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Background/aims <p>Metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD) are emerging hepatocellular carcinoma (HCC) etiologies. Prior-HBV-infection (pHBV) has been linked to HCC in HBsAg-negative populations, but phenotype-specific effects across steatotic liver disease (SLD) remain unclear. We examined whether pHBV modifies 5-year HCC risk by SLD etiology.</p> Methods <p>We analyzed 623 of 1116 patients with hepatic steatosis managed at a single center (2009–2024). pHBV was defined as HBsAg- and HBV DNA-negative status with anti-HBc and/or anti-HBs positivity. The primary endpoint was the 5-year cumulative HCC incidence. Kaplan–Meier, PSM, IPTW, and Cox interaction models were used.</p> Results <p>pHBV was present in 152 patients (24.4%). Overall, pHBV was not associated with 5-year HCC after PSM (150 pairs; 6.58% vs. 5.60%; log-rank <i>P</i> = 0.701) or IPTW (3.80% vs. 4.27%; HR 0.97, 95% CI 0.37–2.54; <i>P</i> = 0.874). In MASLD/cryptogenic SLD, pHBV was associated with lower HCC incidence (PSM 1.32% vs. 9.53%, <i>P</i> = 0.027; IPTW 0.86% vs. 4.35%, <i>P</i> = 0.048). In ALD/MetALD, pHBV showed a borderline higher incidence (PSM 16.17% vs. 3.45%, <i>P</i> = 0.053; IPTW 12.78% vs. 3.99%, <i>P</i> = 0.073). Interaction analyses supported heterogeneity across etiologies (IPTW HR 12.96, <i>P</i> = 0.024; PSM HR 25.87, <i>P</i> = 0.034, Cox HR 7.83, <i>P</i> = 0.057).</p> Conclusions <p>In HBsAg-negative SLD, the association between pHBV and HCC risk appears to differ according to alcohol involvement, with a potentially increased HCC risk in ALD/MetALD and a lower observed HCC incidence in MASLD/cryptogenic disease that requires cautious interpretation.</p> Graphical abstract <p></p>

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Alcohol involvement may modify the association between previous hepatitis B virus infection and hepatocellular carcinoma risk in steatotic liver disease

  • 期刊论文

  • 发表日期：

    2026年6月26日

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  • Naohiro Yasuura,
  • Goki Suda,
  • Masatsugu Ohara,
  • Daisuke Yokoyama,
  • Takatsugu Tanaka,
  • Akimitsu Meno,
  • Takuya Sho,
  • Risako Kohya,
  • Ruixin Deng,
  • Qingjie Fu,
  • Zijian Yang,
  • Osamu Maehara,
  • Shunsuke Ohnishi,
  • Takashi Kitagataya,
  • Naoki Kawagishi,
  • Masato Nakai,
  • Tatsuhiko Kakisaka,
  • Akinobu Taketomi,
  • Naoya Sakamoto

摘要

Background/aims

Metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD) are emerging hepatocellular carcinoma (HCC) etiologies. Prior-HBV-infection (pHBV) has been linked to HCC in HBsAg-negative populations, but phenotype-specific effects across steatotic liver disease (SLD) remain unclear. We examined whether pHBV modifies 5-year HCC risk by SLD etiology.

Methods

We analyzed 623 of 1116 patients with hepatic steatosis managed at a single center (2009–2024). pHBV was defined as HBsAg- and HBV DNA-negative status with anti-HBc and/or anti-HBs positivity. The primary endpoint was the 5-year cumulative HCC incidence. Kaplan–Meier, PSM, IPTW, and Cox interaction models were used.

Results

pHBV was present in 152 patients (24.4%). Overall, pHBV was not associated with 5-year HCC after PSM (150 pairs; 6.58% vs. 5.60%; log-rank P = 0.701) or IPTW (3.80% vs. 4.27%; HR 0.97, 95% CI 0.37–2.54; P = 0.874). In MASLD/cryptogenic SLD, pHBV was associated with lower HCC incidence (PSM 1.32% vs. 9.53%, P = 0.027; IPTW 0.86% vs. 4.35%, P = 0.048). In ALD/MetALD, pHBV showed a borderline higher incidence (PSM 16.17% vs. 3.45%, P = 0.053; IPTW 12.78% vs. 3.99%, P = 0.073). Interaction analyses supported heterogeneity across etiologies (IPTW HR 12.96, P = 0.024; PSM HR 25.87, P = 0.034, Cox HR 7.83, P = 0.057).

Conclusions

In HBsAg-negative SLD, the association between pHBV and HCC risk appears to differ according to alcohol involvement, with a potentially increased HCC risk in ALD/MetALD and a lower observed HCC incidence in MASLD/cryptogenic disease that requires cautious interpretation.

Graphical abstract