ECE2019 Poster Presentations Adrenal and Neuroendocrine Tumours 2 (60 abstracts)
1Department of Endocrinology Diabetes Center, General Hospital of Athens G. Gennimatas, Athens, Greece; 2Endocrinology Department, Athens Naval Hospital, Athens, Greece; 3Athens University Medical School, National Institute of Child Health and Human Development (NICHD), Athens, Greece.
Introduction: The causes of arterial hypertension in diabetic and non-diabetic hypertensive patients are still not clear. However, in recent studies in non-diabetic hypertensive patients (NDHP) we observed dysregulation of aldosterone (ALD) secretion either in the form of autonomous secretion or as hyperesponse to stress. To the best of our knowledge, a similar study in hypertensive patients with type 2 Diabetes Mellitus (DHP) has not been conducted yet.
Objectives: The main aim of this study was to investigate ALD secretion in DHP. Furthermore, to investigate the effect of a sodium-glucose co-transporter type 2 inhibitor (SGLT2i) on renin-angiotensin-aldosterone system (RAAS).
Patients and methods: We included 71 DHP and 60 NDHP who served as controls, with normal renal function. Autonomous ALD secretion was tested using a diagnostic test (DCVT) for both groups, based on the pharmacological blockage of RAAS: midnight administration of dexamethasone (2 mg), captopril (50 mg) and valsartan (320 mg); blood sampling in the next morning for ACTH, cortisol, active renin, ALD and ALD/active-renin-ratio (ARR) estimation. An extra dose of 50mg captopril was given one hour before venipuncture. In addition, 10 mg empagliflozin (SGLT2i) was granted in diabetic patients for a month and active renin, ALD, ARR, ACTH and cortisol levels were estimated before and after treatment initiation. To establish the diagnosis of autonomous aldosterone secretion we used both post-DCVT ALD and ARR simultaneously. Their upper normal limits (UNL) were calculated based on the results of NDHP (control group) as Mean+2SD (ALD: 110 pmol/l and ARR: 10 pmol/mU, sensitivity and specificity: ALD: 100 and 98%, ARR: 10 and 96% respectively).
Results: Autonomous ALD secretion was found in 27.7% (19/71) of DHP. No statistically significant difference in age, systolic/diastolic pressure, basal ARR and potassium/sodium concentrations in serum and 24h-urine, between the two groups (DHP vs NDHP) was found. In contrast, statistically significant difference in the post-DCVT ALD and ARR (Mean±S.E.: ALD:132.2±22.71 vs 51.87±4.54, P<0.0001 and ARR:20.63±10.88 vs 3.74±0.42, P=0.001) between groups was observed. Finally, no effect on RAAS after empagliflozin administration in DHP (ARR:25.59±6.3 vs 27.95±5, P=0.2) was found.
Conclusions: The prevalence of autonomous ALD secretion in diabetic hypertensive patients was found to be particularly high, similar to what was found in non-diabetic hypertensive patients using the same methodology.