The purpose of this study is to determine whether L-Ornithine L-Aspartate is effective for the improvement of Overt Hepatic Encephalopathy.

There is no effective treatment available for hepatic encephalopathy at the moment; therefore we aimed to check the efficacy and safety of L-ornithine L-aspartate(LOLA). It provides critical substrates for ureagenesis and glutamine synthesis, the two primary mechanisms by which the body rids itself of excess ammonia. Ornithine is a specific activator of ornithine carbamyl transferase and carbamylphosphate synthetase, and, in addition, is a substrate for ureagenesis. These reactions are carried out mainly in the periportal portion of the hepatic lobules. Aspartate and ornithine, after conversion to alfa-ketoglutarate, are substrates for glutamine synthesis, which is performed exclusively by a small population of perivenous hepatocytes, the so-called perivenous scavenger cells. The ammonia lowering effect resulting from the stimulation of these two basic mechanisms of ammonia detoxification has been studied in animals and was confirmed in humans in clinical trials.

Inclusion Criteria:

• Cirrhosis, diagnosed on the basis of clinical findings, sonographic, and/or histologic basis,
• Patients >14 years, with HE grades 1 to 4 according to West Haven Criteria,
• Hyperammonemia (fasting venous blood ammonia level >60 µmol/l), and
• Patients with a single reversible precipitating factor of HE such as constipation, hypokalemia, urinary tract infection, respiratory tract infection, spontaneous bacterial peritonitis (SBP), dehydration, or none.

Exclusion Criteria:

• hepatocellular carcinoma,
• severe septicemia,
• active gastrointestinal bleeding,
• hepatorenal syndrome,
• acute superimposed liver injury,
• advanced cardiac or pulmonary disease and end stage renal failure,
• patients with minimal HE
• patients taking sedatives, antidepressants, or benzodiazepines and
• patients with chronic HE on metronidazole or lactulose prior to admission.