To evaluate the clinical efficacy and safety of the IL-1 inhibitor Firsekibart in gout patients with type 2 diabetes (T2D).

Three gout patients with T2D who experienced recurrent arthritis attacks despite prior conventional therapies, including urate-lowering therapy, colchicine, non-steroidal anti-inflammatory drugs, and corticosteroids, were enrolled. All patients received a single subcutaneous injection of Firsekibart 200 mg. Clinical indicators, specifically joint pain assessed by Visual Analogue Scale (VAS), and laboratory parameters including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum uric acid (UA), and fasting plasma glucose (FPG) were collected and compared at baseline and at one month after treatment. Treatment responses and adverse events were also recorded during follow-up.

Three patients with gout complicated by T2D were aged 75, 78, and 79 years. One month after Firsekibart treatment, the baseline joint pain VAS scores (5, 3, 3) decreased to 0 in all patients. Inflammatory markers were significantly reduced. Baseline ESR (76, 132, 86 mm/hr) decreased to 13, 15, and 22 mm/hr post-treatment, and baseline CRP (154.5, 201, 264.9 mg/L) decreased to 1.6, 1.1, and 0.4 mg/L post-treatment. Serum UA levels were effectively managed (baseline: 251.9, 647, 444 μmol/L; post-treatment: 273, 429.9, 320.1 μmol/L), with a notable decline in most cases. FPG levels also decreased substantially, from baseline values of 8.8, 11, and 13.9 mmol/L to 6.8, 6.47, and 6.41 mmol/L post-treatment. All patients achieved clinical remission at the last follow-up, and no adverse events were observed.

For gout patients with T2D who have an inadequate response to conventional anti-inflammatory, analgesic, and urate-lowering treatments, subcutaneous injection of Firsekibart 200 mg can significantly relieve joint pain and reduce systemic inflammatory markers. Moreover, Firsekibart may have a beneficial effect on glycemic control and demonstrates a favorable short-term safety profile. It may therefore represent a potential therapeutic option for refractory gout patients complicated with T2D.