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Jakarta, 28 Jan 2010
The Toxic Effects of NSAIDs on Small Bowel
The gastroduodenal toxicity of conventional non-steroidal anti-inflammatory drugs (NSAIDs) is widely recognized. Side effects involving the more distal portions of the intestinal tract are not only less common, but also frequently underestimated. It is now well established that NSAID-induced toxicity extends to the entire gastrointestinal tract including the small bowel, colon, and rectum.1,2
NSAID-induced lesions may develop either in the healthy gut or at sites of pre-existing bowel disease. Many adverse events involving the lower intestine have been reported, some of them being clinically silent abnormalities that consist of increased intestinal permeability and mucosal inflammation, which are found in most patients on long-term NSAID therapy, and some are potentially life-threatening such as perforation and gut bleeding that may lead to iron-deficiency anemia.
In practice, when iron-deficiency anemia occurs in a patient on NSAID therapy and no cause is found by upper gastrointestinal endoscopy, NSAID-induced enteropathy should be considered. The development of selective COX-2 inhibitors has not provided a definitive solution, and the toxicity of these new agents for the lower intestine still remains. Although in some studies found that gastroprotective agents such as analogue misoprostol had a beneficial short-term effects on markers of clinically enteropathy, but no long-term treatments are capable of preventing NSAID-induced enteropathy due to its well-documented side effects.
Acid secretion plays no role in the pathogenesis of NSAID-induced enteropathy, so that proton pump inhibitors have no protective effect.3
Mucosta® is an anti gastritis and gastropathy drug with Rebamipide as it’s active ingredient. The molecular weight of Rebamipide is 370.79. Mucosta® is classified as anti-inflammatory, anti free-radical drug. As anti-inflammation drug, Mucosta® suppress inflammation process due to the release of inflammatory cytokine, such as IL-8, TNF-α, IL-1ß. By inhibiting the release of free radical, superoxide (O2-) and also scavenge hydroxyl radical (OH-) Mucosta® shows its action as anti free-radical. Mucosta® , a prostaglandin-inducing gastroprotective drug, promotes the synthesis of endogen prostaglandin which helps to reduce the recurrences of ulcer, improve gastroduodenal mucosal defense against aggressive factor, like gastric acid, infection due to H. pylori, NSAIDs, and other stressors.
Mucosta® is indicated in the treatment of gastritis, gastropathy (due to NSAIDs, steroid, or antibiotics), gastric ulcer, and to overcome acute gastroduodenal mucosal lesions due to administration of NSAIDs, steroid, or antibiotics. Mucosta® has strong penetration into gastrointestinal mucosal with minimal systemic effect. Mucosta® does not interact and does not interfere with the absorption of other drugs which often given together (NSAIDs, antibiotics) . In that way, Mucosta® does not affect the effectiveness of those drugs.
Mucosta® is effective, not only to prevent gastric mucosal injuries (gastropathy), but in small intestinal (enteropathy) as well.
Mucosta® is the first choice medication for NSAID gastropathy and enteropathy.
References :
- Bjarnason I, Hayllar J, et al. Side-effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology 1993 ;104 :1832-47.
- Schneider AR, Benz C, Riemann JF. Adverse effects of nonsteroidal anti-inflammatory drugs on the small and large bowel. Endoscopy 1999 ;31 :761-7.
- Thiefin G, Beaugerie L. Toxic effects of nonsteroidal anti-inflammatory drugs on the small bowel, colon, and rectum. Joint Bone Spine 72 (2005): 286-294.
Philip Darmawan, MD., MKT.
Medical Advisor
pdsony@ho.otsuka.co.id
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