Abstract

Hepatic encephalopathy (HE) is a challenging clinical complication of liver dysfunction with a wide spectrum of neuropsychiatric abnormalities that range from mild disturbances in cognitive function and consciousness to coma and death. The uncertainties on the pathogenesis of HE limit the development of specific pharmacological therapies but a key role is thought to be played by circulating gut-derived toxins of the nitrogenous compounds, most notably ammonia. Management of HE primarily involves avoidance of precipitating factors and administration of various ammonia-lowering therapies such as nonabsorbable disaccharides and select antimicrobial agents mostly rifaximin. The nonabsorbable disaccharides include lactulose and lactitol. Nonabsorbable disaccharides are considered the first-line therapy for treatment of acute HE, and improvement in symptoms occurs in 67–87%. Lactitol is comparable to lactulose in the treatment of HE with fewer side effects. Lactulose has also shown to be effective in primary and secondary prophylaxis of HE. Lactulose significantly improves cognitive function and health-related quality of life in patients with minimal hepatic encephalopathy. In a systematic review, the efficacy of nonabsorbable disaccharides was compared with either no intervention or placebo; the overall treatment effect was modest but statistically significant, with a relative risk of no improvement ranging from 0.62 to 0.92.82. There is insufficient evidence to support or refute the use of nonabsorbable disaccharides for HE.KeywordsHepatic encephalopathyDisaccharidesLactulose

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call