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* = Presenting author

P338 Serologic profile and reactivation of Hepatitis B in rheumatic and Inflammatory Bowel Disease patients treated with TNF inhibitors bowel disease

S. Vitor1, L. Meireles1, V. Romão2, C. Freitas1, S. Fernandes*, M.J. Gonçalves2, L. Correia1, M.J. Savedra2, H. Canhão2, J. Fonseca2, J.A. Pereira da Silva2, J. Velosa1

1Hospital Santa Maria, Gastroenterology and Hepatology, Lisbon, Portugal, 2Hospital Santa Maria, Rheumatology, Lisbon, Portugal

Background

TNF inhibitors (TNFi) are widely used in rheumatologic diseases (RD) and inflammatory bowel disease (IBD). However, these drugs have been associated with an increased risk of reactivation of latent infections. The specific risk of hepatitis B (HB) reactivation remains unclear since the low incidence of that infection in the majority of European countries. Our study aims to evaluate the serologic HB profile of patients with RD and IBD who had undergone TNFi therapy in a single centre; and to assess the incidence of HB reactivation in patients with a serological pattern of past HB infection.

Methods

Retrospective study of HB baseline serologic profile in patients with IBD and RD who have started TNFi therapy at our institution. Clinical signs of liver injury and liver injury blood tests were analysed during the treatment in order to identify cases with reactivation. Reactivation was defined as the detection of AgHBs or DNA-VHB.

Results

We analyzed 484 patients with available data on HB serologic profile, 210 men (43.4%) with a mean age of onset of biological therapy of 38 ± 15 years. 258 patients were diagnosed with RD (100 rheumatoid arthritis, 76 ankylosing spondylitis and 82 other RD); 226 patients suffered from IBD (180 Crohn's disease, 41 ulcerative colitis and 5 indeterminate colitis); 273 patients were simultaneously submitted to immunosuppressive treatment with azathioprine, 6-mercaptopurine, corticosteroids or methotrexate, for at least 1 month. At the beginning of the treatment, the HB serologic profile variations were: negative in 63.4%, 31.0% AbHBs+/AbHBc- and 5.8% AbHBc+ (with or without AbHBs+). The 28 AbHBc+ patients did not differ significantly from the overall population in terms of demographic characteristics, diagnosis, follow-up interval and biological therapy. No patient received prophylactic antiviral therapy during the follow-up period (median 8 years and 80 days) and there was only one case of HB reactivation, a Crohn's disease patient treated with infliximab and azathioprine.

Conclusion

In our cohort, there was one case of HB reactivation, corresponding to 3.5% of AbHBc+ patients treated with TNFi. This study highlights the importance of assessing HB serologic profile at the beginning of immunosuppressive therapy. This strategy allows not only the vaccination of serologic negative patients but also the identification of patients at risk of HB reactivation.