Introduction:
Hepatitis B virus (HBV) reactivation remains a potentially serious complication of immunosuppressive and anticancer therapies. While current guidelines classify patients into high-, moderate-, and low-risk categories, this editorial discusses new real-world evidence suggesting that HBV reactivation risk is more dynamic than previously appreciated.
Key Takeaways:
- Current HBV risk stratification remains broadly valid, with anti-CD20 therapies continuing to carry the highest risk of HBV reactivation.
- Clinically meaningful HBV reactivation can still occur in patients considered "low risk," particularly those receiving low-dose or short-term corticosteroids.
- HBV risk is dynamic rather than binary, influenced by cumulative immunosuppression, combination therapies, host factors, and monitoring intensity.
- Tyrosine kinase inhibitors, anthracyclines, and several targeted therapies also demonstrated clinically relevant HBV reactivation risk.
- Even with regular HBV DNA monitoring, some patients progressed to hepatitis, highlighting the limitations of surveillance alone.
- The findings renew the debate over HBV DNA monitoring versus universal antiviral prophylaxis, especially in patients receiving prolonged or multidrug immunosuppressive therapy.
- Treatment decisions should consider the overall immunosuppressive burden rather than relying solely on individual drug-risk categories.
Clinical Impact:
This editorial reinforces current guideline recommendations while emphasizing that "low risk" should never be interpreted as "no risk." Careful HBV screening, individualized risk assessment, close monitoring, and timely antiviral prophylaxis remain essential for patients receiving immunosuppressive therapy.
Bottom Line:
HBV reactivation risk exists across the entire spectrum of immunosuppressive therapy. Rather than depending solely on static drug-based categories, clinicians should adopt a dynamic, patient-centered approach that accounts for cumulative immunosuppression and individual risk factors.