Risk Factors for Postsurgical Gout Flares after Thoracolumbar Spine Surgeries

Abstract

Gouty arthritis is the most common form of inflammatory arthritis and flares frequently after surgeries. Such flares impede early patient mobilization and lengthen hospital stays; however, little has been reported on gout flares after spinal procedures. This study reviewed a database of 6439 adult patients who underwent thoracolumbar spine surgery between January 2009 and June 2021, and 128 patients who had a history of gouty arthritis were included. Baseline characteristics and operative details were compared between the flare-up and no-flare groups. Multivariate logistic regression was used to analyze predictors and construct a predictive model of postoperative flares. This model was validated using a receiver operating characteristic (ROC) curve analysis. Fifty-six patients (43.8%) had postsurgical gout flares. Multivariate analysis identified gout medication use (odds ratio [OR], 0.32; 95% confidence interval [CI], 0.14–0.75; p = 0.009), smoking (OR, 3.23; 95% CI, 1.34–7.80; p = 0.009), preoperative hemoglobin level (OR, 0.68; 95% CI, 0.53–0.87; p = 0.002), and hemoglobin drop (OR, 1.93; 95% CI, 1.25–2.96; p = 0.003) as predictors for postsurgical flare. The area under the ROC curve was 0.801 (95% CI, 0.717–0.877; p < 0.001). The optimal cut-off point of probability greater than 0.453 predicted gout flare with a sensitivity of 76.8% and specificity of 73.2%. The prediction model may help identify patients at an increased risk of gout flare.

Netosis in Surgery

“…18 In acute gout, needle-like MSU microcrystals deposited in tissues and joints are incompletely phagocytosed by monocytes and neutrophils, causing activation of the NLRP3 inflammasome, production of IL-1β, and further neutrophil recruitment. 13,18 Neutrophils are stimulated by MSU crystals and macrophage-derived IL-1β to form aggregated NETs, which are known to be present in gouty tophi. 13 While NETs contribute to tophi formation by densely packing MSU crystals with ecDNA, aggregated NETs can trap and cleave proinflammatory cytokines (TNF-α, IL-1β, and IL-6) FIGURE 3.…”

“…Colchicine binds to tubulin and inhibits microtubule assembly, which is required for neutrophil chemotaxis, adhesion, transmigration and recruitment, GPCR signaling, Ca 2+ influx, NOX2 superoxide production, intracellular transport, nuclear chromatin swelling, organelle trafficking, and NETosis. 13,18 Acute perioperative gout can pose difficulties with arthritis severity, pain management, and patient immobilization. Colchicine is a useful intervention, due to its efficacy and the relative contraindications of perioperative systemic corticosteroid or nonsteroidal anti-inflammatory drug administration.…”

“…Acute exacerbations of recurrent gout are common (17.2%–44.3%) after major surgery, related to fasting, systemic acidosis, blood transfusion, volume depletion, tissue hypoxia, or presurgical hyperuricemia. The risk of perioperative gout is especially increased in males, patients with obesity or diabetes mellitus, previous gout history, high-protein purine-rich diets, after abdominal, orthopedic or bariatric surgery, or perioperative cessation of colchicine gout prophylaxis 18 . In acute gout, needle-like MSU microcrystals deposited in tissues and joints are incompletely phagocytosed by monocytes and neutrophils, causing activation of the NLRP3 inflammasome, production of IL-1β, and further neutrophil recruitment 13,18 .…”

“…The risk of perioperative gout is especially increased in males, patients with obesity or diabetes mellitus, previous gout history, high-protein purine-rich diets, after abdominal, orthopedic or bariatric surgery, or perioperative cessation of colchicine gout prophylaxis 18 . In acute gout, needle-like MSU microcrystals deposited in tissues and joints are incompletely phagocytosed by monocytes and neutrophils, causing activation of the NLRP3 inflammasome, production of IL-1β, and further neutrophil recruitment 13,18 . Neutrophils are stimulated by MSU crystals and macrophage-derived IL-1β to form aggregated NETs, which are known to be present in gouty tophi 13 .…”

“…Inhibition of NETosis by colchicine treatment is also effective in other microcrystal diseases, including gout, pseudogout, and atherosclerosis. Colchicine binds to tubulin and inhibits microtubule assembly, which is required for neutrophil chemotaxis, adhesion, transmigration and recruitment, GPCR signaling, Ca 2+ influx, NOX2 superoxide production, intracellular transport, nuclear chromatin swelling, organelle trafficking, and NETosis 13,18 . Acute perioperative gout can pose difficulties with arthritis severity, pain management, and patient immobilization.…”