SUN-058 Concurrent Hypercortisolism in Primary Aldosteronism Patients at a Tertiary Care Center: 2007-2017

Abstract

Background: Primary aldosteronism patients often have co-morbidities, such as diabetes mellitus and osteopenia/osteoporosis, that are consistent with states of cortisol dysregulation. Recent studies have alluded to co-secretory adrenal states. Methods: Subjects were evaluated under an IRB-approved protocol. Patients seen between 2007 and 2017 identified as having primary aldosteronism with meeting one of the following criteria: saline suppression test with 4-hr aldosterone value >10 ng/dl, 24-hr urinary aldosterone >14mcg/24 hrs on unrestricted salt diet, or prior diagnosis of primary aldosteronism. Abnormal cortisol status was defined as evening diurnal cortisol >1.8 mcg/dl, urinary free cortisol >50mcg/24 hrs, dexamethasone suppression test with post-test cortisol >1.8 mcg/dl, 8mg dexamethasone suppression test with failure to suppress cortisol >68%, or 6-day Liddle’s test (if done) with failure to suppress urinary free cortisol >90% over 6 days or 17-hydroxysteroid >69%. Data are reported as frequencies and percentages, or mean ±standard deviation. Results: The cohort seen between 2007 and 2017 consisted of 130 patients (mean age=49.7±11.5 yrs; 46% female; mean BMI=31.4±6.5). Self-reported race was 46% black, 35% white, 6% Asian, 5% multi-racial, and 8% unknown. At study visit, mean Hemoglobin A1c was 5.9%±1.2. Aldosterone value at 4-hour time point of saline suppression test was 28.8 ± 37.7ng/dl, and 24-hour urinary aldosterone mean was 63.5±54.9mcg/24 hrs. Loss of diurnal cortisol rhythm was seen in 90% (98/109) of patients. 24-hour urinary free cortisol values were elevated in 18% (19/103) patients. 1mg or 2mg dexamethasone suppression test was performed in 63 patients, with 9 (14%) patients with failure to suppress cortisol. 8mg dexamethasone suppression test was performed in 61 patients, with 5 (8%) patients failing to suppress cortisol by >68%. 53 patients underwent the 6-day Liddle’s test, with 52% (13/25) failing to suppress urinary free cortisol by >90%, and 87% (20/23) failing to suppress 17-hydroxysteroids by >69%. Conclusions: The majority of primary aldosteronism patients seen between 2007-2017 demonstrate loss of diurnal cortisol rhythm. Some met criteria for hypercortisolemia, with elevated 24-hour urinary free cortisol or failure to suppress on dexamethasone suppression test, or failure to suppress 17-hydroxysteroids on 6-day Liddle’s test. This is suggestive of autonomous adrenal cortisol secretion, which may explain the detrimental co-morbidities seen in these patients and has implications for the need for earlier diagnosis and treatment and may be an area of further study.