Endocrine Abstracts

Background: Individuals with adrenal insufficiency (AI) receive life-long glucocorticoid (GC) replacement therapy (CGRT), which often exceeds normal daily physiological GC production, leading to detrimental effects on cardiometabolic parameters and bone health.

Objective: Assessment of glucose, lipid and bone metabolism in AI postmenopausal patients in relation to the cause of AI and the CGRT dose.

Methods: 114 AI postmenopausal women were retrospectively studied (37 primary AI [PAI] and 37 secondary AI [SAI] patients and 40 AI patients following Cushing’s syndrome (CS) treatment [post-CS AI]). Biochemical glucose and lipid parameters and bone mineral density (BMD) in lumbar spine (LS) and femoral neck (FN) were evaluated at baseline and at the follow-up (2 years). Additionally, patients were divided in 3 groups based on their total daily hydrocortisone (H/C) doses (TDH/CD); low dose (LD) (TDH/CD ≤ 15 mg) (21 patients), medium dose (MD) (15 mg < TDH/CD ≤ 25 mg) (50 patients) and high dose (HD) (TDH/CD > 25 mg) (43 patients)

Results: At baseline all patients had comparable age, body mass index. duration of AI, age of menopause and. Significantly more PAI patients were on LD and more post-CS AI ones on HD. Although mean daily GC dose was equal among groups, PAI patients received significantly less GC per body surface area (BSA) (P=0.045). Additionally, they had P1NP levels (P=0.013) and lower HbA1c, TChol and LDL values compared with the other ones (P=0.043, 0.018 and 0.001, respectively). After 2 years’ time, TDH/CD decreased among all patients. Furthermore, P1NP values remained higher and TChol and LDL values lower among the PAI patients. Regarding TDH/CD, at baseline HD patients had worse lipid profile, increased bone turnover and lower BMD and T-Score in FN and LS. At 2 years follow-up, HD patients continued to exhibit deteriorated lipid values, elevated b-cross laps and lower BMD and T-Score in LS but not in FN in comparison to the other patients.

Conclusions: PAI patients had increased bone formation and better glucose and lipid profile compared to SAI and post-CS AI patients, and this difference persisted during the two years follow-up. This possibly related to the use of lower GC doses per BSA in PAI patients. Additionally, HD therapy in AI patients exerts a longitudinal and persistent negative effect on the glucose and lipid profile and the bone metabolism. Our data enforce the need for the lowest possible GC replacement dose and the routine follow up for all AI patients.