https://orcid.org/0000-0001-7005-0474
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Abstract
Introduction
Acetaminophen-induced hepatotoxicity can result in hyperammonemia, but it is not clear if elevated ammonia concentrations predict encephalopathy.
Methods
We retrospectively studied patients with acetaminophen toxicity at a liver transplant center over 8 years (January 1, 2010–December 31, 2017), who developed hepatotoxicity (AST and/or ALT >1000 IU/L) or hyperammonemia (ammonia > 40 µmol/L). We recorded baseline characteristics, laboratory data, documented grade of encephalopathy, and treatments administered. Sensitivity and specificity values were calculated for varying ammonia concentrations.
Results
A total of 102 patient encounters were included with 75 having ammonia concentrations. On presentation, 40% (30/75) of patients had concentrations greater than 100 µmol/L. However, an [ammonia] > 100 µmol/L was neither sensitive (46 % [95% CI: 26–67%]) nor specific (63% [48 − 76%]) for encephalopathy. Only an increasing ammonia concentration had a significant, but small (1.53 (95% CI: 1.06 − 2.20)) positive likelihood ratio for the development of hepatic encephalopathy.
Discussion
Animal models have suggested that in acetaminophen toxicity, encephalopathy may be secondary to an alternative mechanism other than hyperammonemia which may explain the lack of correlation between initial hyperammonemia and encephalopathy in this cohort. Additionally, a lack of empiric treatment for hyperammonemia did not appear to alter the course of any of the patients. None of these patients developed encephalopathy.
Conclusion
In cases of acetaminophen-induced hepatotoxicity, ammonia concentrations do not correlate with encephalopathy and empiric treatment for hyperammonemia does not appear to be beneficial.
Acknowledgements
Landon Curtis helped with the initial data gathering.
The study was completed under the IRB PRO18070695.
Disclosure statement
No potential conflict of interest was reported by the author(s).