Citation

Montgomery JY, Bajaj JS. Curr. Gastroenterol. Rep. 2011; 13(1): 26-33.

Affiliation

Virginia Commonwealth University, Richmond, VA 23249, USA.

Copyright

(Copyright © 2011, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s11894-010-0150-z

PMID

20924726

Abstract

Minimal hepatic encephalopathy (MHE) is a neurocognitive disorder that affects up to 80% of cirrhotic patients. Similar to overt hepatic encephalopathy, ammonia and oxidative stress play key roles in the pathogenesis of MHE. However, MHE is characterized by subtle deficits and psychomotor abnormalities that can only be elicited by specialized psychometric tests. Although no gold standard exists for the diagnosis, MHE remains an important entity for clinicians to recognize because of its negative impact on a patient's health-related quality of life and association with driving impairment and vehicle accidents. MHE has also been associated with an increased rate in the development of overt hepatic encephalopathy and increased mortality; therefore, identification and treatment should not be delayed. Treatment to date has been focused on reducing serum ammonia levels with agents such as lactulose, probiotics, and synbiotics. MHE is a real and growing problem that is epidemic in cirrhosis, and increasing awareness of this condition is necessary for adequate management of these patients.

Language: en