目的 探讨全身免疫炎症指数（SII）、C反应蛋白与白蛋白比值（CAR）及C反应蛋白-白蛋白-淋巴细胞（CALLY）指数与痛风性关节炎（GA）急性发作的关系。 方法 选取成都市第三人民医院2023年2月至2025年5月63例急性发作期GA患者纳入GA急性期组，同期处于疾病临床缓解期（无关节红肿热痛等急性炎症症状）的患者62例作为GA缓解期组，另选取于医院进行健康体检者62例作为健康对照组，对比3组SII、CAR及CALLY指数差异，通过logistic回归分析GA急性发作的危险因素，采用受试者工作特征曲线（ROC）分析SII、CAR及CALLY指数对患者急性发作的评估价值，采用多元线性回归分析治疗前后SII、CAR及CALLY指数变化率（Δ%）与疼痛VAS评分改善值（ΔVAS）间的关系。 结果 GA急性期组外周血SII指数、CAR比值高于GA缓解期组，GA缓解期组高于健康对照组（P < 0.05）；GA急性期组外周血CALLY指数低于GA缓解期组，GA缓解期组低于健康对照组（P < 0.05）；logistic回归分析显示多关节受累、高外周血SII、CAR指数值是GA患者急性发作的独立危险因素，接受规律降尿酸治疗、高外周血CALLY指数是防止急性发作的保护因素（P < 0.05）；外周血CALLY指数鉴别GA急性期与缓解期ROC曲线下面积为0.861，高于SII指数、CAR比值检测曲线下面积0.731、0.736（P < 0.05）；GA急性期患者治疗后外周血SII指数、CAR比值均较治疗前降低，CALLY指数较治疗前升高（P < 0.05）；多元线性回归分析结果显示，在调整了年龄和基线VAS评分后，Δ%SII、Δ%CAR、Δ%CALLY指数均是ΔVAS的独立危险因素（P < 0.05）。 结论 GA患者急性发作期SII指数、CAR比值升高且CALLY指数降低，三者可反映患者治疗后炎症消退及症状改善，且以CALLY指数评估急性发作期效能最优。

Objective To investigate the association between the systemic immune-inflammation index （SII）， C-reactive protein-to-albumin ratio （CAR）， and C-reactive protein-albumin-lymphocyte （CALLY） index and acute exacerbations of gouty arthritis （GA）. Methods This study enrolled 63 patients with GA in the acute phase， 62 patients in clinical remission （absence of acute inflammatory signs such as joint erythema， swelling， and localized heat/pain）， and 62 healthy controls at the Third People's Hospital of Chengdu between February 2023 and May 2025. SII， CAR， and CALLY index levels were compared across the three groups. Logistic regression was used to identify risk factors for acute GA exacerbations. Receiver operating characteristic （ROC） curve analysis evaluated the diagnostic performance of these indices. Multiple linear regression assessed the association between the percentage changes （Δ%） in SII， CAR， and CALLY index following treatment and the change in Visual Analog Scale （VAS） pain scores （ΔVAS）. Results SII and CAR levels were progressively lower across the acute， remission， and healthy control groups （all P < 0.05）， whereas the CALLY index was progressively higher （all P < 0.05）. Logistic regression identified polyarticular involvement and elevated SII and CAR as independent risk factors for acute exacerbations， while regular urate-lowering therapy and a higher CALLY index were independently protective （all P < 0.05）. The CALLY index demonstrated superior diagnostic performance for distinguishing the acute from the remission phase （AUC = 0.861）， significantly outperforming SII （AUC = 0.731） and CAR （AUC = 0.736） （both P < 0.05）. Following treatment， SII and CAR levels significantly decreased， while the CALLY index increased in patients with acute GA （all P < 0.05）. After adjusting for age and baseline VAS， multiple linear regression identified Δ%SII， Δ%CAR， and Δ%CALLY as independent predictors of ΔVAS （all P < 0.05）. Conclusion Elevated SII and CAR， alongside a decreased CALLY index， characterize the acute phase of GA. All three biomarkers effectively track post-treatment inflammatory resolution and clinical improvement， with the CALLY index exhibiting the highest diagnostic accuracy for identifying acute GA exacerbations.