Avancées récentes dans la physiopathologie de l'hyperuricémie et de la goutte. [Recent advances in the pathophysiology of hyperuricemia and gout]

Details

Serval ID
serval:BIB_1288B0936C3B
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Avancées récentes dans la physiopathologie de l'hyperuricémie et de la goutte. [Recent advances in the pathophysiology of hyperuricemia and gout]
Journal
Revue Médicale Suisse
Author(s)
So  A.
ISSN
1660-9379 (Print)
Publication state
Published
Issued date
03/2007
Volume
3
Number
103
Pages
720, 722-4
Notes
English Abstract Journal Article Review --- Old month value: Mar 21
Abstract
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.
Keywords
Gout/*physiopathology Humans Hyperuricemia/*physiopathology Inflammation/physiopathology
Pubmed
Create date
25/01/2008 8:39
Last modification date
20/08/2019 12:40
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