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Vol. 85, No. 3, 2012
Issue release date: May 2012

Risk Assessment of Development of Hepatic Decompensation in Histologically Proven Hepatitis B Viral Cirrhosis Using Liver Stiffness Measurement

Kim B.K. · Park Y.N. · Kim D.Y. · Park J.Y. · Chon C.Y. · Han K.-H. · Ahn S.H.
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Background/Aims: There are few studies regarding the predictive value of liver stiffness measurement (LSM) for development of hepatic decompensation. We assessed the risk of hepatic decompensations in B-viral compensated cirrhosis, using an LSM and LSM-based model (LSM-spleen diameter to platelet ratio score, LSPS = LSM × spleen diameter/platelet count) in a prospective, longitudinal study. Methods: We analyzed 217 patients with histologically proven B-viral cirrhosis, well-preserved liver function, and no history of decompensation. The Kaplan-Meier and Cox regression method were used to examine the major endpoint, time to the first decompensation event, defined as development of ascites, hepatic encephalopathy, variceal hemorrhage, and deterioration of liver function to Child-Pugh class B/C. Results: During follow-up, 26 patients experienced hepatic decompensation, ascites (n = 22), hepatic encephalopathy (n = 11), variceal hemorrhage (n = 9), and deterioration of liver function (n = 20). For risk stratification, patients were grouped as LSM <13, 13–18, and ≥18 kPa, and from multivariate analysis, patients with LSM 13–18 kPa [hazard ratio (HR) 4.547/ p = 0.044] and ≥18 kPa (HR 12.446/p < 0.001) retained independently higher risks than patients with LSM <13 kPa. Similarly, when patients were grouped as LSPS <1.1, 1.1–2.5, and ≥2.5, those with LSPS 1.1–2.5 (HR 5.796/p = 0.004) and ≥2.5 (HR 13.618/p < 0.001) retained independently higher risks than those with LSPS <1.1. Conclusion: LSM and LSPS are useful in risk assessment of hepatic decompensation among complication-naive B-viral cirrhotic patients.

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