- Indian Rheumatology association
The world of Rheumatology has been on an active lookout for drug withdrawal opportunities in rheumatic diseases. Our Norwegian peers have spearheaded this effort in true Viking fashion, with results of the 3-year follow-up to their DMARD tapering ARCTIC-REWIND study.
A total of 160 RA patients in sustained remission for 1 year were included in this open-label, non-inferiority study, and randomized to receive stable csDMARDs, half-dose csDMARDs, or half-dose csDMARDs followed by drug withdrawal.
A greater proportion of patients remained flare-free over 3 years in the stable dose group (80% vs 57% vs 38%, p=0.01), and non-inferiority for withdrawal was not achieved. However, over 90% of patients in each group were in DAS-28 remission at 36 months, underlining that remission was easily achieved following a flare. The cumulative radiographic damage over 3 years was significantly lesser in the stable dose group (vs half-dose), and treatment intensification using bDMARDs was numerically higher in the withdrawal group.
Overall, the attractive concept of truly “drug-free” remission was verified in almost 40% of patients, and return to a remission status following flares was demonstrated for the rest. The crux of the matter remains that disease monitoring is of vital importance during drug tapering, and complete withdrawal of DMARDs cannot yet be justified in RA.
The enigma, “Axial Spondyloarthritis,” (AxSpA) has continued to be a bone of contention among rheumatologists on one prominent issue: can we stop radiographic progression? While terms like radiographic and non-radiographic seem to be part of a continuum, the patient perspective is clear- any drug that will prevent bone fusion is a good drug.
In the era of biologic DMARDs, the GESPIC cohort has recently provided a refreshing insight into the role of NSAIDs in retarding radiographic progression over a 10-year follow-up. This prompted the CONSUL trial, an open-label multicenter RCT comparing Golimumab (GOL) monotherapy to a combination of GOL and Celecoxib (GOL + CEL) over 108 weeks, in patients of AxSpA having baseline risk of progression.
Comparing GOL monotherapy to the combination revealed a non-significant mean mSASSS change difference of 1.7 vs 1.1 (p=0.79), and new syndesmophyte formation (25% vs 11%, p=0.12). Clinical outcomes (BASDAI and ASDAS: mean changes) were similar, and there were no differences in adverse events between the two treatment groups.
These numerical differences in progression, though present, were not significant enough to justify continuous treatment with NSAIDs in a patient already receiving a biologic DMARD for AxSpA. An advantage was the selection of patients for the study based on prior good responses to TNFi therapy, thus providing a semblance of homogeneity in the study population. Practically, these results support the addition of NSAIDs to bDMARDs only in cases where there is inadequate response to the bDMARD, and do not routinely advocate combination therapy for all.
