Firsekibart enables complete steroid withdrawal in 53-year-old with refractory tophaceous gout.

Managing refractory gout is challenging, especially when patients develop glucocorticoid dependence, leading to a cycle of recurrent flares upon steroid tapering. Current standard-of-care often falls short in breaking this cycle, leaving patients vulnerable to long-term steroid side effects. The interleukin-1β (IL-1β) pathway is a key driver of inflammation in gout, making anti-IL-1β agents a promising therapeutic strategy to control flares and potentially facilitate steroid withdrawal.

This case report describes a 53-year-old male with severe tophaceous gout and established glucocorticoid dependence. Despite ongoing urate-lowering therapy (ULT), he experienced frequent gout flares when attempting to reduce methylprednisolone below 16 mg/day. After conventional anti-inflammatory agents proved inadequate, the patient received a single 200-mg subcutaneous dose of firsekibart (an anti-IL-1β monoclonal antibody). The primary endpoint was the cessation of gout flares and the ability to successfully taper and discontinue glucocorticoids.

Following the single intervention, gout flares ceased immediately. This allowed for a successful glucocorticoid taper and complete discontinuation over the subsequent two months. Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate, normalized. Renal function stabilized, and serum urate levels, which were previously elevated despite ULT, also decreased. The patient maintained a flare-free state throughout the follow-up period. This outcome highlights firsekibart's potent anti-inflammatory effects.

A single 200-mg subcutaneous dose of firsekibart led to immediate cessation of gout flares, enabling complete glucocorticoid discontinuation over two months.