Stomach and Duodenum Dyspepsia

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Dyspepsia ("bad digestion") accounts for approximately 5% of all visits to family practitioners and is the most common reason for referral to a gastroenterologist in the United States, accounting for 20% to 40% of consultations (Jones and Lacy, 2004). The term dyspepsia refers to episodic or recurrent pain or discomfort arising from the proximal GI tract related to meals and is associated with heartburn, reflux, regurgitation, indigestion, bloating, early satiety, and weight loss. The lack of a standardized definition affects accurate prevalence data, given the challenge of clearly defining dyspepsia as either functional or nonulcer dyspepsia (~60% of cases), or that caused by structural or biochemical disease (40%) (Dickerson and King, 2004). Regardless of cause, dyspepsia has a profoundly negative impact on patients' health-related quality of life (HRQOL) and results in significant economic burden.

Nonulcer dyspepsia (NUD) is defined in patients who have undergone either formal radiographic or endoscopic evaluation and who do not have an organic lesion (e.g., ulcer, tumor) to explain their symptoms. Potential etiologies for NUD include gastric acid hypersecretion, gastroduodenal dysmotility, visceral hypersensitivity, emotional stress, and psychological factors. As with other functional GI disorders, the potential for underlying psychosocial and lifestyle factors must be addressed. There is no current recommendation on the role of prokinetics, cytoprotectives, or antidepressants in the management of functional dyspepsia; similarly, no clear evidence supports specific diet and lifestyle modifications or psychosocial interventions.

Peptic Ulcer Disease

Key Points

A noninvasive H. pylori "test and treat" strategy is as effective as endoscopy in the initial management of patients under age 45 with uncomplicated dyspepsia.

Eradication of H. pylori infection in patients with a duodenal or gastric ulcer reduces symptom recurrence. Ulcer prophylaxis with an H2RA or PPI should be considered in patients at high risk for NSAID-associated PUD, including those with a history of PUD, elderly patients, and patients taking corticosteroids or anticoagulants.

Peptic ulcer disease (PUD) is the most common cause of upper gastrointestinal bleeding (UGIB) and a leading cause of dyspepsia (Box 38-2), with a cumulative lifetime prevalence of 8% to 14% (Fig. 38-5). Although up to 70% of patients with gastric and duodenal ulcers are 25 to 64 years old, the peak prevalence of complicated ulcer disease requiring hospitalization is age 65 to 74 (Saad and Scheiman, 2004).

Numerous options exist for the management of uninvestigated dyspepsia in primary care (Fig. 38-6). Given the high cost and often limited access to endoscopy testing, not all patients with uninvestigated dyspepsia should undergo an invasive investigation of their symptoms. The presence of "alarm symptoms" for PUD raises concern for a gastric malignancy. The American Gastroenterological Association (AGA, 2005) endorses prompt endoscopic evaluation in any patient over age 45 with new-onset dyspepsia.

The most common complications of PUD include UGIB, perforation, penetration, and gastric outlet obstruction. An upper GI hemorrhage can occur in up to 15% of patients with PUD and is most common in patients older than 60, with mortality as high as 10%. Perforation occurs in approximately 7% of patients with PUD, again classically in elderly patients receiving long-term nonsteroidal anti-inflammatory drugs (NSAIDs). Perforation can be confirmed on plain abdominal radiography; barium contrast studies and upper endoscopy are contraindicated with suspected perforation, and urgent surgical consultation is mandatory. Mortality may be as high as 30% to 50% in patients with perforation, particularly in elderly and debilitated patients. Penetration occurs when the ulcer crater erodes through and into adjacent organs, including the small bowel, pancreas, liver, and biliary tree. Often subtle, it typically presents as acute pancreatitis. Gastric outlet obstruction occurs in 1% to 3% of PUD patients, resulting from acute inflammation or mechanical obstruction caused by scarring at the gastroduodenal junction (Saad and Scheiman, 2004).

Approaches to confirm a diagnosis of PUD include double-contrast barium esophagography (upper GI series) and upper endoscopy. Although the upper GI series has accuracy of 80% to 90%, upper endoscopy is the preferred diagnostic modality, with multiple studies showing consistent diagnostic superiority in identifying gastric and duodenal ulcers. Despite a higher procedural cost and a slightly increased risk in procedure-related complications (bleeding, perforation, oversedation), upper endoscopy should be the initial diagnostic study performed in suspected PUD. Most importantly, upper endoscopy provides the distinct advantage of permitting biopsies and brushings to identify underlying pathology.

Fecal-oral infection with the bacterium Helicobacter pylori is a major risk factor for the development of PUD. Its prevalence and association with PUD is higher in populations who have a lower standard of living than in the United States, especially in Africa and Central America, although this may be declining. Approximately 90% of patients worldwide with duodenal ulcers are infected with the H. pylori pathogen, whereas 30% to 40% of U.S. ulcer patients are infected (Chey and Wong, 2007). The strongest evidence to support the role of H. pylori as an etiology of PUD is the elimination of ulcer recurrence when the infection has been successfully eradicated.

The evidence-based standard of care dictates that patients with dyspepsia and no alarm symptoms should be tested

Box 38-2 Causes of Dyspepsia


GERD (with and without esophagitis) Functional (nonulcer dyspepsia) Peptic ulcer disease

Less commont

Alcohol consumption Biliary colic Celiac sprue

Gastrointestinal malignancy Gastroparesis

Infection (viral, bacterial, spirochetal, parasitic)

Inflammatory and infiltrative processes (esophagus, stomach, small bowel)

Intestinal ischemia Lactose intolerance

Medications (primarily aspirin and NSAIDs)



Other systemic and metabolic disorders

*In order of relative frequency. tAlphabetical order.

Modified from Saad R, Scheiman JM. Diagnosis and management of peptic ulcer disease. Clin Fam Pract 2004;6:569-587.

GERD, Gastroesophageal reflux disease; NSAIDs, nonsteroidal anti-inflammatory drugs.

Figure 38-5 Gastric ulcer. (Courtesy Dr. Erik-Jan Wamsteker.)

for H. pylori infection and then given eradication therapy if positive, ("test and treat") (Chey and Wong, 2007). H. pylori-positive or H. pylori-negative patients who do not undergo endoscopy initially should do so if their symptoms persist. The effectiveness of this approach depends on the prevalence of H. pylori infection in patients with ulcers in the

Management Peptic Ulcer Images

** Alarm symptoms include rectal bleeding or melena, weight loss, anorexia, early satiety, persistent vomiting, anemia. The presence of an abdominal mass, lymphadenopathy, dysphagia, odynophagia, family history of upper GI cancer, personal history of peptic ulcer, prior gastric surgery or malignancy should eliminate consideration of noninvasive approaches.

GERD: gastroesophageal reflux disease ASA: aspirin

NSAIDs nonsteroidal anti-inflammatory drugs PPI: proton pump inhibitor H. pylori: Helicobacter pylori

* Age cutoff is controversial. Risk of pathology increases slightly with age but older age (50-55) cutoff in many guidelines

** Alarm symptoms include rectal bleeding or melena, weight loss, anorexia, early satiety, persistent vomiting, anemia. The presence of an abdominal mass, lymphadenopathy, dysphagia, odynophagia, family history of upper GI cancer, personal history of peptic ulcer, prior gastric surgery or malignancy should eliminate consideration of noninvasive approaches.

Figure 38-6 Evaluation of uninvestigated dyspepsia. (Modified from Saad R, Scheiman JM. Diagnosis and management of peptic ulcer disease. Clin Fam Pract 2004;6:569-587.)

community; as in some geographic areas, prevalence may be too low to make this approach effective.

Nonendoscopic testing for H. pylori includes a quantitative assay for serum immunoglobulin G (IgG) antibodies, the radiolabeled urea breath test, and the stool antigen test. The median sensitivity and specificity for serologic IgG tests are 92% and 83%, respectively (SIGN, 2003). Some patients may have persistently positive IgG antibodies for months to years after eradication therapy, yielding a false-positive result during that period if retested. In comparative studies, urea breath tests are more accurate than serologic tests. The stool antigen test is recommended as the preferred initial noninva-sive diagnostic test. The urea breath test is the recommended standard to determine if H. pylori has been successfully eradicated (Chey and Wong, 2007).

Several medication regimens have been developed for the treatment of confirmed H. pylori infection, based on data from randomized controlled trials (RCTs), meta-analyses, and systematic reviews (Table 38-2). The best evidence-based recommendation for H. pylori eradication is for 14-day triple therapy with the use of a proton pump inhibitor (PPI), clarithromycin, and either amoxicillin or metronidazole, yielding eradication rates from 70% to 85%. The most common salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that 10-day therapy with a PPI, levofloxacin, and amoxicillin is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection (Chey and Wong, 2007).

Another major etiology of PUD is the increasing and widespread use of both NSAIDs and aspirin. The use and overuse of these medications is the most common cause of PUD in H. pylori-negative patients, and up to 60% of unexplained cases of PUD are attributed to unrecognized NSAID use. In a meta-analysis of observational studies of GI bleeding risk from various NSAIDs, a fourfold increased risk associated with NSAID-use persisted throughout therapy and fell to baseline within 2 months of discontinuation of the drug (Hernandez-Diaz and Rodriguez, 2000). Although both H. pylori and aspirin/NSAIDs are involved in the overwhelming majority of PUD cases, other factors contribute to the remaining 1% to 5% (Box 38-3).

Independent risk factors that augment the impact of H. pylori and NSAID-related PUD risk and may promote ulcer complications include advancing age; history of PUD

Table 38-2 First-Line Regimens for Helicobacter pylori Eradication


Duration (days)

Eradication Rates (%)


Standard-dose PPI bid (esomeprazole, qd); clarithromycin, 500 mg, or amoxicillin, 1000 mg



Consider in non-penicillin-allergic patients who have not previously received a macrolide.

Standard-dose PPI bid; clarithromycin, 500 mg, or metronidazole, 500 mg



Consider in penicillin-allergic patients who have not previously received a macrolide or are unable to tolerate bismuth quadruple therapy.

Bismuth subsalicylate, 525 mg qid; metronidazole, 250 mg qid; tetracycline, 500 mg qid; ranitidine, 150 mg bid; or standard-dose PPI qd-bid



Consider in penicillin-allergic patients.

PPI + amoxicillin, 1 g bid, followed by:



Requires validation in North America.

PPI + clarithromycin 500 mg, tinidazole 500 mg bid


Modified from Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol 2007;102:1808-1825. PPI, Proton pump inhibitor.

Box 38-3 Etiology of Peptic Ulcer Disease

Major causes

Helicobacter pylori infection

Nonsteroidal anti-inflammatory drugs (NSAIDs)


Minor causes

Duodenal obstruction from annular pancreas

Use of topically injurious drugs (potassium chloride, nitrogen-containing bisphosphonates)

Immunosuppressants (e.g., mycophenolate) Helicobacter heilmannii infection

Mucosal infection (herpes simplex 1, cytomegalovirus, tuberculosis, syphilis)

Systemic processes (systemic mastocytosis, Crohn's disease, lymphoma, carcinomas)

Radiation involving duodenum

Use of cocaine or "crack" cocaine

Zollinger-Ellison syndrome

From Heidelbaugh JJ. Peptic ulcer disease. In Rakel RE (ed). Essential Family Medicine, 3rd ed. Philadelphia, Saunders-Elsevier, 2006.

or complicated ulcer disease with perforation, penetration, or gastric outlet obstruction; use of multiple NSAIDs (including concomitant use of low-dose aspirin and an NSAID); and concurrent warfarin or corticosteroid use. Evidence suggests that smoking may increase the risk of PUD and ulcer complications by impairing gastric mucosal healing. Alcohol use may increase the risk of ulcer complications in NSAID users, but its overall effect in those patients without concomitant liver disease has not been clearly defined. Currently, no solid evidence implicates dietary factors in the development of PUD.

Use of NSAIDs and aspirin is frequently associated with symptoms of dyspepsia, even in the absence of PUD. Empiric antisecretory therapy with PPIs is an attractive strategy that involves subjecting only those patients to upper endoscopy who fail to respond to a 4-week course of pharmacotherapy. The rationale for this approach is that most patients with dyspepsia do not have H. pylori infection or PUD (most typically have GERD), and their response to antisecretory therapy eliminates the need for further, expensive and invasive diagnostic testing (Saad and Scheiman, 2004).


The most efficacious therapy for H. pylori eradication consists of 14-day triple therapy with a PPI, clarithromycin, and amoxicillin or metronidazole, yielding eradication rates of 70% to 85% (Chey and Wong, 2007) (SOR: A).

Gastroesophageal Reflux Disease Key Points

• The PPIs provide the most rapid symptomatic relief and healing of esophagitis in the highest percentage of patients.

• Although less effective than PPIs, H2RAs given in divided doses may be effective in some patients with less severe symptoms of GERD; continuous therapy to control symptoms and prevent complications is appropriate.

• Chronic acid suppression has been associated with malabsorption of iron, vitamin B12, and calcium; small bowel bacterial overgrowth; increased risk of hip fracture; and community-acquired pneumonia.

A complex, chronic, and relapsing condition, GERD carries a risk of significant morbidity and resultant complications. Population-based studies revealed that 40% of U.S. adults experience heartburn at least once a month; age- and gender-adjusted prevalence of weekly heartburn or acid regurgitation approaches 20% (Heartburn, 1998; Locke 1997). Most patients with GERD self-treat with over-the-counter (OTC) medications and do not seek medical attention for their symptoms.

Most patients with GERD evaluated in primary care practices have nonerosive reflux disease (NERD), although some will progress to erosive esophagitis (Fig. 38-7), and even fewer to more severe disease resulting in esophageal strictures, Barrett's esophagus, and adenocarcinoma of the esophagus (DeVault and Castell, 2005). Patients with NERD are prone to develop atypical or extraesophageal manifestations of disease (Box 38-4). Because of a small risk of disease progression, however, they generally do not require long-term surveillance despite persistent reflux symptoms. Symptom relapse rates in patients with NERD are similar to those in patients with erosive esophagitis, and although many will require continuous pharmacotherapy to control their symptoms, almost all continue to exhibit no definable erosive esophagitis on upper endoscopy (Fass, 2002).

Upper endoscopy is considered the gold standard in assessing esophageal complications of GERD (e.g., erosive esophagitis, Barrett's esophagus) but lacks an appreciable sensitivity and specificity for identifying pathologic reflux. Double-contrast barium radiography has limited usefulness in making an accurate diagnosis of GERD but may be useful in defining the presence of anatomic abnormalities, such as pyloric stenosis, malrotation, and annular pancreas in the vomiting infant, as well as hiatal hernia and esophageal strictures in children and adults.

The goals of GERD treatment are to relieve symptoms, heal erosive esophagitis if present, manage and prevent complications, and avoid recurrence and progression of disease using acid-suppressive medications. Initial empiric pharmacotherapy should consist of either an H2RA or a PPI, without the need for immediate diagnostic testing in the vast majority of cases. Expert opinion supports either step-up or step-down therapy for the initial treatment of patients with GERD (Inadomi, 2002). In patients who incompletely respond to H2RAs, PPIs taken once daily 30 minutes before the first meal of the day are preferred over continuing H2RA therapy because of greater efficacy and faster symptom control with PPIs. An inadequate response to a 4- or 8-week trial of standard-dose PPI may indicate the need for longer treatment, more severe disease, or an incorrect diagnosis (Fig. 38-8). Additional benefit may be obtained by extending treatment for another 4 to 8 weeks with the same or a double dose of PPI (Medical Advisory Panel, 2003).

Diagnostic testing is recommended in patients with GERD who have an inadequate response to PPI therapy, need continuous chronic therapy to control frequent GERD symptoms, have chronic symptoms (>5 years) and are at risk for Barrett's esophagus, have atypical or extraesophageal manifestations suggesting complicated disease, or have alarm symptoms suggesting cancer (Box 38-5).

Lifestyle modifications should be recommended as adjunctive therapy in all patients with GERD (Box 38-6). Evidence is lacking to support the use of nonpharmacologic measures as the sole initial or long-term therapy for GERD, but expert opinion considers these to be of some potential benefit and no proven harm, although not sufficiently effective in treatment.

The basic tenets of antireflux surgery include reduction of the hiatal hernia, repair of the diaphragmatic hiatus, strengthening of the gastroesophageal junction-posterior diaphragm attachment, and strengthening of the antireflux barrier by adding a gastric wrap around the gastroesophageal junction (Nissen/Toupet fundoplication). In controlled studies comparing antireflux surgery to H2RAs and PPIs, surgery has shown marginal superiority as measured by heartburn relief,

Figure 38-7 Esophagitis. (CourtesyDr. Erik-Jan Wamsteker.)

Box 38-4 Atypical or Extraesophageal Manifestations of GERD

Aspiration Asthma Chronic cough Dental enamel loss Globus sensation Noncardiac chest pain Recurrent laryngitis Recurrent sore throat Subglottic stenosis

Modified from Heidelbaugh JJ, Nostrant TT. Medical and surgical management of gastroesophageal reflux disease. Clin Fam Pract 2004;6:547-568.

esophagitis healing, and improved quality of life in patients with erosive esophagitis. Long-term follow-up trials found that over half of patients resumed taking antireflux medications 3 to 5 years after surgery, most likely as a result of poor patient selection and surgical breakdown (Heidelbaugh and Nostrant, 2004).


Acid suppression with PPIs (proton pump inhibitors) is the mainstay of therapy for esophagitis (DeVault and Castell, 2005) (SOR: A). Lifestyle modifications should be recommended as an adjunctive therapy in patients with GERD (DeVault and Castell, 2005) (SOR: B).

Upper Gastrointestinal Bleeding

Key Points

Comorbid risk factors for GI bleeding severity, including advanced age, shock, congestive heart failure, ischemic heart disease, and stigmata of recent hemorrhage, accurately predict the likelihood of death or rebleeding.


Chf Treatment Algorithm
Figure 38-8 Algorithm for the diagnosis and treatment of gastroesophageal reflux disease. (Modified from Heidelbaugh JJ, Nostrant TT. Medical and surgical management of gastroesophageal reflux disease. Clin Fam Pract 2004;6:547-568.)

Box 38-5 Alarm symptoms of GERD Suggesting Complicated Disease

Black or bloody stools Choking

Chronic coughing


Early satiety



Iron deficiency anemia


Weight loss

Modified from Heidelbaugh JJ, Nostrant TT. Medical and surgical management of gastroesophageal reflux disease. Clin Fam Pract 2004;6:547-568.

• UGIB is confirmed by upper endoscopy, permitting direct visualization of the cause and location of the bleeding and allowing an attempt at immediate hemostasis.

Significant UGIB is defined as bleeding that results in hemo-dynamic instability and a decrease in the hemoglobin (Hb) and hematocrit (Hct). Although most patients with UGIB resolve spontaneously, those with an acute UGIB requiring hemostasis often present with a recent history of hematemesis

Box 38-6 Suggested Lifestyle Modifications in GERD Management

Avoid acidic foods (citrus and tomato-based products), alcohol, caf-feinated beverages, chocolate, onions, garlic, salt, and peppermint. Avoid large meals.

Avoid medications that may potentiate GERD symptoms (calcium channel blockers, |-agonists, a-agonists, theophylline, nitrates, sedatives) Avoid recumbency 3 to 4 hours after meals. Avoid tight clothing around the waist Decrease dietary intake of fat. Elevating head of bed 4 to 8 inches (10-20 cm). Losing weight Smoking cessation

*Dietary fibers and physical exercise may be protective

Modified from DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol 1999;94:1434-1442; and Nilsson M, Johnsen R, Ye W, et al. Lifestyle related risk factors in the aetiology of gastro-oesophageal reflux. Gut 2004;53:1730-1735.

(vomiting fresh blood) or "coffee grounds" emesis (black, partially digested blood). UGIB has an incidence of 40 to 150 episodes per 100,000 persons annually in the United States, with mortality of 6% to 10% (Oh and Pisegna, 2004). Box 38-7 lists the most common causes of UGIB.

It is important to characterize patients with risk factors for the development of UGIB to identify potential preventive measures, including aspirin/NSAID use and anticoagulation or antiplatelet therapy. H. pylori infection, erosive esopha-gitis, history of UGIB, perioperative period, intensive care unit (ICU) admission, and Zollinger-Ellison syndrome are also significant risk factors for UGIB. Figure 38-9 outlines an algorithm for the diagnosis and management of acute UGIB. Hemodynamically unstable patients should be admitted to the ICU, have a large-bore intravenous (IV) and nasogastric tube placed, and should not be fed orally.

Confirmation of UGIB is by upper endoscopy, permitting direct visualization of the cause and location of the bleeding and an attempt at immediate hemostasis. During the diagnostic evaluation, the endoscopist can treat the source of UGIB by using electrocautery, injection of 0.9% saline or 100% ethanol, or a combination of these techniques. Alternative methods include laser photoablation, band ligation, and sclerotherapy and balloon tamponade for esophageal and gastric variceal bleeding. The risk of rebleeding after therapy can be predicted by the morphology and size of the ulcer at



Gastric Duodenal Avm

Figure 38-9 Algorithm for the evaluation of acute upper gastrointestinal (GI) bleeding. ASA, Acetylsalicylic acid; AVM, arteriovenous malformation; NSAIDs, nonsteroidal anti-inflammatory drugs; PPI, proton pump inhibitor; PUD, peptic ulcer disease. (Modified from Oh DS, Pisegna JR. Management of upper gastrointestinal bleeding. Clin Fam Pract 2004;6:631-645)

Figure 38-9 Algorithm for the evaluation of acute upper gastrointestinal (GI) bleeding. ASA, Acetylsalicylic acid; AVM, arteriovenous malformation; NSAIDs, nonsteroidal anti-inflammatory drugs; PPI, proton pump inhibitor; PUD, peptic ulcer disease. (Modified from Oh DS, Pisegna JR. Management of upper gastrointestinal bleeding. Clin Fam Pract 2004;6:631-645)

Box 38-7 Common Causes of Upper Gastrointestinal Bleeding

Arteriovenous malformations (AVMs)

Bleeding from the nose or pharynx

Dieulafoy's lesion (ruptured mucosal artery)

Erosive esophagitis (severe)

Esophageal rupture (Boerhaave's syndrome)

Helicobacter pylori infection



Mallory-Weiss tears (esophagogastric mucosal tears) Neoplasm (carcinoma, lymphoma, leiomyoma, leiomyosarcoma, polyps)

Nonsteroidal anti-inflammatory drugs (NSAIDs) Ulcers (gastric, duodenal)

Vascular-enteric fistulas, usually from aortic aneurysm or graft Varices (esophageal, gastric, duodenal)

Modified from Oh DS, Pisegna JR. Pharmacologic treatment of upper gastrointestinal bleeding. Curr Treat Options Gastroenterol 2003;6:157-162.

upper endoscopy. Most cases of rebleeding occur within the first 72 hours after hospital admission; patients at increased risk for upper GI rebleeding should have ICU monitoring during their admission (Oh and Pisegna, 2004). The use of PPIs in reducing the risk of UGI rebleeding was demonstrated in a landmark study with IV omeprazole, showing the clinical efficacy of acid reduction therapy in preventing the complications of PUD rebleeding (Lau et al., 2000).


Clinical symptoms suggesting gastroparesis, or impaired and delayed gastric emptying, include nausea, vomiting, and postprandial abdominal fullness. Most often, gastroparesis is related to poorly controlled diabetes mellitus, autonomic neuropathies, postsurgical conditions (e.g., vagotomy, Billroth pyloroplasty), and anorexia nervosa. Vomiting needs to be differentiated from regurgitation, rumination, and even bulimia; the duration, frequency, and severity of symptoms together should be described along with any associated symptoms.

Gastric-emptying scintigraphy of a radiolabeled solid meal is the most accepted method to test for gastroparesis. Conventionally, the test is performed for 2 hours after ingestion of a radiolabeled meal; however, performing the test for up to 4 hours may increase the yield in detecting delayed gastric emptying in symptomatic patients. Breath testing can be used to measure gastric emptying using the nonradioactive isotope carbon 13 (13C) (Parkman et al., 2004).

Primary treatment of gastroparesis includes dietary manipulation and administration of antiemetic and prokinetic agents. Dietary recommendations include eating more frequent and smaller meals and replacing solid food with liquids, such as soups. Foods consumed should be low in both fat and fiber content. Common antiemetic agents include prochlorperazine, trimethobenzamide, and promethazine. Currently used prokinetic agents include metoclopramide and erythromycin, administered orally or intravenously. Domperidone, a dopamine (D2) receptor antagonist, is not approved in the United States for treatment of gastroparesis but is available in Canada, Mexico, and Europe (Parkman et al., 2004). Endoscopic injection of botulinum toxin into the pyloric sphincter can aid in relaxing pyloric sphincter resistance, allowing more food to empty from the stomach. No placebo-controlled trials have yet been reported for this therapy, and long-term control of gastroparesis should not be expected from using botulinum toxin.

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