-q13) characterized by short stature, hypogonadism leading to\r\nosteoporosis, delayed puberty, central hypocorticism and the most life threatening, excessive appetite which is followed by morbid obesity. Patients with PWS present reduced\r\nGH secretion, hypogonadotropic hypogonadism, abnormal appetite control and high pain threshold suggesting\r\nhypothalamic-pituitary dysfunction. However, all high resolution imaging studies are normal; due to changes in Chr\r\n15, the hypothalamic function is disrupted. All patients with PWS show severe disturbances in appetite control resulting in hyperphagia and obesity. Peptides involved in hypothalamic appetite control as ghrelin, leptin, NPY/AGRP, POMC, and their cognate receptors, are involved in developmental processes, determine the threshold for\r\nsignals of body fat below which increases in energy intake and reductions in energy expenditure. In addition, low GH and IGF1 level, central hypothyroidism, delayed puberty and central hypogonadism may impact upon the body composition. Despite the detailed knowledge about obesity mechanisms regulated at hypothalamic level, the pharmacological intervention is limited currently to substitution of proven\r\nendocrine deficiencies and GH treatment. The PWS brain seems "wired" for a positive energy balance, and very few\r\npathways can counterbalance this genetic imprinting.
  • Case Report

    Bumbacea RS, Ghiordanescu IM, Tudose I, Popa LG, Badiu C, Giurcaneanu C

    Autoimmune Progesterone Dermatitis in a Patient with no Medical History of Hormonal Contraception or Pregnancy

    Acta Endo (Buc) 2015 11(1): 99-102 doi: 10.4183/aeb.2015.99

    Abstract Context. Autoimmune progesterone dermatitis (AIPD) is a rare, cyclical dermatosis, with variable clinical presentation, occurring exclusively or being aggravated during the luteal phase of the menstrual cycle, when levels of progesterone rise. Its pathogenesis is still unclear. AIPD is thought to occur as an autoimmune reaction to endogenous possibly modified progesterone, but it could also be triggered by exogenous progesterone exposure. AIPD is a diagnosis of exclusion. Usually there is no or limited response to oral H1 antihistamines and a partial response to steroids. Ovulation inhibitors represent the specific treatment. Case report. We report a case of AIPD in an 18-year-old nulliparous patient with no medical history of allergic diseases and no exposure to oral contraceptive pills. AIPD was suspected based on the clinical picture (recurrent cyclical eczematous eruption on the face and abdominal area) and confirmed by positive intradermal test and positive progesterone challenge. This diagnosis was supported by the result of the skin biopsy, which also helped to exclude other dermatoses with premenstrual aggravation. The rash responded satisfactorily to treatment with a combination of oral contraceptives, levonorgestrel and estrione, which is currently considered first line therapy. Conclusions. This case is of particular interest due to the lack of previous pregnancy or exposure to progesteron therapy. Recurrent, cyclical eruptions in fertile women should raise the suspicion of AIPD. If early recognized, the patient may benefit from non-invasive treatment that improves significantly the quality of life.
  • Images in Endocrinology

    Hariga CS, Badiu C, Jecan R, Lascar I

    Virginal Gigantomastia

    Acta Endo (Buc) 2016 12(1): 102-103 doi: 10.4183/aeb.2016.102

  • Images in Endocrinology

    Badiu C, Cristofor D

    Brain calcifications

    Acta Endo (Buc) 2006 2(1): 109-109 doi: 10.4183/aeb.2006.109

  • Actualities in medicine

    Dobrescu R, Badiu C

    Actualities in Genetics of Differentiated Thyroid Cancer

    Acta Endo (Buc) 2020 16(1): 118-120 doi: 10.4183/aeb.2020.118

    Genetics of cancer is a hot topic, an excellent example of translational medicine. Risk stratification, selection of cases for surgery in Bethesda categories 3 &4 FNAB are examples of the high impact of genetic evaluation in thyroid neoplasia.
  • General Endocrinology

    Radian S, Bensaada M, Lautier C, Moles JP, Grigorescu F, Gussi I, Badiu C, Nastasia S, Hudita D, Leonte L, Marinescu B, Coculescu M

    Molecular genetics strategies to identify vasotocin coding sequences in humans: family-specific approach using genomic DNA and fetal tissues mRNAs

    Acta Endo (Buc) 2005 1(2): 131-144 doi: 10.4183/aeb.2005.131

    Abstract References
    Vertebrate nonapeptide neurohormones constitute an evolutionarily conserved family, involved in vital functions, such as hydro-osmotic balance regulation, reproduction and social behaviour. Two human members of this family are known, vasopressin (AVP) and oxytocin (OXT), with their highly homologous genes closely located on Chr 20p13. Presence of vasotocin (AVT) in man has been suggested, but remains controversial, and genetic evidence is lacking. AVT activity could be explained by the presence of a third distinct gene for AVT or an RNA-processing mechanism involving products of AVP and/or OXT genes. To test the first hypothesis, we developed bioinformatics and experimental approaches using genomic DNA and fetal tissues mRNAs. Family-specific primers for AVT and neurophysin were designed based on CODEHOP strategy and used in our experiments. Results of bioinformatics and genomic DNA experiments (family-specific and Alu step-out PCR) suggest there is no evidence for an AVT gene in the genome. RNA-based techniques 3?-RACE and Family-Specific Domain Restriction Fragment RTPCR provided evidence for new transcript species that could code for AVT. Further experiments will be needed to characterize them. We discuss potential mechanisms of AVT mRNA generation based on AVP and OXT mRNAs, by alternative splicing, heterologous transsplicing or RNA-editing. While all methods we developed proved feasible, current results suggest there is no AVT gene in the genome, but specific mRNAs could be present in fetal tissues. Their full characterization may potentially allow identification of vasotocin mRNA and shed light on a subject of fundamental scientific interest.
    1. Dale HH. Evidence concerning the endocrine function of the neurohypophysis and its nervous control. In: The Neurohypophysis, editor Heller HH. London: Butterworth?s, 1957, 1-9.
    2. Dantzer R. Vasopressin, gonadal steroids and social recognition. Prog Brain Res. 1998;119:409-14.
    3. Bielsky IF, Young LJ. Oxytocin, vasopressin, and social recognition in mammals. Peptides. 2004;25(9):1565-74. [CrossRef]
    4. Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, Fehr E. Oxytocin increases trust in humans. Nature. 2005;435(7042):673-6. [CrossRef]
    5. Hoyle CH. Neuropeptide families and their receptors: evolutionary perspectives. Brain Res. 1999;848(1-2):1-25. [CrossRef]
    6. Sausville E, Carney D, Battey J.The human vasopressin gene is linked to the oxytocin gene and is selectively expressed in a cultured lung cancer cell line. J Biol Chem. 1985;260(18):10236-41.
    7. Pavel, S. Arginine vasotocin as a pineal hormone. J. Neural. Transmission 1978; 13:135-155.
    8. Coculescu M, Pavel S. Arginine vasotocin-like activity of cerebrospinal fluid in diabetes insipidus. J Clin Endocrinol Metab. 1973;36(5):1031-2. [CrossRef]
    9. Catrina SB, Coculescu M, Andersson M. A chemical method to isolate hypothalamic nonapeptides by coupling cyst(e)in with bimane. J Cell Mol Med. 2001;5(2):195-7. [CrossRef]
    10. Badiu C, Coculescu M, Moller M. Arginine vasotocin mRNA revealed by in situ hybridization in bovine pineal gland cells. Cell Tissue Res. 1999;295(2):225-9. [CrossRef]
    11. Ervin MG, Amico JA, Leake RD, Ross MG, Robinson AG, Fisher DA. Arginine vasotocin and a novel oxytocin-vasotocin-like material in plasma of human newborns. Biol Neonate. 1988;53(1):17-22. [CrossRef]
    12. Pavel S. Evidence for the ependymal origin of arginine vasotocin in the bovine pineal gland. Endocrinology. 1971;89(2):613-4. [CrossRef]
    13. Pavel S, Dorcescu M, Petrescu-Holban R, Ghinea E. Biosynthesis of a vasotocin-like peptide in cell cultures from pineal glands of human fetuses. Science. 1973;181(106):1252-3. [CrossRef]
    14. Rose TM, Schultz ER, Henikoff JG, Pietrokovski S, McCallum CM, Henikoff S. Consensusdegenerate hybrid oligonucleotide primers for amplification of distantly related sequences. Nucleic Acids Res. 1998;26(7):1628-35. [CrossRef]
    15. <>
    16. Fuentes JJ, Pucharcos C, Pritchard M, Estivill X. Alu-splice PCR: a simple method to isolate exoncontaining fragments from cloned human genomic DNA. Hum Genet. 1997;101(3):346-50. [CrossRef]
    17. Siebert PD, Chenchik A, Kellogg DE, Lukyanov KA, Lukyanov SA. An improved PCR method for walking in uncloned genomic DNA. Nucleic Acids Res. 1995;23(6):1087 [CrossRef]
    18. Matz M, Shagin D, Bogdanova E, Britanova O, Lukyanov S, Diatchenko L, Chenchik A. Amplification of cDNA ends based on template-switching effect and step-out PCR. Nucleic Acids Res. 1999;27(6):1558-60. [CrossRef]
    19. Michel G, Levy B, Chauvet MT, Chauvet J, Acher R. Complete amino acid sequence of goose VLDVneurophysin. Traces of a putative gene conversion between promesotocin and provasotocin genes. Int J Pept Protein Res. 1990;36(5):457-64. [CrossRef]
    20. Ruppert S, Scherer G, Schutz G. Recent gene conversion involving bovine vasopressin and oxytocin precursor genes suggested by nucleotide sequence. Nature. 1984 Apr 5-11;308(5959):554-7. [CrossRef]
    21. Pavel S. Evidence for the presence of lysine vasotocin in the pig pineal gland. Endocrinology. 1965 ;77(5):812-7. [CrossRef]
    22. Pavel S. Pineal vasotocin and sleep. Environmental Physiology. Vol. 18 in Advances in Physiological Sciences. Proceedings of the 28th International Congress of Physiological Sciences, Budapest, 1980. Obal, F., and G. Benedek, Eds. Budapest: Akademiai Ki
    23. Coculescu M, Serbanescu A, Temeli E. Influence of arginine vasotocin administration on nocturnal sleep of human subjects. Waking Sleeping. 1979;3(3):273-7.
    24. Mihai R, Coculescu M, Wakerley JB, Ingram CD. The effects of [Arg8]vasopressin and [Arg8]vasotocin on the firing rate of suprachiasmatic neurons in vitro. Neuroscience. 1994 ;62(3):783-92. [CrossRef]
    25. Lefebvre DL, Zingg HH. Novel vasopressin gene-related transcripts in rat testis. Mol Endocrinol. 1991;5(5):645. [CrossRef]
    26. Foo NC, Funkhouser JM, Carter DA, Murphy D. A testis-specific promoter in the rat vasopressin gene. J Biol Chem. 1994;269(1):65.
    27. Caudevilla C, Serra D, Miliar A, Codony C, Asins G, Bach M, Hegardt FG. Natural trans-splicing in carnitine octanoyltransferase pre-mRNAs in rat liver. Proc Natl Acad Sci U S A. 1998;95(21):12185-90. [CrossRef]
    28. Finta C, Zaphiropoulos PG. Intergenic mRNA molecules resulting from trans-splicing. J Biol Chem. 2002;277(8):5882-90. Epub 2001 Nov 28. [CrossRef]
    29. Mohr E, Peters A, Morris JF, Richter D. Somatic nonhomologous crossing-over between neuropeptide genes in rat hypothalamic neurons. Proc Natl Acad Sci U S A. 1994;91(24):11403-7. [CrossRef]
    30. Eisenberg E, Nemzer S, Kinar Y, Sorek R, Rechavi G, Levanon EY. Is abundant A-to-I RNA editing primate-specific? Trends Genet. 2005;21(2):77-81. [CrossRef]
    31. Levanon EY, Eisenberg E, Yelin R, Nemzer S, Hallegger M, Shemesh R, Fligelman ZY, Shoshan A, Pollock SR, Sztybel D, Olshansky M, Rechavi G, Jantsch MF. Systematic identification of abundant Ato- I editing sites in the human transcriptome. Nat Biotechnol [CrossRef]
  • General Endocrinology

    Vladoiu S, Dinu Draganescu D, Botezatu A, Anton G, Oros S, Paun DL, Ianas O, Rosca R, Badiu C

    Correlations between Polymorphisms of Estrogen 1, Vitamin D Receptors and Hormonal Profile in Infertile Men

    Acta Endo (Buc) 2016 12(2): 137-144 doi: 10.4183/aeb.2016.137

    Objective. Estrogen receptor alpha (ESR1) polymorphisms (XbaI and PvuII) and vitamin D receptor (VDR) polymorphisms (FokI, BsmI, ApaI and TaqI) are the most frequently studied regarding the correlations with the infertility in males, but the results are controversial. The purpose of this study is to evaluate possible correlations between hormonal markers, VDR and ESR1 genotypes and semen analysis, in order to bring new data for a better understanding of male infertility. Subjects and Methods. 42 infertile men and 28 controls were enrolled. The polymorphisms of VDR gene (ApaI, TaqI, BsmI and FokI) and ESR1 (XbaI and PvuII) were performed by PCR-RFLP, along with hormonal markers. Results. An important correlation between PvuII polymorphism and infertility status was revealed. A significant difference between control and infertility group regarding the presence of BsmI (A>G) and ApaI (G>T) polymorphisms was observed in infertile group, prolactin and DHEA were found to correlate significantly statistic with BsmI GG genotype, whereas ApaI AA genotype correlates with prolactin and SHBG levels. Conclusions. By a multivariate analysis, we demonstrated a cumulative effect of some genetic variants in the hormonal status of infertile patients. Therefore, we show that specific genetic variants of ESR1 and VDR genes may jointly influence human spermatogenesis.
  • Book Review

    Badiu C

    Hypercalcemia - Clinical Diagnosis and Management

    Acta Endo (Buc) 2022 18(1): 138-138 doi: 10.4183/aeb.2022.138

  • Book Review

    Badiu C

    Oxford Handbook of Clinical Medicine (10 Ed.)

    Acta Endo (Buc) 2019 15(1): 144-144 doi: 10.4183/aeb.2019.144