P048 Cytomegalovirus retinitis in a patient with rheumatoid arthritis on tofacitinib

Abstract

Background/Aims Cytomegalovirus (CMV) retinitis is one of the most common opportunistic ocular infections and has traditionally been associated with immunocompromised individuals. We present a case of CMV retinitis following 3 months of treatment with tofacitinib in conjunction with methotrexate (MTX) for rheumatoid arthritis (RA) in an elderly lady with no other co-morbidities. Methods The case is presented below. Results 69-year-old lady with long standing seronegative, anti-cyclic citrullinated peptide negative, erosive RA since 2016. She was intolerant of sulphasalazine, leflunamide, methotrexate and etanercept. Hydroxychloroquine was avoided due to idiopathic cystoid macular oedema in the right eye with a baseline visual acuity of 6/18. Baseline fundus fluorescein angiogram (FFA) was negative for any vascular, inflammatory or occlusive disease. She was escalated to tofacitinib in August 2019. Approximately 3 months later, she noticed significantly reduced vision in her right eye from 6/18 down to 6/60. She had an FFA and Indocyanine Green Angiography, which showed quite extensive retinal ischaemia and vasculitis. Her bloods revealed a raised serum ACE and a T-spot test from 2018 was reactive followed by a repeat in 2019 which was equivocal. Tofacitinib was discontinued. She was commenced on rifampicin and isoniazid as 3 months prophylaxis for latent tuberculosis (LTBI). Additionally, she was started on oral prednisolone 60mg daily for presumed sarcoid related retinal vasculitis. She failed to improve despite a week’s treatment and subsequently had a vitreous aspirate which was strongly positive for CMV PCR. Her CMV viral load was 267copies/ml. The aspirate was negative for other infectious agents. She was commenced on valganciclovir for CMV retinitis. Unfortunately, her vision remained unchanged despite the viral load becoming undetectable a few weeks later. Despite having LTBI, there was no reactivation of this with her immunosuppressive therapy. Conclusion CMV retinitis is usually associated with immunocompromised individuals and is rarely encountered related to tofacitinib therapy for rheumatoid arthritis. Tofacitinib suppresses T cell function by inhibiting STAT signalling pathways, modulating T cell activation and cytokine production. Our case highlights the preferential development of CMV retinitis over active TB in the presence of LTBI, which is a recognised risk with the use of JAK kinase inhibitors. TB risk has been associated with genetic mutations in IL-12, IFN-γ and STAT1 pathways while CMV activation may be influenced by mutations in HLA ,Toll-like receptors, immunoglobulin light chain antibodies, IFN lambda region as well as alternative transcripts of the CMV viral major immediate early genes. Disclosure K. Beharry: None. S. Kaur: None. E. Papagiannuli: None. S. Moses: None. D. De Lord: None.