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Article: Fibrosis evolution in chronic hepatitis B e antigen‐negative patients across a 10‐year interval

TitleFibrosis evolution in chronic hepatitis B e antigen‐negative patients across a 10‐year interval
Authors
KeywordsFatty liver
Hepatitis B
Liver fibrosis
Metabolic syndrome
Issue Date2019
PublisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2893
Citation
Journal of Viral Hepatitis, 2019, v. 26 n. 7, p. 818-827 How to Cite?
AbstractThe degree of liver fibrosis in chronic hepatitis B (CHB) infection influences outcome and management. Existing data describing the long‐term dynamic changes of liver fibrosis are limited. This study aimed to evaluate the evolution of liver fibrosis in CHB across a 10‐year period. CHB patients with liver stiffness measurement (LSM) by transient elastography 10 years ago were recruited for follow‐up LSM. Fibrosis stages were classified according to EASL‐ALEH guidelines. Fibrosis progression/regression was arbitrarily defined as ≥1 fibrosis stage change from baseline. A total of 459 hepatitis B e antigen (HBeAg)‐negative patients (224 untreated, 235 treated with nucleos(t)ide analogues [NAs]) were recruited. The mean age at baseline LSM was 41.7 ± 9.0 years (56.2% male). Over 10 years, the proportion of patients with advanced fibrosis/cirrhosis significantly reduced from 16.3% to 5.7% (P < 0.001). Fibrosis progression and regression were observed in 8.7% and 37.5%, respectively. No treatment with NAs (OR 2.259, 95% confidence interval [CI]: 1.032‐4.945), metabolic syndrome (OR 4.379, 95% CI: 1.128‐16.999) and hepatic steatosis (OR 7.799, 95% CI: 2.271‐26.776) was associated with fibrosis progression. Liver stiffness decline demonstrated positive correlation with the time after HBsAg seroclearance (r = −0.50, P < 0.001). Median liver stiffness was higher both at baseline (14.0 vs 6 kPa, P < 0.001) and 10 years (9.1 vs 4.9 kPa, P < 0.001) in patients with cirrhosis‐related complications/hepatocellular carcinoma compared with those without. In conclusion, CHB‐related liver fibrosis changed dynamically across 10 years. Metabolic syndrome and hepatic steatosis were associated with fibrosis progression, while antiviral therapy was associated with fibrosis regression. Patients with HBsAg seroclearance demonstrated time‐dependent decline in liver stiffness.
Persistent Identifierhttp://hdl.handle.net/10722/269437
ISSN
2021 Impact Factor: 3.517
2020 SCImago Journal Rankings: 1.329
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMak, LY-
dc.contributor.authorSeto, WK-
dc.contributor.authorHui, RWH-
dc.contributor.authorFung, J-
dc.contributor.authorWong, DKH-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, MF-
dc.date.accessioned2019-04-24T08:07:42Z-
dc.date.available2019-04-24T08:07:42Z-
dc.date.issued2019-
dc.identifier.citationJournal of Viral Hepatitis, 2019, v. 26 n. 7, p. 818-827-
dc.identifier.issn1352-0504-
dc.identifier.urihttp://hdl.handle.net/10722/269437-
dc.description.abstractThe degree of liver fibrosis in chronic hepatitis B (CHB) infection influences outcome and management. Existing data describing the long‐term dynamic changes of liver fibrosis are limited. This study aimed to evaluate the evolution of liver fibrosis in CHB across a 10‐year period. CHB patients with liver stiffness measurement (LSM) by transient elastography 10 years ago were recruited for follow‐up LSM. Fibrosis stages were classified according to EASL‐ALEH guidelines. Fibrosis progression/regression was arbitrarily defined as ≥1 fibrosis stage change from baseline. A total of 459 hepatitis B e antigen (HBeAg)‐negative patients (224 untreated, 235 treated with nucleos(t)ide analogues [NAs]) were recruited. The mean age at baseline LSM was 41.7 ± 9.0 years (56.2% male). Over 10 years, the proportion of patients with advanced fibrosis/cirrhosis significantly reduced from 16.3% to 5.7% (P < 0.001). Fibrosis progression and regression were observed in 8.7% and 37.5%, respectively. No treatment with NAs (OR 2.259, 95% confidence interval [CI]: 1.032‐4.945), metabolic syndrome (OR 4.379, 95% CI: 1.128‐16.999) and hepatic steatosis (OR 7.799, 95% CI: 2.271‐26.776) was associated with fibrosis progression. Liver stiffness decline demonstrated positive correlation with the time after HBsAg seroclearance (r = −0.50, P < 0.001). Median liver stiffness was higher both at baseline (14.0 vs 6 kPa, P < 0.001) and 10 years (9.1 vs 4.9 kPa, P < 0.001) in patients with cirrhosis‐related complications/hepatocellular carcinoma compared with those without. In conclusion, CHB‐related liver fibrosis changed dynamically across 10 years. Metabolic syndrome and hepatic steatosis were associated with fibrosis progression, while antiviral therapy was associated with fibrosis regression. Patients with HBsAg seroclearance demonstrated time‐dependent decline in liver stiffness.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2893-
dc.relation.ispartofJournal of Viral Hepatitis-
dc.subjectFatty liver-
dc.subjectHepatitis B-
dc.subjectLiver fibrosis-
dc.subjectMetabolic syndrome-
dc.titleFibrosis evolution in chronic hepatitis B e antigen‐negative patients across a 10‐year interval-
dc.typeArticle-
dc.identifier.emailMak, LY: lungyi@hku.hk-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.emailFung, J: jfung@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, MF: mfyuen@hku.hk-
dc.identifier.authorityMak, LY=rp02668-
dc.identifier.authoritySeto, WK=rp01659-
dc.identifier.authorityFung, J=rp00518-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, MF=rp00479-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/jvh.13095-
dc.identifier.pmid30895682-
dc.identifier.scopuseid_2-s2.0-85064654619-
dc.identifier.hkuros297414-
dc.identifier.volume26-
dc.identifier.issue7-
dc.identifier.spage818-
dc.identifier.epage827-
dc.identifier.isiWOS:000472774300004-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1352-0504-

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