Aktuelle Rheumatologie 2018; 43(01): 82-87
DOI: 10.1055/s-0043-116663
Übersichtsarbeit
Georg Thieme Verlag KG Stuttgart · New York

Nicht steroidale Antirheumatika und gastrointestinales Risiko

Non-Steroidal Anti-Inflammatory Drugs and Gastrointestinal Risk
Wolfgang W. Bolten
1   Innere Med., Rheumatologie, Klaus Miehlke-Klinik, Wiesbaden
› Author Affiliations
Further Information

Publication History

Publication Date:
20 December 2017 (online)

Zusammenfassung

Bei somatischen muskuloskelettalen Schmerzerkrankungen werden nicht steroidale Antirheumatika (NSAR) mit Erfolg schmerz- und entzündungslindernd eingesetzt. Dazu hemmen sie die parakrine Synthese von Prostaglandinen (PG), die sowohl schmerzvermittelnd wirken, an anderer Stelle aber „house keeping“ Effekte haben. Dem Organismus stehen für die PG Synthese die Isoenzyme COX-1 und die induzierbare COX-2 zur Verfügung. Durch die Hemmung der COX-1 und konsekutiver Senkung der PG- Spiegel entstehen gastrointestinale Nebenwirkungen der GI-Mukosa. Im Gegensatz zu den traditionellen NSAR hemmen Coxibe selektiv die COX-2 und verursachen deshalb weniger GI-Probleme. Die Komedikation mit Protonenpumpenhemmern oder mit einem synthetischen PG-Analogon senkt die Ulkusrate ebenfalls. Auch andere nicht PG-abhängige Mechanismen schützen die Mukosa. Sie können ebenfalls durch NSAR gestört werden. 

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are used successfully to alleviate pain and inflammation in somatic musculoskeletal pain disorders. To this end, they inhibit the paracrine synthesis of prostaglandins (PGs), which induce pain while also having “house-keeping” effects. The COX-1 isoenzymes and the inducible COX-2 enzyme are available for PG synthesis in an organism. Inhibition of COX-1, followed by decreasing PG levels, leads to gastrointestinal side-effects affecting the GI mucosa. Unlike traditional NSAIDs, coxibs selectively inhibit COX-2, thereby causing fewer gastrointestinal problems. Co-medication with proton-pump inhibitors or a synthetic PG analogue also leads to a lower ulcer rate. Other non-PG-dependent mechanisms protect the mucosa. They also may be disrupted by NSAIDs.

 
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