Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 44 EP8 | DOI: 10.1530/endoabs.44.EP8

SFEBES2016 ePoster Presentations (1) (116 abstracts)

Will the routine use of high dose steroids for alcoholic hepatitis result in an increased incidence of clinically significant hypocortisolism in patients with liver cirrhosis?

Priya Karia 1 , Vassiliki Bravis 1, , Victoria Salem 1, , Shiva Radhakrishnan 1 & Dri Choa 1


1Department of Diabetes and Endocrinology, St. Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK; 2Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK.


Introduction: Recent evidence supports the use of high dose steroids for 28 days in acute alcoholic hepatitis. We present a patient with Childs Pugh C liver cirrhosis, who developed adrenal axis suppression following such treatment. We discuss the complex aetiology and biochemistry of hypocortisolism in liver disease.

Case: 48 year-old female admitted with alcoholic hepatitis, treated with a non-tapering 28-day course of 40 mg prednisolone. The patient was re-admitted 4 weeks later with severe, symptomatic hyponatraemia. This resolved only following hydrocortisone replacement therapy.

Results: Serum sodium (mmol/L) • Prior to discontinuation of prednisolone: 131 • At re-admission, 4 weeks later: 104 • Following hydrocortisone replacement: 138

Short Synacthen test (after cessation of prednisolone):

Cortisol (mmol/L) • Basal (09:00am): 44 mmol/L • 30-minute: 107 mmol/L • 60-minute: 137 mmol/L (normal peak on local guidelines >450 nmol/L)

Basal ACTH <5 pg/ml

Cortisol post-hydrocortisone dose: 764 mmol/L

Serum albumin: 26 g/L

Cortisol-binding globulin (CBG): 43.2 mg/L (normal range 31.0-53.4 mg/L)

The free cortisol index (FCI) is a surrogate marker for free cortisol and is defined as total cortisol (nmol/L)/CBG (mg/L). FCI > 12 represents sufficient adrenal reserve2. This patient’s peak, post-synacthen FCI was 9.09.

Learning points: 1. A 28-day course of 40 mg prednisolone induced adrenal suppression in this patient with acute alcoholic hepatitis and liver cirrhosis. 2. Adrenal dysfunction is already prevalent in patients with liver failure. Causes are multifactorial and include pituitary suppression and poor synthetic function of steroid hormones (“hepatoadrenal syndrome”). 3. Biochemical diagnosis should account for changes in circulating albumin. CBG affects the availability of free cortisol. 4. The use of high dose Prednisolone for 28 days in the treatment of alcoholic hepatitis in patients with liver cirrhosis should be used cautiously and be recognised as a risk for subsequent adrenal suppression. Hepatologists should consider adrenal axis interrogation after completion of such courses.

Volume 44

Society for Endocrinology BES 2016

Brighton, UK
07 Nov 2016 - 09 Nov 2016

Society for Endocrinology 

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