Author Of 1 Presentation
P0249 - Demyelinating events following initiation of anti-TNFɑ therapy in the British Society for Rheumatology Biologics Registry in Rheumatoid Arthritis (ID 1695)
Abstract
Background
Anti-tumour necrosis factor-ɑ (anti-TNFɑ) monoclonal antibodies are used to treat a number of autoimmune diseases. They have been associated with de novo central nervous system (CNS) demyelination and increased relapse rate in MS. The British Society for Rheumatology Biologics Register in Rheumatoid Arthritis (BSRBR-RA) is a large, prospective pharmacovigilance study which aims to monitor the safety of anti-TNFɑ.
Objectives
To establish the clinical characteristics, timing and incidence of demyelination in patients who have received anti-TNFɑ therapy.
Methods
BSRBR-RA data were used to identify adverse events reported in patients receiving anti-TNFɑ therapies. MedDRA codes and associated verbatim reports were searched for terms related to CNS demyelination. Patients with no reported demyelination prior to BSRBR-RA entry with at least one completed follow-up form were included. Demyelinating events were classified as definite, probable or possible based on available clinical information, with reference to MacDonald 2017 criteria. Crude rates of demyelination were calculated. Exploratory analyses calculated standardised incidence rates (SIRs) compared to the English population (HES/GPRD data; Mackenzie 2014) in the whole cohort and limited to those with definite/probable demyelination.
Results
38 individuals with demyelinating events were identified from a total pool of 12,980. Median age at study entry was 47 years and median disease duration 8 years; 69% were female. Median age at demyelinating event was 51. Events occurred a median of 3 (IQR 1-5) years from start of first anti-TNF therapy; 27 (71%) occurred within 5 years. Kaplan Meir plots indicated a steady event rate. 28 events occurred in individuals still taking anti-TNFɑ therapy; of the other 10, 6 were within 90 days of drug withdrawal. The crude incidence of demyelination was 21.4/100,000 patient years (95%CI 15.1-29.4). SIR in the whole population was 1.50 (95%CI 1.06-2.05) and 0.91 (0.57-1.36) when limited to definite/probable cases. Males showed a higher point estimate than females in both analyses.
Conclusions
Patients receiving biological therapy for the treatment of RA show a marginally increased SIR; this signal is lost when restricting to those with probable or definite demyelination. The BSRBR-RA provides a robust resource for pharmacovigilance. Patients concerned about demyelination associated with anti-TNFɑ can be relatively reassured that new development of demyelination is unlikely.