Endocrine Abstracts

Introduction: Glycogenic hepatopathy (GH) has been reported as a very rare and under recognized complication in longstanding poorly controlled type 1 diabetes patients. GH is characterised by transient elevation of liver transaminase and hepatomegaly caused by reversible and excessive glycogen accumulation in hepatocytes. Here we report a 20 years old type 1 poorly controlled diabetic female patient with elevated transaminases.

Clinical presentation: A 20-year-old type 1 diabetic female with poor glycaemic control, complicated by recurrent diabetic ketoacidosis (DKA) was admitted, with symptoms of fatigue, nausea, abdominal pain, and vomiting. Her glycaemia had been poorly controlled with several episodes of DKA for several years. Her physical examination revealed hepatomegaly. Abdominal US showed mild fatty change of liver and mild hepatomegaly. Her HbA1c, 14.2%, SGOT: 79 (0–35) U/l, SGPT: 97 (0–35) U/l, ALP: 125 (47–119) U/l, and GGT: 247 (4–24) U/l. Auto-antibody including anti-nuclear antibody (ANA), smooth muscle antibodies (ASMA), and mitochondrial antibodies (AMA) were all negative. Thyroid function test, serum cupper, alfa1 antitripsin, and serum ceruloplasmin were also normal. The serologic findings for viral infection such as IgM anti-HAV, HBsAg, anti-HCV, HCV-RNA, cytomegalovirus, and Epstein–Barr virus were also all negative. Serum albumin and coagulation tests remained normal. She was not an alcohol or drug consumer and was not taking any medication except insulin. In addition, she did not show any symptom and sign compatible with acute hepatitis. So, we recommend her for a liver biopsy to elucidate the cause of acute elevation of liver enzyme. In hematoxylin and eosin stain, liver biopsy showed normal liver architecture, however, the hepatocytes were diffusely swollen with pale cytoplasm. The periodic acid-Schiff (PAS) staining showed abundant glycogen accumulation within hepatocytes. So, histologically, it was diagnosed as a glycogenic hepatopathy. Six weeks later, her transaminases were drooped to high normal levels via glycaemic control.

Conclusion: GH is a rare cause of increased transaminases in diabetic patients. Clinician awareness of GH should prevent diagnostic delay and will provide better insight into the prevalence of GH.