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Subject: Ammonia (Blood NH3, NH3, NH4)
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Ammonia is derived mostly from protein degradation. Most of the ammonia in the blood comes from the intestine, where colonic bacteria use ureases to breakdown urea to ammonia and CO2. Eight-five percent of blood from the intestine is carried directly to the liver via the portal vein and 85% of ammonia is converted back to urea and excreted by the kidneys and colon. Helicobacter pylori in the stomach appears to be an important source of ammonia in patients with cirrhosis.
Normal range: <50 μmol/L.
In the diagnosis of hepatic encephalopathy and hepatic coma in the terminal stages of liver cirrhosis, hepatic failure, acute and subacute necrosis, and Reye syndrome. Hyperammonemia in infants may be an indicator of inherited deficiencies of the urea cycle metabolic pathway.
Should be measured in cases of unexplained lethargy and vomiting, encephalopathy, or any neonate with unexplained neurologic deterioration.
Not useful to assess the degree of dysfunction (e.g., in Reye syndrome, hepatic function improves and the ammonia level falls, even in patients who finally die of these disorders).
Certain inborn errors of metabolism (e.g., defects in urea cycle, organic acid defects).
Transient hyperammonemia in newborn; unknown etiology; may be life threatening in the first 48 hours.
May occur in any patient with severe liver disease (e.g., acute hepatic necrosis, terminal cirrhosis, and after portacaval anastomosis). Increased in most cases of hepatic coma but correlates poorly with degree of encephalopathy. Not useful in known liver disease but may be useful in encephalopathy of unknown cause.
Moribund children: Moderate increases (≤300 μmol/L) without being diagnostic of a specific disease.
GU tract infection with distention and stasis.
Some hematologic disorders, including acute leukemia and after bone marrow transplantation.
Total parenteral nutrition.
Smoking, exercise, valproic acid therapy.
Hyperornithinemia (deficiency of ornithine aminotransaminase activity) with gyrate atrophy of the choroid and retina
Atmospheric ammonia may cause falsely elevated results.
The presence of ammonium ions in anticoagulants may produce falsely elevated results.
Ammonia levels are not always high in all patients with urea cycle disorders.
High-protein diet may cause increased levels.
Ammonia levels may also be elevated with GI hemorrhage.
Ammonia increases due to cellular metabolism: 20% in 1 hour and 100% by 2 hours.
Prolonged tourniquet application can falsely raise blood ammonia levels.