Lymphocytic gastritis

Lymphocytic gastritis is characterized by the presence of large numbers of mature lymphocytes infiltrating the surface and foveolar epithelium.

Clinical Manifestations

In his original report of this condition, Haot suggested that lymphocytic gastritis corresponded to the endoscopic entity previously known as varioliform gastritis. The histological features of lymphocytic gastritis may also be found in endoscopically normal stomachs and in patients with celiac disease, and the varioliform aspect (numerous thickened folds capped by small nodules that contain a central erosion or ulceration) can be found in H.pylori–infected stomachs.

Lymphocytic gastritis is rare, found in 1% to 3% of persons who undergo endoscopy with biopsy sampling. It is most commonly diagnosed in the sixth decade and appears to affect men and women equally.

In contrast to patients with chronic active gastritis, patients with the varioliform type of lymphocytic gastritis are often symptomatic; rapid weight loss and anorexia are reported in about half of affected patients, whereas epigastric pain is less common. Hypoproteinemia, hypoalbumin­emia, and peripheral edema suggesting protein-losing gastroenteropathy have been documented in approximately 20% of patients. Lymphocytic gastritis is a chronic disease, but there have been few case reports of spontaneous resolution. When it is associated with gluten enteropathy, the signs, symptoms, and clinical course are those of celiac disease.

Pathogenesis

Both the etiology and the pathogenesis of most lymphocytic gastritides are unknown. Because virtually all intraepithelial lymphocytes are CD8 + suppressor T cells, the same cells that form the intraepithelial infiltrate in celiac disease, an allergic pathogenesis has been proposed. This hypothesis is supported by the increasingly apparent association between a subtype of lymphocytic gastritis and celiac disease. The relationship with H.pylori, initially enthusiastically embraced, then vigorously rejected, is now viewed with an agnostic attitude by most investigators.

Macroscopic and Endoscopic Appearance

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.