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Alpha‐fetoprotein is a predictor of outcome in acetaminophen‐induced liver injury
Author(s) -
Schmidt Lars E.,
Dalhoff Kim
Publication year - 2005
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.20511
Subject(s) - medicine , alpha fetoprotein , gastroenterology , acetaminophen , predictive value , alanine aminotransferase , liver injury , anesthesia , hepatocellular carcinoma
An increase in alpha‐fetoprotein (AFP) following hepatic necrosis is considered indicative of hepatic regeneration. This study evaluated the prognostic value of serial AFP measurements in patients with severe acetaminophen‐induced liver injury. Prospectively, serial measurements of AFP were performed in 239 patients with acetaminophen intoxication and a peak alanine aminotransferase (ALT) level above 1,000 U/L. AFP was measured using an enzyme‐linked immunoassay (EIA) with a detection limit below 0.4 μg/L. The optimum threshold of AFP to discriminate nonsurvivors was identified. An increase in AFP above 4 μg/L occurred in 158 (79%) of 201 survivors compared with 11 of 33 nonsurvivors (33%; P < .00001). The increase in AFP occurred a mean of 1.0 days (range, −2 to +6 days) after peak ALT in survivors compared with 4.1 days (range, +2 to +7 days) in nonsurvivors ( P < .00001). Starting on the day of peak ALT, AFP values were significantly higher in survivors than in nonsurvivors. A threshold AFP of 3.9 μg/L on day +1 after peak ALT to identify nonsurvivors had a sensitivity of 100%, a specificity of 74%, a positive predictive value of 45%, and a negative predictive value of 100%. In conclusion , an increase in AFP was strongly associated with a favorable outcome in patients with acetaminophen‐induced liver injury. AFP may be useful as a supplement to existing prognostic criteria. We suggest that the introduction of highly sensitive EIAs for the detection of AFP will require a reevaluation of AFP as a prognostic marker in acute nonneoplastic liver disease. (H EPATOLOGY 2005;41:26–31.)