Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication

Aim. The success of direct-acting antivirals (DAAs) against hepatitis C virus is a major breakthrough in hepatology. Previous studies have shown that chitinase 3-like protein 1 (CHI3L1) was a marker for staging of liver fibrosis caused by HCV. In this investigation, we used CHI3L1 as a surrogate mar...

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Main Authors: Qian Kang, Jianhong Chen, Hao Luo, Ning Tan, Hui Gao, Xiaxia Zhang, Min Yu, Dan Liu, Hongli Xi, Yaoyu An, Yifan Han, Ran Cheng, Xiaoyuan Xu
Format: Article
Language:English
Published: Hindawi Limited 2020-01-01
Series:Disease Markers
Online Access:http://dx.doi.org/10.1155/2020/8539804
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language English
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author Qian Kang
Jianhong Chen
Hao Luo
Ning Tan
Hui Gao
Xiaxia Zhang
Min Yu
Dan Liu
Hongli Xi
Yaoyu An
Yifan Han
Ran Cheng
Xiaoyuan Xu
spellingShingle Qian Kang
Jianhong Chen
Hao Luo
Ning Tan
Hui Gao
Xiaxia Zhang
Min Yu
Dan Liu
Hongli Xi
Yaoyu An
Yifan Han
Ran Cheng
Xiaoyuan Xu
Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
Disease Markers
author_facet Qian Kang
Jianhong Chen
Hao Luo
Ning Tan
Hui Gao
Xiaxia Zhang
Min Yu
Dan Liu
Hongli Xi
Yaoyu An
Yifan Han
Ran Cheng
Xiaoyuan Xu
author_sort Qian Kang
title Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
title_short Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
title_full Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
title_fullStr Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
title_full_unstemmed Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV Eradication
title_sort decrease in chitinase 3-like protein 1 levels reflects improvement in liver fibrosis after hcv eradication
publisher Hindawi Limited
series Disease Markers
issn 0278-0240
1875-8630
publishDate 2020-01-01
description Aim. The success of direct-acting antivirals (DAAs) against hepatitis C virus is a major breakthrough in hepatology. Previous studies have shown that chitinase 3-like protein 1 (CHI3L1) was a marker for staging of liver fibrosis caused by HCV. In this investigation, we used CHI3L1 as a surrogate marker to compare dynamic hepatic fibrosis variations following the elimination of HCV among cases receiving sofosbuvir (SOF)-based regimens and pegylated interferon/ribavirin (PR) treatments. Methods. The study enrolled 105 patients, including 46 SOF-based regimens treated patients, 34 PR-experienced patients, and 25 untreated patients. Serum samples and clinical data were obtained at the baseline, the end of treatment, and at weeks 24 and 48 after treatments. Results. First, we found that serum level of CHI3L1 correlated moderately but significantly with LSM (r=0.615, P<0.001) at the baseline, and diagnosed liver cirrhosis at baseline with high accuracy (AUC=0.939) by ROC analysis. So we explored CHI3L1 as a sensitive biomarker to monitor the regression of liver fibrosis after HCV eradication. We found that the serum CHI3L1 level of CHC cases receiving SOF-based regimen treatments was markedly reduced immediately after treatment compared with that at the baseline (123.79 (118.55) vs. 118.20 (103.68), P=0.001). For cases undergoing PR treatment, the serum CHI3L1 decreased significantly at week 24 posttreatment compared with that at the baseline (69.98 (51.44) vs 89.15 (110.59), P=0.016). For the untreated cirrhotic patients, CHI3L1 levels increased at week 96 follow-up compared with that at the baseline (194.73 (172.46) vs. 89.50 (242.97), P=0.048), reflecting continued worsening of liver fibrosis. Conclusion. CHI3L1 is suggested to be the sensitive marker to monitor fibrosis variations in weeks during treatments and after achieving SVR. It has the potential to allow the identification of early treatment failure for a timely switch to alternative treatment and to allow monitoring progression of fibrosis as a risk factor for liver cirrhosis.
url http://dx.doi.org/10.1155/2020/8539804
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spelling doaj-c700284781f942fc8c580d4e10f552d42020-11-25T04:00:59ZengHindawi LimitedDisease Markers0278-02401875-86302020-01-01202010.1155/2020/85398048539804Decrease in Chitinase 3-Like Protein 1 Levels Reflects Improvement in Liver Fibrosis after HCV EradicationQian Kang0Jianhong Chen1Hao Luo2Ning Tan3Hui Gao4Xiaxia Zhang5Min Yu6Dan Liu7Hongli Xi8Yaoyu An9Yifan Han10Ran Cheng11Xiaoyuan Xu12Departments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartment of Gastroenterology, Capital Medical University Affiliated Beijing Shijitan Hospital, Beijing 100038, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartment of Gastroenterology, Capital Medical University Beijing Tiantan Hospital, Beijing 100070, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaDepartments of Infectious Diseases, Peking University First Hospital, NO.8, Xishiku Street, Xicheng District, Beijing 100034, ChinaAim. The success of direct-acting antivirals (DAAs) against hepatitis C virus is a major breakthrough in hepatology. Previous studies have shown that chitinase 3-like protein 1 (CHI3L1) was a marker for staging of liver fibrosis caused by HCV. In this investigation, we used CHI3L1 as a surrogate marker to compare dynamic hepatic fibrosis variations following the elimination of HCV among cases receiving sofosbuvir (SOF)-based regimens and pegylated interferon/ribavirin (PR) treatments. Methods. The study enrolled 105 patients, including 46 SOF-based regimens treated patients, 34 PR-experienced patients, and 25 untreated patients. Serum samples and clinical data were obtained at the baseline, the end of treatment, and at weeks 24 and 48 after treatments. Results. First, we found that serum level of CHI3L1 correlated moderately but significantly with LSM (r=0.615, P<0.001) at the baseline, and diagnosed liver cirrhosis at baseline with high accuracy (AUC=0.939) by ROC analysis. So we explored CHI3L1 as a sensitive biomarker to monitor the regression of liver fibrosis after HCV eradication. We found that the serum CHI3L1 level of CHC cases receiving SOF-based regimen treatments was markedly reduced immediately after treatment compared with that at the baseline (123.79 (118.55) vs. 118.20 (103.68), P=0.001). For cases undergoing PR treatment, the serum CHI3L1 decreased significantly at week 24 posttreatment compared with that at the baseline (69.98 (51.44) vs 89.15 (110.59), P=0.016). For the untreated cirrhotic patients, CHI3L1 levels increased at week 96 follow-up compared with that at the baseline (194.73 (172.46) vs. 89.50 (242.97), P=0.048), reflecting continued worsening of liver fibrosis. Conclusion. CHI3L1 is suggested to be the sensitive marker to monitor fibrosis variations in weeks during treatments and after achieving SVR. It has the potential to allow the identification of early treatment failure for a timely switch to alternative treatment and to allow monitoring progression of fibrosis as a risk factor for liver cirrhosis.http://dx.doi.org/10.1155/2020/8539804