Dyspepsia1 1Loren Laine, M.D.Clinical Management EditorUniversity of Southern CaliforniaLos Angeles, California
2003; Elsevier BV; Volume: 125; Issue: 4 Linguagem: Inglês
10.1016/j.gastro.2003.07.001
ISSN1528-0012
Autores Tópico(s)Gastroesophageal reflux and treatments
ResumoA 44-year-old man presents with a 1-year history of intermittent pain in the epigastric region, which often occurs one hour after meals. The pain does not radiate and he has no weight loss, vomiting, or symptoms of GI bleeding. He denies early satiety, bloating, constipation, or diarrhea. He reports heartburn about twice a month, typically when he goes to bed soon after eating a large meal. He is otherwise healthy, is not obese, and takes no medications. Dyspepsia is currently defined as discomfort or pain centered in the upper abdomen; there are often accompanying symptoms including fullness, bloating, or early satiety.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar More recently, it has been proposed that weight loss is a specific dyspepsia symptom, suggesting that the current nosology may need revision.3Tack J. Piessevaux H. Coulie B. Caenepeel P. Janssens J. Role of impaired gastric accommodation to a meal in functional dyspepsia.Gastroenterology. 1998; 115: 1346-1352Abstract Full Text Full Text PDF PubMed Scopus (923) Google Scholar The exclusion of heartburn from dyspepsia continues to be debated.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar Our patient has uninvestigated dyspepsia, which is a very common complaint everywhere.4Talley N.J. Zinsmeister A.R. Schleck C.D. Melton III, L.J. Dyspepsia and dyspepsia subgroups a population-based study.Gastroenterology. 1992; 102: 1259-1268PubMed Google Scholar, 5Talley N.J. Weaver A.L. Zinsmeister A.R. Melton 3rd, L.J. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders.Am J Epidemiol. 1992; 136: 165-177PubMed Google Scholar, 6Agréus L. Svardsudd K. Nyren O. Tibblin G. Irritable bowel syndrome and dyspepsia in the general population overlap and lack of stability over time.Gastroenterology. 1995; 109: 671-680Abstract Full Text PDF PubMed Scopus (634) Google Scholar In the United States, the point prevalence is approximately 25%, excluding those people who have dominant symptoms of gastroesophageal reflux disease (GERD).4Talley N.J. Zinsmeister A.R. Schleck C.D. Melton III, L.J. Dyspepsia and dyspepsia subgroups a population-based study.Gastroenterology. 1992; 102: 1259-1268PubMed Google Scholar The incidence is more poorly documented,5Talley N.J. Weaver A.L. Zinsmeister A.R. Melton 3rd, L.J. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders.Am J Epidemiol. 1992; 136: 165-177PubMed Google Scholar, 6Agréus L. Svardsudd K. Nyren O. Tibblin G. Irritable bowel syndrome and dyspepsia in the general population overlap and lack of stability over time.Gastroenterology. 1995; 109: 671-680Abstract Full Text PDF PubMed Scopus (634) Google Scholar but in Scandinavia, in a 3-month period, dyspepsia developed in 0.8% of subjects without previous dyspepsia.6Agréus L. Svardsudd K. Nyren O. Tibblin G. Irritable bowel syndrome and dyspepsia in the general population overlap and lack of stability over time.Gastroenterology. 1995; 109: 671-680Abstract Full Text PDF PubMed Scopus (634) Google Scholar Notably, the number of subjects who develop dyspepsia appears to be matched by a similar number of subjects who lose their symptoms, so the prevalence remains stable from year to year.5Talley N.J. Weaver A.L. Zinsmeister A.R. Melton 3rd, L.J. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders.Am J Epidemiol. 1992; 136: 165-177PubMed Google Scholar The pattern of individual symptom cycling in dyspepsia has not as yet been adequately documented, but symptom relapse is the rule.5Talley N.J. Weaver A.L. Zinsmeister A.R. Melton 3rd, L.J. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders.Am J Epidemiol. 1992; 136: 165-177PubMed Google Scholar Dyspepsia is a costly, chronic condition, and drug costs in particular are rising rapidly.7Agréus L. Borgquist L. The cost of gastro-oesophageal reflux disease, dyspepsia and peptic ulcer disease in Sweden.Pharmacoeconomics. 2002; 20: 347-355Crossref PubMed Scopus (84) Google Scholar While only a minority with dyspepsia actually consult (25%), this represents a very large number of patients in primary care and gastroenterology practice in the United States.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar Very few studies have investigated dyspepsia subjects from the community by esophagogastroduodenoscopy (EGD) and other tests, to determine the underlying causes of the symptoms, but most have no obvious cause for their symptoms. In a population-based study from northern Norway, among those with epigastric pain only 9% had a peptic ulcer; 14% had reflux esophagitis.8Johnsen R. Bernersen B. Straume B. Forde O.H. Bostad L. Burhol P.G. Prevalences of endoscopic and histological findings in subjects with and without dyspepsia.BMJ. 1991; 302: 749-752Crossref PubMed Scopus (216) Google Scholar The rest were classified as having functional dyspepsia, but how many had endoscopy negative reflux disease is uncertain.8Johnsen R. Bernersen B. Straume B. Forde O.H. Bostad L. Burhol P.G. Prevalences of endoscopic and histological findings in subjects with and without dyspepsia.BMJ. 1991; 302: 749-752Crossref PubMed Scopus (216) Google Scholar Peptic ulcer disease is declining but still accounts for 1 in 10 cases of dyspepsia although this varies depending on the underlying prevalence of H. pylori infection and nonsteroidal anti-inflammatory drug (NSAID) use.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar Malignancy of the upper gastrointestinal tract remains a relatively rare cause of dyspepsia in primary care.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar A number of drugs can theoretically induce dyspepsia, including alendronate, certain oral antibiotics such as erythromycin, the anti-obesity agent orlistat, theophylline, potassium supplements, and the antidiabetic agent acarbose.2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar However, data supporting the role of drugs aside from NSAIDs in the genesis of dyspepsia in the population are lacking.9Hallas J. Bytzer P. Screening for drug related dyspepsia an analysis of prescription symmetry.Eur J Gastroenterol Hepatol. 1998; 10: 27-32Crossref PubMed Scopus (46) Google Scholar If a patient is taking a regular NSAID or aspirin, endoscopy to rule out ulcer disease has been recommended1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar although many physicians would consider just stopping the NSAID and only endoscoping those whose symptoms failed to resolve.2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar The Cox II selective NSAIDs may induce dyspepsia and delay ulcer healing.10Hawkey C.J. Langman M.J. Non-steroidal anti-inflammatory drugs: overall risks and management. Complementary roles for COX-2 inhibitors and proton pump inhibitors.Gut. 2003; 52: 600-608Crossref PubMed Scopus (164) Google Scholar Herbal products or home remedies have sometimes been implicated in dyspepsia although good data are lacking. It has been suggested that identifying the predominant or major symptom is helpful clinically in distinguishing GERD from dyspepsia.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar However, dominant heartburn is not alone an adequate predictor of GERD. If the prevalence of GERD is 25% in dyspepsia, then based on the published sensitivity and specificity of dominant heartburn for identifying GERD (defined by 24-hour pH testing), the probability of GERD in the setting of dominant heartburn is little better than tossing a coin (54%).11Moayyedi P. Axon A.T. The usefulness of the likelihood ratio in the diagnosis of dyspepsia and gastroesophageal reflux disease.Am J Gastroentrol. 1999; 94: 3122-3125Crossref PubMed Google Scholar The frequency of GERD symptoms may help improve discrimination; infrequent GERD symptoms (less than twice a week) do not usually impair quality of life and are unlikely to be associated with serious pathology.12Dent J. Jones R. Kahrilas P. Talley N.J. Management of gastro-oesophageal reflux disease in general practice.BMJ. 2001; 322: 344-347Crossref PubMed Scopus (100) Google Scholar, 13Carlsson R. Dent J. Bolling-Sternevald E. Johnsson F. Junghard O. Lauritsen K. Riley S. Lundell L. The usefulness of a structured questionnaire in the assessment of symptomatic gastroesophageal reflux disease.Scand J Gastroenterol. 1998; 33: 1023-1029Crossref PubMed Scopus (418) Google Scholar In primary care practice, the vast majority with GERD do not have esophagitis, but in gastroenterology practice the pretest probability of esophagitis is higher.12Dent J. Jones R. Kahrilas P. Talley N.J. Management of gastro-oesophageal reflux disease in general practice.BMJ. 2001; 322: 344-347Crossref PubMed Scopus (100) Google Scholar Individual dyspeptic symptoms cannot be used to help identify peptic ulcer disease in uninvestigated dyspepsia.14Bytzer P. Talley N.J. Dyspepsia.Ann Intern Med. 2001; 134: 815-822Crossref PubMed Google Scholar Expert groups have suggested subdividing dyspepsia into subgroups based on symptom patterns to help identify underlying structural disease, as well as more homogenous populations that would respond to targeted medical therapy.2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar Our patient has an “ulcer-like” pattern. However, symptom subgroups and symptom scoring systems have all failed miserably in distinguishing organic from functional dyspepsia.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar, 4Talley N.J. Zinsmeister A.R. Schleck C.D. Melton III, L.J. Dyspepsia and dyspepsia subgroups a population-based study.Gastroenterology. 1992; 102: 1259-1268PubMed Google Scholar, 14Bytzer P. Talley N.J. Dyspepsia.Ann Intern Med. 2001; 134: 815-822Crossref PubMed Google Scholar Biliary colic can be distinguished from dyspepsia; the pain is usually severe, unpredictable, and prolonged.14Bytzer P. Talley N.J. Dyspepsia.Ann Intern Med. 2001; 134: 815-822Crossref PubMed Google Scholar The diagnostic yield of an ultrasound is low in dyspepsia.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 2Drossman D.A. Corazziari E. Talley N.J. Thompson W.G. Whitehead W.E. Rome II Multinational Working Teams, ed.The functional gastrointestinal disorders.in: Diagnosis, Pathophysiology and Treatment a Multinational Consensus. 2nd ed. McLean, Virginia, Degon2000Google Scholar A past history of peptic ulcer disease can be highly relevant; even if H. pylori infection in this setting has been diagnosed and successfully treated, one-third of “cured” ulcer patients develop non-ulcer dyspepsia.15Forbes G.M. Glaser M.E. Cullen D.J. Warren J.R. Christiansen K.J. Marshall B.J. Collins B.J. Duodenal ulcer treated with Helicobacter pylori eradication seven-year follow-up.Lancet. 1994; 343: 258-260Abstract PubMed Scopus (346) Google Scholar The American College of Physicians in 1985 published a guideline that suggested that patients with dyspepsia over the age of 45 deserved referral for prompt endoscopy.16AnonymousEndoscopy in the evaluation of dyspepsia. Health and Public Policy Committee, American College of Physicians.Ann Intern Med. 1985; 102: 266-269Crossref PubMed Scopus (158) Google Scholar The major rationale for this strategy remains that gastric cancer is very rare below the age of 45 years but it increases thereafter.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar, 14Bytzer P. Talley N.J. Dyspepsia.Ann Intern Med. 2001; 134: 815-822Crossref PubMed Google Scholar, 17Voutilainen M. Mantynen T. Kunnamo I. Juhola M. Mecklin J.P. Farkkila M. Impact of clinical symptoms and referral volume on endoscopy for detecting peptic ulcer and gastric neoplasms.Scand J Gastroenterol. 2003; 38: 109-113Crossref PubMed Scopus (31) Google Scholar Other data have suggested that the age threshold can be raised to 55 years because gastric cancer is rare in younger patients.18Gillen D. McColl K.E. Does concern about missing malignancy justify endoscopy in uncomplicated dyspepsia in patients aged less than 55?.Am J Gastroenterol. 1999; 94: 2329-2330Crossref PubMed Scopus (14) Google Scholar The World Congresses of Gastroenterology sensibly recommended an age threshold of 50 years, matching the age screening threshold for colon cancer, but recognized that a small number of patients with gastric cancer will still be missed applying such an age threshold (or indeed any other) in the United States.19Talley N.J. Axon A. Bytzer P. Holtmann G. Lam S.K. Van Zanten S. Management of uninvestigated and functional dyspepsia a Working Party report for the World Congresses of Gastroenterology 1998.Aliment Pharmacol Ther. 1999; 13: 1135-1148Crossref PubMed Scopus (102) Google Scholar In addition to older age, other alarm features are listed in Table 1. There is evidence that the absence of alarm features in patients who are young with dyspepsia is a reliable indicator that malignancy is not present.14Bytzer P. Talley N.J. Dyspepsia.Ann Intern Med. 2001; 134: 815-822Crossref PubMed Google Scholar, 18Gillen D. McColl K.E. Does concern about missing malignancy justify endoscopy in uncomplicated dyspepsia in patients aged less than 55?.Am J Gastroenterol. 1999; 94: 2329-2330Crossref PubMed Scopus (14) Google Scholar A U.K. study found in a population of 940,000 that 169 patients under the age of 55 years had gastric or esophageal cancer; only 5 had no alarm symptoms and these were all advanced cancers and hence, not amenable to cure18Gillen D. McColl K.E. Does concern about missing malignancy justify endoscopy in uncomplicated dyspepsia in patients aged less than 55?.Am J Gastroenterol. 1999; 94: 2329-2330Crossref PubMed Scopus (14) Google Scholar (Figure 1). However, the positive predictive value of alarm features remains relatively poor. Notably, intermittent dysphagia is a common symptom in the general population and is unlikely alone to indicate serious disease although this is not widely recognized20Locke 3rd, G.R. Talley N.J. Fett S.L. Zinsmeister A.R. Melton 3rd, L.J. Prevalence and clinical spectrum of gastroesophageal reflux a population-based study in Olmsted County, Minnesota.Gastroenterology. 1997; 112: 1448-1456Abstract Full Text PDF PubMed Scopus (1913) Google Scholar; however, progressive dysphagia would be a worrying symptom. A long history of symptoms should make cancer unlikely but a symptom duration threshold has not been defined in the literature.Table 1Alarm Features for Dyspepsia≥45 years (new onset)Progressive dysphagia or odynophagiaRectal bleeding or melenaFamily history of upper GI cancerWeight loss of >10% of body weightPrevious gastric surgery or malignancyPrevious history of peptic ulcerAnorexia/early satietyJaundicePersistent vomitingAnemia or bleedingAbdominal mass or lymphadenopathy Open table in a new tab There are a number of management options that can be considered. The choice applied very much depends on both individual patient characteristics and where one practices. The “gold standard” option is to offer the patient a prompt EGD. This will enable therapy to be directed to any underlying disease detected including peptic ulcer, reflux esophagitis, or cancer. However, patients with nonerosive reflux disease cannot be distinguished from functional dyspepsia by EGD,12Dent J. Jones R. Kahrilas P. Talley N.J. Management of gastro-oesophageal reflux disease in general practice.BMJ. 2001; 322: 344-347Crossref PubMed Scopus (100) Google Scholar and in patients at low risk of a serious underlying disease based on age and a lack of alarm features, this approach probably offers little over noninvasive strategies. Obviously, if the patient is particularly anxious or irrationally fearful of underlying serious disease, then endoscopy may be helpful in providing reassurance. However, data to support the reassurance value of EGD are extremely limited. The psychological general well-being index has been shown to improve in the week following endoscopy in patients with dyspepsia, which was presumed to reflect patient reassurance from the procedure, but the durability of improvement was not determined.21Wiklund I. Glise H. Jerndal P. Carlsson J. Talley N.J. Does endoscopy have a positive impact on quality of life in dyspepsia?.Gastrointest Endosc. 1998; 47: 449-454Abstract Full Text Full Text PDF PubMed Scopus (95) Google Scholar One randomized controlled trial reported prompt endoscopy was associated with greater patient satisfaction compared with empiric H2 receptor antagonist therapy, but these results may have been biased by patient expectation on entry into this management trial.22Bytzer P. Hansen J.M. Schaffalitzky de Muchadell O.B. Empirical H2-blocker therapy or prompt endoscopy in management of dyspepsia.Lancet. 1994; 343: 811-816Abstract PubMed Scopus (316) Google Scholar The cost of endoscopy also needs to be considered here. The patient may or may not be covered by health insurance and may or may not be easily able to afford the procedure. Decision analysis suggests endoscopy in younger patients with no alarm features is not cost effective in the United States; the total cost of EGD would need to be under $500 for this management approach to dominate other strategies.23Fendrick A.M. Chernew M.E. Hirth R.A. Bloom B.S. Alternative management strategies for patients with suspected peptic ulcer disease.Ann Intern Med. 1995; 123: 260-268Crossref PubMed Scopus (200) Google Scholar, 24Silverstein M.D. Petterson T. Talley N.J. Initial endoscopy or empirical therapy with or without testing for Helicobacter pylori for dyspepsia a decision analysis.Gastroenterology. 1996; 110: 72-83Abstract Full Text PDF PubMed Scopus (175) Google Scholar I am not convinced that use of small caliber endoscopes transnasally would make endoscopy a more attractive option; it is my bias most patients still prefer to be sedated. A popular approach would be to prescribe an empiric trial of antisecretory therapy. While acid secretion is normal in functional dyspepsia, acid hypersensitivity theoretically may induce symptoms or possibly sensitize patients.25Samsom M. Verhagen M.A. vanBerge Henegouwen G.P. Smout A.J. Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients.Gastroenterology. 1999; 116: 515-520Abstract Full Text Full Text PDF PubMed Scopus (233) Google Scholar, 26Lee K.J. Vos R. Janssens J. Tack J. Influence of duodenal acidification on the sensorimotor function of the proximal stomach in man.Am J Physiol Gastrointest Liver Physiol. 2003; (in press)Google Scholar For example, installation of acid into the duodenum induced nausea in patients with duodenal dysmotility presumably because the acid was unable to be cleared25Samsom M. Verhagen M.A. vanBerge Henegouwen G.P. Smout A.J. Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients.Gastroenterology. 1999; 116: 515-520Abstract Full Text Full Text PDF PubMed Scopus (233) Google Scholar; acid infusion into the duodenum also increased gastric hypersensitivity and inhibited gastric accommodation in healthy volunteers.26Lee K.J. Vos R. Janssens J. Tack J. Influence of duodenal acidification on the sensorimotor function of the proximal stomach in man.Am J Physiol Gastrointest Liver Physiol. 2003; (in press)Google Scholar Abnormal dumping of acid into the duodenum could theoretically aggravate dyspepsia in some cases. It is also conceivable that physiological gastroesophageal reflux could induce epigastric pain in patients with esophageal hypersensitivity, and this explains some cases of functional dyspepsia. Randomized controlled trials in the primary care setting have shown that proton pump inhibitors (PPIs) are superior to H2 receptor antagonists, antacid alginate, and placebo in relieving symptoms in uninvestigated dyspepsia.27Delaney B.C. Innes M.A. Deeks J. Wilson S. Cooner M.K. Moayyedi P. Oakes R. Hobbs F.D. Forman D. Initial management strategies for dyspepsia (Cochrane Review).Cochrane Database Syst Rev. 2001; 3: CD001961PubMed Google Scholar However, these studies have been limited by their inclusion of patients with undiagnosed ulcer disease and symptomatic GERD mislabeled as dyspepsia. In patients with documented functional dyspepsia, which our patient is most likely to suffer with, the data on the benefits of potent acid suppression are mixed. Moreover, it is controversial whether “ulcer-like functional” dyspepsia responds better to antisecretory agents compared with the remainder of patients presenting with dyspepsia. A randomized controlled trial in Chinese patients, where reflux disease is rare, failed to show any benefit of lansoprazole 30 or 15 mg over placebo regardless of dyspepsia subgroup.28Wong W.M. Wong B.C. Hung W.K. Yee Y.K. Yip A.W. Szeto M.L. Fung F.M. Tong T.S. Lai K.C. Hu W.H. Yuen M.F. Lam S.K. Double blind, randomised, placebo controlled study of four weeks of lansoprazole for the treatment of functional dyspepsia in Chinese patients.Gut. 2002; 51: 502-506Crossref PubMed Scopus (106) Google Scholar Other studies have reported a significant benefit of omeprazole 20 mg once or twice daily over placebo, but on secondary analyses this benefit appeared to be confined to patients with ulcer-like dyspepsia.29Talley N.J. Lauritsen K. The potential role of acid suppression in functional dyspepsia the BOND, OPERA, PILOT, and ENCORE studies.Gut. 2002; 50: 36-41Google Scholar The problem with empiric antisecretory therapy in uninvestigated dyspepsia is that treatment with a PPI can promote healing of undiagnosed peptic ulcer disease, leaving the patient at risk of ulcer recurrence and complications in the future once acid suppression is stopped. On the other hand, the cost effectiveness of empiric proton pump inhibitor therapy in the setting of a low background prevalence of ulcer disease and H. pylori is quite compelling.30Spiegel B.M.R. Vakil N.B. Ofman J.J. Dyspepsia management in primary care a reappraisal of competing strategies.Gastroenterology. 2002; 122: 1270-1285Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar Notably, the prevalence of peptic ulcer disease (and H. pylori) varies widely across the United States31Jones M.P. Evaluation and treatment of dyspepsia.Postgrad Med J. 2003; 79: 25-29Crossref PubMed Scopus (19) Google Scholar (Figure 2). Location, race, and socioeconomic status should influence the management pathway; H. pylori infection is much less likely in younger, middle class Caucasians than in Hispanics or blacks, for example. Hence, if H. pylori is relatively uncommon, empiric antisecretory therapy makes sense, but if the background prevalence of H. pylori is 20% or higher, patients should never be offered empiric antisecretory therapy without first testing for the infection in my view. What about high-dose proton-pump inhibitor therapy? Consider this approach if the patient has failed to respond to standard PPI doses. Even in patients with nonpredominant heartburn, they could still have underlying gastroesophageal reflux disease that has been missed, a reasonable rationale for high-dose PPI testing. A potential disadvantage of empiric antisecretory therapy is acid rebound. This has been documented to occur with both H2 receptor antagonists and PPIs, but with PPIs it appears to be a more important problem in H. pylori-negative cases and can persist.32Gillen D. McColl K.E. Problems related to acid rebound and tachyphylaxis.Best Pract Res Clin Gastroenterol. 2001; 15: 487-495Abstract Full Text PDF PubMed Scopus (54) Google Scholar However, the clinical implications of acid rebound remain inadequately documented (and have been ignored in decision analyses and management trials), although theoretically acid rebound could lead to difficulties in withdrawing patients with dyspepsia from PPI therapy. Testing for H. pylori infection, using a locally validated noninvasive H. pylori test and treating the patient if infected, is the alternative that is currently recommended by the American Gastroenterological Association.1Talley N.J. Silverstein M.D. Agreus L. Nyren O. Sonnenberg A. Holtmann G. AGA technical review evaluation of dyspepsia.Gastroenterology. 1998; 114: 582-595Abstract Full Text Full Text PDF PubMed Scopus (394) Google Scholar The rationale here is that test and treat usually eliminates underlying ulcer disease. In management trials, H. pylori test-and-treat has been shown to be equivalent in terms of outcome compared with prompt endoscopy27Delaney B.C. Innes M.A. Deeks J. Wilson S. Cooner M.K. Moayyedi P. Oakes R. Hobbs F.D. Forman D. Initial management strategies for dyspepsia (Cochrane Review).Cochrane Database Syst Rev. 2001; 3: CD001961PubMed Google Scholar, 33Lassen A.T. Pedersen F.M. Bytzer P. Schaffalitzky de Muckadell O.B. Helicobacter pylori test-and-eradication versus prompt endoscopy for management of dyspepsia patients a randomised trial.Lancet. 2000; 356: 455-460Abstract Full Text Full Text PDF PubMed Scopus (212) Google Scholar, 34McColl K.E. Murray L.S. Gillen D. Walker A. Wirz A. Fletcher J. Mow C. Henry E. Kelman A. Dickson A. Randomised trial of endoscopy with testing for Helicobacter pylori compared with non-invasive H. pylori testing alone in the management of dyspepsia.BMJ. 2002; 324: 999-1002Crossref PubMed Google Scholar and superior to a short course of proton pump inhibitor therapy alone.35bManes G. Menchise A. De Nucci C. Balzano A. Empirical prescribing for dyspepsia randomised controlled trial of test and treat versus omeprazole treatment.BMJ. 2003; 326: 1118Crossref PubMed Google Scholar, 36Chiba N. Van Zanten S.J. Sinclair P. Ferguson R.A. Escobeda S. Grace E. Treating Helicobacter pylori infection in primary care patients with uninvestigated dyspepsia the Canadian adult dyspepsia empiric treatment-Helicobacter pylori positive (CADET-Hp) randomised controlled trial.BMJ. 2002; 324: 1012-1016Crossref PubMed Scopus (202) Google Scholar Notably, some trials of test-and-treat33Lassen A.T. Pedersen F.M. Bytzer P. Schaffalitzky de Muckadell O.B. Helicobacter pylori test-and-er
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