Abstract
Background
The management of acute gout flares in elderly patients with multiple comorbidities remains a significant clinical challenge. Although interleukin-1β (IL-1β) inhibitors are recommended for refractory gout when conventional therapies are unsuitable, evidence remains limited regarding their use in patients with active malignancy and moderate-to-severe renal impairment. This case addresses the knowledge gap in balancing potent anti-inflammatory therapy with complex oncological and renal risks.
Case Description
We report a case of a 73-year-old male patient with refractory gout, a disease duration exceeding 20 years, and extensive tophus formation. The patient was concomitantly diagnosed with acinar adenocarcinoma of the prostate, stage 3 chronic kidney disease (CKD), coronary artery disease, and grade 3 hypertension. Due to recurrent acute gout flares, impaired renal function, and a high risk of bleeding, standard anti-inflammatory therapeutic options were contraindicated. After a comprehensive assessment of the potential risks and benefits, treatment was initiated with firsekibart, a novel fully human monoclonal antibody targeting IL-1β, administered as a single 200 mg subcutaneous injection, in combination with a short course of low-dose glucocorticoids. Urate-lowering therapy with febuxostat was subsequently introduced. Marked relief of joint pain and swelling was observed within 24 hours of treatment. During the 3-month follow-up period, inflammatory markers improved substantially, with high-sensitivity C-reactive protein decreasing from 62.36 to 0.9 mg/L. Target serum urate levels were achieved (444.9 µmol/L), and renal function showed improvement, as evidenced by an increase in the estimated glomerular filtration rate from 36.4 to 44.9 mL/min/1.73 m2. No evidence of tumor progression, serious infections, or major cardiovascular adverse events was observed in the follow-up period.
Conclusions
This case suggests that firsekibart may provide rapid and effective inflammation control in high-risk gout populations where standard treatments are limited. These findings highlight the potential of IL-1β targeted therapy as a precision medicine approach for complex patients; however, larger prospective studies are required to validate the long-term oncological and renal safety profile of firsekibart in this population.
Keywords: Gout, firsekibart, interleukin-1β (IL-1β), prostate cancer, case report
Highlight box.
Key findings
• This case highlights the effective use of firsekibart, an anti-interleukin-1β (IL-1β) monoclonal antibody, in the treatment of acute gout flares in an elderly patient with multiple comorbidities, including prostate cancer, stage 3 chronic kidney disease, and cardiovascular disease. The patient showed rapid improvement in joint pain, inflammatory markers, and renal function with no significant adverse events.
What is known, and what is new?
• Gout in elderly patients with comorbidities poses therapeutic challenges, as non-steroidal anti-inflammatory drugs and glucocorticoids are associated with significant risks. IL-1β inhibitors have been shown to be effective in the management of acute gout when traditional therapies are not suitable.
• This case provides real-world evidence of the efficacy of firsekibart in an elderly, high-risk patient, demonstrating rapid symptom relief and improvement in both inflammatory and renal markers.
What is the implication, and what should change now?
• Firsekibart may represent a viable treatment option for gout in elderly patients with comorbidities, in whom conventional treatments are contraindicated. Further studies and clinical trials are needed to validate its long-term safety and efficacy in similar patient populations. Clinicians should consider targeted therapies such as firsekibart in the management of complex gout cases.
Introduction
Gout in elderly patients is frequently characterized by a high tophaceous burden and a cluster of complex comorbidities, including chronic kidney disease (CKD), cardiovascular disease (CVD), and malignancies (1-3). These concurrent conditions create a therapeutic bottleneck, as first-line anti-inflammatory agents—such as non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine—are often strictly contraindicated in patients with renal insufficiency or high bleeding risks (4,5). Although glucocorticoids may provide rapid symptom relief, their prolonged or high-dose administration has been associated with fluctuations in blood glucose and blood pressure, as well as an increased risk of infection, thereby restricting their use in patients with concomitant diabetes or hypertension (6,7). Consequently, identifying therapeutic strategies that can achieve rapid anti-inflammatory effects while maintaining an acceptable safety profile remains a major clinical challenge in the management of refractory gout complicated by multiple comorbidities.
Evidence suggests that NLRP3 inflammasome activation and the subsequent release of interleukin-1β (IL-1β) are central mechanisms driving the inflammatory cascade in acute gout attacks (8,9). Based on this pathophysiological rationale, both the Chinese Guidelines for the Diagnosis and Management of Hyperuricemia and Gout (2024 update) (10) and the American College of Rheumatology (ACR) guidelines (11) recommend IL-1β inhibitors for patients in whom conventional therapies are ineffective or contraindicated.
Firsekibart is a novel fully human monoclonal antibody targeting IL-1β that was independently developed in China. Previous clinical studies have demonstrated its pronounced anti-inflammatory efficacy in the treatment of acute gout flares (12,13). Nevertheless, real-world clinical experience with firsekibart in patients presenting with complex conditions, such as concomitant malignancy and renal dysfunction, remains limited.
The decision to use biological targeted therapy in the context of active cancer is particularly complex. While some evidence suggests that IL-1β inhibition might modulate cancer-related inflammation, its clinical impact on the tumor microenvironment and potential interactions with ongoing oncological treatments require careful observation (14,15). Furthermore, the tolerability and clinical response of such agents in patients with stage 3 CKD remain insufficiently documented in clinical practice.
This report describes a 73-year-old male patient with tophaceous gout complicated by prostate cancer, stage 3 CKD, and severe CVD. Treatment with firsekibart was followed by rapid alleviation of articular symptoms, normalization of inflammatory markers, and improvement in renal function, thereby providing valuable insights into the multidisciplinary management of such high-risk gout patients under complex clinical constraints. We present this article in accordance with the CARE reporting checklist (available at https://tau.amegroups.com/article/view/10.21037/tau-2026-0406/rc).
Case presentation
Patient information
A 73-year-old male with a history of gout exceeding 20 years was admitted to The First Affiliated Hospital of Jinan University on July 23, 2025, due to an acute flare of bilateral knee pain that had worsened over the preceding 4 days. His gout had been diagnosed over two decades ago, initially affecting the first metatarsophalangeal joint, ankles, and both knees. Despite intermittent treatment with NSAIDs and colchicine, the disease was poorly controlled, and acute flares remained frequent. One year prior, the patient was prescribed febuxostat, but his serum uric acid level fluctuated around 440 µmol/L. The current flare had begun 4 days earlier, without a specific trigger, leading to severe bilateral knee pain, restricted joint movement, and hospitalization for management. The patient had no history of recent vaccination, including the recombinant zoster vaccine, which has been identified as a potential trigger for NLRP3-mediated gout flares in elderly populations.
The patient’s past medical history included: (I) malignancy: acinar adenocarcinoma of the prostate diagnosed 1 year earlier; (II) renal disease: stage 3 CKD diagnosed 1 year earlier, following an episode of acute pyelonephritis, associated with elevated serum creatinine and right renal calculi; (III) CVD: grade 3 hypertension, coronary artery disease, and a history of cerebral infarction, all diagnosed more than 10 years earlier; and (IV) metabolic: type 2 diabetes mellitus and hyperlipidemia.
Clinical findings
The patient was stable at admission, with a body mass index of 23.8 kg/m2. Musculoskeletal examination revealed bilateral knee swelling, increased local skin temperature, and palpable tophi around both wrists, knees, and ankles, along with osteophyte formation at the distal interphalangeal joints of both hands. Laboratory tests showed markedly elevated inflammatory markers, including high-sensitivity C-reactive protein (hsCRP) of 62.36 mg/L (reference: 0–10 mg/L) and an erythrocyte sedimentation rate of 82 mm/h (reference: 0–15 mm/h). To evaluate the physiological and immune context prior to biological therapy, baseline nutritional and immune status were assessed. The patient’s serum albumin (ALB) was 34.6 g/L (reference: 40–55 g/L), total protein (TP) was 70.2 g/L (reference: 65–85 g/L), and globulin (GLB) was 35.60 g/L (reference: 20–40 g/L); the mild hypoalbuminemia was consistent with his chronic inflammatory state and concurrent CKD. His baseline immune profile showed a white blood cell (WBC) count of 7.99×109/L, with an absolute neutrophil count (ANC) of 4.81×109/L [reference: (1.8–6.3)×109/L] and absolute lymphocyte count (ALC) of 1.81×109/L [reference: (1.1–3.2)×109/L]. The monocyte count was 0.85×109/L. These results indicated a stable baseline immune function, providing a safety basis for the administration of the IL-1β inhibitor while on enzalutamide therapy.
Renal function was compromised, as reflected by a serum creatinine level of 159.5 µmol/L (reference: 57–111 µmol/L) and an estimated glomerular filtration rate (eGFR) of 36.4 mL/min/1.73 m2 (reference: 80–120 mL/min/1.73 m2). Serum uric acid was elevated at 484.0 µmol/L (reference: 208–428 µmol/L), and the patient exhibited mild anemia, with a hemoglobin level of 97.0 g/L (reference: 130–175 g/L). Imaging studies revealed bilateral knee joint effusion and synovial hyperplasia on ultrasound, along with tophus formation and bone erosions. X-ray examinations showed gouty arthritic changes, including nodular high-density shadows around the knees and right wrist.
Differential diagnosis
Given the markedly elevated inflammatory markers (hsCRP >60 mg/L) and previous history of pyelonephritis, a thorough differential diagnosis was performed to rule out septic arthritis and pseudogout [calcium pyrophosphate deposition (CPPD)] (1). Exclusion of pseudogout: The patient had a chronic disease course exceeding 20 years with recurrent polyarticular flares and multiple palpable tophi. Bilateral knee X-rays revealed no evidence of chondrocalcinosis. Furthermore, multi-site joint ultrasonography showed characteristic hyperechoic masses and the pathognomonic “double-contour sign” (hyperechoic enhancement on the hyaline cartilage surface), which are specific to monosodium urate crystal deposition and distinguish it from the fibrocartilage calcification seen in CPPD (2). Exclusion of septic arthritis: septic arthritis typically presents with acute monoarticular redness, swelling, heat, and pain, often accompanied by fever and marked elevation of peripheral blood leukocytes. This patient had chronic polyarticular disease, with baseline complete blood count showing normal WBC and absolute neutrophil counts, no fever or signs of systemic infection. Considering the patient’s advanced age, comorbid CKD and prostate cancer, invasive joint aspiration would have increased the risk of infection and bleeding as well as physical burden. Given the typical history of gout, documented hyperuricemia, characteristic imaging findings, and presence of tophi, the clinical diagnosis of gout was clear; therefore, joint fluid aspiration and polarized light microscopy were not performed.
Diagnosis
Based on these findings, the patient was diagnosed with gouty arthritis with an acute flare and multiple tophi, along with acinar adenocarcinoma of the prostate, stage 3 CKD, hypertension, type 2 diabetes, coronary atherosclerotic heart disease, and hyperlipidemia.
Therapeutic intervention
Given the patient’s advanced age, stage 3 CKD, and multiple comorbidities, NSAIDs were contraindicated, and long-term glucocorticoid therapy posed a significant risk. To break the cycle of pain, inflammation, and renal injury, an individualized treatment regimen was developed. For anti-inflammatory and analgesic therapy, a single subcutaneous injection of firsekibart (200 mg), a novel anti-IL-1β monoclonal antibody, was administered, in accordance with the Chinese Guidelines for the Diagnosis and Management of Hyperuricemia and Gout (2024 update) and the 2020 ACR Guideline. This was complemented by a targeted 2-day bridge of oral low-dose triamcinolone (16 mg/day for 2 days) to manage the acute pain while transitioning to biological therapy, followed by firsekibart monotherapy for ongoing inflammation control.
Following the resolution of the acute flare, urate-lowering therapy was initiated with a slow titration of febuxostat, targeting a stable serum urate level of <300 µmol/L within 6 to 12 months to facilitate the dissolution of existing tophi. To support renal function, uremic clearance granules and compound α-keto acid tablets were added to reduce the renal burden. For comorbidity management, anti-tumor therapy with enzalutamide was continued, while aspirin was replaced with clopidogrel hydrogen sulfate to balance the cardiovascular benefits and bleeding risks. Additionally, atorvastatin and controlled-release nifedipine were maintained to manage the cardiovascular risks.
Outcome and follow-up
One day after firsekibart administration, marked improvement in bilateral knee pain, swelling, erythema, and warmth was observed. The patient’s general condition remained stable, and no treatment-related adverse events were reported.
At the 1-month follow-up (Figure 1), significant resolution of knee joint swelling and normalization of local skin temperature were documented. At the 3-month follow-up (Figure 2), with the patient on febuxostat 40 mg/day, hsCRP decreased from 62.36 to 0.9 mg/L, indicating effective suppression of systemic inflammation; serum creatinine decreased from 159.5 to 134.2 µmol/L; the eGFR increased from 36.4 to 44.9 mL/min/1.73 m2, suggesting renal functional improvement. The serum uric acid level decreased to 444.9 µmol/L at this stage. Since the urate target had not yet been achieved, the dosage of febuxostat was further up-titrated under close monitoring. By the 6-month follow-up, with febuxostat increased to 80 mg/day, the serum uric acid level decreased to 399 µmol/L. As the treat-to-target goal of <300 µmol/L for tophaceous gout remained unmet, the patient was advised to enhance lifestyle interventions and continue regular follow-up for further dose adjustment.
Figure 1.
Changes in joint manifestations before treatment (A) and 1 month after treatment (B), demonstrating significant improvement in joint swelling and local inflammatory signs.
Figure 2.
Changes in renal function, inflammatory markers, and serum uric acid levels before and after treatment. eGFR, estimated glomerular filtration rate; hsCRP, high-sensitivity C-reactive protein; SCr, serum creatinine.
All procedures performed in this study were in accordance with the ethical standards of The First Affiliated Hospital of Jinan University and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.
Discussion
The pathophysiological hallmark of acute gout flares is macrophage NLRP3 inflammasome activation by monosodium urate crystals, which promotes the maturation and release of IL-1β, thereby initiating and amplifying local and systemic inflammatory cascades (10,16). Unlike NSAIDs, which exert anti-inflammatory effects through cyclooxygenase inhibition, or colchicine, which disrupts microtubule polymerization, firsekibart is a novel fully human monoclonal antibody that directly neutralizes IL-1β, targeting a critical upstream mediator of the inflammatory response. Through this mechanism, sustained amplification of inflammatory signaling can be effectively suppressed at its source (17,18).
In the present case, markedly elevated inflammatory markers at admission (hsCRP >60 mg/L) indicated a severe inflammatory state. Rapid clinical improvement was observed within 24 hours following a single administration of firsekibart, suggesting its prompt onset of action in interrupting IL-1β-driven inflammatory cascades (19). The selection of the 200 mg dose, rather than a lower 100 mg dose, was based on evidence from Phase II/III clinical trials demonstrating that 200 mg provides more potent and sustained suppression of IL-1β-driven inflammatory cascades in patients with a high tophaceous burden (17-19). From a pharmacological perspective, as a fully human IgG monoclonal antibody, firsekibart is primarily cleared through intracellular proteolytic degradation rather than renal excretion (20). This ensures a stable pharmacokinetic profile in patients with moderate renal impairment, making dose adjustment unnecessary even with an eGFR of 36.4 mL/min/1.73 m2. Furthermore, a strategic sequential approach was implemented using a 2-day “bridge” of low-dose triamcinolone. This specific duration was designed to cover the pharmacokinetic window before firsekibart reaches peak plasma concentration (typically 3–5 days post-injection), ensuring immediate symptom control during the hyperacute phase. Unlike conventional prolonged steroid regimens, this ultra-short-term exposure was tailored to minimize systemic metabolic and infectious risks—such as glycemic fluctuations and blood pressure instability—which are critical considerations for elderly patients with concurrent malignancy, diabetes, and CKD (21). This “steroid-sparing” targeted strategy achieved rapid resolution of acute inflammation while maintaining long-term therapeutic stability without compromising the patient’s complex comorbidity profile.
A notable clinical observation in this case was the improvement in renal function, as evidenced by an increase in the eGFR from 36.4 to 44.9 mL/min/1.73 m2. Traditionally, gout-related renal impairment has been primarily attributed to mechanical injury resulting from urate crystal deposition in renal tubules, commonly referred to as gouty nephropathy. However, growing evidence has highlighted the crucial role of persistent low-grade or chronic inflammation in the initiation and progression of CKD (22,23). In the present case, given the contraindication to NSAIDs, insufficient control of joint inflammation would likely have led to the sustained elevation of proinflammatory mediators, including IL-1β and IL-6. These cytokines have been shown to contribute to endothelial dysfunction and promote renal interstitial fibrosis, thereby accelerating renal function deterioration (24).
The observed renal recovery should be interpreted as a multifactorial clinical outcome. Beyond the direct alleviation of cytokine-mediated injury to glomerular and tubular structures by firsekibart, the rapid resolution of the systemic inflammatory “storm” (hsCRP >60 mg/L) likely had a profound impact on renal hemodynamics. The suppression of intense systemic inflammation can stabilize vascular tone and improve renal perfusion, which is often compromised during acute inflammatory responses. Furthermore, the therapeutic benefit was likely augmented by the synergistic effect of comprehensive supportive care. The concurrent administration of compound α-keto acid tablets provided critical metabolic support by reducing urea nitrogen production and alleviating the renal workload. Additionally, effective pain relief decreased the patient’s reliance on potentially nephrotoxic analgesic agents, while the controlled initiation of febuxostat facilitated improved interactions between uric acid metabolism and renal function. This combined approach incorporating targeted biological therapy and standardized renal support likely contributed to disrupting the vicious cycle characterized by declining renal function and progressive hyperuricemia, ultimately leading to improved renal outcomes.
When biologic agents are considered for patients with concomitant malignancies and CVDs, safety remains a central concern in clinical decision-making. Although prostate cancer was present in this patient, previous studies have demonstrated that IL-1β plays a role in promoting angiogenesis and mediating immunosuppressive processes in the tumor microenvironment (25). Exploratory analyses from several clinical investigations, most notably the CANTOS trial, have further suggested that IL-1β inhibition may be associated with reduced incidence of certain malignancies or decreased cancer-related mortality (26,27). However, the intersection of IL-1β inhibition and prostate cancer therapy involves complex mechanistic considerations. Emerging evidence suggests that IL-1β can act as a repressor of androgen receptor (AR) expression in prostate cancer cells (15); thus, neutralizing this cytokine could theoretically alleviate this repression and impact the efficacy of AR-targeted therapies like enzalutamide. In the present case, this potential risk was carefully balanced against the clinical necessity of controlling the patient’s severe refractory gout. Notably, the patient’s tumor status remained stable and no clinical evidence of tumor progression was observed throughout the follow-up period. These findings preliminarily indicate that firsekibart may exhibit an acceptable short-term safety profile in patients with solid tumors complicated by gout. Nevertheless, given the theoretical interplay between IL-1β and the AR axis, the long-term oncological outcomes of IL-1β-targeted therapy require validation through larger cohorts and extended follow-up.
In relation to cardiovascular safety, gout has been recognized as an independent risk factor for cardiovascular events, while chronic low-grade inflammation has been identified as a key contributor to the development and progression of atherosclerosis. The targeted inhibition of the IL-1β pathway by firsekibart enables the rapid suppression of systemic inflammatory activity, which may theoretically contribute to improvements in endothelial function and reductions in residual inflammatory cardiovascular risk. In the present case, the patient’s blood pressure and lipid profiles remained stable throughout the follow-up period, and no new cardiovascular or cerebrovascular events occurred, thereby providing clinical support for the feasibility of this therapeutic approach in individuals with high cardiovascular risk (28).
Conclusions
This case illustrates a favorable clinical response and promising tolerability of firsekibart in a 73-year-old patient with refractory tophaceous gout complicated by active prostate cancer and CKD. Beyond the rapid alleviation of articular symptoms, targeted anti-inflammatory therapy was associated with an improvement in renal function, highlighting its potential role in the precision-based management of complex gout. These findings suggest that firsekibart may represent a promising therapeutic option within a multidisciplinary framework for high-risk gout populations with limited conventional treatment options.
Supplementary
The article’s supplementary files as
Acknowledgments
None.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of The First Affiliated Hospital of Jinan University and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.
Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tau.amegroups.com/article/view/10.21037/tau-2026-0406/rc
Funding: None.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-2026-0406/coif). Y.J. and Y.L. are from GeneScience Pharmaceuticals Co., Ltd. The other authors have no conflicts of interest to declare.
(English Language Editor: L. Huleatt)
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