ECEESPE2025 Rapid Communications Rapid Communications 1: Adrenal and Cardiovascular Endocrinology (5 abstracts)
Metabolic phenotype in non-aldosterone producing adrenal adenomas (NAPACAs) with co-existent polycystic ovaries syndrome (PCOS): a joint ENSAT project
Ariadni Spyroglou 1 , Panagiota Konstantakou 2 , Marianna Minnetti 2 , Barbara Altieri 3 , Elisabeth Nowak 4 , Petros Papalexis 5 , Anna Angelousi 5 , Dimitra Vasiliadi 6 , Otilia Kimpel 3 , Djuro Macut 7 , Lorenzo Tucci 8,9 , Francesca Donnarumma 8,9 , Guido Di Dalmazi 8,9 , Andrea Isidori 2 , Martin Reincke 4 , Manousos Konstadoulakis 1 , George Mastorakos 1 , Gregory Kaltsas 10 & Krystallenia Alexandraki 1
1National and Kapodistrian University of Athens; 2nd Department of Surgery, Aretaieio Hospital, Athens, Greece; 2Sapienza University of Rome, Department of Experimental Medicine, Rome, Italy; 3University of Würzburg, Division of Endocrinology and Diabetes, Department of Medicine, University Hospital, Würzburg, Germany; 4LMU University Hospital, LMU Munich, Department of Medicine IV, Munich, Germany; 5National and Kapodistrian University of Athens, First Department of Internal Medicine, Unit of Endocrinology, Laikon General Hospital, Athens, Greece; 6European Reference Network on Rare Endocrine Conditions (ENDO-ERN), Evangelismos Hospital, Department of Endocrinology, Diabetes and Metabolism, Athens, Greece; 7University Clinical Centre of Serbia, Faculty of Medicine, University of Belgrade, Clinic for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia; 8IRCCS Azienda Ospedaliero-Universitaria di Bologna, Division of Endocrinology and Diabetes Prevention and Care, Bologna, Italy; 9Alma Mater Studiorum University of Bologna, Department of Medical and Surgical Sciences (DIMEC), Bologna, Italy; 10National and Kapodistrian University of Athens, 1st Propaedeutic Department of Internal Medicine, Athens, Greece
JOINT1779
Non-aldosterone producing-adrenal-adenomas (NAPACAs) and polycystic ovaries syndrome (PCOS) are associated with hyperinsulinemia and insulin-resistance and thereby with increased prevalence of several aspects of the metabolic syndrome. Whether the co-existence of the two disease entities leads to accentuated prevalence of the metabolic syndrome remains unclear. Aim of the present study is the assessment of cardiovascular risk factors and insulin resistance indices in women with NAPACAs with and without PCOS. We conducted a retrospective multicenter study including adult premenopausal women categorized as NAPACA (n=44), PCOS (=19) or NAPACA+PCOS (n=24), excluding women with hormonally active adenomas other than mild autonomous cortisol excess (MACS), congenital adrenal hyperplasia, diabetes, systemic steroid medication or active malignancy and analyzed clinical, biochemical and hormonal data of the respective patients. As expected from the disease natural history, NAPACA patients were significantly older than the other two groups (NAPACA 41.02±1.1, PCOS 31.05±1.5, NAPACA+PCOS 33.83±1.4 years old, P<0.001). PCOS patients displayed the lowest (26.88±1.8 kg/m2) and NAPACA+PCOS the highest body-mass-index (31.83±1.9 kg/m2, P=0.05), but patients of the three groups did not differ in their waist-to-height ratio (P=0.12), systolic (P=0.51) and diastolic blood pressure (P=0.16), HbA1c (P=0.49) and fasting plasma glucose levels (P=0.51). Interestingly, NAPACA+PCOS patients displayed significantly higher fasting insulin levels (NAPACA 9.38±1.1, PCOS 12.93±2.9, NAPACA+PCOS 25.52±9.1 μU/ml, P<0.05). NAPACA+PCOS patients displayed significantly increased insulin resistance as calculated by the glucose-to-insulin ratio (GIR, P<0.05), the HOMA index (P<0.05) the QUICKI index (P<0.05) and the MATSUDA index (P<0.05). NAPACA+PCOS patients also presented lower HDL levels (NAPACA 58.67±2.6, PCOS 58.21±3, NAPACA+PCOS 48.05±2.5 mg/dl, P<0.05). Although the cortisol levels upon 1 mg-dexamethasone suppression test (DST) did not differ among the groups (P=0.1), the DHEA-S (P<0.05), androstenedione (P<0.01) and testosterone levels (P<0.01) were significantly higher in the two groups including PCOS patients. Free androgen index levels positively correlated with the insulin resistance in NAPACA (GIR R -0.56, P<0.01, HOMA R 0.52, P<0.05, QUICKI R -0.52, P<0.05, MATSUDA R -0.49, P=0.09) and PCOS patients (GIR R -0.68, P<0.01, HOMA R 0.67, P<0.01, QUICKI R -0.67, P<0.01, MATSUDA R -0.82, P<0.001), while cortisol after 1mg-DST positively correlated with the insulin resistance in the NAPACA+PCOS group (GIR R -0.48, P=0.05, HOMA R 0.58, P<0.05, QUICKI R -0.58, P<0.05, MATSUDA R -0.67, P<0.05). These data provide hints that NAPACA+PCOS patients represent a distinct phenotype compared to NAPACA or PCOS patients, with a worse metabolic profile, and further studies with larger patient cohorts will be necessary to elucidate this observation.
Volume 110
Article tools
My recent searches
My recently viewed abstracts
Authors
Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
© Bioscientifica 2025 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more