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Mucosal Diseases of the Stomach: Differentiating Benign from Malignant
Malignant Mucosal Processes
Etiology
A wide range of benign disease processes can affect the mucosa of the stomach, including inflammatory, infectious, hereditary, and autoimmune processes. What these processes have in common is that they affect one of the primary defenses of the stomach wall—the mucosal layer.
In considering the radiologic appearance of these entities, it is helpful to divide them into their primary mucosal manifestations—ulcers, polyps and masses, and diffuse mucosal processes. Some of the more common processes include the following:
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Ulcers: Infections ( Helicobacter pylori, cytomegalovirus), erosive gastritis (nonsteroidal antiinflammatory drugs [NSAIDs], alcohol, stress, radiation, direct trauma), Crohn's disease, autoimmune (Behçet's) disease, sarcoidosis
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Polyps and masses: Hyperplastic and adenomatous polyps (also seen in Cronkhite-Canada syndrome and familial polyposis of the colon), hamartomas (Peutz-Jeghers syndrome, Cowden's disease), heterotopic pancreatic tissue, lymphoid hyperplasia
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Diffuse mucosal processes: Acute gastritis, atrophic gastritis, eosinophilic and lymphocytic gastritis, Zollinger-Ellison syndrome, Ménétrier's disease, and those that cause a linitis plastica appearance (corrosives, radiation, Crohn's disease, tuberculosis, sarcoidosis, syphilis)
In this chapter, the discussion is tailored to each of these categories, with a description of the most common entities.
Prevalence and Epidemiology
Benign Diseases Causing Mucosal Ulcerations
The most common benign cause of mucosal ulcerations is peptic ulcer disease. Although decreasing in overall incidence with the routine use of histamine-2 (H 2 ) blockers, the overall death rate from peptic ulcer disease has remained stable. The vast majority of cases of gastric ulcers (70% to 90%) and duodenal ulcers (up to 90%) are due to H. pylori infection.
Other causes of gastric ulcers include NSAIDs and aspirin. Chronic NSAID users have a prevalence of peptic ulcer disease of 25%. Less common causes of benign gastric mucosal ulcers include stress ulcers in burn patients (Curling's ulcers) and head trauma patients (Cushing's ulcer), crack cocaine and alcohol abuse, Crohn's disease, sarcoidosis, cytomegalovirus infection, and Behçet's disease.
Benign Diseases Causing Polyps and Masses
Polypoid lesions of the stomach include hyperplastic (regenerative), adenomatous, hamartomatous, and inflammatory polyps, as well as heterotopic pancreatic tissue. The most common benign polyps are hyperplastic polyps, which can commonly occur in the setting of gastritis. Unlike adenomatous polyps, which can degenerate in a fashion similar to that of colonic adenomas, hyperplastic polyps have almost no malignant potential.
Hamartomatous polyposis syndromes are rare and include Peutz-Jeghers syndrome, multiple hamartoma/Cowden's disease, juvenile polyposis, Cronkhite-Canada syndrome, and Bannayan-Riley-Ruvalcaba syndrome. Whereas hamartomatous polyps are themselves without malignant potential, they are frequently associated with adenomatous polyps. More importantly, these syndromes can be associated with extraintestinal malignancies, and diagnosis is essential so the patient can be undergo screening.
Benign Diseases Causing Diffuse Mucosal Abnormalities
The most common diseases that affect the gastric mucosa diffusely are acute gastritis and chronic and atrophic gastritis. Acute gastritis, most commonly secondary to H. pylori infection, can progress to a chronic state if left untreated. Other causes of acute gastritis include NSAID-induced gastritis, caustic ingestion, and granulomatous disease (sarcoidosis, tuberculosis), as well as less common causes such as cytomegalovirus infection, herpesvirus infection, and syphilis.
Chronic gastritis can progress to atrophic gastritis, which is characterized by loss of the normal mucosal glands and is categorized by the portion of the stomach involved. Type A chronic and atrophic gastritis, which affects predominantly the fundus and body, has been termed autoimmune gastritis and is the least common of the two types. This form is associated with pernicious anemia, caused by destruction of the parietal cells and loss of intrinsic factor, which leads to vitamin B 12 deficiency and megaloblastic anemia. More common is type B chronic/atrophic gastritis, which affects predominantly the antrum and is associated with chronic H. pylori infection.
Other causes of gastritis are less common. Eosinophilic gastritis is characterized by blood eosinophilia and eosinophilic gastric wall infiltrates. The antrum is predominantly involved, and mucosal fold thickening can become severe enough to cause gastric outlet obstruction. Bowel involvement can occur and is termed eosinophilic gastroenteritis .
Diffuse gastric fold thickening can occur as a result of inflammation or infiltration. In Ménétrier's disease there is hypertrophy of the mucus-producing cells of the stomach mucosa, causing marked fold thickening. This rare disorder is of unknown cause and can mimic malignancy as well as severe gastritis or an infiltrative process. In addition to the usual clinical presentation of pain, weight loss, and occasional bleeding, the disorder is characterized by hypoalbuminemia secondary to loss of proteins.
Pathology
In general, entities that affect the stomach mucosa can be divided into a few broad categories: infectious, inflammatory, infiltrative, autoimmune, and hereditary. Those processes causing ulcers can fall into any of these categories, but polypoid lesions tend to represent either inflammatory or hereditary causes.
Infectious causes, including most commonly H. pylori, all begin by circumventing the stomach mucosa's natural defenses. Because of its highly acidic environment, the stomach is able to withstand infection from a wide range of ingested bacteria. However, in H. pylori, the bacteria have adapted mechanisms to neutralize the acidic environment by creating sodium bicarbonate and ammonia from the enzyme urease. Once it has colonized the stomach, H. pylori causes an increase in gastric acid production through a variety of mechanisms, including inhibition of the production of somatostatin by the antral D cells. Because somatostatin is a potent inhibitor of antral G cell gastrin production, this leads to an overall increase in acid secretion. This acid hypersecretion is thought to be the primary mechanism for H. pylori —induced gastritis and ulcer formation.
Other infectious agents, including herpesvirus and cytomegalovirus, involve direct viral infection of the mucosal cells. Clinically, these affect immunocompromised patients. Cytomegalovirus infection is characterized by intranuclear inclusions seen on biopsy. Syphilitic involvement of the stomach is rare but has been seen with increasing frequency in immunocompromised patients. In early disease, gastritis is characterized pathologically by perivascular and mucosal mononuclear infiltration. In later stages of the disease, gummatous involvement of the stomach can occur, as well as scarring and stricture.
Inflammatory causes of gastritis include NSAID-induced gastritis, as well as caustic ingestion. The most common of these disorders is NSAID-induced gastritis. NSAIDs cause a decrease in stomach mucus and bicarbonate production by inhibiting prostaglandins. This leads to a breakdown in the defensive barrier of the stomach lining to gastric acid, which in turn leads to gastritis and ulcer disease.
Infiltrative causes tend to result in a diffuse abnormality of the stomach mucosa. These include eosinophilic and lymphocytic gastritis, Ménétrier's disease, sarcoidosis, and tuberculosis. The pathologic hallmark is infiltration of mucosa or submucosa with abnormally increased cells (in the case of eosinophilic and lymphocytic gastritis, as well as Ménétrier's disease) or reactive tissue (in the case of granulomas of sarcoidosis and tuberculosis).
Benign polypoid and mucosal mass lesions of the stomach are most commonly hyperplastic and seen in the setting of gastritis. These have a low potential for malignancy. Adenomatous polyps, which can be seen in the setting of polyposis syndromes mentioned previously, have a higher potential for malignancy and can be either tubular or villous. Finally, hamartomatous polyps, also seen in the setting of polyposis syndromes, are the least common of the subtypes.
Imaging
Ulcers
Gastric ulcer disease typically manifests as symptoms of epigastric or abdominal pain, which is worse with eating. These clinical symptoms are nonspecific and can be seen in a variety of abdominal pathologic processes, not just referable to the stomach. Magnetic resonance imaging (MRI), ultrasonography, and positron emission and computed tomography (PET/CT) are not generally useful in the diagnosis.
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