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

  • Case Report

    Simsek T, Tatar OC, Guler SA, Canturk NZ, Cakir O, Gurbuz YS

    Adrenal Arteriovenous Malformation Masquerading as an Adrenal Adenoma

    Acta Endo (Buc) 2023 19(2): 245-248 doi: 10.4183/aeb.2023.245

    Abstract
    Arteriovenous malformations of adrenal gland are extremely rare. We report a case of an adrenal arteriovenous malformation, mimicking an adrenal tumor in preoperative imaging. A 48-year-old woman presented to our clinic with abdominal pain. A 9x7 cm right adrenal tumor was detected. Based on the imaging findings, adrenal adenoma was suspected. However, clinical symptoms and endocrine abnormalities were absent, the lesion was thought to be non-functional. Laparoscopic right adrenalectomy was performed. Pathologically, this was diagnosed as an adrenal arteriovenous malformation. To the best of our knowledge, this is the first reported case of an adrenal arteriovenous malformation in the current literature.
  • Case Report

    Hayta SB, Guner R, Cam S, Akyol M

    Rosacea is Associated with Thyroid Autoimmunity: A Case Control Study

    Acta Endo (Buc) 2018 14(2): 248-251 doi: 10.4183/aeb.2018.248

    Abstract
    Background and aims. There are numerous intrinsic and extrinsic factors associated with the pathophysiology of rosacea, including immune dysregulation. The aim of this study is to determine the relationship between rosacea and thyroid autoimmunity. Methods. Seventy-two patients with rosacea and 62 rosacea-free control subjects were included in the study. Serum free triiodothyronine (fT3), free thyroxine (fT4), thyrotropin releasing hormone (TSH), antithyroidperoxidase antibody (ATPO), antithyroglobulin (anti-Tg), prolactin, dehydroepiandrosterone sulfate (DHEAS), basal cortisol, serum CRP concentrations and erythrocyte sedimentation rate were measured. Results. The number of the cases with high levels of CRP, anti-M and prolactin in rosacea group were significantly higher than the controls (p<0.05), there was no significant difference according to other parameters in both groups (p>0.05). There was no significant difference according to the presence of a thyroid disease in both groups (p>0.05). The decrease in the CRP parameter in patients with the disease duration of 1-5 years was found to be statistically significant (βCRP=-0.251, pCRP<0.05). There was no statistically significant difference according to disease severity or disease duration (p>0.05). Conclusions. Rosacea may be associated with high thyroid autoantibodies, prolactin and CRP levels, in which immune-endocrine interactions are important.
  • Endocrine Care

    Mitu F, Dumitriu I.L., Schiriac C.E. , Vata L.G., Gurzu B

    Effect of Supervised Lifestyle Changes on Metabolic Syndrome-Associated Inflammation

    Acta Endo (Buc) 2013 9(2): 249-262 doi: 10.4183/aeb.2013.249

    Abstract
    Background. Weight loss associated with long-term lifestyle changes has significant beneficial effects on metabolic syndrome (MetS) features on obese patients; unfortunately, the weight recidivism rate is high and the weight fluctuations could increase the cardiovascular and metabolic risk. On the other hand, there are many data about the endocrine role of adipose tissue. Objective. Taking into account the imbalance between pro-inflammatory and anti-inflammatory cytokines secreted by adipose tissue on obese patients, this study assessed the effects of one month-long supervised lifestyle change (SLC) program without weight loss on the MetS-associated inflammatory status. Methods. The study included 29 obese adults with MetS. The SLC program included supervised moderate physical activities and diet for one month. The levels of adipocytokines, lipids and inflammatory markers were analyzed before and after one month SLC program, and 2 months later at follow-up. Results. At follow-up, the leptin, vascular endothelial growth factor (VEGF), and hsCRP levels decreased, whereas the interleukin-4 (IL-4) and high-density lipoprotein (HDL) cholesterol levels increased from their baseline levels. So, an SLC program, even in the absence of weight loss, could have an extended antiinflammatory effect by decreasing the proinflammatory adipocytokines. Conclusion. Our data furthermore emphasize the importance of the adipocytokines gender-related variation for a more personalized evaluation protocol on obese patients.
  • Notes & Comments

    Kobylinska L, Ghita MA, Caruntu C, Gabreanu G, Tataru CP, Badescu SV, Geicu O, Neagu M, Constantin C, Dobrescu I, Zagrean L

    Preliminary Insights in Oxytocin Association with the Onset of Diabetic Neuropathy

    Acta Endo (Buc) 2017 13(2): 249-253 doi: 10.4183/aeb.2017.249

    Abstract
    Diabetes is one of the most prevalent chronic disorders, associating numerous somatic and behavioral modifications. Oxytocin has been widely studied for its involvement in social behavior and psychiatric disorders. This pilot study presents a series of 3 patients with type 1 diabetes and diabetic neuropathy in which the values of plasma oxytocin, neurotensin, β-endorphins, α-MSH, substance P and orexin A were measured in comparison to 3 healthy controls with matching ages. In the diabetic patients group, there was a strong negative correlation between the value of plasma glucose and oxytocin (r=-0.99, p=0.04), respectively neurotensin (r=- 0.99, p=0.03). These values did not correlate in the control group. The results suggest that oxytocin, in conjunction with neurotensin, could be investigated as a potential early detection marker of diabetic neuropathy and, to our knowledge, this is the first report focusing on plasma oxytocin levels in patients with diabetic neuropathy.
  • Case Report

    Isik S, Berker D, Aydin Y, Ozuguz U, Tutuncu Y, Simsek Y, Guler S

    Severe hyperkalemia without electrocardiographic changes in a patient with Addison disease

    Acta Endo (Buc) 2010 6(2): 251-255 doi: 10.4183/aeb.2010.251

    Abstract
    Objective. Hyperkalemia is one of the most common acute life-threatening metabolic emergencies. Alterations in serum potassium (K+) levels can have dramatic effects on\r\ncardiac cell conduction and may lead to electrocardiographic (ECG) changes. But in some\r\npatients ECG changes do not accompany serum K+ abnormalities. Severe hyperkalemia secondary to Addison Disease (AD) is rare.\r\nCase. A 40-year-old woman with AD was admitted to emergency service with generalized pain. The patient?s serum K+ level was found to be at the highest level that can be detected in our laboratory (>10.0 mmol/L, normal 3.5-4.5 mmol/L) and repeated serum K+ confirmed the previous result. Results of repeated ECGs have revealed a normal sinus rhythm. Our case is particularly interesting because it demonstrates an Addison patient that has an extremely high level of K+ (>10 mmol/L) without any accompanying ECG changes.\r\nConclusion. Our case confirms that diagnostic ECG changes do not always accompany severe hyperkalemia. Therefore, clinicians should be careful that ECG may look\r\nnormal in the presence of severe hyperkalemia.
  • Notes & Comments

    Akbas A, Dagmura H, Gul S, Dasiran F, Daldal E, Okan I

    Management Principles of Incidental Thyroid 18F-FDG Uptake Identified on 18F-FDG PET/CT Imaging

    Acta Endo (Buc) 2022 18(2): 253-257 doi: 10.4183/aeb.2022.253

    Abstract
    Purpose. The purpose of this study is to determine the clinical significance of incidental thyroid 18F-FDG PET/ CT uptake in oncology patients with the focus achieving the most appropriate management of this challenging situation. Materials and method. Two thousand five hundred and eighty 18F-FDG PET/CT studies performed at our institute in the past 4 years were retrospectively reviewed. Patients with incidental FDG uptake in the thyroid gland were further analysed. Results. The prevalence of incidental FDG uptake in thyroid gland was 7.6% (129 patients). 26 patients (20.1%) had diffuse 18F-FDG PET/CT uptake, 103 patients (79.1%) had nodular uptake in thyroid gland. All diffuse uptake patients who were further examined diagnosed to be a benign condition. 53 patients in the nodular uptake group were further examined and the final histopathology examinations revealed an 18.8% malignancy rate. SUV max values ranged from 2 to 21.8 with a significant highness in malignant lesions. Conclusion. 18F-FDG PET/CT uptake in the thyroid gland may be diffuse or nodular. Diffuse uptake needs no further examination as it usually accompanied by benign thyroid disorders. Patients with nodular uptake whose general condition is good should be further examined due to high rates of malignancy.
  • Case Report

    Goren TA, Kilimci DD, Yigit Y, Yildirim AT, Gulen H, Ersoy B

    Episode of Acute Hemolysis Due to Undiagnosed Glucose-6-Phosphate Dehidrogenase Deficiency in an Adolescent with Newly Diagnosed Type 1 Diabetes Mellitus: Case Report and Review of Literature

    Acta Endo (Buc) 2023 19(2): 256-259 doi: 10.4183/aeb.2023.256

    Abstract
    Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is common in the community. The most important clinical manifestation of G6PD deficiency is acute hemolytic anemia due to oxidative stressors. Diabetes Mellitus (DM) can precipitate hemolysis in patients with G6PD deficiency. Here, we described a 15-year-old male with newly diagnosed type 1 DM (T1DM) and unknown G6PD deficiency who suffered from hemolytic anemia during normalization of blood glucose. On admission, the patient did not have ketoacidosis. After the patient's blood sugars were regulated with insulin therapy, he presented five days later with hemolytic anemia. The cause of hemolytic anemia was G6PD deficiency. The patient had no previous episodes of hemolysis and had no relevant family history. Hypoglycemia did not occur during blood glucose regulation. The return of blood sugar to normal after a long period of hyperglycemia was thought to be the possible cause of hemolysis. In conclusion, G6PD deficiency should be considered when there is an episode of hemolysis in newly diagnosed children and adolescents with T1DM, especially in the absence of ketoacidosis and hypoglycemia.
  • Perspectives

    Koseoglu D, Ozdemir Baser O, Berker D, Guler S

    Exenatide Treatment Reduces Thyroid Gland Volume, but Has No Effect on the Size Of Thyroid Nodules

    Acta Endo (Buc) 2020 16(3): 275-279 doi: 10.4183/aeb.2020.275

    Abstract
    Context. Exenatide is a Glucagon-like Peptide-1 receptor agonist, which is widely used for type 2 diabetes mellitus (T2DM). Limited and conflicting results are present about the effect of exenatide on the thyroid gland. Objective. The aim of this study was to evaluate the effect of exenatide treatment on structural and functional features of the thyroid gland in patients with T2DM. Design. The study was a prospective study, performed between 2015 and 2017. The laboratory values and thyroid ultrasonography features were compared before and after exenatide treatment. Subjects and Methods. The study included 39 obese diabetic patients. After inclusion to the study exenatide was started and patients were followed up for 6 months. Total thyroid volume, thyroid function tests, serum carcinoembryonic antigen (CEA) and calcitonin levels, the size and appearance of thyroid nodules were compared between baseline and after 6 months of treatment. Results. Exenatide at a dose of 5μg bid was started, increased to 10 μg bid after 4 weeks. We found a statistically significant decrease in thyroid volume (p=0.043) and serum thyroid stimulating hormone (TSH) levels (p=0.007), whereas serum ATPO. ATGl, fT4, fT3, CEA and calcitonin levels did no change with 6 months of exenatide treatment. There were no significant differences in the size and appearance of the thyroid nodules with treatment. The thyroid volume decrease was not correlated with TSH, body mass index and HbA1c reduction. Conclusion. Exenatide treatment for 6 months decreased serum TSH levels and thyroid volume, but had no effect on thyroid nodules and serum CEA and calcitonin levels.
  • General Endocrinology

    Genes D, Pekkolay Z, Simsek M, Saracoglu H, Turgut M, Tekes S, Tuzcu AK

    Comparison of C-Peptide Levels in Monogenic Forms of Diabetes with other Types of Diabetes: a Single-Center Study

    Acta Endo (Buc) 2023 19(3): 281-285 doi: 10.4183/aeb.2023.281

    Abstract
    Objective. This study aimed to evaluate the utility of C-peptide levels in the differentiation of monogenic forms of diabetes from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in clinical practice. Subjects and Methods. A total of 104 patients aged >16 who visited the Dicle University’s Faculty of Medicine between April 2011 and December 2020 and were diagnosed with monogenic diabetes by genetic analysis or with T1DM and T2DM were randomly selected for retrospective evaluation. The C-peptide levels of these patients at the time of diagnosis of diabetes were compared. Results. Of the 104 patients, 24 (23%) were diagnosed with maturity-onset diabetes of the young (MODY), 40 (38.5%) with T1DM, and 40 (38.5%) with T2DM. Median C-peptide levels (ng/mL) (interquartile range) were 1.78 (1.24–2.88) in MODY group, 0.86 (0.34– 1.22) in T1DM group, and 2.38 (1.58–4.27) in T2DM group. Conclusions. There was a difference in C-peptide levels between MODY and T1DM groups but not between MODY and T2DM groups. As per clinical evaluations, although C-peptide levels of patients with MODY are similar to those of patients with T2DM patients, the possibility of C-peptide levels being similar to those required for T1DM diagnosis should also be considered.
  • Endocrine Care

    Gheorghiu ML, Gussi I, Lutescu I, Galoiu S, Hortopan D, Caragheorgheopol A, Coculescu M

    Mantaining physiological levels of serum prolactin in prolactinomas treated with dopamine agonists throughout pregnancy prevents tumor growth

    Acta Endo (Buc) 2005 1(3): 281-298 doi: 10.4183/aeb.2005.281

    Abstract References
    Introduction: Prolactinomas may grow during pregnancy. Dopamine agonists (DA) prevent tumor growth, but usually suppress prolactin (PRL) both in mother and fetus. Possible long-term consequences on fetal development remain unknown.\r\nAim: to assess whether DA treatment throughout pregnancy in a dosage able to maintain physiological gestational serum levels of prolactin (PRL) still prevents prolactinoma growth.\r\nPatients and methods: We evaluated 68 pregnancies in 49 women with prolactinoma (PRM) and 46 pregnancies in healthy women as controls. Thirty-three pregnancies were recorded in 27 women treated throughout pregnancy with bromocriptine (BRC) (n = 25) or cabergoline (CAB) (n = 2) divided in 2 groups: group A (22 pregnancies in 18 patients) had suppressed serum PRL (below the 5th percentile of the control group Z during the last trimester); group B (11 pregnancies in 10 patients) had physiological serum PRL levels. Other 26 pregnancies in 21 patients were incompletely evaluated and included only in the pregnancy outcome and cure rate analysis. Treated patients were compared with the control group Y 8 women with PRM who discontinued DA after pregnancy induction (9 pregnancies) and a control group Z of 46 healthy pregnant women, randomly selected from two departments of Obstetrics. Patients with multiple pregnancies were recorded in each corresponding study group.\r\nResults: In the control group Y, tumor size showed an increase in 2 (intrasellar macroPRM) out of 8 cases (25%). DA treatment throughout gestation in 27 women with PRM prevented the growth in all cases and induced a shrinkage of more than 30% of tumor mass in 8/14 macroPRM (57.1%), i.e., in 4/7 (57.1%) of macroPRM with physiological serum PRL levels during pregnancy, and in 5/8 (62.5%) of macroPRM with suppressed PRL levels (p = NS) (1 patient had pregnancies in both groups). Low dose DA (BRC 2.5 ? 5 mg/day or CAB 0.5 mg/week) maintains physiological PRL levels in 6/12 (50%) macroPRM, but suppressed PRL in 80% of microPRM. Cure was recorded in 6/49 (12.2%) of patients. Two patients with PRM-induced neuroophthalmic syndrome were successfully treated with DA throughout 1 and respectively 3 pregnancies.\r\nConclusions: Some women with prolactinomas showed a tumour size increase if they were not treated with dopamine agonists throughout pregnancy. Maintaining physiological serum PRL levels during pregnancy (frequently with low doses of DA) prevented tumor growth, avoiding a PRL suppression that may have subtle influence on long-term foetal development.
    1. Sobrinho LG, Nunes MC, Santos MA, Mauricio JC. Radiological evidence for regression of prolactinoma after treatment with bromocriptine. Lancet 1978; 2(8083):257-258. [CrossRef]
    2. McGregor AM, Scanlon MF, Hall R, Hall K. Effects of bromocriptine on pituitary tumour size. Br Med J 1979; 2(6192):700-703. [CrossRef]
    3. Colao A, Annunziato L, Lombardi G. Treatment of prolactinomas. Ann Med 1998; 30(5):452-459. [CrossRef]
    4. Coculescu M, Simionescu N, Oprescu M, Alessandrescu D. Bromocriptine treatment of pituitary adenomas. Evaluation of withdrawal effect. Endocrinologie 1983; 21(3):157-168.
    5. Schlechte JA. Clinical practice. Prolactinoma. N Engl J Med 2003; 349(21):2035-2041. [CrossRef]
    6. Passos VQ, Souza JJ, Musolino NR, Bronstein MD. Long-term follow-up of prolactinomas: normoprolactinemia after bromocriptine withdrawal. J Clin Endocrinol Metab 2002; 87(8):3578-3582. [CrossRef]
    7. Coculescu M, Anghel R, Badiu C, Caragheorgheopol A, Hortopan D, Dumitrascu A et al. Additional effects of radiotherapy to dopamine agonists in the treatment of macroprolactinomas. Acta Endocrinologica (Buc) 2005; 1(1):43-60. [CrossRef]
    8. Colao A, Di Sarno A, Cappabianca P, Di Somma C, Pivonello R, Lombardi G. Withdrawal of longterm cabergoline therapy for tumoral and nontumoral hyperprolactinemia. N Engl J Med 2003; 349(21):2023-2033. [CrossRef]
    9. Robert E, Musatti L, Piscitelli G, Ferrari CI. Pregnancy outcome after treatment with the ergot derivative, cabergoline. Reprod Toxicol 1996; 10(4):333-337. [CrossRef]
    10. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]
    11. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]
    12. Alessandrescu D, Coculescu M, Oprescu M, Brotea G, Zagrean L, Petrenciuc O. Pregnancy induced and maintained under 2-Br-alfa-ergocryptin in a patient with evolutive prolactinoma (in Romanian). Obstetrica si Ginecologia 1981; 29:209-215.
    13. Briggs GG, Freeman RK, Yaffe SJ. Bromocriptine. Drugs in pregnancy and lactation. Philadelphia: Lippincott Williams & Wilkins, 2002: 143-145.
    14. Kletzky OA, Rossman F, Bertolli SI, Platt LD, Mishell DR, Jr. Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy. Am J Obstet Gynecol 1985; 151(7):878-884.
    15. Ben Jonathan N, Hnasko R. Dopamine as a prolactin (PRL) inhibitor. Endocr Rev 2001; 22(6):724-763. [CrossRef]
    16. Bigazzi M, Ronga R, Lancranjan I, Ferraro S, Branconi F, Buzzoni P et al. A pregnancy in an acromegalic woman during bromocriptine treatment: effects on growth hormone and prolactin in the maternal, fetal, and amniotic compartments. J Clin Endocrinol Me [CrossRef]
    17. Handwerger S, Freemark M. Role of placental lactogen and prolactin in human pregnancy. Adv Exp Med Biol 1987; 219:399-420.
    18. American College of Obstetricians and Gynecologists CoTB. Early pregnancy loss. ACOG Technical Bulletin 212. 1995.
    19. Elster AD, Sanders TG, Vines FS, Chen MY. Size and shape of the pituitary gland during pregnancy and post partum: measurement with MR imaging. Radiology 1991; 181(2):531-535.
    20. Gonzalez JG, Elizondo G, Saldivar D, Nanez H, Todd LE, Villarreal JZ. Pituitary gland growth during normal pregnancy: an in vivo study using magnetic resonance imaging. Am J Med 1988; 85(2):217-220. [CrossRef]
    21. Scheithauer BW, Sano T, Kovacs KT, Young WF, Jr., Ryan N, Randall RV. The pituitary gland in pregnancy: a clinicopathologic and immunohistochemical study of 69 cases. Mayo Clin Proc 1990; 65(4):461-474.
    22. Kupersmith MJ, Rosenberg C, Kleinberg D. Visual loss in pregnant women with pituitary adenomas. Ann Intern Med 1994; 121(7):473-477.
    23. Molitch ME. Pregnancy and the hyperprolactinemic woman. N Engl J Med 1985; 312(21):1364-1370. [CrossRef]
    24. Crosignani P, Ferrari C, Mattei AM. Visual field defects and reduced visual acuity during pregnancy in two patients with prolactinoma: rapid regression of symptoms under bromocriptine. Case reports. Br J Obstet Gynaecol 1984; 91(8):821-823.
    25. Konopka P, Raymond JP, Merceron RE, Seneze J. Continuous administration of bromocriptine in the prevention of neurological complications in pregnant women with prolactinomas. Am J Obstet Gynecol 1983; 146(8):935-938.
    26. Coculescu M, Hudita D, Gussi I, Gheorghiu M, Hortopan D, Caragheorgheopol A. Tumor size changes in prolactinomas treated with minimum bromocriptine throughout gestation . Gynecological Endocrinology 2000; 14(suppl 2):50.
    27. Canales ES, Garcia IC, Ruiz JE, Zarate A. Bromocriptine as prophylactic therapy in prolactinoma during pregnancy. Fertil Steril 1981; 36(4):524-526.
    28. Shanis BS, Check JH. Relative resistance of a macroprolactinoma to bromocriptine therapy during pregnancy. Gynecol Endocrinol 1996; 10(2):91-94. [CrossRef]
    29. Liu C, Tyrrell JB. Successful treatment of a large macroprolactinoma with cabergoline during pregnancy. Pituitary 2001; 4(3):179-185. [CrossRef]
    30. de Turris P, Venuti L, Zuppa AA. [Long-term treatment with cabergoline in pregnancy and neonatal outcome: report of a clinical case]. Pediatr Med Chir 2003; 25(3):178-180.
    31. Verhelst J, Abs R, Maiter D, van den BA, Vandeweghe M, Velkeniers B et al. Cabergoline in the treatment of hyperprolactinemia: a study in 455 patients. J Clin Endocrinol Metab 1999; 84(7):2518-2522. [CrossRef]
    32. Cannavo S, Curto L, Squadrito S, Almoto B, Vieni A, Trimarchi F. Cabergoline: a first-choice treatment in patients with previously untreated prolactin-secreting pituitary adenoma. J Endocrinol Invest 1999; 22(5):354-359.
    33. Ciccarelli E, Grottoli S, Razzore P, Gaia D, Bertagna A, Cirillo S et al. Long-term treatment with cabergoline, a new long-lasting ergoline derivate, in idiopathic or tumorous hyperprolactinaemia and outcome of drug-induced pregnancy. J Endocrinol Inves
    34. Jones J, Bashir T, Olney J, Wheatley T. Cabergoline treatment for a large macroprolactinoma throughout pregnancy. J Obstet Gynaecol 1997; 17(4):375-376.
    35. Divers WA, Jr., Yen SS. Prolactin-producing microadenomas in pregnancy. Obstet Gynecol 1983; 62(4):425-429.
    36. Luthman M, Bremme K, Eneroth P, Werner S. Women with prolactin-producing pituitary adenoma show decreased serum placental lactogen during pregnancy. Gynecol Obstet Invest 1993; 35(2):80-85. [CrossRef]
    37. Kubota T, Nagae M, Yaoi Y, Kumasaka T, Saito M. Prolactin-releasing system in maternal, fetal, and amniotic compartments during labor. Obstet Gynecol 1986; 68(1):80-85.
    38. Yuen BH, Moon YS, Shin DH. Inhibition of human chorionic gonadotropin production by prolactin from term human trophoblast. Am J Obstet Gynecol 1986; 154(2):336-340.
    39. Leav I, Merk FB, Lee KF, Loda M, Mandoki M, McNeal JE et al. Prolactin receptor expression in the developing human prostate and in hyperplastic, dysplastic, and neoplastic lesions. Am J Pathol 1999; 154(3):863-870. [CrossRef]
    40. Gussi I, Gheorghiu M, Lutescu I, Hortopan D, Caragheorgheopol A, Hudita D et al. Maintaining physiological profile of prolactin throughout pregnancy in women with prolactinomas on dopamine agonists. Rom J Endocrinol Metab 2002; 1(suppl 4):23.
    41. Molitch ME. Pituitary tumors and pregnancy. Growth Horm IGF Res 2003; 13 Suppl A:S38-S44.
    42. Ahmed M, al Dossary E, Woodhouse NJ. Macroprolactinomas with suprasellar extension: effect of bromocriptine withdrawal during one or more pregnancies. Fertil Steril 1992; 58(3):492-497.
    43. Daya S, Shewchuk AB, Bryceland N. The effect of multiparity on intrasellar prolactinomas. Am J Obstet Gynecol 1984; 148(5):512-515.
    44. Fujimoto M, Yoshino E, Mizukawa N, Hirakawa K. Spontaneous reduction in size of prolactinproducing adenoma after delivery. Case report. J Neurosurg 1985; 63(6):973-974. [CrossRef]
    45. Hammond CB, Haney AF, Land MR, van der Merwe JV, Ory SJ, Wiebe RH. The outcome of pregnancy in patients with treated and untreated prolactin-secreting pituitary tumors. Am J Obstet Gynecol 1983; 147(2):148-157.
    46. Yamada M, Miyake A, Koike K, Ikegami H, Aono T, Tanizawa O. Spontaneous pregnancy after a pregnancy induced by treatment in hyperprolactinemic women. Eur J Obstet Gynecol Reprod Biol 1990; 35(2-3):125-129. [CrossRef]
    47. Bergh T, Nillius SJ, Larsson SG, Wide L. Effects of bromocriptine-induced pregnancy on prolactin-secreting pituitary tumours. Acta Endocrinol (Copenh) 1981; 98(3):333-338.