Patients with IBD, rheumatoid arthritis, and psoriasis are commonly treated using biologic agents such as infliximab, tofacitinib, and ustekinumab.
While there is concern over hepatitis B virus (HBV) reactivation in patients exposed to biologics, new research shows reactivation is not common.
A team, led by Ilkay Ergenc, Marmara University School of Medicine, assessed the reactivation rate in biologic exposed patients within surface antigen negative phase of HBV infections.
The data was presented during the 16th Congress of European Crohn's and Colitis Organisation (ECCO).
Biologics have become a prominent treatment for immune mediated inflammatory diseases in recent years. However, despite the prevalence in use, there is an unknown risk for hepatitis B reactivation in hepatitis B surface antigen (HBsAg) negative phase of HBV exposed patients.
The researchers examined 8266 patients who were followed up with at gastroenterology, rheumatology, and dermatology out-patient clinics with a diagnosis of IMID from clinical charts, 2484 of which were exposed to biologic agents with a negative HBsAg and positive Anti-HBc IgG. Of this group, 221 patients were included in the final analysis with a mean age of 54.08 ± 11.69 years old.
The most common diagnosis that led to biologic exposure include psoriasis (n = 57; 25.8%), rheumatoid arthritis (n = 55; 24.9%), and spondylarthritis (n = 76; 34.4%). Less than 10% of the patients were diagnosed with inflammatory bowel disease, Bechet’s disease, Takayasu arteritis, Still disease, and temporal arteritis.
More than 10% of patients were exposed to infliximab, adalimumab, and etanercept, while less than 10% were exposed to certolizumab, golimumab, ustekinumab, secukinumab, abatacept, ixekizumab, tocilizumab, and tofacitinib.
The investigators sought primary outcomes of HBV reactivation, defined as reverse seroconversion of HBsAg.
The median amount of different biologic subtype use was 1 and the mean biologic agent exposure time was 55 months.
In addition there were 152 (68.8%) patients using concomitant immunomodulatory agents and 84 (38.0%) participants exposed to corticosteroids during biologic use.
The results were positive as for the entire cohort there was no hepatitis B reactivation with a reverse seroconversion of HBsAg positivity.
In addition, antiviral hepatitis B prophylaxis was given to 48 (21.7%) participants with entecavir, tenofovir, or lamivudine.
Prior to biologic exposure, HBV-DNA was screened in 56 (25.3%) patients and 2 patients had HBV-DNA reactivation with a negative HBsAg during exposure to the biologic agent.
“Though only 21.7% of our patients used prophylaxis, we found only two reactivations (1%) and no HBsAg seroconversion in our cohort,” the authors wrote. “Our results suggest a re-assessment of antiviral prophylaxis for anti-HBc Ag (+) patients exposed to biologic agents. Current guidelines would be updated in the light of future studies.”
In a separate study presented at ECCO, researchers found biologics do not lead to an increased risk of HBV flares when compared to steroids and thiopurines for IBD patients.
The use of thiopurine (aHR, 2.56; 95% CI, 1.54-4.26; P <0.001) and ever being exposed to steroids (aHR, 2.73; 95% CI, 1.30-5.72; P = 0.008) were identified risk factors for hepatitis flare after adjustment of baseline ALT level.
On the other hand, the use of biological therapy was not linked to an increase risk of hepatitis flare (aHR, 1.79; 95% CI, 0.79-3.99; P = 0.14). Exposure to steroids was associated with an increased risk of hepatitis flare regardless of the peak dose (<20mg prednisolone daily, 20-40mg daily, or >40mg daily) [aHR, 2.34–4.18].
Finally, 15 patients (4.1%) developed severe icteric hepatitis flare (ALT > 120U/L and bilirubin >38 mmol/L) and the cumulative incidence of severe icteric hepatitis flare were 2.7%, 7.2% and 8.4% at 12 months, 36 months, and 60 months respectively.
The study, “Hepatitis B reactivation under biologic therapy in patients with HBsAg negative phase of chronic HBV infection,” was published online by the European Crohn’s & Colitis Organisation.