Synovial Fluid Analysis for Diagnosis of Intercritical Gout

Pascual, Eliseo; Batlle-Gualda, Enrique; Martínez, Agustín; Rosas, Jose Armando Alvarado; Vela, Paloma

doi:10.7326/0003-4819-131-10-199911160-00007

Cited by 221 publications

(119 citation statements)

References 12 publications

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“…The capacity to nucleate and grow crystals is clearly an important variable. However, other factors besides the presence of crystals must be involved, because crystals can be detected in asymptomatic joints (2)(3)(4)(5) and at sites of experimental intracutaneous crystal injection after erythema has resolved (12). One possibility is that crystals are coated with protective proteins, such as apolipoproteins, that reduce the inflammatory potential of crystals following uptake by polymorphonuclear cells (18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

“…In patients with gout, monosodium urate monohydrate (MSU) crystals are readily detectable in asymptomatic joints (2) and during the intercritical phase (3). In contrast with joints of patients with acute gout, which have intense neutrophilic infiltration of the synovium, asymptomatic joints of patients with gout have a predominantly mononuclear cell infiltrate (4).…”

mentioning

confidence: 99%

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Safe disposal of inflammatory monosodium urate monohydrate crystals by differentiated macrophages

Landis¹,

Yagnik²,

Florey³

et al. 2002

Arthritis & Rheumatism

146

102

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Objective. Although monosodium urate monohydrate (MSU) crystals have been recognized since the 18th century as the etiologic agent of gout, it is still unknown why certain hyperuricemic individuals remain asymptomatic, and how an acute attack of gout spontaneously resolves. We hypothesized that mononuclear phagocytes hold the key to these questions, and that the state of monocyte/macrophage differentiation is critical.Methods. Human peripheral blood monocytes were differentiated for 1-7 days in vitro and examined with respect to 1) uptake of MSU crystals, 2) expression of macrophage, dendritic cell, and activation markers, 3) secretion of tumor necrosis factor ␣ (TNF␣), interleukin 1␤ (IL-1␤), IL-6, and IL-10, 4) activation of endothelial E-selectin expression, and 5) enhancement of secondary neutrophil recruitment by endothelial cells.Results. MSU crystals induced TNF␣, IL-1␤, and IL-6 (but not IL-10) secretion in undifferentiated monocytes, which in turn promoted endothelial cell E-selectin expression and secondary neutrophil capture under shear flow. In contrast, differentiation over 3-5 days led to development of a noninflammatory phenotype characterized by a lack of proinflammatory cytokine secretion, lack of endothelial cell activation, and lack of secondary neutrophil recruitment. Acquisition of the noninflammatory phenotype correlated with expression of macrophage antigen but not with expression of dendritic cell marker or activation marker. Monocytes and macrophages were similarly phagocytic, and a control particle, zymosan, elicited secretion of the full panel of cytokines in both cell types. However, coincubation with MSU led to a significant suppression of zymosaninduced TNF␣ secretion (P ‫؍‬ 0.009) from macrophages but not monocytes.Conclusion. These findings imply that differentiated macrophages provide a safe-disposal mechanism for the removal of inflammatory urate crystals. This may be of clinical relevance to the maintenance of asymptomatic hyperuricemia and the resolution of acute gout.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Safe disposal of inflammatory monosodium urate monohydrate crystals by differentiated macrophages

Landis¹,

Yagnik²,

Florey³

et al. 2002

Arthritis & Rheumatism

146

102

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“…The inclusion criteria were the following: (1) diagnosis of gout proven by presence of MSUr crystals in the synovial fluid [17] or otherwise complying with the American Rheumatism Association criteria [18]; (2) pre-treatment with benzbromarone monotherapy of 100-200 mg/day for at least 2 months with available sUr efficacy results; (3) no relevant liver disease and (4) no relevant renal disease, defined as glomerular filtration rate (GFR) >50 ml min −1 1.73 m −2 .…”

Section: Methodsmentioning

confidence: 99%

Biochemical effectiveness of allopurinol and allopurinol-probenecid in previously benzbromarone-treated gout patients

et al. 2007

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“…In the absence of clinical intervention, acute gouty arthritis usually resolves within a few days. However, monosodium urate monohydrate (MSU) crystals can persist in joints following acute inflammation and have been identified within mononuclear cells in synovial fluid aspirated from clinically quiescent knee and metatarsophalangeal joints (1)(2)(3). A possible beneficial role of macrophages in gout has been demonstrated with the observation that mouse macrophage cell lines and human in vitro-differentiated macrophages ingest MSU crystals without proinflammatory cytokine secretion or endothelial cell activation (4,5).…”

mentioning

confidence: 99%

Macrophage release of transforming growth factor β1 during resolution of monosodium urate monohydrate crystal–induced inflammation

Yagnik¹,

Evans²,

Florey³

et al. 2004

Arthritis & Rheumatism

116

102

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Objective. It has previously been shown that as monocytes differentiate into macrophages, they lose the ability to secrete proinflammatory cytokines in response to monosodium urate monohydrate (MSU) crystals. The purpose of this study was to investigate whether MSU crystals induce macrophages to secrete antiinflammatory factor instead.Methods. Human monocyte or macrophage isolates were prepared from samples obtained from healthy volunteer donors either by differentiation of blood monocytes in vitro or by collecting cells from skin blisters during the early or late phase of the dermal inflammatory response to cantharidin. Monocyte or macrophage isolates were then incubated with MSU crystals for 24 hours, and culture supernatants were assayed for candidate antiinflammatory mediators (by enzyme-linked immunosorbent assay) and for the capacity to activate or suppress endothelial cell E-selectin expression and secondary neutrophil recruitment under shear flow.Results. Analysis of supernatants from in vitrodifferentiated macrophages revealed that transforming growth factor ␤1 ( The mechanisms behind the spontaneous resolution of gout remain incompletely explained. In the absence of clinical intervention, acute gouty arthritis usually resolves within a few days. However, monosodium urate monohydrate (MSU) crystals can persist in joints following acute inflammation and have been identified within mononuclear cells in synovial fluid aspirated from clinically quiescent knee and metatarsophalangeal joints (1-3). A possible beneficial role of macrophages in gout has been demonstrated with the observation that mouse macrophage cell lines and human in vitro-differentiated macrophages ingest MSU crystals without proinflammatory cytokine secretion or endothelial cell activation (4,5). Such quiescent behavior is in marked contrast to less well-differentiated monocytic isolates, which secrete tumor necrosis factor ␣ (TNF␣), interleukin-1␤ (IL-1␤), IL-6, and IL-8, activate E-selectin expression, and promote secondary neutrophil capture by endothelial cells under physiologic flow in response to MSU crystal uptake (5-9).

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Synovial Fluid Analysis for Diagnosis of Intercritical Gout

Abstract: Arthrocentesis of asymptomatic knees and first metatarsophalangeal joints and synovial fluid analysis are simple procedures that facilitate the diagnosis of gout during intercritical periods.

Cited by 221 publications

References 12 publications

Safe disposal of inflammatory monosodium urate monohydrate crystals by differentiated macrophages

Safe disposal of inflammatory monosodium urate monohydrate crystals by differentiated macrophages

Biochemical effectiveness of allopurinol and allopurinol-probenecid in previously benzbromarone-treated gout patients

Macrophage release of transforming growth factor β1 during resolution of monosodium urate monohydrate crystal–induced inflammation

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