title: [Options in the treatment of hepatic encephalopathy].
abstract: Hepatic encephalopathy is a result of insufficient liver function, with grave consequences for the patients. It is primarily caused by disturbed hepatic elimination of the neurotoxin, ammonia (NH3). Aside from dietetic measures, treatment rests on drugs designed to reduce the NH3 burden. The primary options, lactulose and the practically unabsorbable antibiotic rifaximin are suitable to decrease the bacterial NH3 generation in the intestine. Other antibiotics like neomycin at best have a place in acute treatment. L-ornithine-L-aspartate (LOLA) and branched-chain amino acids (valine, leucine, isoleucine) aim at supporting the scavenge of NH3 in glutamine; however, the final balance of this pathway is unfavourable. In addition, the constituents of LOLA enhance the capacity of the urea cycle and, ultimately, the elimination of NH3. As the evidence from available studies--is not unequivocal in each case, the current place of LOLA in treatment is that of an option for patients, who do not respond to standard therapy.
authors.forename: Karl-Uwe
authors.initials: KU
authors.lastname: Petersen
mesh_terms: D000597:Amino Acids, Branched-Chain / Q000627:therapeutic use; D000641:Ammonia / Q000378:metabolism; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D004151:Dipeptides / Q000627:therapeutic use; D006501:Hepatic Encephalopathy / Q000378:metabolism / Q000628:therapy*; D006801:Humans; D012294:Rifamycins / Q000627:therapeutic use; D000078262:Rifaximin
chemical_list: D000597:Amino Acids, Branched-Chain; D000900:Anti-Bacterial Agents; D004151:Dipeptides; D012294:Rifamycins; D000641:Ammonia; C002939:ornithylaspartate; D000078262:Rifaximin