Dyspepsia
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| ICD-10 | K30. | |
|---|---|---|
| ICD-9 | 536.8 | |
| DiseasesDB | 30831 | |
| MeSH | C23.888.821.236 | |
Dyspepsia (from the Greek "δυς-" (Dys-), meaning hard or difficult, and "πέψη" (Pepsi), meaning digestion) refers to disorders of the stomach involving symptoms such as heartburn, nausea, pain, or general discomfort.
Many cases of dyspepsia are caused by stomach ulcers which are diagnosed with a barium meal test or gastroscopy. Most cases of ulcer dyspepsia are caused by Helicobacter pylori infection. However, some studies also suggest non-ulcer dyspepsia may be resolved from eradicating this infection. In some situations (such as in ulcers), high levels of gastric acid may irritate the stomach lining and cause dyspeptic symptoms. Dyspepsia may also be a side effect from drugs treating other diseases.
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[edit] Treatment of Functional Dyspepsia
Functional dyspepsia is defined as chronic or recurrent pain or discomfort centered in the upper abdomen[1]. For the sake of this discussion, it is important to clarify that functional dyspepsia often is a diagnosis of exclusion, meaning that endoscopy for other conditions such as GERD or PUD is negative, and the patient is Helicobacter pylori-negative.
Traditional therapies used for this diagnosis include lifestyle modification, antacids, H2-receptor antagonists (H2-RAs), prokinetic agents, and antiflatulents. It is has been noted that one of the most frustrating aspects of treating functional dyspepsia is that these traditional agents have been shown to have little or no efficacy[2].
Antacids and sucralfate were found to be no better than placebo in a literature review[1]. H2-RAs have been shown to have marked benefit in poor quality trials (30% relative risk reduction[1]), but only a marginal benefit in good quality trials[2]. Prokinetic agents would empirically seem to work well since delayed gastric emptying is considered a major pathophysiolgoical mechanism in functional dyspepsia[2]. They have been shown in a meta-analysis to produce a relative risk reduction of up to 50%, but the studies evaluated to come to this conclusion used the drug cisapride which has since been removed from the market (now only available as an investigational agent[3]) due to serious adverse events such as torsades¬, and publication bias has been cited as a potential partial explanation for such a high benefit[1]. Modern prokinetic agents such as metoclopramide, erythromycin and tegaserod have little or no established efficacy and often result in substantial side effects[1]. Simethicone has been found to be of some value, as one trial suggests potential benefit over placebo and another shows equivalence with cisapride[1]. So, with the somewhat recent advent of the proton pump inhibitor (PPI) class of medications, the question of whether these new agents are superior to traditional therapy has arisen.
Currently, PPIs are, depending on the specific drug, FDA indicated for erosive esophagitis, gastroesophageal reflux disease (GERD), Zollinger-Ellison syndrome, eradication of H. pylori, duodenal and gastric ulcers, and NSAID-induced ulcer healing and prevention, but not functional dyspepsia. There are, however, evidence-based guidelines and literature that evaluate the use of PPIs for this indication. A helpful chart summarizing the major trials is available from the functional dyspepsia guidelines published in the World Journal of Gastroenterology in 2006[2].
The CADET study was the first to compare a PPI (omeprazole 20mg daily) to both an H2-RA (ranitidine 150mg BID) as well as a prokinetic agent (cisapride 20mg BID) alongside placebo[4]. The study evaluated these agents in patients at 4 weeks and 6 months and noted that omeprazole had a significantly better response at 6 months (31%) than cisapride (13%) or placebo (14%) (p = 0.001) while it was just above the cutoff for being statistically significantly better than ranitidine (21%) (p = 0.053). Omeprazole also showed a significant increase in quality of life scores over the other agents and placebo in all but one category measured (p = 0.01 to 0.05).
The ENCORE study, which was a follow-up of patients from the OPERA study, showed responders to omeprazole therapy had fewer clinic visits than non-responders (1.5 vs 2.0) over a three month period (p < 0.001)[5][6].
[edit] References
- ^ a b c d e f Talley NJ, Vakil N; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the management of dyspepsia. Am J Gastroenterol. 2005 Oct;100(10):2324-37.
- ^ a b c d Monkemuller K, Malfertheiner P. Drug treatment of functional dyspepsia. World J Gastroenterol. 2006 May 7;12(17):2694-700.
- ^ Anonymous. Information regarding withdrawal of Propulsid (cisapride) by Janssen Pharmaceutica. From FDA website (http://www.fda.gov/medwatch/safety/2000/safety00.htm#propul).
- ^ Veldhuyzen van Zanten SJ, Chiba N, Armstrong D, Barkun A, Thomson A, Smyth S, Escobedo S, Lee J, Sinclair P. A randomized trial comparing omeprazole, ranitidine, cisapride, or placebo in helicobacter pylori negative, primary care patients with dyspepsia: the CADET-HN Study. Am J Gastroenterol. 2005 Jul;100(7):1477-88.
- ^ Talley NJ, Meineche-Schmidt V, Pare P, Duckworth M, Raisanen P, Pap A, Kordecki H, Schmid V. Efficacy of omeprazole in functional dyspepsia: double-blind, randomized, placebo-controlled trials (the Bond and Opera studies). Aliment Pharmacol Ther. 1998 Nov;12(11):1055-65.
- ^ Meineche-Schmidt V, Talley NJ, Pap A, Kordecki H, Schmid V, Ohlsson L, Wahlqvist P, Wiklund I, Bolling-Sternevald E. Impact of functional dyspepsia on quality of life and health care consumption after cessation of antisecretory treatment. A multicentre 3-month follow-up study. Scand J Gastroenterol. 1999 Jun;34(6):566-74.
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