Recurrent gout flares are a major clinical burden of gout, and despite available uric acid-lowering therapies, the risk of recurrent gout remains high. Sixty-seven percent of patients who have already had a previous gout flare would have at least one flare within a year [7]. Surgery is an important trigger for gout flares, with studies finding that 17.2% of patients with gout will experience a gout flare after surgery, and observers in China have found this flare rate to be as high as 40.3% [8, 9].

No previous studies have included endovascular interventional procedures to analyze, and our study found that endovascular interventional procedures were an important risk factor for postoperative gout flares. There may be several reasons for this: (1) Inflammation from mechanical endothelial injury caused by endovascular interventional procedures may lead to gout flares. It has been found that percutaneous coronary intervention (PCI) causes mechanical endothelial injury and endothelial denudation, resulting in elevated inflammatory markers such as hyper-sensitivity CRP (hs-CRP), and this significantly raised inflammatory markers after the procedure suggests a close association with poor prognosis [10, 11]. Similar results have been found in radiofrequency ablation, and studies have shown that the concentration of vascular hemophilia factor (vWF), an important plasma component that is elevated when endothelial cells are injured or receive stimulation, is elevated 24 h after radiofrequency ablation, thus suggesting that radiofrequency ablation can also cause endothelial injury [12, 13]. Initial endothelial activation was related to leukocyte recruitment, which would release intracellular serine proteases [e.g., neutrophil elastase, histone G, and proteinase 3 (PR3)] in response to cell recruitment, causing MSU crystal-mediated cell injury and death, and secrete IL-1β to increase inflammation [14, 15]. Therefore, we speculate that endothelial damage induced by interventional procedures may recruit leukocytes and accelerate the inflammatory response caused by urate crystals, thus causing gout flares [16]. (2) Coronary microembolization (CME) is a common complication of percutaneous coronary intervention (PCI) [17]. It has been found that inflammatory responses in the myocardium after CME involved TLR4/MyD88/NF-κB signaling and the NLRP3 inflammasome, with increased expression levels of pro-inflammatory factors TNF-α, IL-1β [18]. Also, the TLR4/NF-κB pathway plays an important role in the pathogenesis of gout as well. The priming signal effectively promotes the transcriptional activation of NLRP3 inflammasome-containing genes such as NLRP3, pro-IL-1β, and pro-IL-18 in a TLR4/NF-κB pathway-dependent manner [19, 20].

The traditional anti-inflammatory and analgesic drugs for gout treatment include colchicine, NSAIDs, and glucocorticoids [21]. Our study showed that only taking colchicine before surgery was a protective factor for postoperative gout flares, which is consistent with previous findings [9, 22, 23]. The mechanism of colchicine is mainly to bind to β-microtubulin and inhibit cytoskeletal microtubule polymerization, thereby inhibiting the formation of NLPR3 inflammasomes and suppressing the inflammatory response to gout [21, 24]. This may be the reason why colchicine reduces gout flares after endovascular interventional procedures. Besides, colchicine has an endothelial protective effect [25], which can increase plaque stability and decrease plaque progression [26]. Adding low-dose (0.5 mg/day) colchicine to the optimal medical treatment significantly reduced the risk of acute coronary events, cardiovascular death, and resuscitated cardiac arrest [27, 28]. Therefore, prophylactic treatment with colchicine (0.5–1.0 mg/day) can prevent not only postoperative gout flares but also cardiovascular events, which we used if appropriate as a first-line option.

Previous studies have found that the rate of achieving target uric acid in patients with gout in China is low, with only 39.2% of patients reaching the target uric acid (6 mg/dl), even among those who have received long-term uric acid lowering therapy [29]. Therefore, we chose 7 mg/dl (the diagnosis of hyperuricemia) rather than 6 mg/dl as the cutoff. Our results suggested that presurgical uric acid level of ≥ 7 mg/dl before operation was a risk factor for postoperative gout flares, but taking uric acid-lowering agents was not associated with gout flares, which is consistent with previous findings [30]. Therefore, even though target uric acid (6 mg/dl) is difficult to achieve in the short term, controlling preoperative uric acid levels below 7 mg/dl remains an important method of preventing postoperative gout flares.

The limitations of this study are as follows. First, the study was a cross-sectional design with a single race and a small sample size. Second, in the collection of study data, although the exact risk factors were studied extensively, surgery-related factors (e.g., preoperative preparation, surgical technique, postoperative management) was not included. Third, ophthalmologic surgery was not included due to limitations in data collection. Therefore, the results of this study may not be fully applicable to all surgical options. A future well-designed study is needed to investigate the pathogenesis of postoperative gout flares.