Neue Erkenntnisse zur Pathophysiologie und Therapie der Gicht [New knowledge on the pathophysiology and therapy of gout]

Détails

Ressource 1Télécharger: serval:BIB_6C79E25BFF3B.P001 (298.90 [Ko])
Etat: Public
Version: de l'auteur
Licence: Non spécifiée
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ID Serval
serval:BIB_6C79E25BFF3B
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Neue Erkenntnisse zur Pathophysiologie und Therapie der Gicht [New knowledge on the pathophysiology and therapy of gout]
Périodique
Zeitschrift für Rheumatologie
Auteur(s)
So A.
ISSN
0340-1855
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
66
Numéro
7
Pages
562-567
Langue
allemand
Résumé
Gout is caused by the deposition of monosodium urate crystals (MSU) in tissue and provokes a local inflammatory reaction. It is the most common form of inflammatory arthritis in the elderly. The formation of MSU crystals is facilitated by hyperuricemia. In the last two decades, both hyperuricemia and gout have increased markedly and similar trends in the epidemiology of the metabolic syndrome have been observed. Recent studies provide new insights into uric acid metabolism in the kidneys as well as possible links between hyperuricemia and hypertension. MSU crystals provoke inflammation by activating leukocytes to produce inflammatory cytokines and other inflammatory mediators. The uptake of MSU crystals by monocytes involves interactions with Toll-like receptors (TLR-2 and TLR-4) and CD14, components of the innate immune system. Intracellularly, MSU crystals activate inflammasomes to activate pro-IL-1 (interleukin 1) processing to yield mature IL-1beta. The inflammatory effects of MSU are IL-1-dependent and can be blocked by IL-1 inhibitors. These advances provide new therapeutic targets to treat hyperuricemia and gout.
Mots-clé
Animals, Arthritis, Gouty, Endothelium, Humans, Hyperuricemia, Inflammation Mediators, Interleukin-1beta, Kidney, Leukocytosis, Monocytes, Synovial Membrane, Uric Acid
Pubmed
Web of science
Open Access
Oui
Création de la notice
03/03/2009 10:46
Dernière modification de la notice
01/10/2019 7:18
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