Radiological presentation of gastric Crohn's disease
During a barium swallow X-ray examination, upper GI involvement in Crohn's disease demonstrates a highly specific pattern. The inflammatory process predominantly affects the distal segments.
In the antrum of the stomach, multiple superficial mucosal defects—so-called aphthous erosions—are visualized. Extension of the pathological process to the duodenum is accompanied by marked thickening of its folds. They acquire a characteristic nodular structure, forming a specific mucosal relief pattern that in classical diagnostic radiology is described as the "cobblestone mucosa" sign (cobblestone mucosa).
Differential diagnosis: Ménétrier disease
A special place in the differential diagnosis of conditions with thickened folds is occupied by Ménétrier disease (Ménétrier Disease). This condition leads to protein-losing enteropathy (protein-losing enteropathy) and can cause severe, disabling symptoms.
Barium fluoroscopy and CT visualize massively thickened, often bizarre and lobulated gastric folds. The changes are most pronounced in the proximal part of the organ and along the greater curvature.
- Classical description: involvement of the gastric body with a completely spared antrum.
- Real practice: up to 50% of cases are accompanied by involvement of the antrum, i.e., diffuse involvement is observed.
- Additional radiological sign: increased fluid accumulation in the small bowel lumen, which may prevent adequate coating of the mucosa by the barium suspension.
Key differential diagnostic sign from gastric cancer: in Ménétrier disease, giant folds remain elastic and pliable, whereas in the development of carcinoma, the gastric wall becomes infiltrated, rigid, and completely aperistaltic.
Endocrine syndromes and hypersecretion
Thickening of the gastric folds may result from excessive stimulation of the mucosa.
Hypertrophic Gastritis (Hypertrophic Gastritis) Radiographs reveal characteristic enlargement and prominence of the gastric areas (areae gastricae). This radiological sign strictly correlates with an increased rate of gastric hypersecretion and the development of peptic ulcer disease (PUD).
Zollinger-Ellison Syndrome (Zollinger-Ellison Syndrome) The etiology of the syndrome is associated with gastrinomas—non-$\beta$-cell tumors of the pancreatic islets. They secrete excess gastrin, radically stimulating hydrochloric acid hypersecretion. X-ray imaging reveals prominent, thickened gastric folds and overt signs of increased fluid secretion in the lumen.
Features of tumors in Zollinger-Ellison syndrome:
- Localization: 75% are located in the pancreas, 15% in the duodenal wall, and the rest have extraintestinal locations.
- Malignancy: tumors possess high malignant potential; metastases (predominantly to the liver) are present in nearly 50% of cases.
- Associations: the syndrome is a manifestation of multiple endocrine neoplasia type 1 (MEN-1 / MEN type I, Wermer syndrome). This syndrome also includes tumors of the parathyroid glands, pituitary, and adrenals, and is sometimes associated with carcinoid tumors.
Infiltrative and toxic lesions
Eosinophilic Gastroenteritis (Eosinophilic Gastroenteritis) The pathomorphology is based on focal or diffuse infiltration of various GI segments by eosinophils. The disease is common in patients with concurrent atopy or bronchial asthma and is accompanied by peripheral eosinophilia. Clinically, it presents with spasmodic abdominal pain, bloating, persistent diarrhea, and vomiting.
Any GI segment may be affected, but preferred sites are the stomach (especially the antrum) and the proximal small intestine. The radiological picture strictly depends on which wall layers are involved (mucosal, muscular, or subserosal). Fluoroscopy reveals thickening of the gastric and small bowel folds. Narrowing and rigidity of the antrum combined with mucosal nodularity are frequently detected. With transmural wall involvement, eosinophilic ascites is often observed.
Corrosive Ingestion (Corrosive Ingestion) Ingestion of caustic chemicals causes severe damage to the mucosa and deeper layers, which can lead to total gastric necrosis, wall perforation, and patient death. It is important to remember a simple toxicology rule: acids cause more severe and deeper damage specifically to the stomach and duodenum, unlike alkalis, which primarily damage the esophageal wall.
Briefly: answers to topical questions
What diseases are included in the full differential diagnosis of conditions causing pronounced thickening of the gastric folds?
In the presented sources, pathologies described with gastric fold thickening include:
- Ménétrier disease — massively thickened, often bizarre and lobulated gastric folds.
- Zollinger-Ellison syndrome — thickened gastric folds and signs of increased gastric secretion.
- Eosinophilic gastroenteritis — thickening of the gastric and small bowel folds.
- Infectious gastritis in tuberculosis, histoplasmosis, and syphilis — ulcerations, fold thickening, mucosal nodularity.
- Diffuse erosive gastritis — thickened nodular folds with erosions.
- Gastric lymphoma — in some patients, diffuse thickening of gastric folds, the picture may resemble hypertrophic gastritis.
What specific blood and gastric juice laboratory changes are characteristic of Ménétrier disease?
Ménétrier disease is characterized by blood laboratory changes associated with protein loss, whereas gastric juice parameters are not described. The sources indicate the following manifestations:
- Protein-losing enteropathy (protein-losing enteropathy) — leads to a decrease in the body's protein levels.
- Hypoalbuminemia — clinically manifests as hypoalbuminemic edema.
Specific changes in gastric juice parameters are absent in the provided materials.
What late radiological signs and complications develop in the stomach after a chemical acid burn?
Following a chemical burn from concentrated acids, severe damage to the stomach and duodenum develops. Among the described complications are the following conditions:
- Gastric necrosis.
- Perforation of the organ wall.
- Fatty outcome (death).
Late radiological signs of chemical acid burns are not presented in these materials; only acute life-threatening consequences of corrosive ingestion are described.
Rule of GI chemical burns: "Acids strike the stomach and duodenum, while alkalis destroy the esophagus."
Class and exam questions
How to differentiate Ménétrier's disease from gastric carcinoma on imaging?
The main differential diagnostic criterion lies in tissue elasticity. In Ménétrier disease, even massively thickened folds remain pliable and elastic, whereas in carcinoma, the gastric wall thickens, becomes rigid, and loses normal peristalsis.
Where are gastrinomas most commonly localized in Zollinger-Ellison syndrome?
In the vast majority of cases (about 75%), gastrinomas are localized in the pancreas. About 15% of tumors are found in the duodenum, and the rest have an extraintestinal location.
What is the "cobblestone" sign?
This is a specific mucosal relief pattern revealed on barium fluoroscopy. In Crohn's disease, duodenal folds thicken and acquire a pronounced nodular structure, externally resembling a cobblestone pattern (cobblestone mucosa).
What determines the radiological picture in eosinophilic gastroenteritis?
Clinical and radiological signs directly depend on the depth of infiltration: whether only the mucosal, muscular, or subserosal layer of the GI wall is involved. In total (panmural) involvement, eosinophilic ascites frequently develops.
What else to study on this topic
- Radiological criteria for the differential diagnosis of antral rigidity (carcinoma vs. eosinophilic gastroenteritis).
- Radiological semiotics of multiple endocrine neoplasia type 1 syndrome (MEN-1 / Wermer syndrome).
- Pathogenesis of protein-losing enteropathy in Ménétrier's disease.
- CT presentation of panmural involvement in eosinophilic gastroenteritis and assessment of ascites.
- Assessment of gastric areas (areae gastricae) in hypertrophic gastritis.
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