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The measurement of ammonia is a standard request for patients hospitalised in critical care units and is of considerable usefulness in managing hepatic impairment for monitoring the onset of encephalopathy, particularly in paediatric units.1
However, its measurement presents difficulties for the laboratory due to preanalytical and analytical issues. There are multiple preanalytical issues that can cause false increases in ammonia in the sample due to deterioration phenomena related to protein catabolism. The sample's stability limit is 1 h, and the sample needs to be kept refrigerated and sealed throughout the process, including pre-centrifugation, to avoid external contamination and evaporation.2
The most extensively used laboratory methodology in laboratories is enzymatic determination (glutamate dehydrogenase (GLDH)). Interference from various factors has been reported, including products resulting from hepatic damage. Haemolysis also causes a false increase in ammonia, although it is not clear whether this increase is due to the release of intracellular content or to some other mechanism. It is therefore recommended that a sample blank be employed.3
In the laboratory, we perform the ammonia measurement in lithium-heparin plasma, using the enzymatic method (without a sample blank or reagent blank), which uses GLDH and a stabilised hydroxymethylglutaryl-CoA reductase (NADPH) analogue (Dimension Vista 1500, Siemens HD, Tarrytown, New York, USA). There has been a recent change in the formulation of the reagent, with a reduction in the limit of detection from 25 to 10 µmol/L.
New reagent has a microbial source of the enzyme (GLDH), …
Contributors MJA and RG-R conceived of the study. MJA, RG-R and PL initiated the study design and PF-C and PO helped with implementation. RG-R provided statistical expertise. All authors contributed to refinement of the study protocol and approved the final manuscript.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.