european crystal network workshop



    Cesar Diaz-Torne (1), Maria A. Ortiz (2), Sicylle Jeria-Navarro (1), Andrea Garcia-Guillem (1), Lluis Sanz (1), Susana Hernandez (1), Silvia Vidal (2)

    (1). Servei De Reumatologia. Hospital De La Santa Creu I Sant Pau. ( 2). Servei D’immunologia. Institut De Recerca Sant Pau.


    Introduction: Gout is a chronic inflammatory deposition disease related to an increase of cardiovascular (CV) events and mortality. Subclinical chronic inflammation has been demonstrated in this patients but not its relation with the monosodium urate (MSU) crystal deposit size and the number of CV risk factors.


    Objective: To study subclinical inflammation in intercritical gout patients and its relation to the estimated size of the MSU crystals deposit and the number of CV risk factors.


    Methods: To analyze subclinical inflammation in intercritical gout patients we performed a secretome analysis and a cytokine and adiponektine plasma levels quantification (IL-1β, IL-18, IL-6, sIL-6R, TNFα, CXCL-5, RANTES, leptin, resistin and adiponectin). As nowadays it is not feasible to determinate the whole body deposit of MSU crystals we created three different MSU crystal deposit size patient groups using an indirect clinical classification to estimate it. Then we compared cytokine levels between healthy donors and gout patients. We also compared levels between patients with different crystal deposit estimated size and studied its association to the number of CV risk factors.


    Results: Ninety consecutive patients attending a Crystal Arthritis Unit were studied. Mean age was 68.27 (28-101) years. 81.1% were male. Clinical gout evolution was of 10.1±9.8 years. 77.5% were on urate lowering treatment. 24% has tophaceous gout. Mean uric acid was 6.3±2.1 mg/dl with 47.1% of them being on target. Hypertension was present in 68.9%, diabetes mellitus in 18.9%, dislipemia in 48.9%, BMI>30 in 32,9%, abdominal obesity in 50% and 16,1% suffered from ischemic heart disease. From the 102 molecules studied in the secretome analysis in 56 there was at least a 20% difference between donors group and any group of intercritical gout patients. In 74% of them gouty patients secreted lower levels. IL-18, sIL-6R, RANTES, leptin and adiponectin were higher in patients than in healthy donors. IL-18, sIL6-R, RANTES and CXCL5 levels were associated to the size of the crystal deposits. IL-18, sIL-6R, RANTES and leptin were higher in gout groups with CV risk factors. IL-18, sIL6-R, RANTES and leptin were higher in gout patients with no risk factors when compared to healthy donors with no risk factors. No differences were found when comparing urate lowering treated and non-treated patients.


    Conclusion: Our results demonstrate that some proinflammatory cytokines and metabolic proteins are raised in intercritical gout patients. Some of them are different from the flare/inflammasome expected ones. In some cytokines this elevation is related to the size of the monosodium urate crystal deposit or to the number of cardiovascular risk factors. This cytokine changes could help to explain the increase of the cardiovascular events in gout patients.