Inflammatory bowel disease (IBD), an umbrella term for Crohn’s disease and ulcerative colitis, is becoming an increasingly significant public-health challenge worldwide. The burden is rising particularly rapidly in developing countries, including China, where changes in diet, urbanization, environmental exposures and improved diagnosis are contributing to a growing number of cases. For patients with moderate to severe IBD, biologic medicines have transformed treatment by suppressing the immune pathways that drive chronic intestinal inflammation. Among the most widely used of these medicines is infliximab, an antibody that blocks tumor necrosis factor-alpha (TNF-α), a central inflammatory signaling molecule.
By inhibiting TNF-α, infliximab can reduce intestinal inflammation, promote mucosal healing and limit patients’ dependence on corticosteroids. In many cases, treatment also lowers the likelihood of hospitalization and surgery. However, TNF-α has important functions in host defense, particularly in the control of intracellular pathogens and the maintenance of immune surveillance. Suppressing this pathway can therefore create an opportunity for otherwise controlled infections to re-emerge. One of the most serious concerns is hepatitis B virus (HBV) reactivation, a complication that can cause severe hepatitis, liver failure and, in extreme cases, death.
HBV reactivation occurs when viral replication resumes or increases in a person whose infection was previously controlled. It may affect people with persistent infection, identified by the presence of hepatitis B surface antigen (HBsAg), as well as individuals with resolved or occult infection. Patients who are HBsAg-negative but anti-hepatitis B core antibody-positive may retain HBV genetic material in liver cells even after apparently clearing the infection. Under normal immune conditions, viral replication remains suppressed. Immunosuppressive treatment can weaken this control, allowing HBV DNA levels to rise before liver injury becomes clinically apparent.
The risk of reactivation is well established in some immunosuppressed populations, particularly patients receiving intensive chemotherapy or B-cell-depleting therapies such as rituximab. Less certain has been the scale of the problem among people with IBD treated with TNF-α inhibitors. This question is especially important in China, which has intermediate HBV endemicity and an estimated 70 million chronic carriers. In this setting, a substantial number of patients beginning biologic treatment may have chronic HBV infection, previous exposure or no knowledge of their infection status.
A nationwide real-world study has examined HBV infection, reactivation and HBV-associated liver dysfunction among Chinese patients with IBD receiving infliximab. The investigation drew on patients from multiple centers across the country, aiming to reflect routine clinical practice rather than the highly selected conditions of a controlled clinical trial. Before infliximab treatment began, patients underwent HBV screening, and those receiving therapy were monitored through measurements of HBV DNA and liver-function indicators. This approach enabled researchers to evaluate viral behavior alongside the clinical course of intestinal disease and the immunosuppressive treatments used.
The study quantified the occurrence of HBV reactivation in this treatment population and examined factors that may influence individual risk. Baseline HBV serology was a central consideration, distinguishing patients with active or chronic infection from those with evidence of previous exposure. The analysis also considered concurrent immunosuppression and the activity of IBD, both of which may alter the balance between viral replication and immune control. These factors are clinically relevant because infliximab is often used alongside corticosteroids, immunomodulators or other therapies that can intensify overall immune suppression.
The investigators also characterized liver dysfunction linked to HBV in patients receiving infliximab. HBV-related injury is not caused simply by the presence of viral DNA; it commonly reflects an immune response against infected liver cells after viral replication has accelerated. As a result, alanine aminotransferase and other liver enzymes may rise during or after reactivation, sometimes progressing to jaundice, impaired hepatic function or acute liver failure. Regular laboratory surveillance can identify these changes earlier, although monitoring is most effective when it is paired with timely HBV DNA testing and a clear plan for antiviral intervention.
The findings support universal HBV screening before biologic therapy is initiated in patients with IBD. Screening generally involves HBsAg, antibodies to hepatitis B surface antigen and anti-HBc, with HBV DNA testing used to clarify infection and replication status when indicated. Patients who are HBsAg-positive should be assessed for antiviral prophylaxis or treatment before immunosuppression begins. For patients with resolved infection, the appropriate strategy may depend on viral DNA status, the intensity and duration of immunosuppression, and the feasibility of close laboratory follow-up. Preventive antiviral therapy or pre-emptive treatment can reduce the likelihood that silent viral persistence will develop into clinically significant hepatitis.
The study further emphasizes that HBV safety cannot be managed by gastroenterologists alone. Coordinated care involving hepatologists, infectious-disease specialists and primary clinicians can help ensure that serological results are interpreted correctly, antiviral medicines are started when necessary and monitoring continues throughout and after infliximab treatment. Patients should also be informed that reactivation may occur even when they have no symptoms initially, and should be instructed to report jaundice, dark urine, severe fatigue, nausea or abdominal discomfort. As biologic treatment expands across China and other regions where HBV remains common, integrating viral screening and surveillance into IBD care will be essential for preserving the benefits of immune-targeted therapy while limiting preventable liver complications.
Article Title: Hepatitis B virus infection or reactivation and HBV-related liver dysfunction in patients with inflammatory bowel disease receiving infliximab: a nationwide real-world study
Web References: https://doi.org/10.1007/s11684-026-1208-0
Image Credits: Higher Education Press
Keywords: Hepatitis B virus, HBV reactivation, inflammatory bowel disease, Crohn’s disease, ulcerative colitis, infliximab, TNF-α inhibitors, biologic therapy, liver dysfunction, antiviral prophylaxis
Tags: Global trends in IBD and hepatitis BHepatitis B reactivation risk during infliximab therapyImpact of biologic therapies on liver healthInflammatory bowel disease treatment challengesLiver dysfunction in IBD patients on biologicsLiver-related adverse events in biologic therapyManaging infection risks in immunosuppressive treatmentsNationwide study on hepatitis B and infliximSafety concerns with infliximab in hepatitis B carriersTNF-alpha inhibitors and infection re-emergence
