eMedicine Specialties > Radiology > Gastrointestinal

Gastric Ulcer

Isaac Hassan, MB, ChB, FRCR, DMRD, Former Senior Consultant Radiologist, Department of Radiology, St Bernard's Hospital, Gibraltar

Updated: Mar 5, 2009

Introduction

Background

Peptic ulcers are mucosal breaks of 3 mm or greater and are common, occurring in about 10% of adults in Western countries.¹ Gastric ulcers account for about one third of peptic ulcers, and duodenal ulcers account for the remainder.¹ Because a small percentage (<5%) of gastric ulcers are caused by ulcerated gastric carcinomas, all gastric ulcers must be carefully assessed to differentiate benign lesions from malignant lesions.

This erect chest radiograph shows free gas under the diaphragm from a perforated gastric ulcer.

This image from an upper gastrointestinal series shows gastric ulceration with coarse irregular mucosal folds. Histologic evaluation revealed an adenocarcinoma.

Pathophysiology

Helicobacter pylori infection² and the use of nonsteroidal anti-inflammatory drugs (NSAIDs)^3,4 are the 2 main factors in the pathogenesis of peptic ulcers. H pylori infection occurs in 75% of gastric ulcers and 90% of duodenal ulcers.¹ Other possible factors include the use of steroids or aspirin, smoking, alcohol or coffee consumption, stress, delayed gastric emptying, and duodenogastric bile reflux.^5,6

Diseases and conditions that are associated with an increased risk of peptic ulceration include cirrhosis, chronic pulmonary disease, renal failure, and renal transplantation.

Frequency

United States

Approximately 15% of the US population has evidence of a peptic ulcer at some time.¹ Of those ulcers, about 5% are gastric and the rest are duodenal. Overall, the incidence of gastric ulcers has been decreasing over the past 3-4 decades.

International

The frequency of gastric ulcers in other countries is variable and is determined primarily by the association of gastric ulcers with their major causes—namely, H pylori infection and NSAID use.

Mortality/Morbidity

The mortality rate for gastric ulcers has slightly decreased in the past few decades to approximately 1 case per 100,000 population.¹ The hospitalization rate is approximately 30 cases per 100,000 population.

Sex

The prevalence has shifted from a male predominance to similar incidences in males and females.

Age

In contrast to the occurrence of duodenal ulcers in adults of all ages, gastric ulcers occur mainly in adults older than 40 years.

Anatomy

The stomach consists of the cardia (which is adjacent to the gastroesophageal junction), fundus, body, antrum, and pylorus. The fundus is dome shaped and extends above and to the left of the cardia toward the left hemidiaphragm. The body extends from the fundus to the lower end of the lesser curve, which is known as the incisura angularis. The antrum extends from the incisura to the pyloric canal.

The stomach is lined by peritoneum; the lesser omentum and greater omentum are double layers of peritoneum that extend from the lesser curve and greater curve, respectively.

Blood is supplied to the stomach by the right and left gastric, right and left gastroepiploic, and short gastric arteries, which originate from all 3 branches of the celiac trunk. The veins drain into the portal vein or 1 of its branches. The lymphatic vessels drain into the celiac lymph nodes surrounding the celiac trunk.

Presentation

The patient's history may include the following features:

• Typically, pain occurs less than 2 hours after meals, is localized in the epigastrium, and is gnawing, burning, or aching in nature. However, the pain may also be in the right upper abdominal quadrant, chest, or back.
• Anorexia, weight loss, belching, bloating, nausea, and/or heartburn may occur.
• Vomiting may be related to partial or complete gastric outlet obstruction.
• Hematemesis or melena may result from gastrointestinal (GI) bleeding.

Physical examination findings may include the following:

• In uncomplicated gastric ulcer, clinical findings are few and nonspecific.
• Epigastric tenderness may be present.
• Guaiac-positive stool may result from occult blood loss.
• Melena resulting from acute or subacute GI bleeding.
• A succussion splash resulting from partial or complete gastric outlet obstruction.

Complications of gastric ulcer disease include the following⁷ :

• Hemorrhage occurs in 20-30% of ulcers.¹
  • Endoscopy is the investigation of choice, with a sensitivity of more than 90% in the detection of the bleeding site.
  • Double-contrast barium studies are limited by poor mucosal coating in the presence of bleeding. Nevertheless, the bleeding site may be detected in as many as 75% of cases. A filling defect caused by a blood clot may be seen at the base of the barium-filled ulcer (see Images 1-2).
• Gastric outlet obstruction occurs in 5% of patients with peptic ulcers.¹
  • It is most common in duodenal ulcers, but it also occurs in antral or pyloric-channel ulcers.
  • The differential diagnosis includes malignant lesions, Crohn disease, and tuberculosis.
  • Nasogastric suction of the large gastric residue is required before performing the upper GI series.
    • The images typically show narrowing and deformity of the pylorus or duodenal cap.
• Perforation occurs in as many as 10% of patients with peptic ulcer disease but is less common in gastric ulcers.¹
  • Most perforations arise from ulcers in the anterior aspect of the duodenal cap and, less commonly, from the anterior aspect of the lesser curve of the stomach.
  • In 75% of cases, free gas is present in the peritoneum; this is best shown on an erect chest radiograph (see Image 3) rather than on an erect or supine abdominal radiograph (see Image 4).
  • An upper GI series performed with water-soluble contrast agent may demonstrate the presence and site of the perforation and whether it has sealed.
  • Subphrenic collections are common sequelae of a perforated peptic ulcer. They may be depicted on plain radiographs (see Image 5), but they are best assessed with ultrasonography or computed tomography (CT) scanning (see Image 6).
• Penetrating posterior-wall gastric and duodenal ulcers result in a walled-off perforation.
  • An abscess may form in the lesser sac.
  • The pancreas is involved in two thirds of cases.
  • A liver abscess may result from a penetrating ulcer in the lesser curve of the stomach.
• Gastroduodenal fistula, or a double-channel pylorus, is caused by a penetrating ulcer in the distal antrum that erodes directly into the base of the duodenal cap, or bulb. Twin channels communicate between the antrum and pylorus: the true pyloric canal and the fistula.
• Gastrocolic fistulas caused by carcinoma of the stomach or transverse colon have become less common than NSAID- or aspirin-induced ulcers in the greater curve. As these ulcers enlarge, they penetrate inferiorly into the gastrocolic ligament, later forming the gastrocolic fistula.

Preferred Examination

• Begin the evaluation with history taking and physical examination.
• Perform blood tests, including a full blood count and liver function tests.
• Inspect the stool, and test it for the presence of occult blood.
• Perform either fiberoptic endoscopy or a double-contrast barium study of the upper GI tract.
  • Endoscopy has become the diagnostic procedure of choice for patients with suspected duodenal ulcer. However, endoscopy is more invasive and costly than double-contrast barium study.
  • Double-contrast examinations of the upper GI tract remain a useful alternative to endoscopy but have a lower sensitivity, especially in the detection of small duodenal ulcers.
• Test for the presence of H pylori infection. This is essential in all patients with peptic ulcers.
  • Endoscopic or invasive tests include rapid urease, histopathologic, and culture tests.
    • Rapid urease tests are considered the endoscopic diagnostic test of choice. In gastric mucosal biopsy specimens, H pylori is detected by testing for the bacterial product urease. If H pylori is present, bacterial urease converts urea to ammonia, which changes the pH and produces a color change.
    • Histopathologic evaluation, often considered the criterion standard in the diagnosis of H pylori, requires a trained pathologist.
    • Cultures are used mainly in research studies.
  • Nonendoscopic or noninvasive tests include H pylori antibody detection and urea breath tests.
    • Levels of antibodies, such as immunoglobulin G (IgG), to H pylori can be measured in serum, plasma, or whole-blood samples. Whole-blood test samples are obtained with finger sticks, but the results are less reliable than those of other methods.
    • Urea breath tests are used to detect H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, carbon dioxide labeled with the heavy isotope, carbon-13 (¹³ C), or the radioactive isotope,¹⁴ C, is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.

Limitations of Techniques

Endoscopy has become the diagnostic procedure of choice in patients with suspected gastric ulcer. Biopsy samples obtained during endoscopy enable histologic diagnosis. Endoscopy with biopsy has a sensitivity of 95%.¹ However, endoscopy is more invasive and costly than a double-contrast study, and multiple biopsy samples are needed to avoid sampling errors.

Single-contrast barium studies have an overall sensitivity of 75%, but double-contrast barium examinations have a sensitivity of as high as 95% in the detection of gastric cancer.¹ These results are comparable to those of endoscopy, and double-contrast barium examination remains a useful alternative to endoscopy. Barium studies have a disadvantage in that biopsy specimens of the lesion cannot be obtained to test for H pylori infection or to evaluate for the presence of malignancy.

Differential Diagnoses

Crohn Disease
Gastric Carcinoma
Gastrointestinal Stromal Tumors - Leiomyoma/Leiomyosarcoma
Tuberculosis, Gastrointestinal
Zollinger-Ellison Syndrome

Other Problems to Be Considered

The most important differential diagnoses are a benign gastric ulcer; an ulcerated gastric carcinoma; and, less commonly, a gastric lymphoma.

Radiography

Image from an upper gastrointestinal series. A 5-cm ulcer crater in the lesser curve of the stomach is depicted en face. The filling defects in the ulcer crater are caused by a blood clot from recent bleeding.

This erect chest radiograph shows free gas under the diaphragm from a perforated gastric ulcer.

This radiograph depicts a subphrenic collection resulting from a perforated gastric ulcer.

Image from an upper gastrointestinal series. A 1-cm lesser-curve ulcer is depicted en face. Note the radiating mucosal folds.

Findings

Technique of double-contrast barium study

The biphasic technique of double-contrast barium study combines double-contrast views of the stomach obtained using effervescent granules and a high-density barium suspension with subsequent prone or erect single-contrast compression views obtained using a low-density barium suspension. Glucagon 0.1 mg is administered intravenously as a hypotonic agent. Ulcers in the posterior wall or lesser curve are depicted well on double-contrast supine or oblique views. However, prone compression views are required to visualize anterior wall ulcers because they do not fill on supine or oblique projections.

Radiologic features

Gastric ulcers are usually seen as round or ovoid collections of barium (see Images 7-9), but they can also be linear or rod or star shaped. Linear ulcers are often observed in the healing stages.

Ulcers smaller than 5 mm may not be detected on barium studies. The availability of effective medical therapy, commenced before barium study, has been associated with a prevalence of ulcers smaller than 10 mm. Ulcers may vary from 3 mm to > 5 cm in diameter. Giant ulcers (>3 cm) have a greater risk of complications such as bleeding and perforation (see Images 1-2). A gastric diverticulum, which usually arises from the posterior wall of the fundus (see Image 10), should not be confused with a large ulcer.

Most benign ulcers are located in the lesser curve or posterior wall of the antrum or body of the stomach. Only about 5% of benign ulcers are located in the anterior wall or greater curve. Antral ulcers are associated with younger patients and upper lesser-curve ulcers associated with the elderly.¹

The incidence of multiple gastric ulcers varies with the imaging technique. Single-contrast studies are associated with an incidence of 2-8%; double-contrast studies, about 20%; and endoscopy, as high as 30%.¹ Multiple ulcers are more common in patients using aspirin or NSAIDs. Multiple gastric ulcers are usually located in the antrum or body.

Lesser-curve ulcers

The smooth, round, or oval ulcer crater projects beyond the contour of the adjacent gastric wall (see Image 8). Areae gastricae adjacent to the ulcer may be enlarged because of edema, and undermining of the mucosa in the base of the ulcer results in the appearance of a thin radiolucent line called the Hampton line, dividing the barium in the ulcer crater from that in the body of the stomach. If the rim of mucosa becomes edematous, a wider radiolucent band or ulcer collar may be observed. Less commonly, the edema and swelling around the ulcer may produce an ulcer mound with poorly defined outer borders.

This image (same patient as in Image 7 in Multimedia) shows a small, lesser-curve gastric ulcer in profile.

This image from an upper gastrointestinal series shows a small lesser-curve ulcer with regular radiating mucosal folds. Histologic evaluation revealed no evidence of malignancy.

Hourglass deformity caused by fibrosis. This large lesser-curve ulcer is healing, with fibrosis dividing the body of the stomach into 2 compartments.

Another image obtained in the same patient as in Image 12 in Multimedia.

Greater-curve ulcers

Benign greater-curve ulcers are usually located in the distal half of the stomach and are strongly associated with aspirin and NSAID use; the dissolving aspirin tablets collect in the most dependent part of the stomach and cause focal ulceration and gastric erosions (see Image 14).

This image from an upper gastrointestinal series shows aspirin-induced gastric erosions in the body and antrum.

Posterior wall ulcers

Posterior wall ulcers may fill with barium and have the typical appearance of an ulcer crater; shallow ulcers may appear as ring shadows.

This image from an upper gastrointestinal series shows a small lesser-curve ulcer with regular radiating mucosal folds. Histologic evaluation revealed no evidence of malignancy.

Anterior wall ulcers

Anterior wall ulcers are depicted as ring shadows; barium coats the rim of the unfilled ulcer crater. These ulcers fill in when the patient is in the prone position.

Pyloric channel ulcers

Most pyloric channel ulcers are smaller than 1 cm in diameter and are located in the lesser-curve aspect or anterior wall of the pylorus (see Images 15-16).

This image from an upper gastrointestinal series shows a pyloric canal ulcer.

This image (same patient as in Image 15 in Multimedia) shows the pyloric canal ulcer in detail.

Appearances suggestive of a benign ulcer

About 95% of gastric ulcers are benign.¹ The double-contrast technique allows differentiation between benign and malignant gastric ulcers in most cases.

The following features are associated with a benign ulcer:

• The ulcer projects beyond the healthy lumen on the profile view (see Image 8).
• The margin of the ulcer crater is sharply defined and smooth en face (see Image 11 and Image 13).
• Any filling defect that surrounds the ulcer, as a result of edema, is smooth and symmetrical and merges with the healthy mucosa (see Image 11).
• The mucosal folds radiate to the edge of the ulcer (see Image 11).

Benign ulcers that do not have these typical features are classified as indeterminate, and endoscopy and biopsy are required, as they are for ulcers that appear malignant. Reports of single-contrast studies before 1975 showed that 6-16% of gastric ulcers with benign appearances were actually malignant.¹ This finding accounts for the common practice of performing endoscopy and biopsy for gastric ulcers that appear benign despite the low incidence of malignancy (5%).¹

Appearances suggestive of malignancy

The following features are associated with a malignant ulcer:

• The ulcer crater has an intraluminal location. Exceptions are ulcers in the antrum or greater curve, where benign ulcers are often drawn inward because of muscle spasm in the adjacent stomach wall.
• The margins of the ulcer crater may be irregular and nodular.
• The ulcer crater is surrounded by an asymmetrical mass that has an abrupt outer border with the healthy mucosa.
• Clubbed mucosal folds terminate short of the ulcer crater (see Image 17).
• Ulcers in the fundus are rare, and almost all are malignant.

Ulcer healing and scarring

Ulcer healing is demonstrated at follow-up studies as a decrease in ulcer size and, often, a change in shape from round to linear. Complete healing or disappearance of the ulcer is usually observed 8 weeks after medical treatment and confirms its benign nature. Endoscopy and biopsy are indicated if any residual nodularity or irregularity is present.

Posterior wall ulcers are often associated with radiating mucosal folds that converge to form a shallow pit. This appearance may be mistaken for an ulcer crater; however, its margins slope more gradually than that of an ulcer crater, and its appearance does not change on follow-up images.

Hourglass deformity caused by fibrosis. This large lesser-curve ulcer is healing, with fibrosis dividing the body of the stomach into 2 compartments.

Another image obtained in the same patient as in Image 12 in Multimedia.

Degree of Confidence

Single-contrast views have a sensitivity of about 75%, as compared with the combined double-contrast technique, which has a sensitivity of 95% (Levine, 2000). Although most benign ulcers may be identified with double-contrast studies, as many as 6-16% of ulcers diagnosed as benign with single-contrast studies before 1975 were actually malignant. An ulcerating gastric carcinoma must not be mistaken for a benign gastric ulcer, and endoscopy and biopsy are mandatory whenever the radiographic appearances are indeterminate or suggestive of malignancy.¹

False Positives/Negatives

Ulcers smaller than 5 mm may be missed with both single- and double-contrast techniques.

Large gastric diverticulum in the fundus.

Computed Tomography

Findings

CT scanning has no part in the primary detection of gastric ulcers⁸ ; however, this modality has a role in the detection of subphrenic and other collections that may occur after a perforation of a gastric ulcer (see Image 6).

Multidetector row CT (MDCT) scanning⁹ and three-dimensional (3-D) imaging are expected to overcome the limitations in cancer staging by offering rapid and accurate information for space perception, detailed hemodynamics, and real-time 3-D processing of volumetric data sets. In particular, virtual endoscopic imaging may be helpful for detecting early gastric cancer.

Ultrasonography

Findings

The main role of ultrasonography is in the detection of other causes of upper abdominal pain, such as gallstones and pancreatitis. Sonograms depict subphrenic and other collections resulting from a perforated gastric ulcer.

Intervention

Embolization of small branches of the gastric arteries with strips of Gelfoam (Pharmacia & Upjohn Company, Kalamazoo, Mich) or 6-cyanoacrylate has been successful in the management of gastric hemorrhage.^10,11,12

Medicolegal Pitfalls

• Failure to diagnose gastric ulceration and eradicate H pylori infection
• Failure to assess complete healing of the gastric ulcer and exclude a malignant ulcer
• Failure to recognize and treat the complications of hemorrhage, perforation, and obstruction, especially in elderly patients

Multimedia

Media file 1: Image from an upper gastrointestinal series. A 5-cm ulcer crater in the lesser curve of the stomach is depicted en face. The filling defects in the ulcer crater are caused by a blood clot from recent bleeding.

Media file 2: This lateral view (same patient as in Image 1 in Multimedia) shows poor mucosal coating caused by recent bleeding.

Media file 3: This erect chest radiograph shows free gas under the diaphragm from a perforated gastric ulcer.

Media file 4: This supine abdominal radiograph (same patient as in Image 3 in Multimedia) shows a pneumoperitoneum.

Media file 5: This radiograph depicts a subphrenic collection resulting from a perforated gastric ulcer.

Media file 6: Computed tomography scan. Subphrenic collection with gaseous and liquid components. Note the interface between the edge of the liver and the collection.

Media file 7: Image from an upper gastrointestinal series. A 1-cm lesser-curve ulcer is depicted en face. Note the radiating mucosal folds.

Media file 8: This image (same patient as in Image 7 in Multimedia) shows a small, lesser-curve gastric ulcer in profile.

Media file 9: A 1.5-cm ulcer is depicted en face in the lesser curve of the stomach.

Media file 10: Large gastric diverticulum in the fundus.

Media file 11: This image from an upper gastrointestinal series shows a small lesser-curve ulcer with regular radiating mucosal folds. Histologic evaluation revealed no evidence of malignancy.

Media file 12: Hourglass deformity caused by fibrosis. This large lesser-curve ulcer is healing, with fibrosis dividing the body of the stomach into 2 compartments.

Media file 13: Another image obtained in the same patient as in Image 12 in Multimedia.

Media file 14: This image from an upper gastrointestinal series shows aspirin-induced gastric erosions in the body and antrum.

Media file 15: This image from an upper gastrointestinal series shows a pyloric canal ulcer.

Media file 16: This image (same patient as in Image 15 in Multimedia) shows the pyloric canal ulcer in detail.

Media file 17: This image from an upper gastrointestinal series shows gastric ulceration with coarse irregular mucosal folds. Histologic evaluation revealed an adenocarcinoma.

References

1. Levine MS. Peptic ulcers. In: Gore RM, Levine MS, Bralow L, eds. Textbook of Gastrointestinal Radiology. 2nd ed. Philadelphia, Pa: WB Saunders;. 2000: 514-45.

2. Levine MS, Rubesin SE. The Helicobacter pylori revolution: radiologic perspective. Radiology. Jun 1995;195(3):593-6. [Medline].

3. Lanas A, Serrano P, Bajador E, et al. Evidence of aspirin use in both upper and lower gastrointestinal perforation. Gastroenterology. Mar 1997;112(3):683-9. [Medline].

4. Lanza FL. NSAIDs and the gastrointestinal tract. Abdom Imaging. Jan-Feb 1997;22(1):1-4. [Medline].

5. Bas G, Eryilmaz R, Okan I, Sahin M. Risk factors of morbidity and mortality in patients with perforated peptic ulcer. Acta Chir Belg. Jul-Aug 2008;108(4):424-7. [Medline].

6. Koivisto TT, Voutilainen ME, Färkkilä MA. Symptoms, endoscopic findings and histology predicting symptomatic benefit of Helicobacter pylori eradication. Scand J Gastroenterol. 2008;43(7):810-6. [Medline].

7. Uppalapati SS, Boylan JD, Stoltzfus J. Risk Factors Involved in Patients with Bleeding Peptic Ulcers: A Case-Control Study. Dig Dis Sci. Jul 22 2008;[Medline].

8. Grassi R, Romano S, Pinto A, Romano L. Gastro-duodenal perforations: conventional plain film, US and CT findings in 166 consecutive patients. Eur J Radiol. Apr 2004;50(1):30-6. [Medline].

9. Kim HJ, Kim AY, Oh ST, et al. Gastric cancer staging at multi-detector row CT gastrography: comparison of transverse and volumetric CT scanning. Radiology. Sep 2005;236(3):879-85. [Full Text].

10. Wayne JD, Bell RH Jr. Limited gastric resection. Surg Clin North Am. Oct 2005;85(5):1009-20, vii.

11. Yee YK, Cheung TK, Gu Q, Chan P, But D, Hung IF, et al. Factors affecting physicians' practices related to Helicobacter pylori infection: effect of experience and mode of practice. Digestion. 2008;78(2-3):77-81. [Medline].

12. Zippi M, Febbraro I, De Felici I, Mattei E, Traversa G, Occhigrossi G. [Diagnosis and treatment of bleeding peptic ulcer: our experience]. Clin Ter. Jul-Aug 2008;159(4):249-55. [Medline].

13. Befrits R, Sjostedt S, Tour R, et al. Long-term effects of eradication of Helicobacter pylori on relapse and histology in gastric ulcer patients: a two-year follow-up study. Scand J Gastroenterol. Nov 2004;39(11):1066-72. [Medline].

14. Glickman MG, Szemes G, Loeb P, Margulis AR. Peptic ulcer of the pyloric region. Am J Roentgenol Radium Ther Nucl Med. Sep 1971;113(1):147-58.

15. Levine MS. Erosive gastritis and gastric ulcers. Radiol Clin North Am. Nov 1994;32(6):1203-14. [Medline].

16. Levine MS, Creteur V, Kressel HY, et al. Benign gastric ulcers: diagnosis and follow-up with double-contrast radiography. Radiology. Jul 1987;164(1):9-13. [Medline].

17. Lim CH, Chalmers DM. Upper gastrointestinal haemorrhage. Postgrad Med J. Aug 2004;80(946):492, 494. [Medline]. [Full Text].

18. Pattison CP, Combs MJ, Marshall BJ. Helicobacter pylori and peptic ulcer disease: evolution to revolution to resolution. AJR Am J Roentgenol. Jun 1997;168(6):1415-20. [Medline].

19. Peek RM Jr, Blaser MJ. Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med. Feb 1997;102(2):200-7. [Medline].

20. Peura DA. Prevention of nonsteroidal anti-inflammatory drug-associated gastrointestinal symptoms and ulcer complications. Am J Med. Sep 6 2004;117 (suppl 5A):63S-71S.

21. Schulman A, Simpkins KC. The accuracy of radiological diagnosis of benign, primarily and secondarily malignant gastric ulcers and their correlation with three simplified radiological types. Clin Radiol. Jul 1975;26(3):317-25.

Keywords

gastric ulcer, peptic ulcer, stomach ulcer, Helicobacter pylori, H pylori, mucosal break, nonsteroidal anti-inflammatory drugs, NSAIDs

Contributor Information and Disclosures

Author

Isaac Hassan, MB, ChB, FRCR, DMRD, Former Senior Consultant Radiologist, Department of Radiology, St Bernard's Hospital, Gibraltar
Isaac Hassan, MB, ChB, FRCR, DMRD is a member of the following medical societies: American Roentgen Ray Society and Royal College of Radiologists
Disclosure: Nothing to disclose.

Medical Editor

John L Haddad, MD, Clinical Associate Professor, Department of Radiology, Weill Medical College of Cornell University; Director of Body MRI, Department of Radiology, Methodist Hospital in Houston
John L Haddad, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

David Andrew Nicholson, BM, BS, FRCR, Honorary Lecturer, Department of Radiology, University of Manchester; Consultant Gastrointestinal Radiologist, Department of Radiology, Hope Hospital, Salford Royal Hospital NHS Trust
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

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