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Article: Inverse relationship between hepatic steatosis and hepatitis B viremia: Results of a large case-control study

TitleInverse relationship between hepatic steatosis and hepatitis B viremia: Results of a large case-control study
Authors
KeywordsCAP
HBV
NAFLD
controlled attenuation parameter
liver stiffness
Issue Date2018
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, 2018, v. 25 n. 1, p. 97-104 How to Cite?
AbstractThe potential interaction between chronic hepatitis B (CHB) and nonalcoholic fatty liver disease (NAFLD), two of the most prevalent liver diseases worldwide, has not been well defined. We performed liver stiffness (LS) and controlled attenuation parameter (CAP) measurements using transient elastography in 1202 CHB patients. Of these, 601 steatotic patients were matched with nonsteatotic controls in a 1:1 ratio by age, gender, nucleoside analogue treatment status, and treatment duration. Severe fibrosis was defined according to EASL-ALEH criteria, and steatosis was defined as CAP ≥222 dB m-1 . Anthropometric measurements and metabolic-related parameters were recorded. The mean age of the 1202 patients (51.4% male) was 51.8 years. 696 patients (57.9%) were on nucleoside analogues for a median duration of 76.2 months. Among treatment-naïve patients, median serum HBV DNA was lower in steatotic individuals than in controls (3.0 vs 3.4 log IU mL-1 , P < .05), with this inverse relationship remaining significant in multivariate analysis (odds ratio 0.859, 95% CI 0.743-0.994, P < .05). With increased steatosis severity, there was a stepwise decrease in median HBV DNA levels (3.1 and 2.6 log IU mL-1 in no steatosis and severe steatosis, respectively, P = .032). Steatosis was associated with a higher median LS (5.4 kPa vs 5.0 kPa, P < .001). Severe steatosis, when compared to mild/moderate steatosis, was associated with an increased percentage of severe fibrosis (23.2% and 12.6%, respectively, P = .005). We conclude that severe steatosis was associated with increased fibrosis in CHB patients. Increasing steatosis was independently associated with lower serum HBV DNA levels, suggesting its potential negative effects on viral replication.
Persistent Identifierhttp://hdl.handle.net/10722/246565
ISSN
2019 Impact Factor: 3.561
2015 SCImago Journal Rankings: 1.815
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHui, RWH-
dc.contributor.authorSeto, WKW-
dc.contributor.authorCheung, KSM-
dc.contributor.authorMak, LY-
dc.contributor.authorLiu, SHK-
dc.contributor.authorFung, JYY-
dc.contributor.authorWong, DKH-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, RMF-
dc.date.accessioned2017-09-18T02:30:43Z-
dc.date.available2017-09-18T02:30:43Z-
dc.date.issued2018-
dc.identifier.citationJournal of Viral Hepatitis, 2018, v. 25 n. 1, p. 97-104-
dc.identifier.issn1352-0504-
dc.identifier.urihttp://hdl.handle.net/10722/246565-
dc.description.abstractThe potential interaction between chronic hepatitis B (CHB) and nonalcoholic fatty liver disease (NAFLD), two of the most prevalent liver diseases worldwide, has not been well defined. We performed liver stiffness (LS) and controlled attenuation parameter (CAP) measurements using transient elastography in 1202 CHB patients. Of these, 601 steatotic patients were matched with nonsteatotic controls in a 1:1 ratio by age, gender, nucleoside analogue treatment status, and treatment duration. Severe fibrosis was defined according to EASL-ALEH criteria, and steatosis was defined as CAP ≥222 dB m-1 . Anthropometric measurements and metabolic-related parameters were recorded. The mean age of the 1202 patients (51.4% male) was 51.8 years. 696 patients (57.9%) were on nucleoside analogues for a median duration of 76.2 months. Among treatment-naïve patients, median serum HBV DNA was lower in steatotic individuals than in controls (3.0 vs 3.4 log IU mL-1 , P < .05), with this inverse relationship remaining significant in multivariate analysis (odds ratio 0.859, 95% CI 0.743-0.994, P < .05). With increased steatosis severity, there was a stepwise decrease in median HBV DNA levels (3.1 and 2.6 log IU mL-1 in no steatosis and severe steatosis, respectively, P = .032). Steatosis was associated with a higher median LS (5.4 kPa vs 5.0 kPa, P < .001). Severe steatosis, when compared to mild/moderate steatosis, was associated with an increased percentage of severe fibrosis (23.2% and 12.6%, respectively, P = .005). We conclude that severe steatosis was associated with increased fibrosis in CHB patients. Increasing steatosis was independently associated with lower serum HBV DNA levels, suggesting its potential negative effects on viral replication.-
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.rightsThis is the peer reviewed version of the following article: Journal of Viral Hepatitis, 2018, v. 25 n. 1, p. 97-104, which has been published in final form at http://dx.doi.org/10.1111/jvh.12766. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectCAP-
dc.subjectHBV-
dc.subjectNAFLD-
dc.subjectcontrolled attenuation parameter-
dc.subjectliver stiffness-
dc.titleInverse relationship between hepatic steatosis and hepatitis B viremia: Results of a large case-control study-
dc.typeArticle-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.emailCheung, KSM: cks634@hku.hk-
dc.identifier.emailLiu, SHK: drkliu@hku.hk-
dc.identifier.emailFung, JYY: jfung@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityCheung, KSM=rp02532-
dc.identifier.authorityFung, JYY=rp00518-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, RMF=rp00479-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/jvh.12766-
dc.identifier.pmid28772340-
dc.identifier.scopuseid_2-s2.0-85028355364-
dc.identifier.hkuros277296-
dc.identifier.hkuros302525-
dc.identifier.volume25-
dc.identifier.issue1-
dc.identifier.spage97-
dc.identifier.epage104-
dc.identifier.isiWOS:000418760500012-
dc.publisher.placeUnited Kingdom-

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