Published online May 21, 2021. doi: 10.3748/wjg.v27.i19.2312
Peer-review started: January 24, 2021
First decision: February 23, 2021
Revised: February 27, 2021
Accepted: April 22, 2021
Article in press: April 22, 2021
Published online: May 21, 2021
Hepatitis B virus reactivation (HBVr) can occur in patients treated with immunosuppressive medications. Risk stratification for HBVr based on hepatitis B virus (HBV) serology and viral load is an important strategy to determine appropriate HBV monitoring and antiviral prophylaxis use. Recent advances in the understanding of pathophysiology of autoimmune diseases have led the development of cytokine-targeted therapies. Tumor necrosis factor (TNF)-α inhibitors have been widely used for patients with inflammatory bowel disease, psoriasis, and rheumatic diseases. Further, the clinical benefits of interleukin (IL)-12/23, IL-17, or Janus kinases inhibitors have been demonstrated in these patients. It is well known that TNF-α inhibitor use can lead to HBVr, however, the risk of HBVr in patients undergoing non-TNF-targeted biologics have not been fully understood. In this review, we discuss the risk of HBVr in patients treated with non-TNF-targeted biologics, and immunological mechanisms of these medications causing HBVr.
Core Tip: Although the risk of hepatitis B virus reactivation (HBVr) in patients undergoing non-tumor necrosis factor (TNF)-targeted biologics have not been fully understood, some previous studies showed that the risk of HBVr in patients with non-TNF-targeted biologics might be higher than that in patients with TNF-α inhibitors. While patients with chronic hepatitis B virus (HBV) should receive antiviral prophylaxis when they start non-TNF-targeted biologics, antiviral prophylaxis may be a favorable strategy rather than the pre-emptive strategy in patients with resolved HBV. Large-scale studies are needed to ascertain the differential risk of HBVr between patients with TNF-α inhibitors and non-TNF-targeted biologics.