Volume 7, Issue 11 , Pages 1230-1235, November 2009
Levels and Initial Course of Serum Alanine Aminotransferase Can Predict Outcome of Patients With Budd–Chiari Syndrome
Background & Aims
Patients with Budd–Chiari syndrome can present with acute, subacute, or chronic disease; the definitions and significance of these variants have been disputed. An increased level of serum alanine aminotransferase (ALT) is an objective marker for acute liver injury. We analyzed the significance of changes in ALT levels in Budd–Chiari syndrome patients.
Methods
We performed a retrospective analysis of data from 96 consecutive Budd–Chiari syndrome patients.
Results
A threshold peak ALT level that was 5-fold the upper limit of normal distinguished 2 groups of patients: patients with high levels of ALT (40% of patients) presented with more severe liver disease, less frequent liver fibrosis, and more frequent liver cell necrosis, compared with those with ALT levels below this threshold. Patients with levels of ALT that started out high but slowly declined (<50% of starting concentration within 3 days) had significantly lower odds of survival than those with a rapid decline and those with low levels of ALT (40 months transplantation-free survival, 31%, 63%, and 71%, respectively). When ALT level and the velocity of its decline are used as criterion, these data add significant prognostic information to Child–Pugh, to Clichy, and to Rotterdam Budd–Chiari syndrome scores.
Conclusions
Determination of ALT levels at patient presentation allows 2 variants of Budd–Chiari syndrome to be distinguished. High levels of ALT reflect acute, severe, but potentially reversible, ischemic liver cell necrosis. High levels of ALT that decrease slowly predict a poor outcome for patients and might justify rapid aggressive management.
Abbreviations used in this paper: ALT, alanine aminotransferase, BCS, Budd-Chiari syndrome, IQR, interquartile range, TIPS, transjugular intrahepatic portosystemic shunting, ULN, upper limit of normal
Conflicts of interest The authors disclose no conflicts.
PII: S1542-3565(09)00580-1
doi:10.1016/j.cgh.2009.06.011
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
Volume 7, Issue 11 , Pages 1230-1235, November 2009


