Avancées récentes dans la physiopathologie de l'hyperuricémie et de la goutte. [Recent advances in the pathophysiology of hyperuricemia and gout]
Détails
ID Serval
serval:BIB_1288B0936C3B
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
Avancées récentes dans la physiopathologie de l'hyperuricémie et de la goutte. [Recent advances in the pathophysiology of hyperuricemia and gout]
Périodique
Revue Médicale Suisse
ISSN
1660-9379 (Print)
Statut éditorial
Publié
Date de publication
03/2007
Volume
3
Numéro
103
Pages
720, 722-4
Notes
English Abstract Journal Article Review --- Old month value: Mar 21
Résumé
Gout is due to the formation and tissue deposition of MSU crystals. Hyperuricemia promotes crystal formation and results from the disequilibrium between the synthetic and elimination rates of uric acid. Recent studies have elucidated the mechanisms of renal handling of uric acid by specific transporters (URATI and OAT) which play a role in uric acid excretion. MSU crystals provoke inflammation by activating leukocytes to produce inflammatory cytokines. One mechanism is through the TLR2 and TLR4 receptors, which form part of the innate immune system. MSU crystals can also activate a protein complex called the inflammasome, which in turn activates IL-1 processing to yield the secreted mature form of IL- 1beta. The inflammatory effects of MSU can be blocked by IL-1 inhibitors. These advances could provide new targetted therapeutic approaches to treat hyperuricemia and gout.
Mots-clé
Gout/*physiopathology Humans Hyperuricemia/*physiopathology Inflammation/physiopathology
Pubmed
Création de la notice
25/01/2008 9:39
Dernière modification de la notice
20/08/2019 13:40