Endocrine Abstracts

Non-alcoholic steatohepatitis is part of the spectrum of non-alcoholic fatty liver disease. It is characterised by triglyceride deposition in the liver associated with a lobular hepatitis and elevated circulating aminotransferases. It is associated with insulin resistance and commonly occurs in Type 2 diabetes but is much less widely recognised in patients with Type 1 diabetes.

A 29 year old Caucasian male with longstanding Type 1 diabetes presented with right upper quadrant abdominal pain. His diabetes was poorly controlled (HbA1c 10.6% to 11.1%) on a basal bolus insulin regime of Novorapid and Glargine. He had background retinopathy but no evidence of peripheral neuropathy or nephropathy. There was no family history of diabetes. His alcohol intake was 5 units weekly and he smoked 20 cigarettes daily. He was not on any medications known to cause hepatic steatosis. His body mass index was 24.6 kg m⁻². There were no clinical stigmata of insulin resistance, but his 24 hour insulin requirement was 120 units. He had smooth tender hepatomegaly. Transaminases were elevated with an ALT of 287 iu/L (<40), AST of 607 u/L (<40) and GGT of 218 u/L (11–50). He was dyslipidaemic with a total cholesterol of 6.47 mmol/l (<5.00), HDL cholesterol of 0.99 mmol/l (>1.00) and triglycerides of 7.73 mmol/l (<2.30). Liver autoimmune and viral serology were negative. Liver ultrasound showed gross hepatomegaly with evidence of fatty infiltration and focal fatty sparing. Liver biopsy showed large droplet fatty change with lobular inflammation consistent with non-alcoholic steatohepatitis.

In patients with poorly controlled Type 1 diabetes who present with elevated liver enzymes and hepatomegaly, non-alcoholic steatohepatitis should be considered in the differential diagnosis. Abdominal pain, hepatomegaly and liver enzymes may improve dramatically with intensive treatment of diabetes. Good long term control of blood sugars should help to prevent progressive liver disease.