Ammonia (and selected ACLF-associated metabolic biomarkers) (NH₃)

Ammonia is a small nitrogenous compound involved in normal nitrogen metabolism but becomes neurotoxic when elevated—as often occurs in liver failure due to impaired urea cycle activity. In ACLF, ammonia is a central factor in the development of hepatic encephalopathy and has been shown to promote multi-organ failure via induction of hepatocyte death, immune dysfunction, and systemic inflammatory responses[3][1][4][6]. Other ACLF-associated metabolites reflect broader metabolic derangement—including altered amino acid pathways (kynurenine), energy metabolism (glycolysis, methionine cycle), and redox balance—all contributing to the characteristic acute inflammatory and multiorgan dysfunction profile of ACLF[5][2][8]. Both ammonia and specific metabolites are increasingly recognized as *biomarkers* of prognosis and severity, and represent therapeutic targets in ongoing research.

Other names

AmmoniaNH₃hyperammonemiablood ammoniakynureninehexanoylcarnitineD-galacturonic acid

Ammonia-lowering therapies: Decrease intestinal ammonia production (lactulose, rifaximin), increase ammonia clearance (L-ornithine L-aspartate), enhance renal excretion (dialysis), inhibit metabolic pathways contributing to ammonia accumulation. Other metabolite-targeting drugs: Modulation of metabolic pathways (e.g., inhibition of kynurenine pathway by statins/rifaximin)