Author information
1Department of Medicine, Virginia Commonwealth University, Central Virginia Veterans Healthcare System, Richmond, Virginia. Electronic address: jasmohan.bajaj@vcuhealth.org.
2Department of Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
3Department of Medicine, Baylor University Medical Center, Dallas, Texas.
4Salix Pharmaceuticals, Bridgewater, New Jersey.
5Department of Medicine, Medical University of South Carolina, Charleston, South Carolina.
Abstract
Although ammonia is involved in the pathophysiology of hepatic encephalopathy (HE), the use of ammonia levels in clinical practice is problematic.1-3 For example, in a study of 551 patients with overt HE (OHE) receiving lactulose who had ammonia levels tested, only 60% had an increased ammonia level (defined as >72 μmol/L).2 Overall, there was no correlation observed between lactulose dose and whether ammonia levels were obtained (ie, presence/absence of increased ammonia level did not guide therapy), or between time to OHE resolution and ammonia levels.2Additionally, there is substantial interlaboratory variability in sample handling and processing, which may affect ammonia measurements.4.
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