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Epithelial polyps are rare in the stomach. Three types occur: hyperplastic polyps (70%), fundic gland polyps (20%), and adenomatous polyps (10%). The risk of carcinoma is moderate in adenomatous polyp, slight in hyperplastic polyp, and nil in fundic gland polyps. Few gastric carcinomas arise in polyps; even when the two are associated, carcinoma commonly occurs not in the polyp but in adjacent mucosa. Gastric polyps appear as small pedunculated lesions, often multiple, that can be removed endoscopically. Large polyps are very rare.
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Mesenchymal Neoplasms
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Benign mesenchymal neoplasms are uncommon. They include leiomyomas and neurofibroma. Also presenting as a gastric tumor is heterotopic pancreas (also called choristoma but not a true neoplasm; see Chapter 17: Neoplasia: I. Classification, Nomenclature, & Epidemiology of Neoplasms). All of these present as intramural or submucosal nodules that rarely cause symptoms.
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Gastric Adenocarcinoma
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Adenocarcinoma accounts for over 90% of malignant neoplasms of the stomach. The incidence of gastric carcinoma is five to ten times higher in Japan than in the United States. The incidence is also high in Iceland and Chile. In the United States, the incidence has declined since 1950; presently, about 25,000 new cases occur every year. There is an increased prevalence in the USA among Native Americans, Native Hawaiians, and Latino Americans.
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Studies in Japanese immigrants to the United States show a decreased incidence from generation to generation, strongly suggesting that some environmental factor causes gastric cancer in Japan. It has been postulated that polycyclic hydrocarbons in smoked fish may be responsible.
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The declining incidence of gastric carcinoma in the United States has been attributed to better refrigeration of meat, thereby decreasing the need for preservatives such as nitrites. Nitrites are converted to nitrosamines, which have been shown to cause gastric carcinoma in experimental animals. Antibiotic usage, which reduces Helicobacter pylori infection, may also have contributed to the decline in incidence over time.
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Gastric carcinoma is statistically more common in individuals with blood group A. There is no significant familial tendency.
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Gastric carcinoma occurs with increased frequency (1) in patients with chronic atrophic gastritis associated with pernicious anemia (high risk); (2) in those with chronic atrophic gastritis associated with H pylori infection, particularly when there is intestinal metaplasia (uncertain risk); (3) in those with adenomatous and hyperplastic polyps (low risk); and (4) in patients who have had subtotal gastrectomy, when the residual gastric stump is believed to be at increased risk. Chronic peptic ulcers of the stomach were at one time believed to carry an increased risk of carcinoma, but that view is no longer held.
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Early gastric cancer (defined as gastric carcinoma restricted to the mucosa and submucosa) is increasingly recognized. In Japan, where the incidence is high, population screening for gastric cancer is carried out, and early gastric cancer accounts for 30% of cases. In the United States, the incidence is much lower, and screening is not attempted; consequently, less than 10% of cases are detected at this early stage. Early gastric cancer appears as a small, flat mucosal thickening that may have a minimal polypoid and ulcerative component (Figure 38-8). It is thought that there may be a long period (months to years) before invasion of the muscle occurs.
Late gastric cancer (defined as a gastric carcinoma that has invaded the muscle wall) is the stage at which the tumor is commonly diagnosed in the United States. It may present in various ways: (1) as a fungating mass that protrudes into the lumen; (2) as a malignant ulcer with raised, everted edges (Figure 38-9); (3) as an excavated ulcer resembling a chronic peptic ulcer; or (4) as a diffusely infiltrating lesion that causes thickening and contraction of the stomach wall with relatively little mucosal involvement (linitis plastica, or leather-bottle stomach). Differentiation of benign peptic ulcer and ulcerative carcinoma may be difficult without histologic examination (Figure 38-10). Any gastric ulcer that does not heal as expected should be biopsied to rule out carcinoma.
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Microscopic Appearance
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Gastric carcinomas are adenocarcinomas of varying differentiation. The most common form is poorly differentiated (diffuse type), with cells distended by intracellular mucin (signet ring cell carcinoma;Figure 38-11). Well-differentiated (intestinal type) adenocarcinoma is less common. A reactive fibrosis is commonly present in relation to the neoplastic cells.
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(Figure 38-12.) Gastric carcinoma infiltrates the submucosa and invades through the muscle wall into the omental fat. Involvement of the serosa leads to spread of tumor cells in the peritoneal fluid (transcoelomic spread). Such metastasis occurs to the ovary (Krukenberg tumor) and rectovesical pouch. Involvement of submucosal lymphatics by tumor results in microscopic satellite nodules, often some distance from the main mass. Microscopic examination of frozen sections of the resection margins is therefore very important at the time of surgical removal of tumor. Lymphatic involvement also leads to metastasis to lymph nodes around the stomach. Later, extension of tumor up the thoracic duct may lead to involvement of the left supraclavicular nodes (Virchow's node). Lymph node metastases are present in about 50% of cases at the time of diagnosis. Hematogenous spread to the liver and lungs also occurs early.
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Gastric carcinoma is asymptomatic in its early stages and can be detected only by screening of high-risk populations. A few patients with early gastric cancer have symptoms resembling chronic peptic ulcer. Biopsy of a nonhealing gastric ulcer is essential because some of these patients prove to have carcinoma.
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Late gastric cancer presents with anorexia, anemia (due to blood loss), and weight loss. Early satiety may occur in a patient with a large mass or a contracted (linitis plastica) stomach. Hematemesis and melena may occur. Tumors near the pylorus may cause gastric outlet obstruction.
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Diagnosis may be established by endoscopy and biopsy, which provides a histologic diagnosis; and by radiologic examination—particularly computerized tomography—which provides information about the extent of spread and surgical resectability. Note that radiologic diagnosis of carcinoma must always be confirmed by endoscopic biopsy.
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The prognosis depends almost entirely on the depth of invasion of the neoplasm. Early gastric cancer restricted to the mucosa and submucosa has a 5-year survival rate of about 85%. Tumors that have invaded the muscle wall (late gastric cancer) but have not involved lymph nodes have only a 30% 5-year survival rate. When there is extension of tumor through the full thickness of the wall and lymph node involvement is present, the 5-year survival rate drops to about 5%.
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Histologic features and degree of differentiation are of little prognostic importance.
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Gastric lymphoma accounts for about 5% of malignant tumors of the stomach. Two common types occur: (1) low-grade malignant lymphoma, arising in mucosa-associated lymphoid tissue (MALT lymphoma); and (2) high-grade aggressive B-cell lymphomas, most commonly B-immunoblastic lymphoma.
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Gastric lymphomas present as polypoid masses, ulcers, thickened mucosal folds, and large intramural masses (Figure 38-13). The diagnosis is difficult on clinical grounds. Histologic examination of endoscopic biopsies can provide a diagnosis in both MALT lymphomas and in high-grade lymphoma. In MALT lymphomas, differentiation from reactive lymphoid proliferation can be very difficult; large biopsies to demonstrate immunoglobulin gene rearrangement may be needed. In high-grade lymphoma, the mucosa is infiltrated by large malignant cells. Differentiation from poorly differentiated carcinoma may require special stains. Lymphoma cells are negative for mucin and keratin and positive for common leukocyte antigen (CD45). MALT lymphomas are commonly restricted to the stomach (no systemic involvement) and are cured by surgical resection. High-grade lymphomas respond to chemotherapy, which is the primary treatment method. They have a 5-year survival rate of about 60% when the lymphoma is localized to the stomach at presentation.
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Malignant Gastric Stromal Neoplasms
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Malignant gastric stromal neoplasms, although they are the most common mesenchymal neoplasm in the stomach, account for only 2% of gastric malignancies. They arise from undifferentiated mesenchymal cells in the gastric wall. They present as large masses that originate in and involve the wall, usually protruding both into the mucosa and outward as an extragastric mass. Mucosal ulceration and cavitation of the central part of the tumor occur commonly. Although it forms a large mass, the tumor has less tendency to infiltrate and metastasize than gastric carcinoma. Surgical resection is therefore more successful than with carcinoma.
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Microscopically, gastric stromal neoplasms are composed of spindle cells that show varying cellularity, pleomorphism, and mitotic activity. In very large tumors, hemorrhage and necrosis are common. Most are undifferentiated; some show smooth-muscle differentiation (positive staining for desmin and actin); some show neural differentiation (S100 protein positivity). Most show positivity for the antigen CD34. These tumors can be divided into low-grade neoplasms (< 10 mitotic figures per 10 hpf), with a low metastatic potential; and high-grade neoplasms (> 10 mitoses per 10 hpf, with necrosis), with a high incidence of metastasis.
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Patients present with bleeding, blood loss anemia, or a palpable mass. The diagnosis is usually suggested by radiologic appearances. Endoscopic biopsy of the intramural mass is frequently negative for tumor, which is located deep to the submucosa. With surgical resection, over 50% of patients survive for 5 years. Failures may be due either to local recurrence or to distant metastases.
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Carcinoid tumors of the stomach are discussed along with other intestinal carcinoid tumors in Chapter 41: The Intestines: III. Neoplasms.