Arthritis und Rheuma 2004; 24(04): 122-126
DOI: 10.1055/s-0037-1618469
Rheuma und Darm
Schattauer GmbH

Enteroirritation und Enteroprotektion bei der Rheumatherapie

Enteroirritation and enteroprotection in the treatment of rheumatic diseases
Wolfgang W. Bolten
1   Rheumaklinik Wiesbaden, Klaus Miehlke-Klinik
› Author Affiliations
Further Information

Publication History

Publication Date:
23 December 2017 (online)

Zusammenfassung

Traditionelle nichtsteroidale Antirheumatika (tNSAR) und Acetylsalicylsäure (ASS) schädigen die Schleimhaut des gesamten Intestinaltrakts. Schwere Läsionen, Ulzera und Perforationen, Blutungen und Strikturen führen zur Hospitalisation und gegebenenfalls zum Tod. Besonders bei älteren Patienten über 65 Jahre und bei Patienten mit schweren Allgemeinerkrankungen ist das Blutungsund Perforationsrisiko erhöht. Magen-Darm-Ulzera oder gastrointestinale (GI-) Blutungen in der Anamnese oder die Komedikation mit Antikoagulanzien, Kortikosteroiden und nicht zuletzt hohe tNSAR-Dosierungen oder Multi-tNSAR-Therapien lassen das GI-Komplikationsrisiko mit jedem Faktor weiter ansteigen. Ein erst in letzter Zeit besser analysierter Risikofaktor ist ASS, auch in der niedrigen Dosierung zur kardiovaskulären Prophylaxe. Ein bereits bestehendes tNSAR-Ulkus kann mit Protonenpumpenhemmern (PPI) erfolgreich zur Abheilung gebracht werden, ohne dass die tNSAR-Therapie abgesetzt werden muss. In jedem Fall muss die niedrigste mögliche noch wirksame tNSAR-Dosis gewählt werden. Bei Risikopatienten sollten Präventivmaßnahmen ergriffen werden, z. B. eine Komedikation mit dem allerdings mit Nebenwirkungen belasteten Prostaglandinanalogon Misoprostol oder die Behandlung mit hochdosierten H2-Rezeptorantagonisten. Am besten wirken als Kotherapeutika aber PPI. In gleichem Maß wie durch PPI kann die Ulkusrate auch mit COX-2-selektiven Inhibitoren (Coxibe) anstelle der tNSAR erniedrigt werden. Outcomestudien mit über 8000 Patienten belegen das verminderte GI-Komplikationsrisiko unter Coxiben.

Trotz des großen wissenschaftlichen Fortschritts werden die Möglichkeiten der sicheren Schmerztherapie unzureichend ausgeschöpft. Die Ergebnisse der Forschung müssen effizienter an die behandelnden Ärzte weitergegeben werden.

Summary

Traditional nonsteroidal anti-inflammatory drugs (tNSAIDs) and acetylsalicylic acids (ASA) damage the mucous membrane of the entire intestinal tract. Severe lesions, ulcera and perforations, bleeding and strictures lead to hospitalisation and in some cases death. There is an increased risk of bleeding and perforation particularly in elderly patients over 65 and patients with acute general illnesses. Gastroduodenal ulcera or gastrointestinal (GI) bleeding in the anamnesis or the taking of anticoagulants, corticosteroids and not least of all high tNSAID dosages or multi tNSAID treatments at the same time make the risk of GI complications further increase in every factor. A risk factor which was not more deeply analysed until recently is ASA, also in low dosage for cardiovascular prophylaxis.

An already existing tNSAID ulcer can be successfully healed with proton pump inhibitors (PPI) without having to abandon tNSAID therapy. The lowest possible effective tNSAID dose should always be selected. Preventative measures should be taken for patients who are at risk, e.g. the taking of the prostaglandin analogue Misoprostol which have side effects or the treatment with high dose H2 receptor antagonists.

PPI are most effective as a co-therapeutics. The ulcer rate can also be lowered with cyclooxygenase-2-inhibitors instead of with tNSAIDs to the same extent as with PPI. Outcome studies with over 8,000 patients prove the reduced risk of GI complications using cyclooxygenase-2-inhibitors.

Despite significant scientific progress, the possibilities for safe analgesic therapy are becoming insufficiently exhausted. Research results will have to be more efficiently passed on to physicians.

 
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