Summary
DOI: 10.1373/clinchem.2010.144527
A 31-year-old woman was admitted into a regional hospital for abdominal pain, decreased appetite, malaise, confusion, and tea-colored urine. Investigations showed acute liver failure with a markedly decreased liver function characterized by greatly increased aminotransferases, bilirubin concentration, prothrombin time, and international normalized ratio. There was no history of liver disease or intake of herbal medicines or over-the-counter medications. Her condition worsened 2 days later, and she was transferred to our hospital for further management and the possibility of liver transplantation. A physical examination revealed a jaundiced woman in a fair general condition and with a soft but tender right upper quadrant with no guarding or rebound tenderness of the abdomen. She went into a semicomatose state 1 day later.
Student Discussion
Student Discussion Document (pdf)
Bonnie Mei-wah Fong, Tak Shing Siu, and Sidney Tam*
Division of Clinical Biochemistry, Queen Mary Hospital, Hong Kong.
* Address correspondence to this author at: Clinical Biochemistry, Queen Mary Hospital, LG 131, Block K, Queen Mary
Hospital, 102 Pokfulam Road, Pokfulam, Hong Kong SAR. Fax: 852-28559915; e-mail [email protected].
Case Description
A 31-year-old woman was admitted into a regional hospital for abdominal pain,
decreased appetite, malaise, confusion, and tea-colored urine. Investigations showed
acute liver failure with a markedly decreased liver function characterized by greatly
increased aminotransferases, bilirubin concentration, prothrombin time and international
normalized ratio. There was no history of liver disease or intake of herbal medicines or
over-the-counter medications. Her condition worsened 2 days later, and she was
transferred to our hospital for further management and the possibility of liver
transplantation. A physical examination revealed a jaundiced woman in a fair general
condition and with a soft but tender right upper quadrant with no guarding or rebound
tenderness of the abdomen. She went into a semicomatose state 1 day later. Routine
laboratory testing of a blood sample obtained on her arrival in the hospital revealed the
following results: bilirubin, 1210 μmol/L (reference interval, 7–19 μmol/L); alanine
aminotransferase, 6170 U/L (reference interval, 5–31 U/L); aspartate aminotransferase,
5080 U/L (reference interval, 12–28 U/L); alkaline phosphatase, 150 U/L (reference
interval, 34–104 U/L); ammonia, 171 μmol/L (reference interval, 0–33 μmol/L); lactate
dehydrogenase, 6830 U/L (reference interval, 200–360 U/L); prothrombin time, 39.7 s
(reference interval, 11.3–13.2 s); international normalized ratio, 3.3; acetaminophen, 121
μmol/L (therapeutic up to 100 μmol/L). Other results were unremarkable. A serologic
evaluation was negative for hepatitis A and B. The plasma acetaminophen concentration
prompted the clinical suspicion of drug overdose, but she denied taking acetaminophen.
The patient’s liver enzymes, prothrombin time, international normalized ratio, and
acetaminophen concentrations were monitored on subsequent days. Her general condition
and liver function gradually improved, but her plasma acetaminophen concentration
remained >100 μmol/L. Failure of the liver to metabolize the drug was suspected, and liver transplantation was contemplated at that juncture.
Questions to Consider
- What are common causes of acute liver failure?
- What is the usual pharmacokinetic pattern of acetaminophen after ingestion, and how does overdose cause liver injury?
- What methods are available to measure acetaminophen concentrations?
- What factors interfere with acetaminophen measurement?
Final Publication and Comments
The final published version with discussion and comments from the experts appears
in the January 2011 issue of Clinical Chemistry, approximately 3-4 weeks after the Student Discussion is posted.
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DOI: 10.1373/clinchem.2010.144527
Copyright © 2011 American Association for Clinical Chemistry