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Macroscopic and Endoscopic Appearance

CLINICOPATHOLOGICAL APPROACH TO GASTRITIS | Biopsy Protocol | TOOLS TO DIAGNOSE AND CLASSIFY GASTRIC CONDITIONS | Clinical Manifestations | Disease-Specific” Virulence Factors | Invasive Tests | Noninvasive Tests | Treatment of Helicobacter pylori Infection | Evolution and Associations of Helicobacter pylori Gastritis | Clinical Manifestations |


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Approximately 80% of patients in whom a histopathological diagnosis of lymphocytic gastritis is made have endoscopic lesions described as varioliform, aphthous, verrucous, or chronic erosive gastritis. The appearance is that of a complex pattern of enlarged folds, pre­dominantly in the corpus, which are covered by thick mucus, are crossed by large erosions, and may be crested with clusters of elevated aphthoid nodules. Flat erosions may be found in the antrum. The remaining 20% of patients (including those with celiac disease and collagenous gastritis) have less dramatic lesions, with only scattered superficial erosions in the corpus or antrum. Some patients have an endoscopically normal stomach. This last group of patients with a normal-appearing stomach may have a pathogenetically distinct condition, even though the histopathological features are indistinguishable. Some authors have suspected a relationship between lymphocytic gastritis and Ménétrier disease.

Histopathology and Diagnosis

Because the endoscopic appearance of varioliform gastritis may result from either H.pylori infection or lymphocytic gastritis, the diagnosis can be suspected clinically, but it can be confirmed only by histopatholo­gists. In biopsy specimens from these patients, a substantial increase in intraepithelial lymphocytes, particularly in the corpus, is associated with a histopathological spectrum ranging from marked chronic inflammatory cell infiltration of the lamina propria, activity, and focal erosions to a minor increase in chronic inflammatory cells with no activity. In most cases, the histological picture can be readily distinguished from that of chronic H.pylori gastritis, in which few intraepithelial lymphocytes are present (rarely more that 5 or 6 per 100 epithelial cells). The diagnostic threshold for lymphocytic gastritis is generally accepted as more than 25 intraepithelial lymphocytes per 100 epithelial cells, but in most cases the counts are much greater, between 25 and 50 lymphocytes. If H.pylori infection is present, immunohistochemistry to detect CD8 + T cells may be helpful: in pure lymphocytic gastritis, most intraepithelial lymphocytes are CD8 +, whereas a heterogeneous infiltrate characterizes H.pylori gastritis.

Therapy

When concurrent H.pylori infection is present, eradication of the infection may resolve the inflammation and is therefore recommended. Patients with gluten enteropathy will benefit from the standard dietary limitations recommended to restore the small intestinal integrity. For patients with “pure” lymphocytic gastritis and severe gastric mucosal lesions, there are no consistently effective therapies. The use of proton pump inhibitors has resulted in healing of the ulcers and erosions in some patients. Therapy with glucocorticosteroids or sodium cromoglycate, often successfully used for the treatment of eosinophilic gastroenteritis, has obtained unclear results.


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Endoscopic Appearance| Clinical Manifestations and Pathogenesis

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