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Título:	Proinflammatory cytokines and C-reactive protein in uveitis associated with Behçet's disease
Autor/a:	Mesquida, Marina; Molins Monteys, Blanca; Llorenç, Victor; Sainz de la Maza, Maite; Hernandez, Maria Victoria; Espinosa Garriga, Gerard; Adán Civera, Alfredo
Notas:	The aim of the present study was to determine the serum cytokine profile and levels of high sensitivity C-reactive protein (hsCRP) in patients with uveitis associated with Behcet's disease (BD) and to compare them with those obtained from healthy control subjects. We determined the serum concentration of interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta), IL-12p70, IL-17A, tumor necrosis factor-alpha (TNF-alpha), and hsCRP in 13 patients with active uveitis associated to BD, 24 inactive BD patients, and 20 controls. In a subgroup of 10 active patients, a second serum sample was obtained when the disease was inactive. Cytokine profiles and hsCRP levels were correlated with disease activity, severity, complications, and visual outcome. Levels of IFN-gamma and TNF-alpha were significantly increased in patients with active uveitis associated to BD compared to controls (P < 0.05). IFN-gamma, TNF-alpha, and hsCRP were significantly higher during active uveitis associated to BD compared to inactive disease (P < 0.05). Furthermore, IL-17A was significantly increased in patients with active BD without pharmacological treatment compared to controls (P < 0.05). No significant correlations were found with specific cytokine profiles and disease severity, visual outcome, or complications. In summary, increased serum levels of IFN-gamma, TNF-alpha, IL-17A, and hsCRP were associated with active uveitis associated with BD and might serve as markers of disease activity.
Materia(s):	-Citoquines -Proteïnes de la sang -Uveïtis -Malaltia de Behçet -Inflamació -Cytokines -Blood proteins -Uveitis -Behçet's disease -Inflammation
Derechos:	cc-by (c) Mesquida, Marina et al., 2014 http://creativecommons.org/licenses/by/3.0/es
Tipo de documento:	Artículo Artículo - Versión publicada
Editor:	Hindawi Publishing Corporation
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