Tofacitinib in Polymyalgia Rheumatica (EAST PMR Study) Save

An open-label, uncontrolled pilot trial has shown that JAK signaling is involved in the pathogenesis of PMR and that tofacitinib is as effective as glucocorticoids (GC) in patients with polymyalgia rheumatica (PMR).

A single center study from China recruited treatment-naïve PMR patients (September 2020 to September 2022). In the first cohort, they studied gene expression patterns in the peripheral blood mononuclear cells (PBMCs) of 11 PMR patients compared to 20 healthy controls. The found increased expression of IL6R, IL1B, IL1R1, JAK2, TLR2, TLR4, TLR8, CCR1, CR1, S100A8, S100A12, and IL17RA. Moreover, in vitro tofacitinib suppressed the IL-6R and JAK2 expression of CD4+T cells from PMR patients. 

A second cohort of 76 PMR patients were randomized to be treated with either tofacitinib (39) or glucocorticoids (37) for 24 weeks. The primary endpoint was the number of patients with PMR-AS ≤10 at weeks 12 and 24. Only 67 PMR patients completed the 24-week intervention.

There were no statistically significant between group differences in primary or secondary outcomes at weeks 12 and 24; with all patients achieving a PMR-AS <10.  Significant decreases in PMR-AS, CRP, and ESR were also seen.

These data suggest the potential utility of tofacitinib in treating PMR and merits a larger, blinded, randomized clinical trial.