Acta Medica Medianae
Vol. 52, No 2, June, 2013
UDK 61
ISSN 0365-4478(Printed version)
ISSN 1821-2794(Online)
 

Correspondence to:

Lidija Popović Dragonjić

Clinic for Infectious Diseases

Clinical Centre Niš

Dr Zoran Đinđić Boulevard 48

18000 Niš

E-mail: lidija_popovic2003@yahoo.com

Review article                                                                      

UDC: 616.831-008:616.36

doi:10.5633/amm.2013.0208

Recent theories of pathogenesis of hepatic encephalopathy in hepatitis C viral infection

Lidija Popović Dragonjić^1,2, Dane Krtinić¹, Ivan Dragonjić³

Hepatic encephalopathy is potentially reversible, or progressive neuropsychiatric syndrome characterized by changes in cognitive function, behavior and personality changes, and transient neurologic symptoms and characteristic electroencephalographic patterns associated with acute and chronic liver failure. For some time, there has been controversy regarding the origin of toxins responsible for the change of mental state. It was found that the occurrence of hepatic encephalopathy is responsible for multiple organ peripheral changes (intestinal changes, abnormalities of portal-systemic circulation, liver failure, loss of muscle tissue), changes in brain intracellular communication (osmotic changes, astrocytes and axonal abnormalities in communication, changes in cerebral perfusion) and ammonia, endogenous benzodiazepines, gamma amino butyric acid, derivatives of methionine and false neurotransmitters. The aforementioned metabolic factors that contribute to the development of hepatic encephalopathy are not mutually exclusive and multiple factors may be present at the same time. Acta Medica Medianae 2013;52(2):51-55.

      Key words: hepatic encephalopathy, pathogenesis