Management of NSAID-Induced Gastrointestinal Toxicity

Abstract

The association between NSAIDs and the presence of upper gastrointestinal (GI) complications is well established. Evidence that acid aggravates NSAID-induced injury provides a rationale for minimizing such damage by acid suppression. Proton pump inhibitors (PPIs) appear to be very effective in treating NSAID-related dyspepsia, and also in healing gastric and duodenal ulcers in patients continuing to receive the NSAID. An analysis of data from comparative studies of PPIs versus ranitidine, misoprostol and sucralfate shows a therapeutic advantage in favour of the PPI. Several studies now confirm the efficacy of co-therapy with PPIs in the short- and long-term prevention of NSAID-induced upper GI injury. PPIs are more effective than histamine H(2)-receptor antagonists at standard dosages in reducing the risk of gastric and duodenal ulcer, and are superior to misoprostol in preventing duodenal but not gastric lesions. However, when balancing effectiveness and tolerance, PPIs may be considered the treatment of choice in the short- and long-term prevention of NSAID-related mucosal lesions. To date, there are only a few published articles dealing with the role of PPIs in the prevention of upper GI complications. Recent epidemiological and interventional studies provide some evidence that PPIs are of benefit. However, more controlled studies using clinical outcomes are needed to establish the best management strategy (PPIs combined with traditional NSAIDs or with cyclo-oxygenase-2 selective inhibitors) especially in patients with multiple risk factors, in patients using concomitant low-dose aspirin, corticosteroids or anticoagulants (high risk group), or in patients with a history of ulcer complications (very high risk group). Furthermore, it should be underlined that Helicobacter pylori infection positively interacts with the gastroprotective effect of PPIs; therefore, the true efficacy of these drugs in preventing NSAID-related ulcer complications should be reassessed without the confounding influence of this microorganism.

Drug utilization study of co-administration of nonsteroidal anti-inflammatory drugs and gastroprotective agents in an orthopaedics outpatients department of a tertiary care hospital in West Bengal

“…In any case, similar or even better efficacy is obtained by proton pump inhibitors in preventing and/or treating NSAID-induced peptic ulcers. 16,17 There was no prescription of sucralfate as gastroprotective agents.…”

Co-Administration of Nonsteroidal Ant-Inflammtory Drugs and Gastropotective Drugs in Orthopaedic Out Patient Department of a University Hospital in Kashmir

“…Antacids are indicated only for symptomatic relief of pain and are associated with a number of drug interactions,thereby restricting their use [11].Misoprostol,the drug indicated for the prophylaxis of high risk individuals,were not used at all.This may be because of various reasons including the higher cost,frequent side effects and the need for multiple daily dose of Misoprostol.In any case,similar or even better efficacy is obtained by proton pump inhibitors in preventing and/or treating NSAID-inuced peptic ulcers [16,17].Sucralfate was not used as gastroprotective drug in our series.…”

Effects of Ibuprofen, and Some Analogues, on the Muscle Tone of Isolated Segments of the Common Digital Artery of the Fallow Deer (<b><i>Dama dama</i></b>)

“…Due to the fact that their use is so widespread, and because of a lack of viable alternatives, solutions to the problem have been hard to come by. Co-therapy with the PGE 1 analogue misoprostol or proton pump inhibitors such as omeprazole [11,14] have been partially successful in reducing GI toxicity, by decreasing the acidity of the stomach. But use of these gastro-protective agents substantially increases the cost of patient management and adverse reactions [14] from these agents, e.g.…”

“…Co-therapy with the PGE 1 analogue misoprostol or proton pump inhibitors such as omeprazole [11,14] have been partially successful in reducing GI toxicity, by decreasing the acidity of the stomach. But use of these gastro-protective agents substantially increases the cost of patient management and adverse reactions [14] from these agents, e.g. diarrhoea [14], hypomagnesaemia [15] and altered intestinal flora with proton pump inhibitors [16].…”

“…But use of these gastro-protective agents substantially increases the cost of patient management and adverse reactions [14] from these agents, e.g. diarrhoea [14], hypomagnesaemia [15] and altered intestinal flora with proton pump inhibitors [16]. Alternative strategies included the development of selective COX-2 inhibitors, based upon the theory that COX-2 was the source of prostaglandins mediating inflammation, and would therefore not interfere with the other homeostatic functions of prostaglandins produced by COX-1 [8,17].…”