Brief Article
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World J Gastroenterol. Feb 28, 2010; 16(8): 966-972
Published online Feb 28, 2010. doi: 10.3748/wjg.v16.i8.966
Increased liver stiffness in alcoholic liver disease: Differentiating fibrosis from steatohepatitis
Sebastian Mueller, Gunda Millonig, Lucie Sarovska, Stefanie Friedrich, Frank M Reimann, Maria Pritsch, Silke Eisele, Felix Stickel, Thomas Longerich, Peter Schirmacher, Helmut Karl Seitz
Sebastian Mueller, Gunda Millonig, Lucie Sarovska, Stefanie Friedrich, Frank M Reimann, Helmut Karl Seitz, Department of Medicine and Center for Alcohol Research, Salem Medical Center, University of Heidelberg, Zeppelinstraße 11-33, 69121 Heidelberg, Germany
Maria Pritsch, Institute of Medical Biometry and Informatics, University of Heidelberg, 69121 Heidelberg, Germany
Silke Eisele, Felix Stickel, Institute of Clinical Pharmacology, University of Bern, 3010 Bern, Switzerland
Thomas Longerich, Peter Schirmacher, Department of Pathology, University of Heidelberg, 69121 Heidelberg, Germany
Author contributions: Mueller S designed and performed the study and wrote the paper; Seitz HK designed the study; Millonig G, Sarovska L, Friedrich S, Eisele S, Stickel F and Reimann FM performed the study; Pritsch M performed statistical analysis; Longerich T and Schirmacher P performed histological analysis.
Supported by The Dietmar Hopp Foundation and the Manfred Lautenschläger Foundation; an Olympia-Morata fellowship of the University of Heidelberg (Millonig G)
Correspondence to: Sebastian Mueller, MD, PhD, Department of Medicine and Center for Alcohol Research, Salem Medical Center, University of Heidelberg, Zeppelinstraße 11-33, 69121 Heidelberg, Germany. sebastian.mueller@urz.uni-heidelberg.de
Telephone: +49-6221-483210 Fax: +49-6221-484494
Received: December 1, 2009
Revised: December 31, 2009
Accepted: January 7, 2010
Published online: February 28, 2010
Abstract

AIM: To test if inflammation also interferes with liver stiffness (LS) assessment in alcoholic liver disease (ALD) and to provide a clinical algorithm for reliable fibrosis assessment in ALD by FibroScan® (FS).

METHODS: We first performed sequential LS analysis before and after normalization of serum transaminases in a learning cohort of 50 patients with ALD admitted for alcohol detoxification. LS decreased in almost all patients within a mean observation interval of 5.3 d. Six patients (12%) would have been misdiagnosed with F3 and F4 fibrosis but LS decreased below critical cut-off values of 8 and 12.5 kPa after normalization of transaminases.

RESULTS: Of the serum transaminases, the decrease in LS correlated best with the decrease in glutamic oxaloacetic transaminase (GOT). No significant changes in LS were observed below GOT levels of 100 U/L. After establishing the association between LS and GOT levels, we applied the rule of GOT < 100 U/L for reliable LS assessment in a second validation cohort of 101 patients with histologically confirmed ALD. By excluding those patients with GOT > 100 U/L at the time of LS assessment from this cohort, the area under the receiver operating characteristic (AUROC) for cirrhosis detection by FS improved from 0.921 to 0.945 while specificity increased from 80% to 90% at a sensitivity of 96%. A similar AUROC could be obtained for lower F3 fibrosis stage if LS measurements were restricted to patients with GOT < 50 U/L. Histological grading of inflammation did not further improve the diagnostic accuracy of LS.

CONCLUSION: Coexisting steatohepatitis markedly increases LS in patients with ALD independent of fibrosis stage. Postponing cirrhosis assessment by FS during alcohol withdrawal until GOT decreases to < 100 U/mL significantly improves the diagnostic accuracy.

Keywords: Alcoholic liver disease, Alcoholic steatohepatitis, Liver cirrhosis, Bilirubin, Tissue elasticity imaging, FibroScan