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INTRODUCTION — Dyspepsia is a common symptom with an extensive differential diagnosis and a heterogeneous pathophysiology. It occurs in approximately 25 percent of the population each year, but most affected people do not seek medical care . Although dyspepsia does not affect survival, it is responsible for substantial health care costs and significantly affects quality of life [2-5].
This topic will review the definition, etiology, and general approach to the evaluation and management of the patient with dyspepsia. The evaluation and recommendations are largely consistent with the American Gastroenterological Association (AGA) guideline for the evaluation of dyspepsia [6,7].
DEFINITION — According to the Rome III criteria, dyspepsia is defined as one or more of the following symptoms :
●Postprandial fullness (classified as postprandial distress syndrome)
●Early satiation (inability to finish a normal sized meal, also classified as postprandial distress syndrome)
●Epigastric pain or burning (classified as epigastric pain syndrome)
ETIOLOGY — Approximately 25 percent of patients with dyspepsia have an underlying organic cause (table 1). However, up to 75 percent of patients have functional (idiopathic or nonulcer) dyspepsia with no underlying cause on diagnostic evaluation [8-10]. (See 'Diagnostic strategies and initial management' below.)
Dyspepsia secondary to organic disease — Although there are several organic causes for dyspepsia, the main causes are peptic ulcer disease, gastroesophageal reflux, gastric malignancy, and nonsteroidal anti-inflammatory drug (NSAID)-induced dyspepsia (table 1).
Peptic ulcer disease — Upper abdominal pain or discomfort is the most prominent symptom in patients with peptic ulcers. Although discomfort from ulcers is usually centered in the epigastrium, it may occasionally localize to the right or left upper quadrants . While the pain may radiate to the back, back pain as the primary symptom is atypical of peptic ulcer disease.
While classic symptoms of duodenal ulcer occur when acid is secreted in the absence of a food buffer (ie, two to five hours after meals or on an empty stomach), peptic ulcers can be associated with food-provoked symptoms. Thus, pain related to the timing of a meal cannot accurately distinguish a duodenal ulcer from a gastric ulcer.
Peptic ulcers can also be associated with postprandial belching, epigastric fullness, early satiation, fatty food intolerance, nausea, and occasional vomiting. (See "Peptic ulcer disease: Clinical manifestations and diagnosis".)
Gastroesophageal reflux — The most common symptoms of gastroesophageal reflux disease (GERD) are retrosternal burning pain and regurgitation . GERD should be suspected when these symptoms accompany dyspepsia and are the predominant complaints . (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)
Gastroesophageal malignancy — Gastroesophageal malignancy is an uncommon cause of chronic dyspepsia in the Western hemisphere but the incidence is higher in patients of Asian, Hispanic, or Afro-Caribbean extraction. The incidence of malignancy also increases with age. When present, abdominal pain tends to be epigastric, vague and mild early in the disease but more severe and constant as the disease progresses. In addition, other symptoms and signs typically evolve with disease progression (eg, anemia, fatigue, weight loss). (See "Epidemiology, pathobiology, and clinical manifestations of esophageal cancer", section on 'Epidemiology' and "Epidemiology of gastric cancer" and "Clinical features, diagnosis, and staging of gastric cancer", section on 'Clinical features'.)
Biliary pain — Classic biliary pain is characterized by episodic acute and severe upper abdominal pain, usually in the epigastrium or right upper quadrant. It is not colicky. The pain typically lasts for at least one hour and may persist for several hours. The pain may radiate to the back or scapula, and is often associated with restlessness, sweating, or vomiting. Episodes are typically separated by weeks to months and patients are completely pain free between attacks.
Drug-induced dyspepsia — NSAIDs and COX-2 selective inhibitors can cause dyspepsia even in the absence of peptic ulcer disease. (See "Nonselective NSAIDs: Overview of adverse effects", section on 'Gastrointestinal effects'.)
Several other drugs have been implicated as causes of dyspepsia. However, data to support the role of these medications in drug induced dyspepsia are limited. These medications include calcium channel blockers, methylxanthines, alendronate, orlistat, potassium supplements, acarbose and certain antibiotics, including erythromycin [14,15].
Other causes — Celiac disease and chronic pancreatitis may rarely present with dyspepsia alone. Other rare causes for dyspepsia include infiltrative diseases of the stomach (eg, eosinophilic gastritis, Crohn disease, sarcoidosis), diabetic radiculopathy, metabolic disturbances (eg, hypercalcemia, heavy metal toxicity), hepatoma, steatohepatitis, celiac artery compression syndrome, superior mesenteric artery syndrome, and intestinal angina (table 1). (See "Pathogenesis, epidemiology, and clinical manifestations of celiac disease in adults", section on 'Gastrointestinal manifestations' and "Clinical manifestations and diagnosis of chronic pancreatitis in adults", section on 'Clinical manifestations' and "Granulomatous gastritis", section on 'Crohn disease' and "Extrapulmonary manifestations of sarcoidosis", section on 'Gastrointestinal' and "Celiac artery compression syndrome" and "Superior mesenteric artery syndrome" and "Chronic mesenteric ischemia", section on 'Clinical features'.)
Functional dyspepsia — Functional (idiopathic or nonulcer) dyspepsia is defined as the presence of one or more of the following: postprandial fullness, early satiation, epigastric pain or burning, and no evidence of structural disease to explain the symptoms . These criteria should be fulfilled for the last three months with symptom onset at least six months before diagnosis.
A diagnosis of functional dyspepsia can therefore only be established after exclusion of other causes of dyspepsia . The pathophysiology and treatment of functional dyspepsia are discussed in detail, separately. (See 'Diagnostic strategies and initial management' below and "Functional dyspepsia in adults".)
INITIAL EVALUATION — A history, physical examination, and laboratory evaluation are the first steps in the evaluation of a patient with new onset of dyspepsia. (See 'History' below and 'Physical examination' below and 'Laboratory tests' below.)
One important goal of the initial evaluation is to identify alarm features for gastroesophageal malignancy (table 2), which will direct the diagnostic approach. (See 'Diagnostic strategies and initial management' below.)
History — A detailed history is necessary to narrow the differential diagnosis and to identify gastroesophageal reflux disease (GERD) and nonsteroidal anti-inflammatory drug (NSAID)-induced dyspepsia, as well as patients with alarm features (table 2).
●A dominant history of heartburn, regurgitation, or cough is suggestive of GERD . (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults", section on 'Clinical manifestations'.)
●NSAID use raises the possibility of NSAID dyspepsia and peptic ulcer disease. Radiation of the pain to the back or personal or family history of pancreatitis may be indicative of underlying chronic pancreatitis. (See "Nonselective NSAIDs: Overview of adverse effects", section on 'Gastrointestinal effects'.)
●Significant weight loss, anorexia, vomiting, dysphagia, odynophagia, and a family history of gastrointestinal cancers suggest the presence of an underlying malignancy. (See "Clinical features, diagnosis, and staging of gastric cancer", section on 'Clinical features'.)
●The presence of severe episodic epigastric or right upper quadrant abdominal pain lasting more than an hour or pain that occurs at any time is suggestive of symptomatic cholelithiasis. (See "Acute cholecystitis: Pathogenesis, clinical features, and diagnosis", section on 'Clinical manifestations'.)
Physical examination — The physical examination in patients with dyspepsia is usually normal, except for epigastric tenderness. The presence of epigastric tenderness cannot accurately distinguish organic dyspepsia from functional dyspepsia. Abdominal tenderness on palpation should be evaluated with the Carnett sign to determine if it is due to pain arising from the abdominal wall rather than due to inflammation of the underlying viscera. The presence of increased local tenderness during muscle tensing (positive Carnett’s sign) suggests the presence of abdominal wall pain. However, if the pain is decreased (negative Carnett’s sign), the origin of pain is not from the abdominal wall and likely from an intra-abdominal organ, as the tensed abdominal wall muscles protect the viscera. The Carnett sign is described in detail separately. (See "Anterior cutaneous nerve entrapment syndrome".)
Other informative findings on physical examination may include: a palpable abdominal mass (eg, hepatoma) or lymphadenopathy (eg, left supraclavicular or periumbilical in gastric cancer), jaundice (eg, secondary to liver metastasis) or pallor secondary to anemia. Ascites may indicate the presence of peritoneal carcinomatosis. Patients may have evidence of muscle wasting, loss of subcutaneous fat, and peripheral edema due to weight loss.
Laboratory tests — Routine blood counts and blood chemistry including liver function tests should be performed to identify patients with alarm features (eg, iron deficiency anemia) and underlying metabolic diseases that can cause dyspepsia (eg, diabetes, hypercalcemia) (table 2). (See "Clinical manifestations of hypercalcemia", section on 'Gastrointestinal abnormalities' and "Diabetic autonomic neuropathy of the gastrointestinal tract".)
DIAGNOSTIC STRATEGIES AND INITIAL MANAGEMENT — The approach to and extent of diagnostic evaluation of a patient with dyspepsia is based on the presence or absence of alarm features (table 2), patient age, and the local prevalence of Helicobacter pylori (H. pylori) infection (algorithm 1 and table 3) .
Patients with gastroesophageal reflux disease (GERD) and nonsteroidal anti-inflammatory drug (NSAID)-induced dyspepsia should be treated with an empiric trial of proton pump inhibitors (PPI) for eight weeks and NSAIDs should be discontinued (table 4). (See "Medical management of gastroesophageal reflux disease in adults" and "Peptic ulcer disease: Management", section on 'Initial management'.)
Further evaluation should be pursued if these patients continue to have symptoms after eight weeks of PPI therapy or earlier if they have alarm features (table 2). (See 'Evaluation of persistent symptoms' below.)
Patient with alarm features or age ≥55 years
Early upper endoscopy — Upper endoscopy should be performed for the evaluation of new onset dyspepsia in patients with alarm features (table 2) or those age ≥55 years. Upper endoscopy provides a gold standard for establishing a specific cause in patients with upper abdominal pain. Biopsies of the stomach should be obtained to rule out H. pylori. Patients with H. pylori should receive eradication therapy in addition to treatment based on the underlying diagnosis. (See "Medical management of gastroesophageal reflux disease in adults" and "Peptic ulcer disease: Management", section on 'Initial management'.)
Multiple studies have evaluated the yield of upper endoscopy in patients with dyspepsia [19-22]. A meta-analysis of nine studies with 5389 patients found that the most prevalent findings in patients with dyspepsia were erosive esophagitis and peptic ulcer disease (pooled prevalence 6 and 8 percent, respectively) .
The diagnostic yield of upper endoscopy increases with age [19,21]. In the absence of alarm features, we perform early endoscopy (within two weeks) in patients of age ≥55 years. These recommendations are largely consistent with the American Gastroenterological Association (AGA) and American College of Gastroenterology (ACG) guidelines [7,24,25]. However, the optimal age cut-off for endoscopic evaluation in patients with dyspepsia (without alarm features) is controversial and is supported by limited evidence that suggests that the risk of malignancy in most United States populations prior to 55 years is low.
Guidelines also suggest that the age cutoff may vary between countries, depending upon the prevalence of gastric cancer . The AGA guidelines suggest that it may be reasonable in some populations in developed nations to consider the age of 60 or 65 years as the threshold age at which endoscopy should be offered to all new dyspeptic patients and an age cutoff of 45 or 50 years may be more appropriate for United States patients of Asian, Hispanic, or Afro-Caribbean extraction or in populations with a high incidence of gastric cancer in young individuals. A European consensus statement recommends endoscopy in adults older than 45 years old who present with persistent dyspepsia . (See "Clinical features, diagnosis, and staging of gastric cancer".) These recommendations highlight the fact that diagnostic evaluation of the patient with dyspepsia need to be individualized based on symptoms, age, ethnic background, family history, and nationality.
If the upper endoscopy is normal, patients with alarm features or persistent symptoms of dyspepsia should undergo further evaluation to exclude other etiologies. However, most patients with a normal upper endoscopy and routine laboratory tests have functional dyspepsia. (See 'Laboratory tests' above and 'Evaluation of persistent symptoms' below and "Functional dyspepsia in adults".)
Patient without alarm features and age <55 years — The two main strategies in patients <55 years without alarm features are to test and treat for H. pylori and to provide empiric antisecretory therapy. The efficacy of the H. pylori test and treat strategy varies based on whether it is employed in primary or secondary care settings and the local prevalence of H. pylori [27,28].
Patients <55 years of age without alarm features should be tested and treated for H. pylori if the local prevalence of H. pylori is >10 percent . Empiric treatment with a proton pump inhibitor (PPI) should be recommended in areas with prevalence <5 percent (table 3 and table 4).
In areas with a prevalence of 5 to 10 percent, the strategies of test and treat H. pylori or empiric PPI therapy may be equivalent in terms of dyspepsia resolution, patient satisfaction, and cost . It is therefore reasonable for clinicians to use clinical judgment in deciding upon noninvasive H. pylori testing or an empiric trial of a PPI. The decision should include consideration of the patient's age, past history, nonsteroidal antiinflammatory drug use, comorbidities, symptom duration, risk factors for gastric or esophageal malignancy and H. pylori infection, availability and cost of diagnostic testing, and patient preference.
Test and treat for Helicobacter pylori — The rationale for H. pylori testing in patients with dyspepsia is based upon the recognition of H. pylori as an etiologic factor in peptic ulcer disease. Testing for H. pylori should be performed with a urea breath test or stool antigen assay. Serologic testing should not be used due to their low positive predictive value .
Patients who test positive for an infection with H. pylori should undergo treatment with eradication therapy. Most dyspeptic patients who are H. pylori positive and who are treated with appropriate antibiotic therapy persist with dyspeptic symptoms; the number needed to treat to successfully relieve dyspeptic symptoms is estimated at 1 in 14.
Patients who have continued symptoms after successful eradication of H. pylori should be treated with antisecretory therapy with a proton pump inhibitor for four to eight weeks (algorithm 1 and table 4) [7,31]. However, some patients may continue to have symptoms of dyspepsia and may require additional evaluation. (See 'Evaluation of persistent symptoms' below.)
Antisecretory therapy — Empiric antisecretory therapy without H. pylori testing/treatment should be recommended in areas of very low prevalence for H. pylori (<5 percent) and may also be considered in areas with prevalence of 5 to 10 percent (table 4) . Proton pump inhibitor therapy is more effective in relieving symptoms of dyspepsia as compared with H2 antagonists [32,33].
Upper endoscopy — Endoscopic evaluation of patients with dyspepsia without alarm features provides a very small additional benefit over a strategy to test and treat for H. pylori and is unlikely to be cost-effective. It is therefore reserved for patients with persistent symptoms despite antisecretory therapy and H. pylori testing/treatment (algorithm 1).
One of the most comprehensive systematic reviews included 17 controlled trials that involved comparison of 20 variations in the treatment strategies . Initial endoscopy was associated with a small reduction in the risk of recurrent dyspeptic symptoms compared with a strategy of initial empiric treatment. H. pylori testing with endoscopy for a positive result increased costs but did not improve symptoms. H. pylori testing followed by eradication appeared to be as effective as initial endoscopy, but reduced costs by decreasing the proportion of patients that ultimately required an endoscopy.
EVALUATION OF PERSISTENT SYMPTOMS — Despite the approaches described above, some patients continue to have symptoms of dyspepsia. Patients with continued symptoms of dyspepsia fall into the following categories: patients with persistent H. pylori infection, patients with an alternate diagnosis, and patients with functional dyspepsia.
Patients with continued symptoms of dyspepsia should be carefully reassessed, paying specific attention to the type of ongoing symptoms, the degree to which symptoms have improved or worsened, and compliance with medications.
An upper endoscopy should be performed in patients with persistent dyspepsia (algorithm 1). Upper endoscopy allows for testing for H. pylori with biopsies for histology in patients who have not previously been tested and culture and sensitivity testing in patients who have previously been treated. Biopsies of the duodenum should also be performed to rule out celiac disease.
In patients with a normal upper endoscopy, further evaluation should be performed based on the type of ongoing symptoms (algorithm 2). An ultrasound of the gallbladder should be performed only in patients with pain suggestive of biliary disease . Distinguishing between patients with true biliary pain and those with coincident but unrelated dyspepsia and cholelithiasis is important, as it may lead to an unnecessary cholecystectomy that is unlikely to relieve dyspepsia.
Delayed gastric emptying has been found in 30 to 50 percent of patients complaining of dyspeptic symptoms . A gastric emptying study for gastroparesis should be considered in patients with persistent nausea and vomiting and in patients with risk factors for delayed gastric emptying (eg, diabetes mellitus). The clinician should be aware that a significant overlap exists between dyspepsia and gastroparesis; treatment directed at accelerating delayed gastric emptying in these patients may not necessarily improve symptoms . (See "Gastroparesis: Etiology, clinical manifestations, and diagnosis" and "Treatment of gastroparesis".)
Diarrhea, constipation, bloating, and flatulence may be associated with inflammatory bowel disease and a colonoscopy and small bowel radiography may be indicated. A diagnosis of chronic intestinal ischemia should be considered in patients with severe peripheral vascular disease or coronary artery disease. In patients with chronic mesenteric ischemia, computed tomography (CT) and magnetic resonance (MR) angiography may demonstrate high grade stenoses in mesenteric vessels. Symptoms suggestive of an anxiety or panic disorder should be sought and treated if present .
Approximately 75 percent of patients have functional (idiopathic or nonulcer) dyspepsia with no underlying cause on diagnostic evaluation. The management of patients with functional dyspepsia is presented in detail, separately. (See "Functional dyspepsia in adults".)
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Stomach ache and stomach upset (The Basics)")
●Beyond the Basics topic (see "Patient education: Upset stomach (functional dyspepsia) in adults (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Dyspepsia is defined as one or more of the following symptoms: postprandial fullness, early satiation, epigastric pain, or burning. Approximately 25 percent of patients with dyspepsia are found to have an underlying organic disease on diagnostic evaluation (table 1). However, approximately 75 percent of patients have functional (idiopathic or nonulcer) dyspepsia.
●A detailed history, physical examination, and laboratory studies are necessary to narrow the differential diagnosis, identify gastroesophageal reflux disease (GERD) and nonsteroidal anti-inflammatory drug (NSAID)-induced dyspepsia, and patients with alarm features (table 2).
●The approach to and extent of diagnostic evaluation of a patient with dyspepsia is based on the presence or absence of alarm features, patient age, and the prevalence of H. pylori infection (table 2 and algorithm 1).
•Patients with GERD and NSAID-induced dyspepsia should be treated with an empiric trial of proton pump inhibitors (PPI) (table 4) for eight weeks and NSAIDs should be discontinued. (See "Medical management of gastroesophageal reflux disease in adults" and "Peptic ulcer disease: Management".)
•Patients <55 years of age without alarm features should be tested and treated for H. pylori if the prevalence of H. pylori is high (>10 percent). Patients who test positive for an infection with H. pylori should undergo treatment with eradication therapy.
Either strategy (test and treat H. pylori or empiric PPI therapy) may be employed in areas of intermediate H. pylori prevalence (5 to 10 percent).
●Testing for H. pylori should be performed with a urea breath test or stool antigen assay.
Patients who test positive for an infection with H. pylori should undergo treatment with eradication therapy. (See "Treatment regimens for Helicobacter pylori".)
In patients who test negative for an infection with H. pylori and those who have continued symptoms after eradication of H. pylori, we suggest treatment with antisecretory therapy with a proton pump inhibitor for four to eight weeks (table 4) (Grade 2A) .
●In patients with continued symptoms of dyspepsia, endoscopic evaluation should be considered in patients who have not previously undergone an upper endoscopy and biopsies should be obtained for H. pylori and to rule out celiac disease (algorithm 1).
Further evaluation for an alternate diagnosis should be considered based on the patient’s symptoms (algorithm 2).
Patients with continued symptoms of dyspepsia for three months with symptom onset at least six months before diagnosis and no evidence of structural disease to explain the symptoms should be diagnosed and treated as functional dyspepsia. (See "Functional dyspepsia in adults".)
- Tack J, Talley NJ, Camilleri M, et al. Functional gastroduodenal disorders. Gastroenterology 2006; 130:1466.
- Kurata JH, Nogawa AN, Everhart JE. A prospective study of dyspepsia in primary care. Dig Dis Sci 2002; 47:797.
- Ford AC, Forman D, Bailey AG, et al. Effect of dyspepsia on survival: a longitudinal 10-year follow-up study. Am J Gastroenterol 2012; 107:912.
- van Zanten SV, Wahlqvist P, Talley NJ, et al. Randomised clinical trial: the burden of illness of uninvestigated dyspepsia before and after treatment with esomeprazole--results from the STARS II study. Aliment Pharmacol Ther 2011; 34:714.
- Lacy BE, Weiser KT, Kennedy AT, et al. Functional dyspepsia: the economic impact to patients. Aliment Pharmacol Ther 2013; 38:170.
- Talley NJ, American Gastroenterological Association. American Gastroenterological Association medical position statement: evaluation of dyspepsia. Gastroenterology 2005; 129:1753.
- Talley NJ, Vakil NB, Moayyedi P. American gastroenterological association technical review on the evaluation of dyspepsia. Gastroenterology 2005; 129:1756.
- Bytzer P, Talley NJ. Dyspepsia. Ann Intern Med 2001; 134:815.
- Koch KL, Stern RM. Functional disorders of the stomach. Semin Gastrointest Dis 1996; 7:185.
- Malagelada JR. Functional dyspepsia. Insights on mechanisms and management strategies. Gastroenterol Clin North Am 1996; 25:103.
- Earlam R. A computerized questionnaire analysis of duodenal ulcer symptoms. Gastroenterology 1976; 71:314.
- Vakil N, van Zanten SV, Kahrilas P, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol 2006; 101:1900.
- Klauser AG, Schindlbeck NE, Müller-Lissner SA. Symptoms in gastro-oesophageal reflux disease. Lancet 1990; 335:205.
- Hallas J, Bytzer P. Screening for drug related dyspepsia: an analysis of prescription symmetry. Eur J Gastroenterol Hepatol 1998; 10:27.
- Talley NJ. Dyspepsia. Gastroenterology 2003; 125:1219.
- Lacy BE, Talley NJ, Locke GR 3rd, et al. Review article: current treatment options and management of functional dyspepsia. Aliment Pharmacol Ther 2012; 36:3.
- Moayyedi P, Axon AT. The usefulness of the likelihood ratio in the diagnosis of dyspepsia and gastroesophageal reflux disease. Am J Gastroenterol 1999; 94:3122.
- Hunt RH, Xiao SD, Megraud F, et al. Helicobacter pylori in developing countries. World Gastroenterology Organisation Global Guideline. J Gastrointestin Liver Dis 2011; 20:299.
- Williams B, Luckas M, Ellingham JH, et al. Do young patients with dyspepsia need investigation? Lancet 1988; 2:1349.
- Wiklund I, Glise H, Jerndal P, et al. Does endoscopy have a positive impact on quality of life in dyspepsia? Gastrointest Endosc 1998; 47:449.
- Vakil N, Talley N, van Zanten SV, et al. Cost of detecting malignant lesions by endoscopy in 2741 primary care dyspeptic patients without alarm symptoms. Clin Gastroenterol Hepatol 2009; 7:756.
- Adang RP, Vismans JF, Talmon JL, et al. Appropriateness of indications for diagnostic upper gastrointestinal endoscopy: association with relevant endoscopic disease. Gastrointest Endosc 1995; 42:390.
- Ford AC, Marwaha A, Lim A, Moayyedi P. What is the prevalence of clinically significant endoscopic findings in subjects with dyspepsia? Systematic review and meta-analysis. Clin Gastroenterol Hepatol 2010; 8:830.
- Talley NJ, Vakil N, Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the management of dyspepsia. Am J Gastroenterol 2005; 100:2324.
- Chey WD, Wong BC, Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol 2007; 102:1808.
- Malfertheiner P, Megraud F, O'Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut 2007; 56:772.
- Manes G, Menchise A, de Nucci C, Balzano A. Empirical prescribing for dyspepsia: randomised controlled trial of test and treat versus omeprazole treatment. BMJ 2003; 326:1118.
- Silverstein MD, Petterson T, Talley NJ. Initial endoscopy or empirical therapy with or without testing for Helicobacter pylori for dyspepsia: a decision analysis. Gastroenterology 1996; 110:72.
- Grad YH, Lipsitch M, Aiello AE. Secular trends in Helicobacter pylori seroprevalence in adults in the United States: evidence for sustained race/ethnic disparities. Am J Epidemiol 2012; 175:54.
- Malfertheiner P, Megraud F, O'Morain CA, et al. Management of Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report. Gut 2012; 61:646.
- Moayyedi P, Delaney BC, Vakil N, et al. The efficacy of proton pump inhibitors in nonulcer dyspepsia: a systematic review and economic analysis. Gastroenterology 2004; 127:1329.
- Jones RH, Baxter G. Lansoprazole 30 mg daily versus ranitidine 150 mg b.d. in the treatment of acid-related dyspepsia in general practice. Aliment Pharmacol Ther 1997; 11:541.
- Mason I, Millar LJ, Sheikh RR, et al. The management of acid-related dyspepsia in general practice: a comparison of an omeprazole versus an antacid-alginate/ranitidine management strategy. Compete Research Group [corrected]. Aliment Pharmacol Ther 1998; 12:263.
- Delaney BC, Innes MA, Deeks J, et al. Initial management strategies for dyspepsia. Cochrane Database Syst Rev 2001; :CD001961.
- Talley NJ. Gallstones and upper abdominal discomfort. Innocent bystander or a cause of dyspepsia? J Clin Gastroenterol 1995; 20:182.
- Lacy BE. Functional dyspepsia and gastroparesis: one disease or two? Am J Gastroenterol 2012; 107:1615.
- Goodwin RD, Cowles RA, Galea S, Jacobi F. Gastritis and mental disorders. J Psychiatr Res 2013; 47:128.