Clinical Significance

Ammonia is generated primarily in the gastrointestinal tract by metabolism of nitrogenous compounds. An excess of ammonia can be toxic to the central nervous system. The Krebs‑Henseleit urea cycle provides a means of disposal of ammonia by metabolizing ammonia to urea in the liver.  

Hyperammonemia in infants can be caused by inherited deficiencies of the urea cycle enzymes or acquired through acute (as in Reye’s syndrome) or chronic (as in cirrhosis) liver disease. In adults, elevated ammonia levels can aid in diagnosis of liver failure or hepatic encephalopathy from advanced liver diseases such as viral hepatitis or cirrhosis. 

_{Source: Roche Cobas NH3L2 Method Sheet Version 3.0 2022-09}