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Background/Aims Hepatitis E virus [HEV] is the most common cause of acute hepatitis in developing countries but rare in the industrialised world. In the vast majority it causes an acute self-limiting infection which is often asymptomatic. It is usually detected due to raised transaminases in liver function tests [LFTs] which are checked as part of DMARD monitoring. There is increasing literature that immunocompromised patients with human immunodeficiency virus or transplant recipients are at risk of developing chronic HEV infection, which can progress to liver failure. It is unclear that immunosuppressed patients who have a rheumatological conditions have similar issues, which we have looked into locally. Chronic infection is defined as having detectable RNA for over 3 months. Methods Retrospective review of patients attending rheumatology outpatient clinic for blood monitoring, who had positive Hepatitis E serology between 2010 and 2021. Results We identified nine patients attending the rheumatology clinic in Sheffield, confirmed as having acute infection with HEV as Hep E IgM antibody was positive. They were all on immunosuppression and hence having regular monitoring bloods and were receiving either prednisolone, DMARDS or biologics or in combination. There were five males and four females, with an age range of 38 to 71 years. Eight patients had acutely abnormal LFTs with a peak ALT [normal &amp;lt;41 IU/L] ranging from 59 to 1651 while in one the LFTs remained normal. Eight out of nine patient's LFTs recovered to baseline over a period ranging from 3 to 6 weeks (one moved out of area). Five patients had HEV RNA tested after the positive IgM. Two patients had HEV RNA detected initially, the rest had undetectable RNAs. Repeat RNA testing 2 months later was undetectable in both patients, suggesting no chronic HEV infection in all patients. No patients were given HEV antiviral treatment. Almost all patients had their immunosuppressant treatment paused, which was recommenced once their LFTs normalised. In all patients LFTs have remained normal even after 5 years with no evidence of reactivation in spite of ongoing immunosuppression. We plan to check HEV RNA if the LFTs were to become abnormal. Conclusion Our case series raises awareness that rheumatologists should consider HEV as a differential in patients with a marked unexpected rise in transaminases. We observed that all our patients cleared HEV infection and there was no evidence of chronicity even with ongoing immunosuppression, which is different from Hepatitis B &amp; C. We recommend that immunosuppressant treatment should be stopped initially following HEV infection and reintroduced once LFTs have normalised and HEV RNA is undetectable. Disclosure C.A. Zollinger-Read: None. M. Raza: None. M.F. Kazmi: None.

P146 Hepatitis E infection in rheumatic disease: no evidence of chronicity