Our study explored the burden and distribution of MSU deposition in symptomatic gout and asymptomatic hyperuricemia with DECT and compared renal function in gout patients in follow-up DECT. We observed the following important results: 1) The MSU deposition in the gout group was significantly higher than that in the hyperuricemia group except for the elbows. 2) MSU deposition in the knees and feet was significantly higher in the gout group than the hyperuricemia group. 3) In the hyperuricemia group, the MSU deposits at the cortical cortex of the knee and foot/ankle were both significantly higher than those in the soft tissue and joint cavity. 4) The extent of MSU burden measured with DECT was not predictive of the renal insufficiency in gout patients in our study.
The lower MSU deposition in hyperuricemia than gout group in this study is in line with the previous study , supporting the concept that urate deposition precedes clinical gout . This also reminds us that DECT can be used to better monitor and manage patients with hyperuricemia in our clinical work. We should pay more attention to the burden of MSU deposition in patients with hyperuricemia, which may has certain clinical indications for predicting the development of hyperuricemia into gout. So is there a cutoff for MSU deposition between asymptomatic hyperuricemia and symptomatic gout? What is the critical value and where does it exist? These questions deserve further exploration in our future research.
While our sample size is large, supporting that the MSU deposition of symptomatic gout in the feet and knees are more frequently than asymptomatic hyperuricemia . This may imply that the distribution of MSU deposits in the knee and foot is more discriminative for patients with asymptomatic hyperuricemia and those with gout. Perhaps the deposition in these parts is more clinically indicative. In normal clinical work, we should pay more attention to the follow-up and observation of the knees and feet of patients with hyperuricemia, so as to precisely prevent, diagnose and treat potential gout in time.
In the hyperuricemia group, the MSU deposits at the cortical cortex of the knee and foot/ankle were both significantly higher than those in the soft tissue and joint cavity. This means that in practice, it will be more clinically meaningful to observe the bone changes and structural functions of these key location(knees, feet and ankles) of patients with hyperuricemia. The research on bone changes in these parts should also be more in-depth, which is not only conducive to refined clinical management, but may also reveal the deeper mechanisms and reasons behind the progression of hyperuricemia to gout.
The MSU crystal deposition of the elbow in patients with hyperuricemia was much higher than that of gout patients, which is contrary to the previous observations [23, 24] and overall results of other anatomical sites. This may be due to the deviation caused by the small sample size of the elbow DECT examinations or the different MSU sedimentary distributions of different diseases. It is possible because our finding is attributed to the long-term use of urate-lowering drugs which can be reported in most gout patients in our study. In the gout group, the MSU burden on the right elbow was the severest, significantly higher than the MSU burden at all other sites, where the deposition of soft tissue was significantly higher than in the bone cortex and joint cavity. While the previous study showed that the elbow, suprapatellar bursa, and ankle collateral ligaments were among the least common of the affected sites . This may be a statistical artefact of outliers due to the small sample size of the elbow and selection bias of anatomical regions.
To the best of our knowledge, this is the largest sample study to estimate the burden of MSU deposition distribution using DECT and the first study to explore whether the extent of MSU burden can be predictive of the renal insufficiency in gout. However, we observed that the extent of MSU burden measured with DECT was not predictive of the renal insufficiency in gout patients.
We have to acknowledge that our study has several limitations. The main shortfall of this study is a selection bias of anatomical regions and patients. There may be a selection bias as we included only patients with DECT. Besides, not all regions were imaged in all patients. This fact must be considered for the analysis, especially when comparing the tophus volume of different anatomical regions. Furthermore, selection bias can be present in our study because our study enrolled the patients from one single hospital.
Besides, our study is retrospective, thus many variables were missing. This resulted in a small sample size in our follow-up study which may not clarify the relationship between the MSU burden and renal function decline during the follow-up. Thus, prospective large cohort study is needed to uncover the role of DECT MSU burden in predicting renal function decline in future. Moreover, the accuracy of DECT is different for different anatomical locations, and the sample size of some anatomical locations is small. Thus, it is rational to collect more anatomical locations to observe MSU distribution. What’s more, for the first time, we divided a single joint into different parts (cortical bone, soft tissue and joint cavity), but whether DECT can fully and accurately distinguish the distribution of MSU in different components lacks corresponding clinical application, and further data support and verification are needed.
Last but not least, the short follow-up duration in this study (the mean follow-up time was 2 years) was not sufficient to verify the relationship between MSU deposition and renal insufficiency in gout patients.