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Endocrine Abstracts (2020) 70 AEP102 | DOI: 10.1530/endoabs.70.AEP102

Adrenal and Cardiovascular Endocrinology

Is glucocorticoid replacement therapy in adrenal insufficiency a risk factor for liver steatosis?

Gesine Meyer, Madeleine Gruendl, Florian Schlereth, Ludmila Gerber, Klaus Badenhoop & Joerg Bojunga


Goethe-University Hospital, Medical Clinic 1, Endocrinology, Frankfurt, Germany


Introduction: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease affecting up to 30% of the population in western countries. Previous studies have demonstrated that increased glucocorticoid levels play an important role in the development of obesity, hyperglycemia, dyslipidemia, insulin resistance, as well as NAFLD. However, the effects of glucocorticoid substitution on the liver in patients with primary or secondary adrenal insufficiency have been rarely examined.

Objective: To investigate the impact of glucocorticoid replacement therapy in patients with primary or secondary adrenal insufficiency on developing NAFLD or liver fibrosis

Methods: Association between the grade of hepatic steatosis and the dose of hydrocortisone replacement therapy was investigated in n = 96 patients suffering from primary or secondary adrenal insufficiency. The grade of liver steatosis was determined by using an ultrasound-based vibration-controlled transient elastography device called controlled attenuation parameter (CAP). CAP was adjusted for body weight, body mass index and waist circumference. Additionally, we examined the association between HOMA-Index, hypertension, hyperglycemia and dyslipidemia and the dose of glucocorticoid replacement therapy.

Results: There was no significant correlation between the grade of liver steatosis measured with CAP and the daily dose of glucocorticoid replacement therapy. There was also no significant correlation between the CAP value and the product from the duration of glucocorticoid intake in years and the daily dose of glucocorticoid replacement in mg hydrocortisone equivalent as a marker for cumulative glucocorticoid dose. However, CAP showed a strong correlation with waist circumference (P < 0.001), BMI (P < 0.001) and body weight (P < 0.001). There was a moderate relationship between CAP and the metabolic syndrome (P < 0.001), hypertension (P = 0.031) and the level of triglycerides (P = 0.008). On multiple regression analysis, only waist circumference (P < 0.001) and dyslipidemia (P = 0.012) remained significantly associated with CAP. HOMA-Index, hypertension, hyperglycemia and dyslipidemia showed no association with the dose of glucocorticoid replacement therapy.

Conclusion: Glucocorticoid replacement therapy in a physiological daily dose of 15 mg to 30 mg hydrocortisone equivalent seams not to raise the risk of developing NAFLD. Patients suffering from liver steatosis mostly have metabolic risk factors such as obesity, dyslipidemia or hypertension.

Volume 70

22nd European Congress of Endocrinology

Prague, Czech Republic
23 May 2020 - 26 Feb 2020

European Society of Endocrinology 

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