Monosodium Urate Deposits Research Articles

A pilot study on dual-energy computed tomography for detection of urate deposits in renal transplant patients with asymptomatic hyperuricemia.

An increasing role of dual-energy computed tomography (DECT) scan in tophaceous gout assessment is recognized, whereas its role in asymptomatic hyperuricemia is unknown. The objective of this study was to assess the prevalence of joint and renal monosodium urate deposits by DECT in asymptomatic hyperuricemia. Among a renal transplant population with at least 1 year of follow-up, we included 27 patients with sustained hyperuricemia and 11 with normal serum uric acid (SUA) levels. We excluded patients with gout or history of monoarthritis or oligoarthritis. We registered demographic data, drugs, hyperuricemia onset, comorbidities, renal function, and SUA. We used a 128-slice dual-source CT system, and the acquisition protocol included the pelvis and imaging of elbows, wrists, hands, knees, ankles, and feet. The reading process was performed by 2 radiologists. The mean age was 43.7 ± 12 years, 57.8% were males, and median follow-up was 7 years. Hyperuricemia presented after a median time of 0.61 years after transplantation and had persisted for a median of 3.2 years (0.5-16.8 years). For the hyperuricemic group, the median SUA at the DECT scan and the maximum SUA levels were 7.9 and 8.9 mg/dL, respectively. Groups were similar in most of the clinical variables. We did not find any articular or renal deposit; conversely, we demonstrated a quadriceps tendon deposition in 1 patient with hyperuricemia (prevalence of 0.03%; 95% confidence interval, 0.006%-0.17%). In these patients with asymptomatic hyperuricemia, the prevalence of monosodium urate deposition assessed by DECT was low; however, larger studies need to be performed for further validation.

SAT0127 Gout and RA: not Such A Rare Coexistence after All?

BackgroundAccording to the current rheumatology literature, the simultaneous occurrence of rheumatoid arthritis (RA) and gout is rare and only a few cases have been reported to date.[1] However, clinical practice...

Le pied métabolique et endocrinien (hors pied diabétique)

Among metabolic arthropathies, crystal-induced arthropathies are the main causes of involvement of the foot. Gout, a deposition disease due to chronic hyperuricemia with monosodium urate deposits in and around joints, is the main culprit. Treatment armatorium is large but patient compliance and therapeutic inertia by physicians are responsible for treatment failures. Calcium pyrophosphate depositon disease is a rare cause of foot and ankle involvement but specific radiographic patterns and crystal identification in the synovial fluid will allow diagnosis. Very rarely, apatite crystals deposits are responsible for pseudo-acute gout attack. Other metabolic disorders including haemochromatosis, lipid depositons, and endocrine diseases such as acromegaly, can involve both the ankle and the foot.

AB0841 Tendon Involvement in Chronic Tophaceous Gout Detected by Dual-Anergy-Computertomography

BackgroundGout is the most prevalent metabolic arthritis and affects about 8,3 million inhabitants in the USA. Epidemiologic data from Europe are comparable and indicate that gouty arthritis or chronic tophaceous...

AB0995 Clinical and Ultrasound Findings in Manual Workers at High Risk of Occupational Disability and Hyperuricemia

BackgroundIn the last decade, the role of musculoskeletal ultrasound in investigating monosodium urate deposition is rapidly evolving since various findings have been described as specific for gout.ObjectivesThe goal of this...

Dual-energy CT for the diagnosis of gout: an accuracy and diagnostic yield study

ObjectivesTo assess the accuracy of dual-energy CT (DECT) for diagnosing gout, and to explore whether it can have any impact on clinical decision making beyond the established diagnostic approach using...

Definition of hyperuricemia and gouty conditions

To define gout conditions and hyperuricemia. Gout is defined as an arthritic condition resulting from the deposition of monosodium urate (MSU) crystals in and/or around joints, following long-standing hyperuricemia. Several recent ultrasound studies disclosed MSU deposits in a large proportion of asymptomatic hyperuricemic patients. A gout condition defined by asymptomatic MSU deposits can therefore be individualized. Such asymptomatic deposits appear to precede the occurrence of flares, which seem to be triggered by mobilization of preformed crystals. Hyperuricemia appears to be the main, if not the only, risk factor for gout. Recent studies also support the view that hyperuricemia is an independent risk factor for renal and cardiovascular diseases. The level at which uricemia becomes abnormal is still disputed. This lack of consensus precludes comparison of studies using different definitions and impairs the understanding of gout by doctors and patients. We propose to define hyperuricemia as greater than 6 mg/dl, as the life-long risk of gout seems to start at this level. This definition is identical to the minimum uricemia target of urate-lowering drugs (ULDs). Asymptomatic MSU crystals deposits can now be identified and precede the onset of gout flares. Defining hyperuricemia as greater than 6 mg/dl would have the advantage to give the same value for normal and ULD-targeted uricemia, which would facilitate patients' adherence to this target.

The Genetic Basis of Gout

Gout results from deposition of monosodium urate (MSU) crystals. Elevated serum urate concentrations (hyperuricemia) are not sufficient for the development of disease. Genome-wide association studies (GWAS) have identified 28 loci controlling serum urate levels. The largest genetic effects are seen in genes involved in the renal excretion of uric acid, with others being involved in glycolysis. Whereas much is understood about the genetic control of serum urate levels, little is known about the genetic control of inflammatory responses to MSU crystals. Extending knowledge in this area depends on recruitment of large, clinically ascertained gout sample sets suitable for GWAS.

Association of Toll-like receptor 2 polymorphisms with gout

Gout is the most common autoinflammatory arthritis characterized by elevated serum urate and recurrent attacks of intra-articular crystal deposition of monosodium urate (MSU) in tissues. The pathogenesis of gout has not been fully determined, although certain genetic factors are involved in the development of gout. Accumulated data suggested that MSU crystal-induced inflammation is a paradigm of innate immunity. As Toll-like receptors (TLRs) are the underlying mechanisms of the innate immune response, the present study aimed to investigate whether TLR2 polymorphisms are associated with gout. Two single-nucleotide polymorphisms (Arg677Trp and Arg753Gln, rs5743708) in TLR2 were genotyped by polymerase chain reaction-restriction fragment length polymorphism and the -196 to -174 del polymorphism was investigated using the allele-specific polymerase chain reaction in 431 individuals (215 patients with gout and 216 healthy controls). TLR2 Arg677Trp and Arg753Gln genotyping indicated that all the positive samples were of the wild-type genotype. No significant differences in genotype (χ2=1.686, P=0.430) and allele (χ2=1.430, P=0.232) frequencies of the -196 to -174 del polymorphism between the patients with gout and the control groups was observed. Our results suggested that the TLR2 Arg677Trp, Arg753Gln and the -196 to -174 del polymorphisms were not associated with susceptibility to primary gouty arthritis.

Study on the anti-gout activity of chlorogenic acid: improvement on hyperuricemia and gouty inflammation.

Gout is a metabolic disorder associated with hyperuricemia resulting in the deposition of monosodium urate (MSU) crystals in joints and tissues. Lowering serum uric acid (Sur) levels and anti-inflammation are highly essential in treating gout. Chlorogenic acid (CA), as one of the most abundant polyphenols in the Chinese medicines, has been rarely reported to have an anti-gout effect. The model of potassium oxonate (PO)-induced hyperuricemia in mice and MSU crystal-induced inflammation in rats has been established in this study. The potential beneficial effects and mechanisms of CA on hyperuricemia and gouty arthritis were elucidated. The results demonstrated that CA significantly decreased the Sur level by inhibiting the xanthine oxidase (XOD) activity but not increasing the urinary uric acid (Uur) level. In addition, CA also exhibited the effect of suppressing paw swelling. Further investigation indicated that CA improved the symptoms of inflammation induced by MSU crystals by inhibiting the production of proinflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). The present study suggests that CA may have a considerable potential for development as an anti-gouty arthritis agent for clinical application.

Mechanisms of Spontaneous Resolution of Acute Gouty Inflammation

Acute gout is an auto-inflammatory disease characterized by self-limiting inflammation in response to the deposition of monosodium urate (MSU) crystals in the joints or tissues. Recognition of MSU triggers activation of the NLRP3 inflammasome, release of active interleukin (IL)-1β, and amplification of the inflammatory response by the surrounding tissue followed by recruitment and activation of inflammatory leukocytes. The shutdown of this inflammatory response is linked to a number of regulatory events ranging from crystal coating and apoptotic cell clearance through to pro-inflammatory cytokine regulation and transforming growth factor β1 (TGFβ1) production. This review will highlight mechanisms that limit acute inflammation triggered by MSU crystals and suggests areas for further research.

Gout with auricular tophi following anti-tuberculosis treatment: a case report

BackgroundAuricular tophi are firm deposits of monosodium urate in crystal form, which may slowly develop in subcutaneous tissue of the ear. Ear is not usual locations for gout tophi, but when this growth does occur, helix and the antihelix are common sites.Case presentationWe present a 64-year-old man who had multiple painless nodules over bilateral helix. An excisional biopsy was performed. Hematoxylin-eosin staining of biopsy specimens revealed a proteinaceous matrix that surrounded dissolved crystals, consistent with gout tophi. Bilateral auricular tophi are not common and may resemble a number of other diseases including squamous cell carcinomas, Kaposi’s sarcoma, epidermal and dermoid cysts, rheumatoid nodules. Biopsy should be performed to rule out malignancy.ConclusionsTophi of the auricle are usually asymptomatic but can become inflamed and occasionally ulcerate through the overlying skin. Chronic tophaceous gout is treated with dietary control and medication. Surgical excision is performed under local anesthetic if symptoms progression or cosmetically deformity is concerned.

Difficult diagnosis of gout: the benefit of dual energy computed tomography, initial experience in routine clinical practice

Gout, one of the most common inflammatory arthritides in humans, is still difficult to diagnose in challenging situations, when fluid for arthrocentesis or an apparent tophus are absent and, for example, an infection as differential diagnosis has to be ruled out. Dual energy computed tomography (DECT) is an established tool for detection and characterisation of uric acid stones in the urinary tract and has recently been used to detect and display urate deposits. Our first experiences with DECT as a diagnostic tool in routine clinical practice show, that DECT is a promising imaging technique which allows the detection of monosodium urate deposits and benefits the routine diagnosis of tophaceous gout particularly in diffuse soft tissue swelling of the limbs, without the possibility of needle aspiration. However, DECT does not seem suitable to detect dissolved urate crystals, neither in vitro nor in vivo.

SAT0347 Cartilaginous Uric Acid Deposition in Advanced Osteoarthritis: Innocent Bystander or Promotor of Cartilage Destruction?

ObjectivesRecent studies have suggested that synovial fluid uric acid could contribute to tissue inflammation, disease severity and progression of osteoarthritis (OA). Intraarticular uric acid has been associated with OA disease...

AB0112 Anisomeles indica and its active principles modulate IL-1BETA

BackgroundGout is a chronic disease induced by the deposition of monosodium urate. It consists with four stages, hyperuricemia, asymptoms, gout flare and tophaceous gout. Current therapies mainly prevent the flare...

SP0018 The Practical Case: Is it Really Easy to Distinguish Gout from CPPD by Ultrasound? Live Case with Patient

Musculoskeletal ultrasound may be useful to discriminate between similar arthritic entities. In case of suspected crystalline arthropathy, sonography may identify calcium pyrophosphate deposition (CPPD) or monosodium urate (MSU) crystals with...

SAT0354 Usefulness of Imaging Techniques in Mixed Crystal Deposition (Pilot Study).

BackgroundThe coexistence of both urate and calcium pyrophosphate (CPP) crystals in the same synovial fluid has been reported by many authors. The evaluation of crystal deposits in mixed microcrystallic arthropathy...

SP0007 Chronic Gout, Chronic Treatment

Gout is a chronic metabolic and inflammatory disease whose sine qua non is hyperuricemia. The acute attacks seen in gout are merely the “tip of the iceberg” and represent the...

AB1080 Effect of serum urate level on prevention of flare in acute gouty arthritis patients with canakinumab

BackgroundLowering serum urate (SU) level is considered to be the mainstay of gouty arthritis (GA) therapy. SU levels below 6mg/dL favor dissociation of monosodium urate deposits (microtophi and visible tophi)...

SP0006 Visualising Crystals: DECT and More

The first human to see monosodium urate (MSU) crystals in his newly invented microscope was the Dutch researcher Antoni van Leeuwenhoek in 1679. Since then, the gold standard to establish...