Prevention of NSAID-Induced Small Intestinal Mucosal Injury: Prophylactic Potential of Lansoprazole

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs), which are used for the treatment of several inflammatory disorders including rheumatoid arthritis, are well known to cause gastroduodenal mucosal lesions as an adverse effect. Recently, the serious problem of NSAID-induced small intestinal damage has become a topic of great interest to gastroenterologists, since capsule endoscopy and double-balloon enteroscopy are available for the detection of small intestinal lesions. Such lesions have been of great concern in clinical settings, and their treatment and prevention must be devised as soon as possible. Proton pump inhibitors (PPI), such as lansoprazole and omeprazole, show a potent anti-secretory effect. PPIs also have a gastroprotective effect, independent of their anti-secretory actions, which is probably mediated by inhibition of neutrophil functions as well as antioxidant actions. Administration of lansoprazole reduced the severity of the intestinal lesions in a dose-dependent manner, but omeprazole had no effect. The amount of heme oxygenase-1 (HO-1) protein in the intestinal mucosa was significantly increased by lansoprazole, but not by omeprazole. These results suggest that lansoprazole, but not omeprazole, ameliorates indomethacin-induced small intestinal ulceration through upregulation of HO-1/carbon monoxide. Therefore, lansoprazole may be useful for preventing the adverse effects of NSAIDs not only in the stomach but also in the small intestine.

Interaction between C-Reactive Protein and Phytochemical(s) from <i>Calotropis procera</i>: An Approach on Molecular Docking

“…ibobrufen, paracetamol, indomethacin etc. for the recovery of pain and inflammation, ultimately lead to severe side effects like ulcer in gastro-intestinal tract [35][36][37]. Interestingly, C. procera is one the plant that contains several phytochemicals and few of these have already been documented for anti-inflammatory properties [9,[38][39], which supported the present computational prediction.…”

“…It leads to internal and external inflammation in tissues, organs etc. There are well established anti-inflammatory synthetic drugs, which help as pain killer as well as recovery of swelling in tissues however, may cause side effect like ulcer in gastrointestinal tract [33][34][35][36][37]. Moreover, aqueous flower extract of C. procera has been documented to arrest pain, fever and inflammation [38][39] while ethanolic extract of root bark showed anti-inflammatory properties without any side effect [9,40].…”

Exacerbation of Nonsteroidal Anti-Inflammatory Drug-Induced Small Intestinal Lesions by Antisecretory Drugs in Rats: The Role of Intestinal Motility

“…Kuroda et al (2006) first reported that LPZ had an inhibitory effect on IND-induced small intestinal lesions in rats and suggested that LPZ prevented intestinal lesions by anti-inflammatory and antioxidant mechanisms, because LPZ inhibited INDinduced increase of myeloperoxidase activity and thiobarbituric acid-reactive substance in the intestinal mucosa. Higuchi et al (2009) and Yoda et al (2010) reported that LPZ, but not OPZ, prevented IND-induced intestinal lesions in rats and suggested that LPZ protected the intestinal mucosa by up-regulation of hemoxygenase-1 production in the mucosa. We reported previously that LPZ protects the gastric mucosa by a mechanism independent from its antisecretory action, and both CSSN and NO are involved in the protective mechanism of LPZ on the gastric mucosa (Murakami et al, 1996).…”

Non-Steroidal Anti-Inflammatory Drug (NSAID)-Induced Small Intestinal Injury

“…Endogenous PGE (2) promotes the healing of small intestinal lesions [42,43]. Lansoprazole prevents indomethacin-induced small intestinal ulceration [44,45]. However opposite results have been reported later on.…”