Aktuelle Rheumatologie 2018; 43(03): 215-223
DOI: 10.1055/s-0043-121141
Übersichtsarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Stoffwechselkrankheit Gicht

The Metabolic Disease of Gout
Monika Reuss-Borst
1   Facharztpraxis am Rehabilitations- & Präventionszentrum, Bad Bocklet
,
Anne-Kathrin Tausche
2   Abteilung Rheumatologie, Med. Klinik und Poliklinik III, Dresden
› Author Affiliations
Further Information

Publication History

Publication Date:
13 March 2018 (online)

Zusammenfassung

Die Gicht ist die häufigste entzündliche Gelenkerkrankung. Ihr liegt mit der Hyperurikämie als Ursache eine metabolische Störung zugrunde. Abgelagerte Harnsäurekristalle führen zu den typischen anfallsartigen Gelenkentzündungen. In den letzten Jahrzehnten ist die Gichtinzidenz zusammen mit anderen metabolischen Erkrankungen zunehmend. Der Rheumatologe ist besonders gefragt, wenn sich die Gicht klinisch nicht typisch manifestiert (oligo- und polyartikulär), also andere Differenzialdiagnosen infrage kommen, wenn bereits Komplikationen aufgetreten sind (fortgeschrittene Arthropathie, tophöse Gicht, zunehmende Nierenfunktionseinschränkung) oder wenn sich die Therapie aufgrund von Komorbiditäten schwierig gestaltet. Im Allgemeinen ist die Diagnostik der Gicht für den erfahrenen Rheumatologen keine Herausforderung, zumal er über Tools wie die Gelenksonografie und Gelenkpunktion mit mikroskopischer Beurteilung von Synovialflüssigkeit verfügt. Auch erscheint die Behandlung der Gicht als „treat-to-target“-Konzept in Analogie zu anderen entzündlich-rheumatischen Erkrankungen und aufgrund effektiver therapeutischer Optionen vergleichsweise übersichtlich. Immer wieder kommt jedoch die Frage nach eventuell modifizierbaren Faktoren bei der Entstehung der Hyperurikämie und Gicht auf. Die vorliegende Arbeit richtet den Fokus auf die Beeinflussung der zugrundeliegenden metabolischen Ursachen unter Berücksichtigung aktueller wissenschaftlicher Erkenntnisse. Ziel ist es, den Fokus von der rein symptomatischen Therapie der Entzündung im Gichtanfall hin auf die kausale Beeinflussung der metabolischen Harnsäure-Homöostase zu richten. Dazu gehört neben diätetischen Maßnahmen auch die Modifikation von Harnsäure-erhöhenden Faktoren wie Komedikationen.

Abstract

Gout is the most common inflammatory joint disease. Its underlying cause is a metabolic condition in the form of hyperuricaemia. Prolonged hyperuricaemia may lead to deposition of monosodium urate crystals in joints and other tissues. The inflammatory response to these crystals results in the typical manifestation of gout flares. During the past few decades, a rising incidence of hyperuricaemia and gout together with other metabolic disorders has been observed. Rheumatologists are frequently consulted if the clinical presentation is not “typical” of gout, suggesting other differential diagnoses (e. g. if arthritis is oligo- or polyarticular), or if complications have occurred (gouty arthropathy, tophi, impaired renal function) and/or if treatment is complicated by co-morbidities. In general, making the right diagnosis is not too difficult for experienced rheumatologists as they have the right tools at hand, e. g. ultrasound and arthrocentesis with microscopic analysis of synovial fluid. Also the treatment of gout seems to be relatively easy as it follows a “treat-to-target” strategy with a manageable amount of therapies. However, one question that keeps coming up concerns possible modifiable factors regarding the development of hyperuricaemia and gout. In due consideration of current scientific evidence, the following article focuses on the causal metabolic aspects and highlights modifiable factors such as dietary habits and co-medications, which influence the homoeostasis of uric acid.

 
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