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Hyperuricemia in Tendons

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 920))

Abstract

Hyperuricemia, particularly gout, and the immune inflammatory response are highly integrated. Both, long standing hyperuricemia and monosodium urate (MSU) crystal deposition can challenge tendon homeostasis because of their potential to cause inflammation to the host. Knowledge is emerging from clinical imaging research depicting where MSU crystals deposit, including patellar tendon, triceps and quadriceps tendons. Remarkably, subclinical tendon inflammation and damage are also present in asymptomatic hyperuricemia. Monosodium urate crystals act as danger activating molecular patterns (DAMPs), activating the inflammasome and inducing the secretion of IL-1beta, a key mediator of the inflammatory response. The crucial role of IL-1beta in driving the inflammatory events during gout attacks is supported by the clinical efficacy of IL-1beta blockade. Some data implicating IL-1beta as an initiator of tendinopathy exist, but the link between hyperuricemia and the development of tendinopathy remains to be validated. Further knowledge about the interactions of uric acid with both innate immune and tendon cells, and their consequences may help to determine if there is a subclass of hyperuricemic-tendinopathy.

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Abbreviations

ADAMTS1:

A Disintegrin-Like And Metalloprotease (Reprolysin Type) With Thrombospondin Type 1 Motif, 1

ADAMTS4:

A Disintegrin-Like And Metalloprotease (Reprolysin Type) With Thrombospondin Type 1 Motif, 4

ADAMTS5:

A Disintegrin-Like And Metalloprotease (Reprolysin Type) With Thrombospondin Type 1 Motif, 5

CRP:

C reactive protein

DAMP:

Danger Associated Molecular patterns

DECT:

dual energy computerized tomography

DNA:

deoxynucleic acid

IL-1beta, IL-1alpha, IL-6, IL-8, IL-18:

Interleukins

MCP-1/CCL2:

macrophage chemotactic protein

MMP-2, MMP-3, MMP-13:

metalloproteinases

MSU:

monosodium urate

NLRP3:

NOD-like receptor protein 3

NSAIDs:

non-steroidal anti-inflammatory drugs

PGE2:

prostaglandin E2

RNA:

ribonucleic acid

TLR2, TLR4:

Toll like receptors

TNF-alpha:

tumor necrosis factor alpha

VEGF:

vascular endothelial growth factor

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Correspondence to Isabel Andia .

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Andia, I., Abate, M. (2016). Hyperuricemia in Tendons. In: Ackermann, P., Hart, D. (eds) Metabolic Influences on Risk for Tendon Disorders. Advances in Experimental Medicine and Biology, vol 920. Springer, Cham. https://doi.org/10.1007/978-3-319-33943-6_11

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