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Article: Reduced hepatic steatosis is associated with higher risk of hepatocellular carcinoma in chronic hepatitis B infection

TitleReduced hepatic steatosis is associated with higher risk of hepatocellular carcinoma in chronic hepatitis B infection
Authors
KeywordsHBV
Hepatocellular carcinoma
NAFLD
Liver stiffness
Controlled attenuation parameter
Issue Date2021
PublisherSpringer (India) Private Ltd. The Journal's web site is located at http://www.springer.com/medicine/internal/journal/12072
Citation
Hepatology International, 2021, v. 15 n. 4, p. 901-911 How to Cite?
AbstractBackground: Concomitant chronic hepatitis B infection (CHB) and non-alcoholic fatty liver disease (NAFLD) is common, but the implications of NAFLD on clinical outcomes of CHB, including hepatocellular carcinoma (HCC), are not well-investigated. Methods: CHB patients were recruited for transient elastography assessment for liver stiffness (LS), and controlled attenuation parameter (CAP), a non-invasive quantification of hepatic steatosis, and were prospectively followed up for development of HCC. Steatosis and severe steatosis were diagnosed by CAP ≥ 248 dB/m and ≥ 280 dB/m respectively, and advanced fibrosis/cirrhosis was diagnosed by LS ≥ 9 kPa. The independent effect of hepatic steatosis on HCC was examined via propensity score matching (PSM) of LS and other significant clinical variables. Results: Forty-eight patients developed HCC among 2403 CHB patients (55.6% male, median age 55.6 years, 57.1% antiviral-treated, median ALT 26 U/L) during a median follow-up of 46.4 months. Multivariate Cox regression analysis showed age (HR 1.063), male (HR 2.032), Albumin-Bilirubin score (HR 2.393) and CAP (HR 0.993) were associated with HCC development. The cumulative probability of HCC was 2.88%, 1.56% and 0.71%, respectively for patients with no steatosis, mild-to-moderate steatosis, and severe steatosis, respectively (p = 0.01). The risk of HCC increased from 1.56 to 8.89% in patients without severe steatosis if advanced fibrosis/cirrhosis was present (p < 0.001). PSM yielded 957 pairs of CHB patients and hepatic steatosis was independently associated with HCC (HR 0.41). Conclusion: Reduced hepatic steatosis was significantly associated with a higher risk of incident HCC in CHB infection. Routine CAP and LS measurements are important for risk stratification.
Persistent Identifierhttp://hdl.handle.net/10722/300947
ISSN
2023 Impact Factor: 5.9
2023 SCImago Journal Rankings: 1.813
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMak, LY-
dc.contributor.authorHui, RWH-
dc.contributor.authorFung, J-
dc.contributor.authorLiu, F-
dc.contributor.authorWong, DKH-
dc.contributor.authorLi, B-
dc.contributor.authorCheung, KS-
dc.contributor.authorYuen, MF-
dc.contributor.authorSeto, WK-
dc.date.accessioned2021-07-06T03:12:26Z-
dc.date.available2021-07-06T03:12:26Z-
dc.date.issued2021-
dc.identifier.citationHepatology International, 2021, v. 15 n. 4, p. 901-911-
dc.identifier.issn1936-0533-
dc.identifier.urihttp://hdl.handle.net/10722/300947-
dc.description.abstractBackground: Concomitant chronic hepatitis B infection (CHB) and non-alcoholic fatty liver disease (NAFLD) is common, but the implications of NAFLD on clinical outcomes of CHB, including hepatocellular carcinoma (HCC), are not well-investigated. Methods: CHB patients were recruited for transient elastography assessment for liver stiffness (LS), and controlled attenuation parameter (CAP), a non-invasive quantification of hepatic steatosis, and were prospectively followed up for development of HCC. Steatosis and severe steatosis were diagnosed by CAP ≥ 248 dB/m and ≥ 280 dB/m respectively, and advanced fibrosis/cirrhosis was diagnosed by LS ≥ 9 kPa. The independent effect of hepatic steatosis on HCC was examined via propensity score matching (PSM) of LS and other significant clinical variables. Results: Forty-eight patients developed HCC among 2403 CHB patients (55.6% male, median age 55.6 years, 57.1% antiviral-treated, median ALT 26 U/L) during a median follow-up of 46.4 months. Multivariate Cox regression analysis showed age (HR 1.063), male (HR 2.032), Albumin-Bilirubin score (HR 2.393) and CAP (HR 0.993) were associated with HCC development. The cumulative probability of HCC was 2.88%, 1.56% and 0.71%, respectively for patients with no steatosis, mild-to-moderate steatosis, and severe steatosis, respectively (p = 0.01). The risk of HCC increased from 1.56 to 8.89% in patients without severe steatosis if advanced fibrosis/cirrhosis was present (p < 0.001). PSM yielded 957 pairs of CHB patients and hepatic steatosis was independently associated with HCC (HR 0.41). Conclusion: Reduced hepatic steatosis was significantly associated with a higher risk of incident HCC in CHB infection. Routine CAP and LS measurements are important for risk stratification.-
dc.languageeng-
dc.publisherSpringer (India) Private Ltd. The Journal's web site is located at http://www.springer.com/medicine/internal/journal/12072-
dc.relation.ispartofHepatology International-
dc.rightsThis version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1007/s12072-021-10218-2-
dc.subjectHBV-
dc.subjectHepatocellular carcinoma-
dc.subjectNAFLD-
dc.subjectLiver stiffness-
dc.subjectControlled attenuation parameter-
dc.titleReduced hepatic steatosis is associated with higher risk of hepatocellular carcinoma in chronic hepatitis B infection-
dc.typeArticle-
dc.identifier.emailMak, LY: lungyi@hku.hk-
dc.identifier.emailHui, RWH: huirex@connect.hku.hk-
dc.identifier.emailFung, J: jfung@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailCheung, KS: cks634@hku.hk-
dc.identifier.emailYuen, MF: mfyuen@hku.hk-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.authorityMak, LY=rp02668-
dc.identifier.authorityFung, J=rp00518-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityCheung, KS=rp02532-
dc.identifier.authorityYuen, MF=rp00479-
dc.identifier.authoritySeto, WK=rp01659-
dc.description.naturepostprint-
dc.identifier.doi10.1007/s12072-021-10218-2-
dc.identifier.pmid34152534-
dc.identifier.scopuseid_2-s2.0-85112190679-
dc.identifier.hkuros323175-
dc.identifier.volume15-
dc.identifier.issue4-
dc.identifier.spage901-
dc.identifier.epage911-
dc.identifier.isiWOS:000664544000001-
dc.publisher.placeIndia-

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