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Liver shunting, technically known as a portosystemic shunt (PSS), refers to an abnormal vascular connection that allows blood from the gastrointestinal tract to bypass the liver and enter the systemic circulation directly (Merck Manuals, 2023). Under normal physiological conditions, the portal vein carries nutrient-rich and toxin-laden blood to the liver for detoxification and metabolic processing. In the presence of a shunt, toxins such as ammonia, which are usually removed by the liver, reach the brain and other organs, often resulting in hepatic encephalopathy (NIH, 2022). Shunts can be congenital, appearing as developmental anomalies, or acquired, typically resulting from portal hypertension associated with chronic liver disease or cirrhosis. Because liver shunting is an anatomical and physiological condition rather than a specific protein, enzyme, or receptor, it is not classified as a molecular therapeutic target. Instead, medical management involves using drugs to mitigate the metabolic consequences of the shunt, such as ammonia-reducing therapies, or performing surgical interventions to close the abnormal vessel (StatPearls, 2023).
Pharmacological agents do not target the shunt itself as it is a macro-vascular structure. Instead, drugs like lactulose and rifaximin target the metabolic consequences by reducing the production and absorption of ammonia in the gut, which the shunted liver cannot detoxify (StatPearls, 2023).
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