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Background <p>Standardized anti-hepatitis B virus (HBV) guidelines for HBV/tuberculosis (TB) co-infected patients during antituberculosis therapy (ATT) are lacking, especially for hepatitis B e antigen (HBeAg)-negative patients with low baseline HBV DNA. It remains unclear whether liver injury during ATT is caused by ATT itself (antituberculosis drug-induced liver injury, AT-DILI) or by HBV reactivation. We aimed to characterize HBV reactivation liver injury in this understudied population and to distinguish it from AT-DILI.</p> Methods <p>We conducted a retrospective multi-center study of 10 consecutive HBeAg-negative HBV/TB co-infected patients with suspected ATT-induced liver injury. HBV reactivation was defined as ≥ 2 log&#xa0;IU/mL HBV DNA increase or conversion from undetectable to detectable. Liver injury was defined as ALT &gt; 3 × ULN with symptoms, or ALT &gt; 5 × ULN, or total bilirubin &gt; 2 × ULN. Key indicators were measured via standardized methods; analyses used SPSS 23.0 and GraphPad Prism 9.0.</p> Results <p>All 10 patients met the criteria for HBV reactivation, with HBV DNA increasing from 3.0 ± 0.6 to 7.4 ± 0.4 log&#xa0;IU/mL (<i>P</i> &lt; 0.001), and 60% developed liver failure. Notably, the median time to liver injury was 18&#xa0;weeks (range 6–40), which is later than typical AT-DILI (usually within the first 8&#xa0;weeks). In comparison, HBV reactivation rates in HBeAg-negative non-TB patients receiving immunosuppressive therapy are reported to be 5–15%, whereas our cohort showed a 100% reactivation rate, suggesting a uniquely high risk in TB patients. Immediate nucleos(t)ide analogue therapy (entecavir/tenofovir) plus ATT adjustment led to 90% 12-month survival, with 80% achieving undetectable HBV DNA and 70% normal ALT by 3&#xa0;months.</p> Conclusion <p>Liver injury during ATT in HBeAg-negative HBV/TB co-infected patients with low baseline HBV DNA is predominantly driven by HBV reactivation rather than AT-DILI. Immediate anti-HBV therapy and regular monitoring are essential. Due to the retrospective case‑series design, our findings are hypothesis‑generating and require validation in prospective cohort studies.</p>

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Hepatitis B virus reactivation liver injury during anti-tuberculosis treatment in HBeAg-negative hepatitis B virus/tuberculosis co-infected patients with low baseline hepatitis B virus DNA

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月15日

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  • Bin Gu,
  • Min Tang,
  • Yulan Zhou,
  • Chenxi Wu,
  • Hengjian Lu,
  • Guozhong Gong

摘要

Background

Standardized anti-hepatitis B virus (HBV) guidelines for HBV/tuberculosis (TB) co-infected patients during antituberculosis therapy (ATT) are lacking, especially for hepatitis B e antigen (HBeAg)-negative patients with low baseline HBV DNA. It remains unclear whether liver injury during ATT is caused by ATT itself (antituberculosis drug-induced liver injury, AT-DILI) or by HBV reactivation. We aimed to characterize HBV reactivation liver injury in this understudied population and to distinguish it from AT-DILI.

Methods

We conducted a retrospective multi-center study of 10 consecutive HBeAg-negative HBV/TB co-infected patients with suspected ATT-induced liver injury. HBV reactivation was defined as ≥ 2 log IU/mL HBV DNA increase or conversion from undetectable to detectable. Liver injury was defined as ALT > 3 × ULN with symptoms, or ALT > 5 × ULN, or total bilirubin > 2 × ULN. Key indicators were measured via standardized methods; analyses used SPSS 23.0 and GraphPad Prism 9.0.

Results

All 10 patients met the criteria for HBV reactivation, with HBV DNA increasing from 3.0 ± 0.6 to 7.4 ± 0.4 log IU/mL (P < 0.001), and 60% developed liver failure. Notably, the median time to liver injury was 18 weeks (range 6–40), which is later than typical AT-DILI (usually within the first 8 weeks). In comparison, HBV reactivation rates in HBeAg-negative non-TB patients receiving immunosuppressive therapy are reported to be 5–15%, whereas our cohort showed a 100% reactivation rate, suggesting a uniquely high risk in TB patients. Immediate nucleos(t)ide analogue therapy (entecavir/tenofovir) plus ATT adjustment led to 90% 12-month survival, with 80% achieving undetectable HBV DNA and 70% normal ALT by 3 months.

Conclusion

Liver injury during ATT in HBeAg-negative HBV/TB co-infected patients with low baseline HBV DNA is predominantly driven by HBV reactivation rather than AT-DILI. Immediate anti-HBV therapy and regular monitoring are essential. Due to the retrospective case‑series design, our findings are hypothesis‑generating and require validation in prospective cohort studies.