Monosodium Urate Research Articles

Mycoplasma hominis–Associated Septic Arthritis Masquerading as Gouty Arthritis

Abstract Septic arthritis caused by M. hominis is exceptionally rare. Here, we report on a 62-year-old man with a medical history of gout and renal cell carcinoma who presented with persistent knee pain and swelling following partial nephrectomy complicated by an abdominal abscess. Arthrocentesis revealed monosodium urate crystals, leading to the initial diagnosis and treatment of gouty arthritis using intra-articular steroid injections, allopurinol, and colchicine. Initial cultures yielded no growth. However, faint transparent colonies grew after discharge, which were eventually identified as M. hominis. Initial antibacterial therapy targeting suspect Mycoplasma spp. was begun with doxycycline, and the patient ultimately completed 12 weeks of doxycycline and clindamycin with cure. This case underscores the importance of maintaining clinical suspicion for fastidious organisms when faced with persistent clinical symptoms without an identifiable organism and highlights a rare clinical presentation of M. hominis.

TINJAUAN SISTEMATIS HISPATOLOGI GOUT ARTRITIS: PERAN SEL IMUN DALAM PROSES INFLAMASI DAN KERUSAKAN JARINGAN

Gout arthritis is a joint inflammation caused by increased uric acid levels, leading to the formation of monosodium urate (MSU) crystals. The study aimed to deepen the understanding of the role of MSU crystals in triggering both acute and chronic inflammatory responses, as well as the formation of tophi, which damage joint and bone tissues. The method used is the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The reviewed articles were obtained from the Science Direct, Semantic Scholar, and PubMed databases using the keywords “Gout Arthritis,” “Histopathology,” “Inflammation,” and “Tophus.” The publication period was limited to 2019-2024. Out of 745 articles found, 12 were selected based on inclusion criteria, which included experimental, observational, and case study reports. The results show that MSU crystals induce inflammation through the infiltration of inflammatory cells such as neutrophils and macrophages. In chronic Gout, the formation of tophi, granulomatous lesions with a crystalline core, leads to bone and joint destruction. Understanding the histopathological aspects is crucial for more accurate diagnosis and more effective management of Gout arthritis. The progression of the disease is related to acute and chronic inflammation, as well as the destructive effects of tophi on joints and bones. In conclusion, MSU crystals play a significant role in triggering inflammation and tissue damage in Gout arthritis, and understanding histopathology can improve diagnostic accuracy and therapeutic efficacy.

Colchicine inhibits monosodium urate crystal-mediated inflammation by influencing F-actin formation

ObjectivesTo understand the mechanism by which colchicine inhibits the inflammatory properties of monosodium urate (MSU) crystal deposits and tophi. MethodsWe investigated the effects of colchicine on the inflammatory properties of monosodium urate (MSU) crystal deposits in several models: (i) In vitro tophus formation by MSU and neutrophils; (ii) MSU-induced peritonitis model; (iii) Alpha-1-antitrypsin-induced peritoneal MSU flare model; (iv) MSU-induced arthritis model. We measured neutrophil numbers, NET formation, IL-1β production and F-actin generation by MSU crystals. In addition, we tested the effect of actin inhibitors SMIFH2, Cytochalasin B and Latrunculin B in the models. ResultsColchicine did not affect neutrophil numbers in all these models. However, colchicine was highly effective to inhibit NET formation, IL-1β production and F-actin generation indicating less pronounced tophus formation, lower inflammatory properties of tophi and reduced conversion from G-actin into F-actin, respectively. F-actin was shown to accumulate in tophi without presence of colchicine and being resistant to degradation by DNase I. Actin inhibitors SMIFH2 and Cytochalasin B significantly reduced IL-1β and neutrophil elastase levels and mitigated MSU-induced arthritis. ConclusionColchicine effects on gout flares are not based on reducing neutrophil numbers but on changing the functional properties of tophi by reducing their DNase-resistant F-actin concentrations and thereby reducing the negative impact of NETs on IL-1β production and the pro-inflammatory state of tophi. Actin inhibitors may be interesting tools to convey anti-inflammatory properties and reduction of flares in gout patients.

Preparation of combined colchicine with loxoprofen sodium loaded in dissolvable microneedles and its anti-gouty arthritis effect

Both colchicine (Col) and loxoprofen sodium (LS) are first-line drugs for gouty arthritis (GA). Dissolvable microneedles (DMNs) represent an innovative transdermal drug delivery system (TDDS) that maximizes the therapeutic effect of drugs. In this paper, a novel TDDS of combined Col with LS loaded in DMNs (Col-LS-DMNS) was prepared to treat GA. To assess the synergistic effects of Col and LS, cell viability assays were conducted using monosodium urate (MSU)-induced HaCaT cells. The optimization of the Col-LS-DMNs formulation was carried out through sealing membrane puncture tests, single-factor experiments, and Box-Behnken response surface methodology. The quality of Col-LS-DMNs was assessed using high-performance liquid chromatography (HPLC), scanning electron microscopy (SEM), sealing membrane puncture tests, in vitro mouse skin puncture experiments, and Franz diffusion cell assays. The therapeutic effect of Col-LS DMNs on GA through animal experiments. Results demonstrated that Col and LS exhibit a synergistic effect, with optimal mass ratio of 1:1. The optimal formulation included PVP K30 and CMC Na at a mass ratio of 10:1, with 63% water content and a mixed dosage of Col and LS of 42 mg. The drug content in Col-LS-DMNs was (19.11±0.65) μg of Col and (20.69±0.89) μg of LS per tablet. SEM imaging revealed that the needle tips were conical. Additionally, Col-LS-DMNs exhibited favorable mechanical properties and caused minimal skin damage. After 24 hours, the cumulative permeation amount was (21.55±19.49) μg/cm2. Col-LS-DMNs significantly reduced MSU-induced ankle swelling and decreased serum concentrations of TNF-α, IL-6, and IL-1β in rats. In conclusion, Col-LS-DMNs represent a promising new treatment modality for GA.

Bone Erosions and Systemic Bone Loss on HR-pQCT in Men With Tophaceous Gout.

Gout, a prevalent inflammatory arthropathy, predominantly affects males and arises from persistent hyperuricemia, resulting in monosodium urate crystal deposition. Hyperuricemia is associated with comorbidities, exacerbating patient morbidity. Conflicting literature exists regarding uric acid's impact on bone mineral density (BMD), with potential proinflammatory effects in gout patients. Localized bone destruction (erosions) is a hallmark of gout, necessitating early detection due to its predictive role in musculoskeletal disability. This cross-sectional study included 26 tophaceous gout patients. Clinical and densitometric parameters were assessed, and high-resolution peripheral quantitative computed tomography (HR-pQCT) was used for bone microarchitecture evaluation, as well as bone erosions in metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints. A healthy control group of 52 age and BMI-matched individuals was included. Despite normal areal bone mineral density (BMD), tophaceous gout patients exhibited impaired HR-pQCT parameters, including lower cortical volumetric BMD (Ct.vBMD) and higher cortical porosity at the distal radius. Similar trends were observed at the tibia. Bone erosions were prevalent (96%), with distribution across MCP and PIP joints. Patients with ≥ 4 erosions displayed increased tophi prevalence and longer uricosuric use. Erosions correlated with compromised microarchitecture, emphasizing their association with disease activity. Despite normal BMD, tophaceous gout patients manifest systemic bone loss, with bone microarchitectural deterioration and localized bone erosions, underscoring the need for detailed clinical approaches to prevent musculoskeletal disabilities, including fragility fractures, in this population.

Optimizing Gout Treatment: A Comprehensive Review of Current and Emerging Uricosurics

Gout is the most common inflammatory arthritis, affecting approximately 5.1% of adults in the United States (US) population. Gout is a metabolic and autoinflammatory disease. Elevated uric acid pools lead to the precipitation of monosodium urate (MSU) crystals in and around joints, as well as other tissues, and the subsequent autoinflammatory response. Since elevated serum urate (SU) levels (hyperuricemia) correspond with gout severity, urate-lowering therapies (ULTs) are the cornerstone of gout treatment.ULTs include xanthine oxidoreductase inhibitors, uricosurics, less commonly used in the US but widely used in Europe and Asia, including benzbromarone, dotinurad, and probenecid (the only US Food and Drug Administration (FDA) approved uricosuric in the US), and uricases, including rasburicase and pegloticase (available only in the US).Over 90% of the daily load of uric acid filtered by the kidneys is reabsorbed through renal transporters. These urate transporters include uric acid transporter 1 (URAT1), glucose transporter 9, and organic anion transporters 1, 3, and 4 (OAT1, OAT3, OAT4). They are the target of approved and in-the-pipeline uricosurics.Any drug that increases renal excretion of uric acid, independently of the mechanism through which it exerts its effect, may be considered a uricosuric drug. This review discusses drugs that increase renal excretion of uric acid, either approved or in development, as well as off-label drugs with uricosuric properties.

Gout: possibilities of treatment optimization

Aim. To consider new mechanisms of gout pathogenesis of and possibilities of influencing the pathological process. Gout is a chronic joint disease caused by the deposition of monosodium urate crystals in various tissues and subsequent inflammation in individuals with hyperuricemia, caused by exocrine and/or genetic factors. In recent years, new knowledge about gout diagnostics, genetics, pathogenesis, comorbidities and various data indicate new strategies to improve control of the disease and its exacerbations, as well as to prevent comorbid conditions. The discovery of new mechanisms concerning sodium monourate crystal-induced inflammation, proposed new methods of treating not only gout, but also other systemic diseases, including renal and cardiovascular diseases using xanthine oxidase inhibitors, including febuxostat. The case of colchicine is very indicative, which recently, taking into account the significant results of laboratory and clinical experiments, received approval from the US Federal Food and Drug Administration for the Prevention of cardiovascular Diseases. This has provided opportunities for the combinedadministration of febuxostat and colchicine to treat gout, recurrent arthritis attacks and reduce the risk of cardiovascular complications.

The Influence of Electronic Health Education Media on Enhancing Self-Management Among Individuals Afflicted with Gout Arthritis: A Comprehensive Scoping Review

Monosodium urate crystals accumulate in Gout Arthritis, resulting in joint inflammation, significant pain, and potential joint damage, which can impair mobility and lead to disability. Additionally, uncontrolled hyperuricemia may result in the formation of kidney stones and diminished kidney function. Therefore, implementing effective management and treatment strategies is crucial for enhancing self-management in individuals diagnosed with Gout Arthritis. This scoping review seeks to provide an overview of the effectiveness of various electronic health education media in improving the self-management of individuals suffering from Gout Arthritis. The study followed the PRISMA guidelines for scoping reviews and involved a comprehensive literature search across ProQuest, Science Direct, Wiley, and Google Scholar, focusing on publications from 2016 to 2022. Ten articles that met the predetermined inclusion criteria were synthesized for this review. The findings suggest that using electronic health education media can significantly enhance self-management practices and medication adherence among Gout Arthritis patients and facilitate favourable changes in uric acid levels. These insights may serve as valuable contributions to managing Gout Arthritis cases

Resolution of acute inflammation induced by monosodium urate crystals (MSU) through neutrophil extracellular trap-MSU aggregate-mediated negative signaling

BackgroundPolymorphonuclear neutrophils (PMN) activation by monosodium urate crystals (MSU) is crucial to acute gouty arthritis and subsequent spontaneous remission within 7–10 days. Activated PMNs release neutrophil extracellular traps (NETs) that entrap MSU crystals, forming NET-MSU aggregates. Whether NET-MSU aggregates contribute to the resolution of acute inflammation remains to be elucidated. This study uses a cell-based approach to unveil their molecular bases.MethodsAll-trans retinoic acid-differentiated HL-60 cells (dHL-60) served as surrogate PMNs. NET release from MSU-activated dHL-60 was confirmed by detecting DNA, neutrophil elastase, and citrullinated histone 3, forming large NET-MSU aggregates. NET area was measured with Fiji software after SYTOX Green staining. Released pro-inflammatory cytokines IL-8 and TNF-α, and the anti-inflammatory cytokine IL-1RA in culture supernatants were quantified to calculate the estimate inflammation score (EIS). Cellular redox state was determined by a FRET-based sensor. Expression of intracellular positive (ERK1/2) and negative (SHP-1 and SHIP-1) cytokine signaling regulators was detected by western blot. qPCR detected mRNA expressions of CISH and SOCS1–SOCS7. Flow cytometry measured neutrophil N1 (CD54) and N2 (CD182) surface markers after staining with fluorescent-conjugated antibodies.ResultsIncubating dHL-60 with MSU for 4 h maximized NET-MSU aggregate formation and acute inflammation with an EIS of 11.6. Prolonging the incubation of dHL-60 + MSU to 22 h gradually raised the EIS to 19.40 without increasing NET area, due to reduced cellular redox capacity. Adding both new dHL-60 and new MSU crystals to the culture, mimicking the clinical scenario, increased NET area but conversely suppressed EIS to 1.53, indicating acute inflammation resolution. The resolution of acute inflammation following prolonged incubation was attributed to decreases in P-ERK and increases in P-SHP-1, SOCS2, SOCS3, and CISH gene expressions, which may suppress pro-inflammatory and enhance anti-inflammatory cytokine production. Moreover, the large NET-MSU aggregates facilitated N1 to N2 polarization, crucial for accelerating inflammation resolution.ConclusionWe explored the potential molecular basis for the spontaneous resolution of MSU induced acute inflammation using a cell-based model in that huge NET-MSU aggregates frustrate the transformation of newly entering PMNs to the N2 phenotype, enhancing the production of the anti-inflammatory cytokine IL-1RA.

Bioinformatics and molecular docking reveal Cryptotanshinone as the active anti-inflammation component of Qu-Shi-Xie-Zhuo decoction by inhibiting S100A8/A9-NLRP3-IL-1β signaling

BackgroundGout is a common type of arthritis marked by monosodium urate (MSU) crystal deposition in joints, triggering an inflammatory response. Qu-Shi-Xie-Zhuo (QSXZ), a traditional Chinese medicine (TCM) formula, has been clinically used for the treatment of gouty arthritis (GA). PurposeThe study sought to examine the impact of QSXZ on GA and to delve into the pharmacological mechanisms that underlie its effects. MethodsThe chemical constituents of QSXZ were analyzed through UPLC-MS. MSU-induced acute gouty arthritis (AGA) and subcutaneous (SC) air pouch models in mice were employed to evaluate the anti-inflammatory properties of QSXZ and its primary active compound, Cryptotanshinone (CTS). To investigate the therapeutic mechanisms of QSXZ, we used MS-based network pharmacology, transcriptomic analysis, molecular docking and multiscale bioassays. ResultsTreatment of QSXZ revealed a significant reduction of inflammatory cell infiltration and the expression of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin -1β (IL-1β). Based on UPLC/MS/MS results, 49 components were considered the active ingredients of QSXZ. Network pharmacology analysis indicated that QSXZ regulates multiple inflammation-related pathways. Subsequent transcriptomic analysis showed that QSXZ regulates gene expression of S100A8 and S100A9. Our investigation observed an increased expression of S100A8 and S100A9 in monocytes derived from gout patients. Molecular docking and molecular dynamics simulation analysis revealed the binding pattern and interaction between QSXZ active compound CTS and S100A8/A9, and subsequent surface plasmon resonance (SPR) and cell thermal shift assay (CETSA) experiments verified the direct interaction between them. To investigate the mechanisms of action, we conducted RT-PCR, Western blotting, immunohistochemistry, flow cytometry, and measured the inflammatory response. Our findings highlight the pathogenic role of S100A8/A9 mediated TLR4-NLRP3 axis in gout and review outstanding therapeutic effects of QSXZ and its primary active compound CTS on MSU-induced experimental models. ConclusionsIn summary, this study substantiates the therapeutic potential of QSXZ and its primary active compound CTS, as promising alternative treatments for GA. Our findings provide valuable insight into the critical pharmacological mechanism of QSXZ in regulating inflammation, highlighting its potential therapeutic effects in GA management.

Disruption of survivin protein expression by treatment with YM155 accelerates the resolution of neutrophilic inflammation.

Prolonged survival of neutrophils is essential for determining the progression and severity of inflammatory and immune-mediated disorders, including gouty arthritis. Survivin, an anti-apoptotic molecule, has been described as a regulator of cell survival. This study aims to examine the effects of YM155 treatment, a survivin selective suppressant, in maintaining neutrophil survival in vitro and in vivo experimental settings of neutrophilic inflammation. BALB/c mice were injected with monosodium urate (MSU) crystals and treated with YM155 (intra-articularly) at the peak of inflammatory response. Leukocyte recruitment, apoptosis neutrophil and efferocytosis were determined by knee joint wash cell morphology counting and flow cytometry. Resolution interval (Ri) was quantified by neutrophil infiltration, monitoring the amplitude and duration of the inflammation. Cytokine production was measured by ELISA. Mechanical hypernociception was assessed using an electronic von Frey aesthesiometer. Efferocytosis was evaluated in zymosan-induced neutrophilic peritonitis. Survivin and cleaved caspase-3 expression was determined in human neutrophils by flow cytometry. Survivin was expressed in neutrophils during MSU-induced gout, and the treatment with YM155 reduced survivin expression and shortened Ri from ∼8 h observed in vehicle-treated mice to ∼5.5 h, effect accompanied by increased neutrophil apoptosis and efferocytosis, both crucial for the inflammation resolution. Reduced IL-1β and CXCL1 levels were also observed in periarticular tissue. YM155 reduced histopathological score and hypernociceptive response. In human neutrophils, lipopolysaccharide (LPS) increased survivin expression, whereas survivin inhibition with YM155 induced neutrophil apoptosis, with activation of caspase-3. Survivin may be a promising therapeutic target to control neutrophilic inflammation.

Gout-associated SNP at the IL1RN-IL1F10 region is associated with altered cytokine production in PBMCs of patients with gout and controls

ObjectivesGout is caused by the response of the innate immune system to monosodium urate (MSU) crystals. A recent gout GWAS identified a signal of genetic association at a locus encompassing IL1RN-IL1F10. Colocalisation analysis using Genotype Tissue Expression Database (GTEx) eQTL data showed that the signal overlaps with genetic control of IL1RN/IL1F10 gene expression. We assess the functional implications of IL1RN rs9973741, the lead gout-associated variant.MethodsWe conducted functional validation of IL1RN rs9973741 in patients with gout and controls. The transcription level of IL1RN/IL1F10 was investigated in unstimulated or MSU-crystal co-stimulated PBMCs. Ex vivo functional assays were performed in PBMCs stimulated with C16 + MSU crystals or LPS for 24 h. Cytokine levels were assessed by ELISA.ResultsIn unstimulated PBMCs, no association of IL1RN rs9973741 (gout risk allele G) to IL1RN expression was observed while IL-1F10 was hindered by low expression at both transcriptional and protein levels. However, G allele carriers showed lower IL1RN expression in PBMCs stimulated with C16/MSU crystal and lower concentrations of circulating IL-1Ra in both controls and gout patients. PBMCs depicted less spontaneous IL-1Ra release in GG homozygous controls and lower IL-1Ra production in response to C16 + MSU crystal costimulation in patients with gout. The G allele was associated with elevated IL-1β cytokine production in response to C16 + MSU crystal stimulation in controls.ConclusionsThe gout risk allele G associates with lower circulating IL-1Ra, lower IL-1Ra production in PBMC assays and elevated IL-1β production in PBMCs challenged with C16 + MSU crystals but not in unchallenged cells. Our data indicate that the genetic signal that associates with gout at IL1RN-IL1F10 region functions to alter expression of IL-1Ra when stimulated by MSU crystals.

Performance of novel multiparametric second-generation dual-layer spectral detector CT in gouty arthritis.

This study aimed to compare the performance of different dual-energy computed tomography (DECT) technologies in detecting monosodium urate (MSU) crystals and evaluate the potential clinical value of novel second-generation dual-layer spectral detector CT (dlDECT) in gouty arthritis. Using data collected from a tertiary hospital, we examined the diagnostic accuracy of different DECT technologies for the diagnosis of MSU. We used two standards: (1) demonstration of MSU crystals in synovial fluid (gold) and (2) 2015 ACR/EULAR gout classification criteria (silver). Furthermore, six novel spectral parameters derived from dlDECT were quantitatively calculated and analyzed for MSU diagnostic efficiency. Of the 243 patients with 387 joints, 68 (27.98%) had synovial fluid analysis. Compared with the gold standard, MSU diagnostic accuracy statistics for dlDECT, dual-source DECT (dsDECT) and rapid kilovolt peak switching DECT (rsDECT) were as follows: area under the curve (AUC): 0.85, 0.80 and 0.75, respectively. Findings were replicated compared with the silver standard. Multiparametric analysis in dlDECT demonstrated the highest MSU detection rate (92.86%), significantly higher than rsDECT (42.08%) and dsDECT (85.80%). Among novel parameters in dlDECT, Calcium-suppressed index 25 (CaSupp-I 25) exhibited the best performance in distinguishing materials (MSU, muscle, and bone), with an AUC of 0.992. The differentiation was also aided by histograms, scatter plots, and attenuation curves. The novel dlDECT is likely not inferior to other DECT technologies in MSU detection, especially its spectral parameter CaSupp-I 25. Multiparameter analysis showed the potential value for detecting MSU crystals in gouty arthritis, providing valuable clinical insights for gout diagnosis. Question The performance of different DECT technologies in detecting monosodium urate (MSU), and the value of dual-layer spectral detector CT (dlDECT) in gouty arthritis remains unclear. Findings The dlDECT was likely not inferior to other DECT technologies in MSU detection, and its multiparametric analysis provided valuable information for MSU diagnosis. Clinical relevance Novel dlDECT may improve the accurate detection of MSU crystals in gouty arthritis compared to other DECT technologies, providing valuable clinical insights and potentially improving patient outcomes for more precise gout diagnosis.

Functional identification of soluble uric acid as an endogenous inhibitor of CD38.

Excessive elevation or reduction of soluble uric acid (sUA) levels has been linked to some of pathological states, raising another subject that sUA at physiological levels may be essential for the maintenance of health. Yet, the fundamental physiological functions and molecular targets of sUA remain largely unknown. Using enzyme assays and in vitro and in vivo metabolic assays, we demonstrate that sUA directly inhibits the hydrolase and cyclase activities of CD38 via a reversible non-competitive mechanism, thereby limiting nicotinamide adenine dinucleotide (NAD+) degradation. CD38 inhibition is restricted to sUA in purine metabolism, and a structural comparison using methyl analogs of sUA such as caffeine metabolites shows that 1,3-dihydroimidazol-2-one is the main functional group. Moreover, sUA at physiological levels prevents crude lipopolysaccharide (cLPS)-induced systemic inflammation and monosodium urate (MSU) crystal-induced peritonitis in mice by interacting with CD38. Together, this study unveils an unexpected physiological role for sUA in controlling NAD+ availability and innate immunity through CD38 inhibition, providing a new perspective on sUA homeostasis and purine metabolism.

Functional identification of soluble uric acid as an endogenous inhibitor of CD38

Excessive elevation or reduction of soluble uric acid (sUA) levels has been linked to some of pathological states, raising another subject that sUA at physiological levels may be essential for the maintenance of health. Yet, the fundamental physiological functions and molecular targets of sUA remain largely unknown. Using enzyme assays and in vitro and in vivo metabolic assays, we demonstrate that sUA directly inhibits the hydrolase and cyclase activities of CD38 via a reversible non-competitive mechanism, thereby limiting nicotinamide adenine dinucleotide (NAD+) degradation. CD38 inhibition is restricted to sUA in purine metabolism, and a structural comparison using methyl analogs of sUA such as caffeine metabolites shows that 1,3-dihydroimidazol-2-one is the main functional group. Moreover, sUA at physiological levels prevents crude lipopolysaccharide (cLPS)-induced systemic inflammation and monosodium urate (MSU) crystal-induced peritonitis in mice by interacting with CD38. Together, this study unveils an unexpected physiological role for sUA in controlling NAD+ availability and innate immunity through CD38 inhibition, providing a new perspective on sUA homeostasis and purine metabolism.

Effects of bariatric surgery on hyperuricemia and gout: a systematic review of the literature.

Gout is the most common form of inflammatory arthritis, and it is due to the deposition of monosodium urate crystals in the articular and extra-articular tissues. Body mass index is strongly correlated with elevated serum uric acid levels and gout is often associated with obesity and metabolic syndrome. Recommended nonpharmacological treatments for hyperuricemia and gout include dietary modifications and weight loss. Many studies have demonstrated that weight loss could reduce serum urate in patients with obesity and it is a commonly recommended treatment for gout. Bariatric surgery-induced weight loss exerts beneficial effects on hyperuricemia and gout, even if a possible raise of gout flares can be observed in patients with hyperuricemia early after surgery. The aim of this review is to systematically analyze all the studies published so far reporting a link between hyperuricemia and/or gout and bariatric surgery to obtain reliable figures on the incidence of this disease and describe the mechanisms underlying this association. Eleven studies accounting for 11,256 patients were included in the review. Mean preoperative prevalence of gout was 4.1%, while the preoperative prevalence of hyperuricemia ranged from 30.6% to 58%. After a mean follow-up of 8.5months, postoperative prevalence of gout significantly decreased to 2.9% (p < .007). The incidence of gout flares after bariatric surgery was higher in the early postoperative phase and progressively decreased over time. Similarly, serum uric acid concentrations showed an increase within the first postoperative month, which was followed by a progressive decrease below the preoperative value.

Material decomposition approaches for monosodium urate (MSU) quantification in gouty arthritis: a (bio)phantom study

BackgroundDual-energy computed tomography (DECT) is a noninvasive diagnostic tool for gouty arthritis. This study aimed to compare two postprocessing techniques for monosodium urate (MSU) detection: conventional two-material decomposition and material map-based decomposition.MethodsA raster phantom and an ex vivo biophantom, embedded with four different MSU concentrations, were scanned in two high-end CT scanners. Scanner 1 used the conventional postprocessing method while scanner 2 employed the material map approach. Volumetric analysis was performed to determine MSU detection, and image quality parameters, such as signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR), were computed.ResultsThe material map-based method demonstrated superior MSU detection. Specifically, scanner 2 yielded total MSU volumes of 5.29 ± 0.28 mL and 4.52 ± 0.29 mL (mean ± standard deviation) in the raster and biophantom, respectively, versus 2.35 ± 0.23 mL and 1.15 ± 0.17 mL for scanner 1. Radiation dose correlated positively with detection for the conventional scanner, while there was no such correlation for the material map-based decomposition method in the biophantom. Despite its higher detection rate, material map-based decomposition was inferior in terms of SNR, CNR, and artifacts.ConclusionWhile material map-based decomposition resulted in superior MSU detection, it is limited by challenges such as increased artifacts. Our findings highlight the potential of this method for gout diagnosis while underscoring the need for further research to enhance its clinical reliability.Relevance statementAdvanced postprocessing such as material-map-based two-material decomposition might improve the sensitivity for gouty arthritis in clinical practice, thus, allowing for lower radiation doses or better sensitivity for gouty tophi.Key PointsDual-energy CT showed limited sensitivity for tophi with low MSU concentrations.Materiel-map-based decomposition increased sensitivity compared to conventional two-material decomposition.The advantages of material-map-based decomposition outweigh lower image quality and increased artifact load.Graphical

Development of gout in people with asymptomatic hyperuricemia: study protocol for a 5-year prospective cohort

IntroductionThe central biochemical cause of gout is hyperuricemia (elevated serum urate levels). Ultrasound features of monosodium urate (MSU) crystal deposition are common in people with asymptomatic hyperuricemia. However, it is...

Assessing Changes in Vascular Inflammation and Urate Deposition in the Vasculature of Gout Patients After Administration of Pegloticase Using Positron Emission Tomography and Dual-Energy Computed Tomography—A Pilot Study

We assessed changes in vascular inflammation and monosodium urate (MSU)-coded deposits after administration of Pegloticase in the vasculature of tophaceous gout patients using 18F-fluorodeoxyglucose (18F-FDG) Positron emission tomography/computed tomography (PET/CT) and dual-energy CT (DECT). Ten patients with tophaceous gout, intolerant or refractory to urate-lowering therapy (ULT), were treated with Pegloticase every two weeks for six months. 18F-FDG PET/CT and DECT were performed at baseline and after Pegloticase therapy to detect vessel wall inflammation (Standard uptake value, SUVmean, and SUVmax) and vascular MSU-coded deposition (MSU volume). Data were summarized using means and standard deviations. Baseline and follow-up values were compared for each variable using mixed-effect models. Significant decreases in SUVmean (p = 0.0003) and SUVmax (p = 0.009) were found with a trend towards a decrease in vessel wall MSU volume after treatment. There was a significant decrease in serum urate, correlating with reduction in SUVmean (R2 = 0.65), with a trend towards a decrease in CRP and blood pressure in all patients. Despite the small sample size, we were able to demonstrate a decrease in vessel wall inflammation and a trend towards a decrease in MSU volume by intensively lowering serum urate. These findings suggest that MSU-coded deposits and hyperuricemia may play a role in vascular wall inflammation. It remains to be seen whether this correlates with a decrease in adverse cardiovascular outcomes.

Physiopathological Aspects of Synovial Fluid and Membrane in Psoriatic Arthritis

Background: Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy characterized by a variety of clinical manifestations, mainly affecting joints and entheses, but also skin, nails, the eye, and the intestine. Objectives: In this review, we describe the essential characteristics of both synovial membranes and synovial fluid (SF) in PsA. Similarly to other inflammatory arthritis, the histological peculiarities in PsA synovitis are lining hyperplasia, neoangiogenesis, and sublining infiltration by immune cells and inflammatory mediators. Synovial effusions are frequent in PsA patients and SF analysis allows us to determine the pathological process occurring in the joint. Routine examinations help clinicians in defining the inflammatory status and possibly the detection of specific cell subsets. In addition, pathogenic crystals including monosodium urate and calcium pyrophosphate may be found in PsA SF. Conclusions: SF represents a potential substrate to identify the biomarkers that are useful to predict disease progression and response to medications in PsA patients, thus guiding the choice of appropriate and tailored pharmacological treatment.