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Objective: To compare the characteristics of monosodium urate (MSU) crystal deposition at specific anatomical sites of the foot detected by dual‐energy computed tomography in patients with different stages of gout. Materials and methods: This study included 101 patients with gout, 64 had early gout (<3 years) and 37 had late gout (>3 years). We retrospectively compared the total volumes of MSU crystals, the detection rates, and the morphology of MSU crystals at specific anatomical sites in the foot of the patients with different gout durations. Results: The total volume of MSU crystals in patients with early gout was significantly smaller than that in patients with late gout (P < 0.05). The detection rates and morphology of MSU crystals in the anterior calf tendons, ankle joints, tarsometatarsal joints, and metatarsophalangeal joints differed significantly between the patients with early and late gout (P < 0.05). There were no significant differences in the detection rates of submillimeter MSU crystals at the other specific anatomical sites, except for the tendons of the anterior calf, the ankle joint, and the metatarsal joint (P > 0.05). The submillimeter MSU crystal deposition was most common in the tendons of the posterior calf, the proportions in patients with early gout and late gout were 85.9% and 70.3%. Only submillimeter deposition existed in 52 patients (81.3%) with early gout and 11 patients (29.7%) with late gout at all sites of the foot. Conclusion: Dual‐energy computed tomography detection of submillimeter MSU crystal deposits in the foot is of great significance for the diagnosis of gout, especially along tendons. [ABSTRACT FROM AUTHOR]

Background: MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation. Methods: In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p. Results: We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P <.05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P <.05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3. Conclusion: The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: This study aimed to explore the regulatory mechanism of the natural soda Shi Han Quan (SHQ) in the development of gout. Methods: Human umbilical vein endothelial cells (HUVECs) were stimulated with monosodium urate (MSU) for 24 h to induce acute gouty inflammation in vitro. HUVECs were divided into four groups: ddH2O group, ddH2O + MSU group, 1/2 ddH2O +1/2 SHQ + MSU group, and SHQ + MSU group. The effects of SHQ on cell viability, concentration and expression of intercellular adhesion molecule‐1 (ICAM‐1), and MSU‐induced release of interleukin (IL)‐1β and IL‐6 were investigated. Additionally, cell viability and ICAM‐1 concentration and expression were detected after HUVECs were incubated with the culture supernatant of THP‐1 cells that had been treated with phorbol 12‐myristate 13‐acetate (PMA), MSU and SHQ for 24 h. Results: The viability of HUVECs was significantly decreased with increasing transfection concentrations of MSU, and MSU treatment resulted in a significant increase of the concentration and expression of ICAM‐1. In addition, SHQ improved the MSU‐induced decrease in cell viability and alleviated MSU‐mediated increase in ICAM‐1 levels. Moreover, SHQ decreased MSU‐induced release of IL‐1β and IL‐6. After HUVECs were incubated with the culture supernatant of THP‐1 cells that had been treated with PMA, MSU and SHQ for 24 h, SHQ also markedly alleviated the effects of MSU, such as by increasing cell viability and decreasing ICAM‐1 levels. Conclusions: Drinking natural soda water may have a significant role in preventing gouty inflammation. [ABSTRACT FROM AUTHOR]