H. pylori infection has been identified as the major cause of chronic gastritis, duodenitis, benign gastric and duodenal ulcers, gastric adenocarcinoma, and MALT lymphoma (4). H. pylori is a gram-negative spiral bacillus that colonizes the stomachs in as many as 80% of individuals in some populations. It will infect only gastric-like epithelium and is usually localized to the gastric antrum, living on the surface epithelial cells beneath the mucous coat. It survives in gastric acid by using a powerful urease enzyme to break down urea into ammonia and bicarbonate, creating a more alkaline environment for itself. The prevalence of infection increases with age (>50% of Americans older than 60 years) and is high in lower socioeconomic populations and in developing countries. Infection is chronic and causes a superficial gastritis, which is most commonly asymptomatic. Approximately 70% of peptic gastric ulcers, 95% of duodenal ulcers, and 50% of gastric adenocarcinoma are caused by this infection. Double-contrast technique demonstrates enlarged areae gastricae in 50% of patients with H. pylori infection. Diagnosis of H. pylori infection is made by serology, urease breath tests, and endoscopic biopsy. Treatment is usually a combination of two to four drugs including one or more antibiotics, H2 blockers to decrease acid secretion, and occasionally a bismuth compound. Cure rates of 90% are reported although antibiotic resistance is emerging. Although spontaneous elimination of infection is rare, treatment of asymptomatic infected individuals is not currently recommended.

Gastric carcinoma is the third most common GI malignancy, following colon and pancreatic carcinoma. Most (95%) are adenocarcinomas; the remainder are diffuse anaplastic (signet-ring) carcinoma, squamous cell carcinoma, or rare cell types (5). Predisposing factors include smoking, pernicious anemia, atrophic gastritis, and gastrojejunostomy. H. pylori infection increases the risk of gastric carcinoma sixfold and is the cause of approximately half of gastric adenocarcinoma cases. The peak age is from 50 to 70 years, with males predominating
2:1. The incidence of gastric carcinoma is as much as five times higher in Japan, Finland, Chile, and Iceland than in the United States. Mortality is high with a 5-year survival rate of 10% to 20%.

The tumor assumes four common morphologic growth patterns. One-third are polypoid masses that present as filling defects within the gastric lumen (Fig. 29.3). Many of these are broad based and papillary in configuration. Another one-third are ulcerative masses presenting as malignant gastric ulcers. The remainder are infiltrating tumors, focal plaque-like lesions with central ulcer, or diffusely infiltrating (15%) with poorly differentiated carcinomatous cells producing bizarre thickened folds and thickened rigid stomach wall, the so-called scirrhous carcinomas (Figs. 29.4, 29.5). The terms “linitis plastica” and “water-bottle stomach” may be applied to describe the resulting stiff narrowed stomach. Additional causes of narrowed stomach are listed in Table 29.1.

The tumor spreads by direct invasion through the gastric wall to involve perigastric fat and adjacent organs, or it may seed the peritoneal cavity. Lymphatic spread is to the regional lymph nodes including perigastric nodes along the lesser curvature, celiac axis, and hepatoduodenal, retropancreatic, mesenteric, and para-aortic nodes (8). Hematogenous metastases involve the liver, adrenal glands, ovaries, and, rarely, bone and lung. Intraperitoneal seeding presents as carcinomatosis or Krukenberg ovarian tumors. PET-CT is most effective in the demonstration of metastatic lymph nodes and distant spread of tumor (8).

Early gastric cancers appear on barium studies as (1) gastric polyps with risk of malignancy increased for lesions larger than 1 cm, (2) superficial plaque-like lesions or nodular mucosa, and (3) shallow, irregular ulcers with nodular adjacent mucosa. These lesions are most sensitively detected on double-contrast studies.

CT and MR are used to determine the extent of tumor to facilitate preoperative planning (Fig. 29.6) (9). Transmural
extension, intraperitoneal spread, or distant metastases limit the treatment to palliative surgery or chemotherapy. Findings include (1) focal, often irregular, wall thickening (>1 cm); (2) diffuse wall thickening due to tumor infiltration (linitis plastica) (contrast enhancement is common); (3) intraluminal soft tissue mass; (4) bulky mass with ulceration; (5) rare, large, exophytic tumor resembling leiomyosarcoma; (6) extension of tumor into perigastric fat; (7) regional lymphadenopathy; and (8) metastases in the liver, adrenal, and peritoneal cavity. Mucinous adenocarcinomas frequently contain stippled calcifications. Findings used to differentiate malignant gastric neoplasms are listed in Table 29.2.

Lymphoma accounts for 2% of gastric neoplasms (10). The stomach is the most common site of involvement of primary GI lymphoma, accounting for approximately 50% of cases. Most (80%) gastric lymphoma is non-Hodgkin, B-cell type (9). Chronic infection of the gastric epithelium with H. pylori is associated with the risk of developing MALT gastric lymphomas, which are more indolent and have a better prognosis than B-cell lymphomas (7). Because lymphoma remains confined to the bowel wall for prolonged periods of time, it has a better prognosis than carcinoma with a 5-year survival rate of 62% to 90%. Lymphoma demonstrates four morphologic patterns: polypoid solitary mass, ulcerative mass, multiple submucosal nodules (Fig. 29.7), and diffuse infiltration (Fig. 29.8). UGI findings include the following: (1) polypoid lesions, (2) irregular ulcers with nodular thickened folds, (3) bulky tumors with large cavities, (4) multiple submucosal nodules that commonly ulcerate and create a target or “bull’s-eye” appearance, (5) diffuse but pliable wall and fold thickening, and (6) rarely, linitis plastica appearance of diffuse, stiff narrowing (Fig. 29.8) (7). Multiplicity of lesions favors MALT lymphoma as the diagnosis.

CT is the primary imaging modality used to stage lymphoma. CT findings that are helpful in differentiating gastric lymphoma from carcinoma include (1) more marked thickening of the wall (may exceed 3 cm) (Fig. 29.9), (2) involvement of additional areas of the GI tract (trans-pyloric spread of lymphoma to the duodenum in 30%), (3) absence of invasion of the perigastric fat, (4) absence of luminal narrowing and obstruction despite extensive involvement, and (5) more widespread and bulkier adenopathy (10).

GI stromal tumors (GISTs) are the most common mesenchymal tumors to arise from the GI tract (11,12). Most, but not all, tumors previously classified as leiomyomas,
leiomyosarcomas, and leiomyoblastomas are now classified as GISTs. Approximately 60% to 70% of GISTs arise in the stomach, and 10% to 30% of these are malignant. True leiomyomas and leiomyosarcomas are very rare in the stomach.