Association of Specific Comorbidities with Monosodium Urate Crystal Deposition in Urate-Lowering Therapy-Naive Gout Patients: A Cross-Sectional Dual-Energy Computed Tomography Study

Abstract

(1) Background: To determine which factors are associated with the volume of monosodium urate (MSU) crystal deposition quantified by dual-energy computed tomography (DECT) in urate-lowering therapy (ULT)-naive gout patients. (2) Methods: In this multicenter cross-sectional study, DECT scans of knees and feet/ankles were prospectively obtained from ULT-naive gout patients. Demographic, clinical (including gout history and comorbidities), and biological data were collected, and their association with DECT MSU crystal volume was analyzed using bivariate and multivariate analyses. A second bivariate analysis was performed by splitting the dataset depending on an arbitrary threshold of DECT MSU volume (1 cm3). (3) Results: A total of 91 patients were included. In the bivariate analysis, age (p = 0.03), gout duration (p = 0.003), subcutaneous tophi (p = 0.004), hypertension (p = 0.02), diabetes mellitus (p = 0.05), and chronic heart failure (p = 0.03) were associated with the total DECT volume of MSU crystal deposition. In the multivariate analysis, factors associated with DECT MSU volumes ≥1 cm3 were gout duration (odds ratio (OR) for each 10-year increase 3.15 (1.60; 7.63)), diabetes mellitus (OR 4.75 (1.58; 15.63)), and chronic heart failure (OR 7.82 (2.29; 31.38)). (4) Conclusion: Specific comorbidities, particularly chronic heart failure and diabetes mellitus, are more strongly associated with increased MSU crystal deposition in knees and feet/ankles than gout duration, regardless of serum urate level.

Why Does Hyperuricemia Not Necessarily Induce Gout?

“…Interestingly, the prevalence of gout flares, irrespective of SUA levels, has been linked to mental disorders [ 45 , 46 ]. Chronic heart failure and diabetes mellitus are more strongly associated with increased MSU crystal deposition in knees and feet/ankles than gout duration [ 47 ]. As reducing SUA may not be the only way to eliminate gout flares [ 48 ], the level of SUA, in essence, should be an indicator of oxidative paradox in vivo.…”

“…Alternatively, targeting MSU crystals could be more useful and efficient in controlling gout flares. Furthermore, as some comorbidities such as chronic heart failure and diabetes mellitus are less influenced by SUA levels [ 47 ], UTL would not be favorable to them. In spite of UA infusion improving endothelial function [ 102 ], quickly lowering SUA could induce an acute gout flare [ 82 ], cardiovascular events [ 103 ], nerve dysfunction [ 104 ], the risk of all-cause death in hemodialysis [ 61 ], vertebral fracture [ 105 ], or heart failure in patients [ 106 ].…”

The role of dual energy computed tomography in the differentiation of acute gout flares and acute calcium pyrophosphate crystal arthritis

“…Other studies have also reported on the difficulties of diagnosing early gout manifestations via DECT [24]. MSU deposits in patients with a short disease duration might be at a stage of development where they are not detectable by DECT, which is limited to a spatial resolution of 0.25 mm [25], although lesions smaller than 1 mm can already be considered artefacts unless present at a typical gout localisation [26]. Similar results were found by Jia et al [27] where the sensitivity of DECT for gout patients with initial onset was 35.7% and patients with a disease duration of less than 24 months yielded a sensitivity of 61.5%.…”

Why Hyperuricemia Does Not Necessarily Induce Gout?

“…Interestingly the prevalence of gout attacks, irrespective of SUA levels, has been linked to mental disorders [45,46]. Chronic heart failure and diabetes mellitus are more strongly associated with increased MSU crystal deposition in knees and feet/ankles than gout duration [47]. As reducing SUA may not be the only way to eliminate gout attack [48], the level of SUA, in essence, should be an indicator of oxidative paradox in vivo, and any means to break such balances may prompt metabolic diseases including gout, despite some causes of hyperuricemia may be irrelevant to a gout attack.nd any means to break such balances may prompt metabolic diseases including gout, despite some causes of hyperuricemia may be irrelevant to gout attack.…”

“…Alternatively, targeting MSU crystals could be more useful and efficient in controlling gout attack/flare. Furthermore, as some comorbidities such as chronic heart failure and diabetes mellitus are less influenced by SUA level [47], UTL would not be favorable to them. In spite of UA infusion could improve endothelial function [102], quickly lowing SUA could induce acute gout attack [82], cardiovascular events [103], nerve dysfunction [104], the risk of all-cause death in hemodialysis [61], vertebral fracture [105] or heart failure patients [106].…”