ECE2020 Audio ePoster Presentations Adrenal and Cardiovascular Endocrinology (121 abstracts)
Adrenal cortex is responsive to human chorionic gonadotropin stimulation in patients with adrenal incidentalomas
Antoan Stefan Sojat 1 , Ljiljana Marina 1,2 , Miomira Ivovic 1,2 , Milina Tancic-Gajic 1,2 , Zorana Arizanovic 1 , Aleksandra Kendereski 1,2 , Natalija Antic 2 , Jelena Milin Lazovic 3 , Sladjana Mihajlovic 2,4 , Dragana Mitrovic 1 & Svetlana Vujovic 1,2
1Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Centre of Serbia, Department for Obesity, Metabolic and Reproductive Disorders, Serbia; 2Faculty of Medicine, University of Belgrade, Serbia; 3Institute of Medical Statistics and Informatics, Faculty of Medicine, University of Belgrade, Serbia; 4University Hospital Centre Dr Dragisa Misovic
Introduction: It is well documented that adrenal tumor tissue is responsive to human chorionic gonadotropin (hCG) as well as to luteinizing hormone (LH) with both hormones sharing a similar physiological role and a mutual receptor.
Objective: The objective of our study was to assess the adrenal steroid response to acute, exogenous hCG stimulation in patients with adrenal incidenatalomas (AI) and for the first time, in a healthy control group.
Methods: Our study group consisted of 39 subjects, 34 patients with AI and 5 age matched healthy controls (63.54 ± 6.91 vs 65.8 ± 3.71 years, P > 0.05). All patients underwent standard AI endocrinological evaluation. The morning after 1mg dexamethasone suppression test (1 mg DST), 10.000 IU hCG was administered intramuscularly to all subjects, starting at 0800 h with measurements of cortisol, dehydroepiandrosterone-sulfate, testosterone and aldosterone every 30 minutes for 3 hours. The partial response to hCG stimulation was considered as a hormone level raise for at least 25% and the full response for at least 50% during the test.
Results: Based on the cortisol level after 1 mg DST, AI patients were divided in two groups: 15 patients withnonfunctional AI (NAI) and 19 patients with (possible) autonomous cortisol secretion ((P)ACS). There was no difference in age nor in sex distribution between the groups. The only hormone which showed response was cortisol in 20 AI patients: 7 with NAI and 13 with (P)ACS. The cortisol response AUC was significantly higher in (P)ACSthen in NAI patients (15075 (9280.5–31224) vs 4134 (3361.5–4894.5), P < 0.001).In the NAI group, 3 patients had partial and 4 had full cortisol response to hCG stimulation, while in the (P)ACS group, 6 patients had partial and 7 had full cortisol response. Although more patients with (P)ACS had a response in cortisol then patients with NAI (13 vs 7), there was no significant difference inthe frequency of partial or full cortisol response between the two groups. This suggests that both patients with NAI and (P)ACS are responsive to hCG stimulation in comparison to healthy controls who showed no response at all in all of the measured hormones.
Conclusion: Our results imply that hCG contributes to the cortisol secretion in both NAI and patients with (P)ACS but not healthy individuals. Patients with (P)ACS showed significantly higher cortisol response than NAI. These findings suggest a possibility of cortisol secretion modulation or control through a suppression of luteinizing hormone secretion or action in patients with (P)ACS.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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