Elevated acetaminophen level: could it be a red herring?

A 34 year old woman, previously healthy and on no medications or supplements, presented with a 5 week history of fatigue and jaundice. She denied alcohol or illicit drug use. She had no encephalopa-thy or ascites, and transaminases were 8 times normal , gamma-glutamyl transpeptidase 9 times normal, alkaline phosphatase 3 times normal, INR 1.7 (normal 0.9-1.1), MCV 97 fL (normal 80-98 fL) and bilirubin and conjugated bilirubin both above upper limit of detection (570 and 180 umol/L, respectively ; normal 3.4-17.1 and < 5.1 umol/L, respectively). Viral and autoimmune serologies, liver imaging, pregnancy screen, slit lamp exam, and urine copper studies were negative. Liver biopsy revealed severe active steatohepatitis with no fibro-sis. Blood acetaminophen level was 5 times the therapeutic limit by colorimetric assay. She received N-acetyl cysteine (NAC) while awaiting a confirma-tory assay for acetaminophen with gas chromato-graphy/mass spectrometry (GC-MS) that was negative. She later admitted to consuming 50 units of alcohol daily in the week prior to the onset of her illness, and she gradually improved with abstinence from alcohol. Patients with a history of drug and alcohol misuse are not always forthcoming in providing an accurate account of what they ingested. Furthermore , patients with severe liver injury may withhold aspects of their psychological or addiction history due to embarrassment or fear of denial of liver transplantation should it be required. Health care practitioners must strive to establish a trusting rapport with a patient, and seek corroborative histories. Given this patient's clinical presentation, a toxicology screen was pertinent. The diagnosis of aceta-minophen hepatotoxicity was appropriately questioned in this case given the subacute rather than acute clinical presentation, and transaminases less than 20 or more times the upper limit of normal , which is more typical with acetaminophen he-patotoxicity when associated with the degree of synthetic dysfunction experienced by this patient. NAC should not be delayed or withheld in any patient with suspected acute acetaminophen induced hepatotoxicity, given prospective data showing its efficacy in reducing hepatotoxicity and mortality when administered within 8 and up to 24 hours of ingestion. 1 Many laboratories utilize colorimetric assays as the initial test to determine acetaminophen concentrations because it is generally reliable, rapid and inexpensive. This methodology relies on detection of indophenol, which is an end product of the hydroly-sis reaction of acetaminophen. 2 The change in ab-sorbance determined by colorimetry is directly proportional to the quantitative acetaminophen level in the …