US EPA

1229595 

Journal Article 

Hyperammonemia: A possible marker for methanol and ethylene glycol intoxication 

Haroz, R; Salzman; Greenberg, MI 

2005 

1 

Clinical Toxicology
ISSN: 1556-3650
EISSN: 1556-9519 

Taylor & Francis Ltd., 11 New Fetter Lane London EC4P 4EE UK, [mailto:info@tandf.co.uk], [URL:http://www.tandf.co.uk] 

43 

6 (Oct 2005) 

689. 

Hyperammonemia associated with methanol ingestion has been reported only once and never reported in association with ethylene glycol ingestion. We are reporting an additional case of hyperammonemia associated with methanol ingestion as well as 2 cases associated with ethylene glycol ingestion and one case demonstrating a normal ammonia level after isopropanol ingestion. Since serum ammonia is not routinely measured after toxic alcohol ingestions and since a plausible mechanism exists for the production of elevated levels of ammonia we raise the possibility of a previously unrecognized association. A 46 year-old-male was unresponsive on presentation with a pH of 6.93, osmolar gap of 402, normal liver functions (LFTs), a serum ammonia level (SAL) of 163 mmol/L and a methanol level of 570 mg/dL. A 55 year-old-male was unresponsive on presentation with a pH of 6.73, anion gap of 30, a SAL of 1100 mmol/L and ethylene glycol level of 38 mg/dL. A 43-year-old-female, unresponsive on presentation after ingesting ethylene glycol had a pH of 6.94, osmolar gap of 60, and a SAL of 158 mmol/L. A 65-year-old female presented, after ingesting isopropanol, with normal LFTs and a SAL of 24 mmol/L. N-acetylglutamate is necessary for the efficient incorporation of ammonia into the urea cycle. Organic acids inhibit the synthesis of N-acetylglutamate. When N-acetylglutamate synthesis is inhibited, ammonia, in turn accumulates. This occurs with certain in-born errors of metabolism and may result as well from the accumulation of acids produced from the metabolism of methanol and ethylene glycol. Hyperammonemia would thus be expected after ethylene glycol and methanol ingestion, but not after isopropanol ingestion. The cases presented corroborate this proposed mechanism for elevation of serum ammonia in the face of methanol or ethylene glycol ingestion. Hyperammonemia may be a previously underrecognized finding in methanol and ethylene glycol intoxication. Ammonia levels are readily obtained and may represent a surrogate marker for methanol or ethylene glycol intoxication.