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

Details

Ressource 1Download: serval:BIB_6C79E25BFF3B.P001 (298.90 [Ko])
State: Public
Version: author
License: Not specified
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
Serval ID
serval:BIB_6C79E25BFF3B
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
Neue Erkenntnisse zur Pathophysiologie und Therapie der Gicht [New knowledge on the pathophysiology and therapy of gout]
Journal
Zeitschrift für Rheumatologie
Author(s)
So A.
ISSN
0340-1855
Publication state
Published
Issued date
2007
Peer-reviewed
Oui
Volume
66
Number
7
Pages
562-567
Language
german
Abstract
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.
Keywords
Animals, Arthritis, Gouty, Endothelium, Humans, Hyperuricemia, Inflammation Mediators, Interleukin-1beta, Kidney, Leukocytosis, Monocytes, Synovial Membrane, Uric Acid
Pubmed
Web of science
Open Access
Yes
Create date
03/03/2009 10:46
Last modification date
01/10/2019 7:18
Usage data