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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

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    Editor-in-Chief
    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
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Original Article

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Liver Cirrhosis, Not Antiviral Therapy, Predicts Clinical Outcome in Cohorts with Heterogeneous Hepatitis B Viral Status

Mi Na Kim1, Seong Gyu Hwang1, Beom Kyung Kim2, Jun Yong Park2, Do Young Kim2, Kwang-Hyub Han2, Seung Up Kim2 , Sang Hoon Ahn2

1Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea, 2Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

Correspondence to: Seung up Kima (https://orcid.org/0000-0002-9658-8050) and Sang Hoon Ahnb
Department of Internal Medicine, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea
aTel: +82-2-2228-1982, Fax: +82-2-393-6884, E-mail: ksukorea@yuhs.ac
bTel: +82-2-2228-1936, Fax: +82-2-393-6884, E-mail: ahnsh@yuhs.ac

Received: May 8, 2018; Revised: August 23, 2018; Accepted: August 24, 2018

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited

Gut and Liver 2019; 13(2): 197-205

Published online March 2, 2019 https://doi.org/10.5009/gnl18204

Copyright © Gut and Liver.

Abstract

Background/Aims

Antiviral therapy (AVT) reduces the risk of hepatocellular carcinoma (HCC) development in patients with chronic hepatitis B (CHB). This multicenter retrospective study investigated the effects of AVT and hepatitis B virus (HBV)-related factors on the risk of HCC development in a cohort with heterogeneous HBV status.

Methods

A total of 1,843 patients with CHB from two institutions were included in this study. Ultrasound and laboratory tests, including the α-fetoprotein test, were conducted regularly to detect HCC development.

Results

The mean age of our study population (1,063 men and 780 women) was 49.4 years. Cirrhosis was identified in 617 patients (33.5%). During follow-up (median, 42.5 months), 81 patients developed HCC (1.39% per person-year). A total of 645 patients (35.0%) received ongoing AVT at enrollment. Ongoing AVT was not significantly associated with the risk of HCC development (all p>0.05). HBV-related variables (HBV DNA level, hepatitis B e antigen status, and alanine aminotransferase level) were also not significantly associated with the risk of HCC development (all p>0.05). In contrast, cirrhosis was significantly associated with the risk of HCC development, regardless of adjustment (adjusted hazard ratio=4.098 to 7.020; all p<0.05). Cirrhosis significantly predicted the risk of HCC development in subgroups with and without ongoing AVT at enrollment, regardless of adjustment.

Conclusions

Our study showed that cirrhosis, not AVT and HBV-related variables, was associated with HCC development in a cohort of patients with heterogeneous HBV status. Our results may help clinicians apply individualized surveillance strategies according to fibrotic status in patients with CHB.

Keywords: Liver cirrhosis, Fibrosis, Antiviral therapy, Hepatitis B, Clinical outcome


Article

Original Article

Gut and Liver 2019; 13(2): 197-205

Published online March 2, 2019 https://doi.org/10.5009/gnl18204

Copyright © Gut and Liver.

Liver Cirrhosis, Not Antiviral Therapy, Predicts Clinical Outcome in Cohorts with Heterogeneous Hepatitis B Viral Status

Mi Na Kim1, Seong Gyu Hwang1, Beom Kyung Kim2, Jun Yong Park2, Do Young Kim2, Kwang-Hyub Han2, Seung Up Kim2 , Sang Hoon Ahn2

1Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea, 2Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

Correspondence to: Seung up Kima (https://orcid.org/0000-0002-9658-8050) and Sang Hoon Ahnb
Department of Internal Medicine, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea
aTel: +82-2-2228-1982, Fax: +82-2-393-6884, E-mail: ksukorea@yuhs.ac
bTel: +82-2-2228-1936, Fax: +82-2-393-6884, E-mail: ahnsh@yuhs.ac

Received: May 8, 2018; Revised: August 23, 2018; Accepted: August 24, 2018

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited

Abstract

Background/Aims

Antiviral therapy (AVT) reduces the risk of hepatocellular carcinoma (HCC) development in patients with chronic hepatitis B (CHB). This multicenter retrospective study investigated the effects of AVT and hepatitis B virus (HBV)-related factors on the risk of HCC development in a cohort with heterogeneous HBV status.

Methods

A total of 1,843 patients with CHB from two institutions were included in this study. Ultrasound and laboratory tests, including the α-fetoprotein test, were conducted regularly to detect HCC development.

Results

The mean age of our study population (1,063 men and 780 women) was 49.4 years. Cirrhosis was identified in 617 patients (33.5%). During follow-up (median, 42.5 months), 81 patients developed HCC (1.39% per person-year). A total of 645 patients (35.0%) received ongoing AVT at enrollment. Ongoing AVT was not significantly associated with the risk of HCC development (all p>0.05). HBV-related variables (HBV DNA level, hepatitis B e antigen status, and alanine aminotransferase level) were also not significantly associated with the risk of HCC development (all p>0.05). In contrast, cirrhosis was significantly associated with the risk of HCC development, regardless of adjustment (adjusted hazard ratio=4.098 to 7.020; all p<0.05). Cirrhosis significantly predicted the risk of HCC development in subgroups with and without ongoing AVT at enrollment, regardless of adjustment.

Conclusions

Our study showed that cirrhosis, not AVT and HBV-related variables, was associated with HCC development in a cohort of patients with heterogeneous HBV status. Our results may help clinicians apply individualized surveillance strategies according to fibrotic status in patients with CHB.

Keywords: Liver cirrhosis, Fibrosis, Antiviral therapy, Hepatitis B, Clinical outcome

Fig 1.

Figure 1.Cumulative incidence rates of hepatocellular carcinoma (HCC) based on antiviral therapy (AVT) status at enrollment. The cumulative HCC incidence rates were not significantly different based on the AVT status at enrollment (p=0.076 by the log-rank test).
Gut and Liver 2019; 13: 197-205https://doi.org/10.5009/gnl18204

Fig 2.

Figure 2.Cumulative incidence rates of hepatocellular carcinoma (HCC) based on cirrhosis. The cumulative incidence rate of HCC in the subgroup with cirrhosis was significantly higher than that of the subgroup without cirrhosis (p<0.001 by the log-rank test).
Gut and Liver 2019; 13: 197-205https://doi.org/10.5009/gnl18204

Table 1 Baseline Characteristics

VariableAll (n=1,843)Yonsei University (n=804, 43.6%)Cha University (n=1039, 56.4%)p-value
Demographic
 Age, yr49.4±11.452.4±10.747.1±11.3<0.001
 Male sex1,063 (57.7)443 (55.1)620 (59.7)0.051
 Diabetes mellitus206 (11.2)44 (5.5)162 (15.6)<0.001
 Cirrhosis617 (33.5)379 (47.1)238 (22.9)<0.001
Laboratory
 α-Fetoprotein, ng/mL6.1±22.45.7±21.56.3±23.10.579
 HBeAg positivity453 (24.6)154 (19.2)299 (28.8)<0.001
 HBV DNA, log IU/mL2.8±2.12.7±2.02.9±2.20.021
 Aspartate aminotransferase, IU/L37.3±57.633.7±43.740.1±66.40.013
 Alanine aminotransferase, IU/L44.4±90.539.2±70.148.5±103.50.022
 Serum albumin, g/dL4.4±0.44.3±0.34.5±0.4<0.001
 Total bilirubin, mg/dL0.8±0.50.9±0.50.8±0.4<0.001
 Platelet count, 109/L174±60168±64178±57<0.001
 Ongoing antiviral therapy645 (35.0)278 (34.6)367 (35.3)0.768

Data are presented as mean±SD or number (%). HBeAg, hepatitis B e antigen; HBV, hepatitis B virus.


Table 2 Comparison of Baseline Characteristics between Patients with and without Ongoing AVT at Enrollment

VariableWith ongoing AVT at enrollment (n=645, 35.0%)Without ongoing AVT at enrollment (n=1,198, 65.0%)p-value
Demographic
 Age, yr50.3±10.448.9±11.80.011
 Male sex387 (60.0)676 (56.4)0.152
 Diabetes mellitus86 (13.3)120 (10.0)0.036
 Cirrhosis276 (42.8)341 (28.5)<0.001
Laboratory
 α-Fetoprotein, ng/mL4.5±14.16.9±25.80.009
 HBeAg positivity176 (27.3)277 (23.1)0.054
 HBV DNA, log IU/mL1.6±1.03.4±2.2<0.001
 Aspartate aminotransferase, IU/L28.3±26.842.2±68.3<0.001
 Alanine aminotransferase, IU/L28.2±31.253.1±109.0<0.001
 Serum albumin, g/dL4.4±0.44.4±0.30.211
 Total bilirubin, mg/dL0.9±0.50.8±0.40.901
 Platelet count, 109/L163±57179±62<0.001

Data are presented as mean±SD or number (%).

AVT, antiviral therapy; HBeAg, hepatitis B e antigen; HBV, hepatitis B virus.


Table 3 HRs of Hepatocellular Carcinoma Development by HBV-Related Variables and Differently Adjusted Models

ModelHBV DNAHBeAgALT



HR95% CIp-valueHR95% CIp-valueHR95% CIp-value
All
 Unadjusted0.9680.865–1.0820.5680.9830.593–1.6290.9471.0000.998–1.0020.764
 Adjusted
  Model 11.0300.920–1.1530.6091.3810.824–2.3130.2211.0010.999–1.0030.368
  Model 21.0310.920–1.1540.7121.3790.823–2.3110.2221.0010.999–1.0030.364
  Model 31.0920.975–1.2230.1291.3690.820–2.2850.2291.0010.999–1.0030.244
  Model 41.0970.947–1.2710.2171.2010.693–2.0840.5141.0000.994–1.0060.800
  Model 51.0570.911–1.2260.4641.0320.599–1.7790.9091.0010.994–1.0070.876
  Model 61.0590.913–1.2270.4511.0460.606–1.8030.8731.0000.993–1.0070.734
Without ongoing AVT at enrollment
 Unadjusted1.0040.877–1.1500.9520.8930.427–1.8660.7631.0010.999–1.0030.549
 Adjusted
  Model 11.0790.941–1.2380.2751.2230.579–2.5810.5981.0010.999–1.0030.306
  Model 21.0800.941–1.2380.2741.2220.579–2.5810.5981.0010.999–1.0030.305
  Model 31.1160.967–1.2880.1341.0900.515–2.3060.8211.0010.999–1.0030.240
  Model 41.1200.942–1.3320.1990.9140.399–2.0950.8311.0020.994–1.0090.674
  Model 51.0570.889–1.2570.5310.6810.303–1.5270.3511.0030.995–1.0110.425
  Model 61.0590.891–1.2600.5140.7020.313–1.5730.3901.0020.994–1.0100.617
With Ongoing AVT at enrollment
 Unadjusted1.0570.803–1.3910.6951.0320.513–2.0720.9311.0000.989–1.0110.991
 Adjusted
  Model 11.1280.850–1.4980.4041.5290.742–3.1510.2501.0030.992–1.0130.648
  Model 21.1260.847–1.4960.4151.5220.738–3.1390.2551.0020.992–1.0130.664
  Model 31.1820.909–1.5360.2121.7210.846–3.5010.1341.0000.987–1.0140.961
  Model 41.0300.722–1.4680.8711.5230.712–3.2600.2780.9940.974–1.0140.556
  Model 51.0300.722–1.4680.8711.5230.712–3.2600.2780.9940.974–1.0140.556
  Model 61.0290.721–1.4700.8741.5170.708–3.2500.2830.9940.974–1.0140.567

HR, hazard ratio; HBV, hepatitis B virus; HBeAg, HBV e antigen; ALT, alanine aminotransferase; CI, confidence interval; AVT, antiviral therapy.

Model 1, age and gender; model 2, model 1 + diabetes mellitus; model 3, model 2 + cirrhosis; model 4, model 3 + α-fetoprotein, HBeAg positivity, HBV DNA, aspartate aminotransferase, alanine aminotransferase, serum albumin, total bilirubin, platelet count, and antiviral therapy AVT at enrollment; model 5, model 4 + AVT initiation after enrollment; model 6, model 5 + institution.


Table 4 HRs of Hepatocellular Carcinoma Development by Ongoing Antiviral Therapy and Differently Adjusted Models

ModelHR95% CIp-value
Unadjusted1.4800.957–2.2910.078
Adjusted
 Model 11.4750.952–2.2830.082
 Model 21.4720.951–2.2800.083
 Model 31.1410.735–1.7710.557
 Model 41.3560.819–2.2450.236
 Model 51.3520.817–2.2370.241

HR, hazard ratio; CI, confidence interval; HBeAg, hepatitis B e antigen; HBV, hepatitis B virus.

Model 1, age and gender; model 2, model 1 + diabetes mellitus; model 3, model 2 + cirrhosis; model 4, model 3 + α-fetoprotein, HBeAg positivity, HBV DNA, aspartate aminotransferase, alanine aminotransferase, serum albumin, total bilirubin, and platelet count; model 5, model 4 + institution.


Table 5 HRs of Hepatocellular Carcinoma Development by Cirrhosis and Differently Adjusted Models (All Study Participants)

ModelHR95% CIp-value
Unadjusted8.4544.825–14.813<0.001
Adjusted
 Model 16.9573.957–12.231<0.001
 Model 27.0203.992–12.347<0.001
 Model 35.2572.795–9.885<0.001
 Model 45.1172.754–9.733<0.001
 Model 54.3372.301–8.177<0.001
 Model 64.0952.148–7.807<0.001

HR, hazard ratio; CI, confidence interval; HBeAg, hepatitis B e antigen; HBV, hepatitis B virus; AVT, antiviral therapy.

Model 1, age and gender; model 2, model 1 + diabetes mellitus; model 3, model 3 + α-fetoprotein, HBeAg positivity, HBV DNA, aspartate aminotransferase, alanine aminotransferase, serum albumin, total bilirubin, and platelet count; model 4, model 3 + AVT at enrollment; model 5, model 4 + AVT after enrollment; model 6, model 5 + institution.


Gut and Liver

Vol.15 No.6
November, 2021

pISSN 1976-2283
eISSN 2005-1212

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