Hepatic encephalopathy (HE) is a serious but usually reversible neuropsychiatric complication of
cirrhosis,
inborn errors of metabolism involving disorders of the
urea cycle, and noncirrhotic portosystemic shunting that most commonly arises from a transjugular intrahepatic portosystemic shunting procedure. Symptoms can include alterations in cognitive function, neuromuscular activity, and consciousness, as well as
sleep disorders and mood changes. HE is associated with significant morbidity and mortality and, if not properly treated, will lead to increased hospital admissions and healthcare costs. Although the standard
therapies of
lactulose and
rifaximin (
Xifaxan, Salix) are effective for most patients, these drugs may be associated with significant adverse effects and expense and, in some patients, inadequate therapeutic response. A need for adjunctive
therapies exists. Drugs that target serum and tissue
ammonia metabolism and elimination may be important adjuncts to drugs that reduce
ammonia production and absorption from the gastrointestinal tract for patients with severe or persistent overt symptoms of HE.
Sodium benzoate is an inexpensive adjunctive agent that can be used in addition to
lactulose and
rifaximin and may provide an option for some select patients with refractory HE who have failed to respond to standard
therapies or who cannot afford them. Although
sodium benzoate does not share the same adverse effect profiles of standard
therapies for HE, its efficacy has not been well established. Given the significant dose-dependent
sodium content of this
therapy, it may not be appropriate for patients with significant fluid retention or kidney dysfunction.