There are many clinical studies using "endoscopic ulcers" as an endpoint. There are far fewer using clinically important outcomes such as a UGI complication. In addition, most of the "endoscopic ulcer" studies did not separate
H. pylori infected patients (which would include a variable number with H. pylori ulcers) from H. pylori negative patients. It has become evident that the prevention of endoscopic ulcers differs between those with and without H. pylori infection. For example, the PPI omeprazole (Prilosec) was superior to low dose ranitidine (Zantac) (150 mg twice daily) or low dose misoprostol (Cytotec) (200 |g twice daily) among those with H. pylori infection. In contrast, omeprazole was less effective and not significantly different from ranitidine among those without H. pylori infection and was actually inferior to low dose misopros-tol. Low dose misoprostol was even superior to omeprazole for healing of "endoscopic" gastric ulcers among those without H. pylori infection (Graham, 2002; Silverstein, 1995). Head-to-head outcome studies using clinically important end points are clearly needed. At the present time it is impossible to determine which combination (H2RAs, PPIs, or misoprostol) is best. It has been suggested that the combination of an antisecretory drug (either an H2RA or PPI) and low dose misoprostol (200 |g twice daily) may provide the best overall protection. The only large scale study showing partial protection used misoprostol, but patients were not stratified in relation to their H. pylori status. It is currently impossible to make recommendations based on data. PPIs are superior to H2RAs for suppression of acid secretion and are generally preferred because they are better tolerated than misoprostol and require only a single daily dose.
Management of NSAID-Associated Dypepsia, Ulcers, and Their Complications NSAID-Associated Dyspepsia
Although dyspepsia does not predict the development of symptomatic ulcer or ulcer complications with NSAID therapy, it is a common problem that often leads to discontinuation oftreatment, repeated endoscopic examinations, and frequent use of gastroprotective agents. Because it is impractical to endoscope every patient with NSAID-associated dyspepsia, we recommend empirical treatment with gastroprotective agents for low to moderate risk patients and endoscopic evaluation for high risk patients (see Table 24-3). For low risk patients, switching to another NSAID or cotherapy with an H2RA often relieves dyspeptic symptoms (see Table 24-3). Antisecretory drugs are useful in patients with reflux-like or ulcer-like dyspepsia. For moderate risk patients, PPIs are preferred to H2RAs because they are more potent, which theoretically should make them more effective (see Table 24-3). However, there are limited comparative data in NSAID users without H. pylori infection, and the data that are available show more similarities with PPIs than differences. Nonetheless, unless cost is a critical issue PPIs are preferred for all but those with minimal risk. If cost is the critical issue, we recommend double dose H2RAs or single dose plus low dose misoprostol.
Although COX-2 inhibitors cause less dyspepsia than conventional NSAIDs, there is no evidence regarding whether substitution for a COX-2 inhibitor can resolve NSAID-associated dyspepsia. Management of dyspepsia in high risk patients (ie, a history of ulcer complication or multiple risk factors) remains difficult and there are remarkably little data to guide the physician. We recommend use of a COX-2 inhibitor and a PPI. If symptoms persist despite receiving combination therapy, we recommend endoscopy to exclude conditions like erosive esophagitis, penetrating ulcers, gastric outlet obstruction, or gastric malignancy (see Table 24-3).
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