Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

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Technique

Contrast Studies

High-density, low-viscosity barium sulfate preparations specially formulated to coat the acidic gastric mucosa are used for doublecontrast upper gastrointestinal studies. Some radiologists routinely induce gastric hypotonia, whereas others believe that any improvement in study quality due to hypotonia is limited. If hypotonia is preferred, in the United States the hypotonic agent glucagon is used, but in many other parts of the world scopolamine methylbromide (Buscopan) is employed, except in elderly patients or those where the side effects of scopolamine contraindicate its use and glucagon is then substituted. Pirenzepine, a selective antimuscarinic drug, appears as effective as scopolamine in inducing gastroduodenal hypotonia but without the undesirable side effects (1).

Water soluble agents are discussed in Chapter 4.

In the United States considerable lowresolution digital radiography equipment has been installed, with the primary justification being ease of filming (radiation dose is a separate and complex issue). High-resolution digital radiography equipment is becoming available; thus digital radiography with a four million pixel charge-coupled device achieves a significant improvement over conventional radiography in detecting gastric cancer (2).

Computed Tomography

Computed tomography (CT) contrast agents suitable for upper gastrointestinal tract opacification are similar to those used in the small bowel.Vomiting after ingesting an oral CT contrast agent is not uncommon. Especially in trauma patients, premedication with metoclopramide results in decreased nausea and vomiting.

A positive oral contrast agent is generally used for most of the gastrointestinal tract, but better gastric wall visualization is achieved with oral water. Water does not obscure subtle gastric wall thickening or enhancement. Using a multislice CT technique and a water-filled gastric lumen, normal gastric wall layers are well outlined during arterial or parenchymal phases.

Multislice three-dimensional (3D) CT of the stomach, often called virtual gastroscopy, is gradually achieving clinical acceptance. Virtual gastroscopy using gas for lumen distention and either a water-soluble agent or barium sulfate for mucosal coating has the potential of being competitive both with barium studies and endoscopy.

Three-dimensional CT rendering using shaded-surface display, ray sum display, and virtual gastroscopy with simultaneous visualization of intraluminal and submucosal components of various gastric tumors provides information not available either with barium studies or endoscopy.

Ultrasonography

A 3D ultrasonography (US) system is on the horizon. A position and orientation sensor mechanism is needed for this system to interface with a scanner head.

Similar to the esophagus, endoscopic US evaluates the gastric wall and adjacent structures and can localize a lesion and outline its extent, but the findings are nonspecific. Thus submucosal fibrosis due to a healing ulcer can mimic the appearance of a neoplasm.

Magnetic Resonance

Oral upper gastrointestinal magnetic resonance (MR) contrast agents are discussed in Chapter 4. The stomach is best studied distended. Hypotonic agents are usually not employed.

Endoscopic MR is under development.

Scintigraphy

Gastric emptying scintigraphy has been available for more than 25 years and is discussed later (see Gastric Emptying Studies). Over time, test meals and techniques have been optimized and standardized, and introduction of digital scintigraphy provides dynamic imaging and allows visualization of antral contractions.

Biopsy/Cytology

Percutaneous CT-guided core needle biopsies are readily obtained from gastric wall tumors. Nonendoscopic gastric biopsy can be performed as part of a double-contrast barium upper gastrointestinal study. Such combined barium-and-biopsy studies readily detect Helicobacter pylori infection and evaluate suspicious findings, eliminating a need for upper endoscopy in most patients.

Percutaneous gastric biopsies, drainage, and gastrostomies can also be performed using CT guidance. Interestingly, comparing CTfluoroscopy with conventional CT gastric interventional procedures, the radiation doses were significantly higher with CT-fluoroscopy, but the yields and procedure times were not significantly different (3).

Endoscopic US-guided fine-needle aspiration biopsy also provides cytologic confirmation of

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suspicious lesions. A multicenter prospective study achieved a fine-needle aspiration cytology sensitivity of 92% and specificity of 93% for lymph node staging, 88% and 95% for identifying extraluminal masses, and 61% and 79% for gastrointestinal wall lesions, respectively (4).

Congenital Abnormalities

Duplication

Gastric duplications are rare. Even rarer is a foregut duplication involving both the esophagus and stomach. Most do not communicate with the true lumen and are located in the antrum, and vary in size considerably. A rare carcinoma has originated in a gastric duplication.

A barium study, US, CT, or magnetic resonance imaging (MRI) should detect most duplications, yet the diagnosis is not always straightforward; a gastric duplication can be misdiagnosed as a pancreatic pseudocyst or a hepatobiliary cystic tumor. Although endoscopic needle aspiration of a gastric duplication cyst is feasible, these mucus-filled duplications tend to recur after simple aspiration. Ultrasonography identifies a multilayered wall, including a hyperechoic mucosa surrounded by hypoechoic muscle layers, findings better seen with endoscopic US.

A congenital double pylorus is rare. A rare double pylorus communicates with a duplication.

Atresia

Agastria and microgastria are very rare anomalies. Microgastria is associated with asplenia. Gastric atresia usually involves the antrum. Antral atresia results in a greatly dilated more proximal stomach and no gas distally, mimicking the appearance of pyloric obstruction (single-bubble sign). Although atresia may be complete, more often it consists of a web-like deformity with a partial opening. In some patients the latter becomes apparent only later in life.

An association has been described between pyloric atresia and epidermolysis bullosa (5).

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The differential diagnosis for partial gastric outlet obstruction in the young includes pyloric stenosis, antral web, antral stenosis, antral duplication, and, rarely, aberrant pancreas.

Vascular Anomalies

Vascular anomalies are common in the stomach and are of interest to the surgeon. To illustrate the scope of vascular anomalies, in a gastric cancer study 44% of patients had vascular anatomy differing from normal, and in 13% a double anomaly was detected (6).

Spontaneous gastric perforation occurs mostly in neonates. The etiology is unknown; possible overdistention or ischemia appears to play a role. Some of these neonates have been on mechanical ventilation or have had attempted nasogastric intubation. The resultant pneumoperitoneum tends to be large. One useful sign of gastric perforation using a horizontal x-ray beam is absence of an air-fluid level in the stomach; a gastric air-fluid level tends to be present with a more distant perforation.

A rare gastric hematoma eventually calcifies (Fig. 2.1).

Trauma

In a setting of CT performed for abdominal trauma, many centers administer routinely either dilute barium or a water-soluble contrast agent either orally or through a nasogastric tube. Done properly, little risk exists of aspiration or other complications.

Gastric perforation is less common than small bowel or colonic perforations,due,in part, to the relatively thick gastric wall. Most traumatic perforations involve a distended stomach. Inadvertent esophageal intubation and gastric ventilation and cardiopulmonary resuscitation have led to gastric perforation. The Heimlich maneuver can also result in gastric rupture. An intrathoracic stomach after gastric herniation into the thorax is also prone to perforate.

Figure 2.1. Gastric wall calcifications (arrow), years after abdominal trauma.

Vomiting

A discussion of vomiting has only indirect relevance to imaging studies, nevertheless, an appropriate imaging study must eventually be selected for a patient experiencing serious vomiting. This topic is best approached by considering likely etiologies in various age groups. More detailed discussions of etiologies and relevant imaging studies are included in this and other appropriate chapters.

Gastroesophageal reflux must be differentiated from vomiting. Reflux implies an incompetent gastroesophageal sphincter. Vomiting, on the other hand, is a complex phenomenon consisting of sudden relaxation of the superior esophageal and gastroesophageal sphincters, pylorospasm, forceful antral muscular contractions, sudden diaphragmatic descent, and abdominal muscle contractions forcing gastric content into the esophagus—mechanisms familiar to radiologists who have observed vomiting under fluoroscopy.

In infants, the gastroesophageal sphincter is incompletely developed and reflux is common. What is “normal” reflux and what constitutes “abnormal” has provoked considerable debate in the pediatric literature and is beyond the scope of this chapter. Especially with upper gastroenteric obstruction, a distinction between reflux and vomiting is often blurred. Esophageal obstruction obviously results in neither reflux nor vomiting, and the condition is generally clinically suspected with first feedings. Bilious vomiting in infants suggests sepsis or obstruction distal to the papilla of Vater, with the most common condition being volvulus secondary to midgut malrotation, a surgical emergency.

Pylorospasm, pyloric stenosis, a duodenal or more distal small bowel web, stenosis or atresia, meconium plug syndrome, and various colonic obstructions are other causes of bowel obstruction and vomiting in infants. Rarer causes of obstruction include large diaphragmatic hernias and gastric volvulus.

Conventional radiography is probably still the most optimal initial imaging study in these infants. At times evidence of a gasless abdomen or gut distention to a certain point suggest a diagnosis, and additional imaging simply delays therapy. At other times this study raises suspicion of a specific diagnosis, and a barium study or US is then performed for confirmation or exclusion.

In an older infant or child with clinically evident gastroesophageal reflux or failure to thrive, a barium study is often obtained both for confirmation of reflux and as screening for other abnormalities.Although reflux can also be studied with a pH probe, US, or scintigraphy, these studies do not exclude other disorders. Scintigraphy is of little use in an infant with projectile vomiting, but it is useful in an older cooperative child.

Causes of vomiting in adults are legion. Central neural, toxic, visceral, and metabolic causes are common; the etiologies are difficult to detect, and most do not require imaging studies. Some visceral causes of vomiting, such as acute cholecystitis, are suspected clinically, and appropriate imaging studies obtained. A major direct role of imaging is to detect an underlying bowel obstruction,traditionally performed with a barium study but currently often supplanted by CT.

Wall Thickening

Infection/Inflammation

Helicobacter Infection

Clinical

Helicobacter pylori, a curvilinear motile gramnegative bacillus, is implicated as a cause of inflammation, ulcers, and a number of neoplasms. Prevalence of H. pylori varies considerably in different populations. Prevalence is higher in non-Caucasians and increases with

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age; H. pylori colonization occurs at about 3% per year and eradication at 1% per year. Although O blood group patients do have a higher prevalence of peptic ulcer disease, H. pylori seroprevalence does not differ between different ABO groups.

H. pylori is easy to diagnose noninvasively and is treatable with antibiotics. A more complex topic is whether all H. pylori should be eradicated (a “kill them all” philosophy more in vogue in the 1990s) or whether there are good, neutral, as well as bad H. pylori. Presumably H. pylori has been a human commensal since time immemorial and produces no known harm in many people. Is it thus worthwhile to suggest blanket antibiotic therapy with its related problems, or should eradication be limited to those at risk for known complications of this infection? Other Helicobacter species also appear to play a role. Thus H. heilmanii is responsible for acute gastritis in some patients.

One interesting observation is that H. pylori infection in Crohn’s disease and ulcerative colitis patients is less prevalent than in controls.

A number of studies have found no statistical difference in patients with symptoms and histologic findings compatible with gastritis or peptic ulcer disease between those positive for H. pylori and those negative. Likewise, gastric emptying times are not related to H. pylori infection. Nevertheless, the relationship between H. pylori and peptic ulcer disease is not straightforward, with more aggressive strains being more common in peptic ulcer disease. Antral H. pylori infection results in an antral gastritis and a derangement of the usual acid inhibition of gastrin production, which leads to an increase in gastrin release, which in turn promotes excess acid secretion by the noninflamed, more proximal part of the stomach. Chronic gastrin elevation results in hyperplasia of both enterochromaffin-like cells and parietal cells, thus further increasing acid secreting capacity. In some patients chronic infection eventually leads to antral atrophy, gastrin production decreases, and hypochlorhydria ensues.

At times H. pylori–induced hypergastrinemia and gastritis suggest Zollinger-Ellison syndrome; eradication of H. pylori results in resolution of findings.

The World Health Organization (WHO) classifies H. pylori as a carcinogen. Its presence

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is associated with a severalfold increased risk of developing a gastric cancer. Carcinogenesis is probably through a sequence of gastritis induction, intestinal metaplasia, dysplasia, and finally development of carcinoma. No difference in prevalence of H. pylori infection exists in patients with Lauren intestinal and diffuse types of carcinomas (the Lauren classification is discussed later; see Adenocarcinoma).

Chronic H. pylori infection promotes mucosa-associated lymphoid tissue (MALT), and primary gastric non-Hodgkin’s MALT lymphoma is strongly associated with H. pylori infection, although the H. pylori strains involved appear to differ from those associated with peptic ulcer disease. Eradication of H. pylori leads to regression of MALT (7) and of lowgrade mucosa-associated lymphomas in their early stages, although several years are needed for gastric mucosa to become normal after H. pylori eradication.

It should be pointed out that MALT develops not only in a setting of H. pylori infection but also in response to other antigen stimulation. Thus reactive lymphoid follicles also develop in the stomach of H. pylori–negative celiac patients.

In the presence of the enzyme urease, urea is hydrolyzed to CO2 and ammonia. H. pylori is a common urease-containing bacterium and will produce CO2 from orally administered urea. The urea breath test consists of having the patient ingest radioactive C-14–labeled urea and then monitoring for the presence of C-14 with a breath analyzer. This test has had limited acceptance. False-positive results are seen in achlorhydria and some other bacterial infection. A serologic test is easier to perform, although the antibody titer remains elevated even after infection has been eliminated.

Imaging

The most common finding of gastric H. pylori infection is thickened folds, presumably representing resultant gastritis rather than H. pylori infection per se. Other findings include antral nodularity and underlying lymphoid hyperplasia, findings often more evident in children than adults. Antral nodularity usually regresses after H. pylori is eradicated.

Gastritis

Clinical

By definition, gastritis signifies inflammation. Some so-called gastritis, such as chemically induced gastritis, often manifests by acute hemorrhage, and histology detects little evidence of inflammation; some authors prefer the term gastropathy rather than gastritis.

Any discussion beyond the superficial quickly evolves into a number of controversies surrounding the definition of gastritis. A symposium of pathologists in Sydney in 1990 established guidelines for classifying and grading gastritis; these guidelines were modified in Houston in 1994 (8).

For convenience, gastritis is usually subdivided into acute, chronic, and a special or distinctive type. Acute gastritis is generally a clinical diagnosis. Pathologists cannot distinguish between acute and active gastritis. No specific radiologic findings are helpful. Acute gastritis is often categorized under discrete types such as chemical (corrosive) injury,stressrelated, phlegmonous, and similar. Chemical gastritis includes not only drugand alcoholinduced gastritis but also gastric changes induced by bile reflux. Stress gastritis is associated with severe trauma, burns, shock, sepsis, and related conditions, and tends to manifest within days of an insult. Acute hemorrhage is a not uncommon clinical presentation with most acute gastritis, and, in fact, in an occasional patient angiographic therapy using vasopressin infusion is necessary for hemorrhage control.

Numerous subdivisions and synonyms are in vogue for chronic gastritis (Table 2.1). Most pathologists divide chronic gastritis primarily into nonatrophic,atrophic,and special types,yet biopsies in some patients, of necessity, still are classified as indeterminate. No essential difference exists between chronic active and acute erosive gastritis, terms commonly used by pathologists.

Of note is that H. pylori is associated with several types of gastritis. H. pylori–associated nonatrophic gastritis almost always involves the antrum, with inflammation extending to the gastric body to a varying degree. With autoimmune gastritis, on the other hand, both inflammation and atrophy spare the antrum.

Source: Adapted from Dixon et al. (8).

Also, H. pylori gastritis almost always is associated with neutrophil infiltration. H. pylori is detected more often in lesions with active rather than chronic inflammation; the presence of H. pylori correlates with degree of lymphocyte infiltration, but not with metaplasia or mucosal atrophy.

Pathologists do not agree on a precise definition of normal. One controversy is the concept of atrophy, with pathologists using a visual scale of mild, moderate, and marked (8). Atrophy implies loss of glandular tissue and is a common pathway for a number of disorders. Thus atrophic gastritis is a descriptive term and not a specific disease. An association between atrophy and metaplasia is not clear, although metaplasia is common in chronic gastritis, regardless of etiology. Some patients with atrophic gastritis develop dysplasia. Follow-up with repeat biopsies reveals that mild dysplasia most often resolves spontaneously, with an occasional one progressing to moderate dysplasia. In summary progression of mild dysplasia is rare, moderate dysplasia changes slowly, and severe dysplasia is an indication for surgery.

Pathologists also gauge activity; thus chronic active gastritis implies the presence of neutrophils, a finding beyond resolution of endoscopy or radiology. Confusing the issue further, some endoscopists do not obtain biopsies but rely on their visual impression to diagnose a specific type of gastritis.

Biopsy tissue, if needed, is usually obtained during endoscopy. An alternate approach is to perform a barium upper gastrointestinal study and at the same time, using a nasogastric tube, obtain fluoroscopically guided gastric biopsies; such fluoroscopic biopsies achieve sensitivities and specificities of over 90% in diagnosing gastritis (9).

Diagnosis

Findings of gastritis on a barium study include aphtha, antral nodularity, thickened folds, coarse areae gastricae, and, at times, lumen narrowing. A number of other disorders, however, have similar findings. Aphtha and coarsened areae gastricae are seen in gastritis, Crohn’s disease, MALT lymphoma, some infections such as herpes and cytomegalovirus, and the rare gastric involvement by Behçet’s disease (Fig. 2.2) or even mastocytosis (Fig. 2.3).

Occasionally gastric lymphoid hyperplasia is a prominent finding of H. pylori gastritis, especially in children. If small, these nodules are difficult to distinguish from aphtha with surrounding inflammation.

Patients ingesting nonsteroidal antiinflammatory drugs on a chronic basis tend to develop gastritis. Some of these patients have a characteristic antral greater curvature flattening.

Aside from biopsy, endoscopists use such macroscopic findings as nodularity, erosions, mucosal hemorrhage, and redness to diagnose

Figure 2.2. Gastric Behçet’s disease. Multiple discrete aphtha are scattered in the antrum. Gastritis and Crohn’s disease can have similar findings.

gastritis, yet considerable controversy surrounds an endoscopic diagnosis of gastritis. In consecutive patients undergoing endoscopy, macroscopic endoscopy findings achieved a

sensitivity of only 40% and a specificity of 84% in detecting H. pylori gastritis (10).

Atrophic/Autoimmune

Patients with autoimmune gastritis tend toward achlorhydria and elevated gastrin levels. Histologically, antral G-cell hyperplasia and an increase in endocrine cells are common. Gastric carcinoids tend to develop in these patients. A relationship with gastric carcinoma is not clear.

Radiology has a limited role in autoimmune gastritis.

Chemical

Acid-induced corrosive gastritis tends to be more severe than the more common causticinduced damage, yet the latter also results in considerable damage, generally in the antrum, at times sufficiently severe to evolve into gastric outlet obstruction. The resultant linitis plas- tica–like appearance tends to have sharply marginated, irregular borders mimicking a gastric carcinoma; a number of these strictures have been resected in the mistaken notion that they are malignant.

Some of these patients undergo either a simple gastrojejunostomy or a Billroth I or II operation and tend to do well, provided no esophageal stricture develops.

Enterogastric reflux of bile and pancreatic secretions is a well-known cause of gastritis both in patients with an intact stomach and after gastric surgery. Such reflux is detected by technetium 99m (Tc-99m)-HIDA scintigraphy, but has no specific imaging appearance.

Lymphocytic

The role of H. pylori in lymphocytic gastritis is not settled; some studies point to no association, whereas others suggest the opposite.

Lymphocytic gastritis is a histologic diagnosis. Histochemical study suggests that lymphocytic gastritis often is part of a generalized lymphocytic gastroenteropathy. In some patients it is associated with celiac disease. It manifests as rugal thickening, nodularity, and erosions. Some authors describe these thickened, serpiginous rugal folds, together with superimposed inflammation, as varioliform gastritis, and at times the imaging appearance suggests Ménétrier’s disease. Some patients develop diffuse gastric ulcerations. Duodenitis is often present. These patients also tend to develop a protein-losing gastroenteropathy. An occasional patient presents with a massive hemorrhage.

Collagenous

The recently described entity of collagenous gastritis is rare. Similar to collagenous colitis, its defining characteristic is fibrous thickening of the subepithelial basement membrane. Etiology and pathogenesis are unknown. There are no specific imaging findings.

Granulomatous

In a setting of chronic gastritis some biopsies yield findings compatible with granulomatous gastritis, although a diagnosis of idiopathic granulomatous gastritis is rare; most of these patients have either Crohn’s disease or sarcoidosis, with an occasional granulomatous gastritis being secondary to infection, foreign bodies, or other gastropathy.

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Peptic Ulcer Disease

Clinical

Peptic ulcers are uncommon in children and rare in infants. Numerous medications induce gastric ulcers. Some nonsteroidal antiinflammatory drugs are associated with giant gastric ulcers. Chemotherapeutic infusion into the hepatic artery for liver neoplasms is occasionally associated with gastric ulcerations. Some of these ulcers tend to be large.

Complications of peptic ulcer disease include stricture and perforation. Anterior wall gastric ulcers tend to perforate into the peritoneal cavity, whereas posterior wall ulcers more often involve the pancreas. A rare gastric ulcer penetrates the spleen or other adjacent structure.

The definition of a giant gastric ulcer varies, but typically an ulcer diameter of 3cm or more is assumed to represent this entity. These giant ulcers are not a separate pathologic entity, but their significance lies in their worse prognosis due to hemorrhage and need for urgent surgery. A giant gastric ulcer led to a pneumopericardium (11).

A double pylorus in most adults is a complication of peptic ulcer disease; a congenital double pylorus is very rare. These ulcers originate either in the duodenal bulb or distal antrum. An occasional benign gastric ulcer evolves into a gastrojejunal or gastrocolic fistula. Other causes of a double pylorus include a necrotic cancer and prior surgery (Fig. 2.4).

Imaging

The appearance of gastric ulcers on an upper gastrointestinal study is familiar to most radiologists and are not discussed here. In general, a finding of a deep U-shaped deformity at the incisura, irregular soft tissue tumor surrounding the ulcer, and prominent converging folds are associated with a significant delay in ulcer healing, even with adequate therapy.

Ultrasonography is not used for ulcer detection, but if US reveals a “target” sign, consisting of hypoechoic gastric wall thickening surrounding a hyperechoic ulcer lumen, the patient can then be referred for a more appropriate study.

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Figure 2.4. Double pyloric channel (arrows). This patient had a prior antrectomy and the two channels were believed to be related to surgery.

Eosinophilic Gastroenteritis

Eosinophilic gastroenteritis is an inflammatory disorder of unknown etiology, considered to be a separate entity from idiopathic hypereosinophilic syndrome, although transitional forms probably exist. Its primary feature is eosinophilic infiltration of discrete or diffuse gastrointestinal tract segments. An occasional patient has eosinophilic infiltration of most if not all of the bowel. About half of these patients have some type of allergy, and a majority have peripheral eosinophilia.

Gastric involvement manifests most often as a narrowed lumen or thickened rugae.

In a rare infant eosinophilic gastroenteritis mimics the clinical findings and US appearance of idiopathic hypertrophic pyloric stenosis.

Eosinophilic gastroenteritis should be differentiated from helminth infestation with its associated eosinophilia.

Crohn’s Disease

Prevalence of gastric involvement in Crohn’s disease is unknown. When Crohn’s disease is evident in the upper gastrointestinal tract,

nearly always concomitant small bowel or colonic involvement is also found.

Although chronic gastritis and duodenitis are common in Crohn’s disease patients, only an occasional biopsy yields granulomas (12). One should keep in mind that granulomas are not pathognomonic for Crohn’s disease; they are also found in sarcoidosis, some infections such as tuberculosis and anisakiasis, as a foreign body reaction, or as an occasional vasculitis. As a practical matter, however, if other causes of granuloma formation are excluded, the presence of noncaseating granulomas is assumed to be due to Crohn’s disease.

The imaging appearance of gastric Crohn’s disease varies from aphthae to strictures (Fig. 2.5). Scintigraphy in Crohn’s patients with nonobstructive disease and no evidence of gastroduodenal disease shows normal gastric emptying, although symptomatic Crohn’s patients develop delayed gastric emptying.

Malacoplakia

Malacoplakia is a granulomatous inflammatory disease involving either the gastrointestinal or genitourinary tract. It is discussed in more detail in Chapter 10.

Malacoplakia is rare in the stomach. It originates either in the gastric wall or adjacent structure and infiltrates the stomach. Its primary significance is that it mimics a neoplasm.

Cytomegalovirus

The prevalence of acute viral gastritis is unknown. The most common is cytomegalovirus infection, which is encountered mostly in immunocompromised individuals and occasionally in children, where it tends to present as thickened rugae similar to Ménétrier’s disease.

Anisakiasis

Anisakiasis is caused by eating raw fish infected with Anisakis larvae. Many reports originate from Japan, but the condition is also encountered in other countries having an acquired culinary taste for raw fish such as sushi and sashimi. Ingestion of undercooked microwaved fish is also implicated. It is uncommon in older individuals and those with prior gastric surgery; rel-