Inflammatory Conditions of the Stomach and Duodenum

PATHOGENESIS

Erosive gastritis is most commonly caused by aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Other less frequent causes include alcohol, stress, trauma, burns, Crohn’s disease, viral or fungal infection, and endoscopic heater probe therapy or other iatrogenic trauma.

It has been well documented that aspirin and other NSAIDs can disrupt the mucosal barrier in the stomach, causing erosive gastritis and gastric ulcers (see Chapter 17 ). Endoscopic studies on healthy volunteers have shown that as few as two aspirin tablets may cause erosive gastritis within 24 hours. ^, Maximal damage usually occurs within 1 to 3 days and healing occurs within 1 week. Thus, NSAID-induced gastric erosions may form and heal rapidly after ingestion of these agents.

CLINICAL FINDINGS

Some patients with erosive gastritis present with dyspepsia, epigastric pain, or signs of upper GI bleeding, but others are asymptomatic. Because erosive gastritis is often detected as an incidental finding on barium studies or endoscopy, it is important to rule out other upper GI abnormalities before assuming this condition is causing the patient’s symptoms.

RADIOGRAPHIC FINDINGS

Two types of erosions, complete and incomplete erosions, are detected on double-contrast studies. Complete or varioliform erosions (by far the most common type) typically occur in the gastric antrum, appearing as punctate or slitlike barium collections surrounded by radiolucent mounds of edema ( Fig. 18.1 ). ^{, ,} In other patients, erosive gastritis may be manifested only by scalloped antral folds ( Fig. 18.2A ) or by varioliform erosions faintly seen on the crests of the folds ( Fig. 18.2B ). Small hyperplastic polyps are occasionally detected at the site of healed erosions as a sequela of chronic erosive gastritis.

In contrast, incomplete erosions are characterized by punctate or slitlike barium collections that have no surrounding mounds of edema ( Fig. 18.3 ). ^, Incomplete erosions are more difficult to detect than varioliform erosions, accounting for less than 20% of all cases of erosive gastritis found on double-contrast studies. ^,

Although no causative significance is generally attributed to the shape or location of gastric erosions detected on double-contrast studies, aspirin and other NSAIDs may occasionally produce incomplete, linear or serpiginous erosions that tend to be clustered in the antrum or body of the stomach on or near the greater curvature ( Fig. 18.4 ). It has been postulated that these erosions result from localized mucosal injury as the dissolving NSAID capsules or tablets collect by gravity in the dependent portion of the stomach. Whatever the explanation, these distinctive linear or serpiginous erosions should be highly suggestive of recent aspirin or other NSAID use. Nevertheless, most patients with NSAID-induced erosive gastritis have typical varioliform erosions. ^, If recent ingestion of NSAIDs is confirmed in symptomatic patients with erosive gastritis, withdrawal of the offending agent usually produces a marked clinical response.

Recurrent episodes of NSAID-induced erosive gastritis may eventually cause flattening and deformity of the greater curvature of the antrum, a radiologic sign of chronic NSAID-related gastropathy ( Fig. 18.5 ). ^,

DIFFERENTIAL DIAGNOSIS

Crohn’s disease involving the stomach may be manifested on double-contrast studies by aphthoid ulcers that are indistinguishable from varioliform erosions, but affected individuals usually have associated ileocolic Crohn’s disease (see later, “Crohn’s Disease”). Gastric erosions can also be mistaken for ulcerated submucosal masses (i.e., bull’s-eye lesions), but the central ulcer of a bull’s-eye lesion is considerably larger than an erosion, and the adjoining mass also is larger than the mound of edema surrounding an erosion (see Chapter 21 ). Bull’s-eye lesions also tend to be more sporadic than erosions and are not aligned on the rugal folds. As a result, it is almost always possible to distinguish these lesions by radiographic criteria.

RADIOGRAPHIC FINDINGS

Most patients with antral gastritis on barium studies have thickened, scalloped, or lobulated folds that are oriented longitudinally in the antrum ( Fig. 18.6A ), but some have thickened transverse antral folds ( Fig. 18.6B ). Crenulation or irregularity of the lesser curvature of the distal antrum is another less common sign of antral gastritis (see Fig. 18.6B ). Other patients have fine transverse striations, or antral striae , as a sign of chronic antral gastritis, although this finding can also be seen as a normal variant. Still others have a single smooth or slightly lobulated fold (also known as a hypertrophied antral-pyloric fold ) that arises on the lesser curvature of the prepyloric antrum and extends into the pylorus or base of the duodenal bulb ( Fig. 18.7 ). ^, Endoscopy is not warranted when a typical antral-pyloric fold is seen on barium studies. If the fold is more lobulated or nodular, however, endoscopic biopsy specimens should be obtained to rule out a plaquelike or polypoid antral carcinoma.

DIFFERENTIAL DIAGNOSIS

Most cases of mild or moderate antral gastritis are readily differentiated from tumor on barium studies. When antral folds are markedly thickened and lobulated in patients with severe antral gastritis, however, the findings can mimic lymphoma or even a submucosally infiltrating gastric carcinoma. In such cases, endoscopic biopsy specimens are required for a definitive diagnosis.

CLINICAL FINDINGS

H. pylori infection is acquired by oral ingestion of the bacterium and is mainly transmitted within families during early childhood. H. pylori is a worldwide pathogen, being most common in developing countries and in lower socioeconomic populations of industrialized countries. The prevalence of H. pylori increases with age; more than 50% of Americans over the age of 60 are infected by this organism. Some people with H. pylori present with dyspepsia, epigastric pain, or other upper GI symptoms, but most are asymptomatic. Even when symptoms are present, it is difficult to prove that the symptoms are caused by H. pylori because of the high prevalence of this infection.

H. pylori gastritis can be eradicated from the stomach by combination therapy with antibiotics and antisecretory agents (proton pump inhibitors). In a consensus development panel sponsored by the National Institutes of Health in 1994 and a subsequent update conference sponsored by the American Digestive Health Foundation in 1997, combination therapy with antibiotics and antisecretory agents was recommended for all H. pylori –positive patients with gastric or duodenal ulcers to accelerate ulcer healing and decrease the rate of ulcer recurrence. ^, However, because of conflicting data about the value of H. pylori eradication therapy in patients with nonulcer dyspepsia, ^, treatment is not generally recommended for this subset of patients. It therefore remains unclear whether combination therapy should be reserved for patients with H. pylori who have gastric or duodenal ulcers or whether patients with H. pylori and nonulcer dyspepsia would also benefit from treatment.

H. pylori gastritis can be accurately diagnosed at endoscopy on histologic specimens, cultures, and a rapid urease test. However, noninvasive tests for H. pylori, such as a urea breath test (using orally administered ¹⁴ C- or ¹³ C-labeled urea) serologic tests, and stool antigen tests have reported sensitivities and specificities of greater than 90% for detecting this infection. ^{, ,}

RADIOGRAPHIC FINDINGS

H. pylori gastritis is the most common cause of thickened folds in the gastric antrum or body on barium studies ( Fig. 18.8 ). ^, However, some patients have diffusely thickened gastric folds or folds that are thickened only in the proximal stomach. Others have markedly thickened, lobulated gastric folds (also known as polypoid gastritis ) in a diffuse ( Fig. 18.9 ) or localized ( Fig. 18.10 ) distribution. ^, Polypoid H. pylori gastritis may be difficult to differentiate from infiltrative conditions or even malignant tumors involving the stomach on barium studies (see later, “Differential Diagnosis”).

Less commonly, H. pylori gastritis is manifested on double-contrast studies by enlarged areae gastricae (≥3 mm in diameter) in the stomach (see Fig. 18.8 ). ^, In the past, enlarged areae gastricae were thought to be associated with duodenal ulcers or hypersecretory states. ^, In retrospect, however, this association was probably related to underlying H. pylori gastritis in most patients. The presence of enlarged areae gastricae should therefore suggest H. pylori gastritis, particularly if associated with thickened gastric folds. ^,

Patients with chronic H. pylori gastritis may gradually acquire lymphoid tissue in the gastric mucosa, resulting in the development of lymphoid follicles containing germinal centers. ^, This lymphoid hyperplasia is characterized on double-contrast studies by innumerable tiny (1–3 mm), round, frequently umbilicated nodules that carpet the mucosa of the gastric antrum or body ( Fig. 18.11 ). The radiographic findings are therefore similar to those of lymphoid hyperplasia in the small bowel or colon.

DIFFERENTIAL DIAGNOSIS

H. pylori gastritis may be indistinguishable on barium studies from hypertrophic gastritis, Ménétrier’s disease, or lymphoma when there are thickened, lobulated folds in a diffuse distribution, and H. pylori gastritis may be indistinguishable from malignant tumors such as lymphoma or a submucosally infiltrating carcinoma when there are enlarged, polypoid folds in a focal distribution. In other patients with H. pylori gastritis, computed tomography (CT) may reveal circumferential thickening of the antrum or focal thickening of the posterior gastric wall, occasionally simulating a gastric carcinoma. Endoscopic biopsy specimens are therefore needed to differentiate polypoid H. pylori gastritis from malignant tumor in these patients.

When H. pylori gastritis is associated with lymphoid hyperplasia, the major consideration in the differential diagnosis is a low-grade gastric MALT lymphoma (see Chapter 21 ). However, gastric MALT lymphoma is characterized on double-contrast studies by multiple round, variably sized, often confluent nodules with poorly defined borders (see Fig. 21.15). In contrast, the nodules of lymphoid hyperplasia have more discrete borders, a more uniform size, and, not infrequently, central umbilications (see Fig. 18.11 ). Lymphoid hyperplasia of the stomach should also be differentiated from enlarged areae gastricae in H. pylori gastritis. ^, However, enlarged areae gastricae have a polygonal or angulated configuration, producing a sharply marginated reticular network (see Fig. 18.8 ), and do not contain central umbilications. If the radiographic findings are equivocal, endoscopic biopsy specimens should be obtained for a definitive diagnosis.

RADIOGRAPHIC FINDINGS

Hypertrophic gastritis is characterized on barium studies by markedly thickened folds, mainly in the gastric fundus and body, because the acid-secreting portion of the stomach is most affected by this condition ( Fig. 18.12 ). In retrospect, however, many if not most cases of previously diagnosed hypertrophic gastritis probably resulted from infection by H. pylori, a much more common cause of thickened gastric folds (see earlier, “ Helicobacter pylori Gastritis”).

DIFFERENTIAL DIAGNOSIS

H. pylori gastritis, Ménétrier’s disease, and lymphoma are the major considerations in the differential diagnosis of thickened, lobulated gastric folds. Polypoid H. pylori gastritis can usually be differentiated from hypertrophic gastritis by noninvasive tests for H. pylori, such as the urea breath test and serologic tests (see earlier, “ Helicobacter pylori Gastritis”). Ménétrier’s disease should be suspected in patients who have normal or decreased acid secretion and a protein-losing enteropathy (see later, “Ménétrier’s Disease”), whereas lymphoma should be suspected when ulcers, masses, or bull’s-eye lesions are also present in the stomach (see Chapter 21 ). Gastric carcinoma is a less common cause of thickened folds and is usually associated with loss of distensibility and decreased or absent peristalsis in the involved portion of the stomach. If the radiographic findings are equivocal, endoscopic biopsy specimens may be required to rule out malignant tumor. Other rare conditions such as Zollinger-Ellison syndrome may also be manifested by markedly thickened gastric folds, but this diagnosis is often suggested by the clinical history and presentation (see Chapter 17 ).

PATHOLOGY

Ménétrier’s disease is characterized histologically by thickening and hyperplasia of the mucosa secondary to cystic dilation and elongation of gastric mucous glands associated with deepening of the foveolar pits. Despite these findings, gastric acid output is decreased or absent in about 75% of cases. Some patients have a protein-losing enteropathy caused by loss of protein from the hyperplastic mucosa into the gastric lumen.

CLINICAL FINDINGS

Ménétrier’s disease tends to occur in older patients and is more common in men than in women. Affected individuals often present with epigastric pain, nausea and vomiting, diarrhea, anorexia, weight loss, and/or peripheral edema. ^, Laboratory studies may reveal hypoalbuminemia due to a protein-losing enteropathy and/or hypochlorhydria due to decreased acid secretion. Rare cases of gastric carcinoma have been reported in patients with Ménétrier’s disease, but it is unclear whether it is a premalignant condition or whether this association is coincidental.

Some patients with Ménétrier’s disease have spontaneous remission of symptoms, whereas others respond to treatment with antisecretory agents, vagotomy, or antibiotics. Unfortunately, most patients have a prolonged illness with intractable symptoms. A total gastrectomy may be required for individuals unresponsive to medical therapy.

RADIOGRAPHIC FINDINGS

Ménétrier’s disease is usually characterized on barium studies by markedly thickened, lobulated folds in the gastric fundus and body with relative antral sparing ( Fig. 18.13A ). ^, In one study, however, the antrum was involved in almost 50% of patients, so diffuse thickening of gastric folds in no way precludes this diagnosis. When the disease is confined to one portion of the stomach, focally enlarged folds may erroneously suggest a polypoid carcinoma or lymphoma ( Fig. 18.13B ).

Ménétrier’s disease is characterized on CT by a markedly thickened gastric wall, with masslike elevations representing giant, heaped-up folds protruding into the lumen ( Fig. 18.13C ). When Ménétrier’s disease is suspected on barium studies or CT, full-thickness endoscopic biopsy specimens are needed to confirm this diagnosis.

DIFFERENTIAL DIAGNOSIS

When H. pylori gastritis produces markedly thickened, lobulated folds, the radiographic findings may be indistinguishable from those of Ménétrier’s disease. Gastric lymphoma may also produce markedly enlarged folds, but neoplastic infiltration should be suggested by associated masses, ulcers, or bull’s-eye lesions (see Chapter 21 ). Occasionally, gastric carcinoma may be manifested by thickened folds, but infiltrating cancers tend to narrow the lumen, whereas the stomach usually remains pliant and distensible in patients with Ménétrier’s disease. Zollinger-Ellison syndrome is also associated with thickened folds, but the presence of increased secretions in the stomach and one or more ulcers in the stomach, duodenum, or even the proximal jejunum should suggest the correct diagnosis (see Chapter 17 ). Other conditions involving the stomach, such as Crohn’s disease, eosinophilic gastritis, sarcoidosis, tuberculosis, and syphilis, may also produce thickened gastric folds, but the correct diagnosis is usually suggested by the clinical history and presentation.