Published online Mar 15, 2015. doi: 10.4239/wjd.v6.i2.321
Peer-review started: August 19, 2014
First decision: September 16, 2014
Revised: October 15, 2014
Accepted: December 18, 2014
Article in press: December 19, 2014
Published online: March 15, 2015
Processing time: 212 Days and 18.2 Hours
Hepatic glycogenosis (HG) is characterized by excessive glycogen accumulation in hepatocytes and represents a hepatic complication of diabetes that particularly occurs in patients with longstanding poorly controlled type 1 diabetes (T1D). HG has been reported to be a very rare disease, although it is believed to be extremely underdiagnosed because it is not possible to distinguish it from non-alcoholic fatty liver disease (NAFLD) unless a liver biopsy is performed. In contrast to HG, NAFLD is characterized by liver fat accumulation and is the more likely diagnosis for patients with type 2 diabetes and metabolic syndrome. The pathogenesis of HG involves the concomitant presence of insulin and excess glucose, which increases glycogen storage in the liver. HG is characterized by a transient elevation in liver transaminases and hepatomegaly. Differentiating between these two conditions is of the utmost importance because HG is a benign disease that is potentially reversible by improving glycemic control, whereas NAFLD can progress to cirrhosis. Therefore, HG should be suspected when liver dysfunction occurs in patients with poorly controlled T1D. The aim of this article is to review the epidemiology, clinical characteristics, pathogenesis and histology of HG.
Core tip: Hepatic glycogenosis (HG) is a complication of diabetes mellitus that is often underdiagnosed. It is defined as pathological glycogen storage in hepatocytes with hepatomegaly and elevated liver enzymes and mainly occurs in patients with longstanding poorly controlled type 1 diabetes. HG cannot easily be distinguished from non-alcoholic fatty liver disease (NAFLD) by history, physical examination or ultrasound; only liver biopsy can provide a definitive diagnosis. The hallmark of this condition is its reversibility with improved glycemic control; in contrast, NAFLD can progress to fibrosis.