Risk assessment of development of hepatic decompensation in histologically proven hepatitis B viral cirrhosis using liver stiffness measurement

Beom Kyung Kim, Young Nyun Park, Do Young Kim, Jun Yong Park, Chae Yoon Chon, Kwang Hyub Han, Sang Hoon Ahn

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)219-227
Number of pages9
JournalDigestion
Volume85
Issue number3
DOIs
Publication statusPublished - 2012 May 1

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Hepatitis B
Liver Cirrhosis
Liver
Hepatic Encephalopathy
Ascites
Spleen
Hemorrhage
Platelet Count
Longitudinal Studies
Fibrosis
Blood Platelets
Multivariate Analysis

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

@article{02bb868d707947e78b5e3bf072d238c1,
title = "Risk assessment of development of hepatic decompensation in histologically proven hepatitis B viral cirrhosis using liver stiffness measurement",
abstract = "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.",
author = "Kim, {Beom Kyung} and Park, {Young Nyun} and Kim, {Do Young} and Park, {Jun Yong} and Chon, {Chae Yoon} and Han, {Kwang Hyub} and Ahn, {Sang Hoon}",
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Risk assessment of development of hepatic decompensation in histologically proven hepatitis B viral cirrhosis using liver stiffness measurement. / Kim, Beom Kyung; Park, Young Nyun; Kim, Do Young; Park, Jun Yong; Chon, Chae Yoon; Han, Kwang Hyub; Ahn, Sang Hoon.

In: Digestion, Vol. 85, No. 3, 01.05.2012, p. 219-227.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Risk assessment of development of hepatic decompensation in histologically proven hepatitis B viral cirrhosis using liver stiffness measurement

AU - Kim, Beom Kyung

AU - Park, Young Nyun

AU - Kim, Do Young

AU - Park, Jun Yong

AU - Chon, Chae Yoon

AU - Han, Kwang Hyub

AU - Ahn, Sang Hoon

PY - 2012/5/1

Y1 - 2012/5/1

N2 - 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.

AB - 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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