Ammonia may be an important factor contributing to the pathogenesis of hepatic encephalopathy, however correlation between plasma ammonia levels and the clinical degree of encephalopathy does not always exist. Increased ammonia is observed in acute hepatic failure, Reye’s syndrome, cirrhosis, gastrointestinal bleeding, and portal-systemic shunting of blood. An increment of ammonia levels is noted at severe inborn metabolic disorders of the urea cycle and related pathways: with increased fasting NH3 (hyperammonemia Type I, argininemia, ornithinemia), with increased protein intake (hyperammonemia Type II, citrullinuria, arginosuccinic aciduria, lysine intolerance, hyperlysinuria, dibasic aminoaciduria Type II). Blood ammonia measurements are useful in monitoring patients on hyperalimentation therapy.

Hyperammonemia may appear in cases of liver malfunction or renal failure. In cases of liver disease, ammonia values rarely surpass 500 μmol/L. Significant hyperammonemia during childhood may be observed in a defective ammonia cycle, organic acidemias, transient neonatal hyperammonemia (THAN), and defective oxidation of fatty acids. In such cases, ammonia levels may often surpass 1000 μmol/L. Some organic acidemias and ΤΗΑΝ may present through symptomatic hyperammonemia from the first day of life. The presence of metabolic acidosis and urine organic acids may assist the distinction between organic acidosis and defective urea cycle. Hyperammonemia may also appear in older infants with defective oxidation of fatty acids. Slight hyperammonemia is relatively common in neonates and can reach values double the normal ones, as it is asymptomatic.

Form: Freeze-dried
Shelf life: 18 months @ 2-8 C
On-Board Stability: 30 days
Sample: Plasma, non hemolysed, EDTA or ammonia-free heparin.
Detection limit: 3.6 μmol/L
Linearity: 5.3-700 μmol/L

For Use On
Please Request Info
2x60 Tests
Please Request Info
2X100 Tests