Abstract

Background. Ammonia has been traditionally viewed as one of the main culprits for the development of hepatic encephalopathy. In the setting of liver cirrhosis or portal-systemic shunting, hepatocytes fail to metabolize ammonia, and thus excess ammonia reaches the systemic circulation, and from there, the brain. Material and methods. We performed a descriptive study involving 28 adult patients with liver cirrhosis. None of the patients had overt hepatic encephalopathy at the time of assessment, as judged by the West Haven criteria. Severity of liver cirrhosis was measured through the Child-Pugh and MELD scores. Serum ammonia was measured by venous sampling. Results. Mean age of the patients was 50±10 years-old. There were 68% males (n=19). Mean MELD score was 17±5 points. Mean Child-Pugh score was 8±2 points. Mean serum ammonia level was 76±37 μmol/L (range: 34-204 μmol/L). Serum ammonia levels correlated significantly with both scores of liver disease severity, more so with MELD (R=0.61, p=0.0005), than with the Child-Pugh score (R=0.38, p=0.04) Conclusions. We reaffirm the importance of measuring blood ammonia in patients with liver cirrhosis, since it is a helpful biomarker which correlates with liver disease severity and hepatic encephalopathy.

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