Diabetes mellitus occurs more frequently in cirrhotic patients than that in the general population. Patients with cirrhosis display two major types of diabetes: 

• Type 2 diabetes mellitus,
• Hepatogenous diabetes (HD). 

HD, an acquired condition, is probably caused by impaired insulin clearance and pancreatic β-cell dysfunction in cirrhotic patients. The pathogenesis of HD involves an increase in the levels of advanced glycation end products and hypoxia-inducible factors. Patients with HD peculiarly have normal fasting glucose, but an abnormal response to an oral glucose tolerance test, which is essential for the diagnosis. Since cirrhosis patients demonstrate a falsely low level of glycated hemoglobin, it disrupts the early diagnosis of HD. 

HD causes an increased rate of cirrhosis complications, decreased 5-year survival rate, and increased risk of hepatocellular carcinoma. Cirrhosis associated with HD shows major complications as hepatic encephalopathy (HE), spontaneous bacterial peritonitis, sepsis, variceal hemorrhage, and renal dysfunction. 

HD is difficult to treat because many antihyperglycemic therapies are linked with an increased risk of cirrhosis; complications, especially hypoglycemia. 

Biguanides, alpha-glucosidase inhibitors, and newer medications like dipeptidyl peptidase-4 inhibitors and sodium-glucose co-transporter 2 inhibitors demonstrate a good safety profile in patients with cirrhosis. Insulin therapy is currently used but its requirement is variable and difficult to predict. Liver transplantation often reverses HD. 

Source:  Indian J Endocrinol Metab. 2018;22(4):552-559. doi:10.4103/ijem.IJEM_79_18