Open AccessAcquired 5‐Oxoprolinuria (Pyroglutamic Acidaemia) as a Cause of Early High Anion Gap Metabolic Acidosis in Acute Massive Paracetamol Overdose
Author(s) -
Leung PSC,
Tsui SH,
Siu TS,
Tam S
Publication year - 2011
Publication title -
hong kong journal of emergency medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.145
H-Index - 12
eISSN - 2309-5407
pISSN - 1024-9079
DOI - 10.1177/102490791101800414
Subject(s) - antidote , metabolic acidosis , medicine , anion gap , acetylcysteine , acetaminophen , emergency department , acidosis , lactic acidosis , anesthesia , toxicity , biochemistry , chemistry , psychiatry , antioxidant
5‐oxoprolinuria is an uncommon and under‐recognised cause of early high anion gap metabolic acidosis after paracetamol overdose. We reported a 30‐year‐old Indian woman with history of chronic alcoholism who ingested 150 g crushed paracetamol tablets for suicide 14 hours before attendance to the A&E Department. Initial arterial blood gas showed a high anion gap metabolic acidosis with respiratory compensation. Serum paracetamol level reached 5004 umol/L and a prolonged course of N‐acetylcysteine was given. She was complicated by hepatotoxicity and 5‐oxoprolinuria (with laboratory confirmation) which reverted after antidote administration. There were no neurological and hepatic sequelae. In case of massive overdose, pathways of drug metabolism are altered prior to the centrilobular hepatic necrosis. A metabolic intermediate of gamma‐glutamyl cycle, 5‐oxoproline, accumulates upon saturation of endogenous glutathione store. The specific antidote N‐acetylcysteine is the only definitive treatment. Prolonged course of antidote may be required in cases of massive overdose and treatment should be individualised. (Hong Kong j.emerg. med. 2011;18:264‐270)