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Research Article
Wai-Kay Seto
Hong Kong University: University of Hong Kong
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9012-313X
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
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 were 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.
Keywords
HBV, hepatocellular carcinoma, NAFLD, liver stiffness, controlled attenuation parameter
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CURRENT STATUS: Under Review
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Posted 05 May, 2021
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Received 23 Apr, 2021
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Subject Areas
Hepatobiliary & Transplant Surgery
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This preprint is under consideration at Hepatology International. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Wai-Kay Seto
Hong Kong University: University of Hong Kong
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9012-313X
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 05 May, 2021
No community comments so far
Reviews received
Received 23 Apr, 2021
Reviewers invited
Invitations sent on 23 Apr, 2021
Editor assigned
On 20 Apr, 2021
First submitted
On 20 Apr, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Hepatobiliary & Transplant Surgery
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
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 were 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.
Figure 1
Figure 2
Figure 3
Figure 4
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