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Foot tendon involvment in gout

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Old 25th January 2013, 04:49 PM
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Default Foot tendon involvment in gout

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Tendon involvement in the feet of patients with gout: a dual-energy CT study.
Dalbeth N, Kalluru R, Aati O, Home E, Doyle AJ et al,
Ann Rheum Dis (2013) 13(1):199.
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Objectives To examine the frequency and patterns of monosodium urate (MSU) crystal deposition in tendons and ligaments in patients with gout using dual-energy CT (DECT).

Methods Ninety-two patients with tophaceous gout had DECT scanning of both feet. Two readers scored the DECT scans for MSU crystal deposition at 20 tendon/ligament sites and 42 bone sites (total 1840 tendon/ligament sites and 3864 bone sites).

Results MSU crystal deposition was observed by both readers in 199/1840 (10.8%) tendon/ligament sites and in 399/3864 (10.3%) bone sites (p=0.60). The Achilles tendon was the most commonly involved tendon/ligament site (39.1% of all Achilles tendons), followed by the peroneal tendons (18.1%). Tibialis anterior and the extensor tendons were involved less commonly (7.6–10.3%), and the other flexor tendons, plantar fascia and deltoid ligaments were rarely involved (<5%) (p<0.0001 between sites). Involvement of the enthesis alone was more common in the Achilles tendon (OR (95% CI) 74.5 (4.4 to 1264), p<0.0001), as was any involvement of the enthesis (OR (95% CI) 6.8 (3.6 to 13.0), p<0.0001).

Conclusions Tendons are commonly affected by MSU crystal deposition in patients with tophaceous gout. The patterns of MSU crystal deposition suggest that biomechanical strain or other local factors may contribute to deposition of MSU crystals.
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Old 25th January 2013, 04:52 PM
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Default Re: Foot tendon involvment in gout

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Last edited by NewsBot : 19th August 2016 at 03:35 AM.
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Old 19th August 2016, 03:34 AM
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Default Re: Foot tendon involvment in gout

Hyperuricemia in Tendons.
Andia I, Abate M
Adv Exp Med Biol. 2016;920:123-32. doi: 10.1007/978-3-319-33943-6_11
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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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