Editorials

Dyspepsia: Relief Not Yet Beyond Belief

Am Fam Physician. 1999 Oct 15;60(6):1649-1656.

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The magnitude of dyspepsia is obvious; up to 40 percent of adults in the Western world have frequent episodes and, in the United States, 2 to 5 percent of primary care visits are for this condition.13 The cost of relevant prescription drugs alone is over $1.3 billion annually in the United States, and the cost of over-the-counter medications is probably at least as much. Yet, despite its prevalence, we are relatively ignorant of the etiology. The symptom of dyspepsia should no longer evoke a differential diagnosis that primarily considers ulcer disease, gallbladder problems, gastritis and “nerves.” As Bazaldua and Schneider3 indicate in their article in this issue of American Family Physician, with the exception of clear-cut gastroesophageal reflux disease (GERD), we cannot rely on the complaint of dyspepsia alone to help us diagnostically.

Because of the ready accessibility of endoscopy and the discovery of Helicobacter pylori and its relationship to peptic ulcer disease, our perception of dyspepsia has changed and, like many things in life, it appears to be more complex than we had anticipated. Most patients with dyspepsia have normal findings on endoscopy.1 The majority of patients colonized with H. pylori are asymptomatic, and patients with dyspepsia have the same or slightly higher colonization rates as persons without symptoms. There are poor correlations between symptoms and histologic gastritis, secondary to H. pylori or other causes, and response of symptoms following H. pylori eradication is unpredictable and relatively small.

Bazaldua and Schneider3 give short shrift to functional or nonulcer dyspepsia which, as they point out, is the most frequent cause of dyspepsia. Their reticence is somewhat understandable in light of the uncertain pathophysiology and, as yet, generally unsatisfactory treatment. Nevertheless, progress is slowly being made in understanding and treating nonulcer dyspepsia. Although motility disturbances were considered the most likely etiology in the recent past, gastric or duodenal hypersensitivity, or both, now appears to more probably account for most symptoms.4,5 There may be an absence of normal postprandial gastric fundus relaxation associated with abnormal antral distension, but this was found in less than one half of subjects tested in one study.6

Although this disorder of relaxation could be primary, it could also be secondary to increased resistance to duodenal filling. Delayed duodenal clearance and hypersensitivity to acid may account for nausea in some patients.7 The hyperalgesia is site-specific and, as with other functional gastrointestinal disorders, these patients have normal somatic pain thresholds. The associated higher frequency of psychiatric disorders may reflect health-care seeking behavior, response to chronic illness and an intrinsic component of the visceral disorder.8,9 Proton pump inhibitors, prokinetic agents, antidepressants, newer kappa opioid agonists and behavioral therapy all appear to be effective in some patients. The high placebo response rate should be viewed as an important part of management.

Bazaldua and Schneider3 are to be commended for the concise presentation in Table 6 in their article, presenting the pros and cons relating to the controversies about treatment of H. pylori colonization in dyspeptic patients. However, they do not mention that there is an increased incidence of GERD after eradication of H. pylori and that the alarming increase of adenocarcinoma of the cardia and esophagus may also be related to this intervention.10,11 The authors favor option 3—testing for and treating H. pylori infections in patients 45 years and younger who have no “alarm” symptoms. Indeed, this approach has considerable support at present.1,12 However, if a patient responds to eradication treatment, is it because an ulcer was healed, gastritis cured, esophagitis curbed or a placebo effect displayed (which may be over 50 percent in functional gastrointestinal disorders)? The patient's risk is about 20 percent for having an ulcer, 15 percent for esophagitis and 30 to 50 percent for functional dyspepsia.

In quoting from the American Gastroenterological Association Technical Review, Bazaldua and Schneider3 note that the benefits of H. pylori eradication in nonulcer dyspepsia “are likely to be small or nonexistent.”12 In two recent studies, 70 to 80 percent of the patients receiving eradication treatment did not respond.13,14 The discordant results in these well-performed studies and others demonstrate that there is no easy answer regarding the optimal management of symptomatic functional dyspepsia in patients with H. pylori colonization.

This organism has been around for a long time, and consideration must be given to the fact that it may also have some protective role.11 We should be circumspect as to the possible implications of eliminating it without regard for the long-term negative consequences that ultimately may be greater than the small and unpredictable short-term benefits of treating nonulcer dyspepsia. Management algorithms can be useful guides but should be used with introspection, realizing there are variables too numerous for simplistic solutions to complex problems.15

Dr. Greenbaum is emeritus professor in the Department of Medicine, College of Human Medicine at Michigan State University in East Lansing, Mich.

Address correspondence to David S. Greenbaum, M.D., Michigan State University, B220 Life Sciences Bldg., East Lansing, MI 48824.

REFERENCES

1. Fisher RS, Parkman HP. Management of nonulcer dyspepsia. N Engl J Med. 1998;339:1376–80.

2. Friedman LS. Helicobacter pylori and nonulcer dyspepsia (editorial). N Engl J Med. 1998;339:1928–30.

3. Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician. 1999;60:1773–88.

4. Malagelada JR. The quest for a physiological answer to dyspepsia (editorial). Gastroenterology. 1998;115:1586–8.

5. Fisher RS. Altered visceral perception is responsible for functional (nonulcer) dyspepsia. Practical Gastroenterology. May 1999:57–61.

6. Tack J, Piessevaux H, Coulie B, Caenepeel P, Janssens J. Role of impaired gastric accommodation to a meal in functional dyspepsia. Gastroenterology. 1998;115:1346–52.

7. Samsom M, Verhagen MA, Henegouwen GP, Smout AJ. Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients. Gastroenterology. 1999;116:515–20.

8. Read NW. Functional dyspepsia: a case of indecision. Gastroenterology. 1999;116:761–2.

9. Kapadia CR. The curse of the functional dyspeptic: too sensitive a visceral afferent nervous system. Gastroenterology. 1999;116:495–7.

10. Spechler SJ. Adenocarcinoma of the gastroesophageal junction. Clin Perspectives Gastroenterology. March/April 1999;2:95–7.

11. Blaser MJ. In a world of black and white, Helicobacter pylori is gray (editorial). Ann Intern Med. 1999;130:695–7.

12. Talley NJ, Silverstein MD, Agreus L, Nyren O, Sonnenberg A, Holtmann G. American Gastroenterological Association technical review: evaluation of dyspepsia. Gastroenterology. 1998;114:582–95.

13. McColl K, Murray L, El-Omar E, Dickson A, el-Nujumi A, Wirz A, et al. Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med. 1998;339:1869–74.

14. Blum AL, Talley NJ, O'Morain C, van Zanten S, Labenz J, Stolte M, et al. Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med. 1998;339:1875–81.

15. Go MF, Vakil N. Helicobacter pylori infection. Clin Perspectives Gastroenterology. May/June 1999;2:141–53.


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