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Isolated collagenous gastritis is a rare disease with a varied presentation including non-alarming symptoms such as dyspepsia. It is characterized by a nodular appearance on endoscopy and a sub epithelial collagen band thicker than 10 micrometres on histopathology examination. The available therapeutic options are mostly symptomatic. Here, we present a case of collagenous gastritis, incidentally diagnosed in a patient being evaluated for dyspepsia.

A 59 year old female presented with history of nausea, vomiting and abdominal bloating after eating spicy or oily food along with reduced appetite and weight loss of 6-7 kgs over 2 years. She was on intermittent proton pump inhibitors (PPIs) and prokinetics for the same with no symptom relief. She is a known diabetic and hypertensive for the past 10 years. Her diabetes was under good control with oral hypoglycemic drugs.

Her BMI is 25 and her physical examination was normal. Routine labs (hemogram, HbA1c, C reactive protein (CRP) and Erythrocyte Sedimentation Rate (ESR) were normal. Ultrasonography revealed cholelithiasis. Upper GI endoscopy was done, which showed friable nodular mucosa in mid and distal body and antrum and duodenal lymphangiectasia with nodular mucosa. (Figure 1a & 1b) Multiple biopsies were taken for histopathology examination. 

Gastric biopsies showed a subepithelial collagen band with irregular contour with a ragged interface with lamina propria. There was expansion of the lamina propria by inflammatory cells (lymphocytes, plasma cells and few eosinophils). Muscularis mucosa was unremarkable. Masson’s trichome staining showed this subepithelial collagen band. These features were consistent with collagenous gastritis. (Figure 1c & 1d). Colonoscopy was done to rule out collagenous colitis. (Figure 2a & 2b). 

This patient was started on Budesonide along with PPIs and prokinetics, following which she had significant improvement in her symptoms and weight gain of 2 kgs.

However, subsequent endoscopy after 3 months showed persistence of the endoscopic appearance, with biopsy examination showing same pattern.

At 6 months of follow up, upper GI endoscopy showed further decrease in distensibility of antrum with luminal narrowing. (Figure 3a) Histopathology examination showed similar findings as before with decrease in thickness of the collagen band and increase fibrosis beneath surface epithelium and lamina propria. Muscularis mucosa was also thickened and splayed. Findings were consistent with atrophic pattern of collagenous gastritis. (Figure 3b & 3c).

Collagenous gastritis is a rare disease with less than 100 cases described in literature. Collagenous colitis and collagenous sprue present with similar histological patterns and all three are considered to be a part of the same disease entity. However, they are commoner, with collagenous colitis being a frequent cause of diarrhoea in older patients (1.1 to 5.2 cases per 100000 population³).

Clinically, a patient of collagenous gastritis can have a varied presentation with abdominal pain, anaemia, diarrhoea, the more common symptoms, and less often with nausea and vomiting, weight loss, gastrointestinalbleeding, dyspepsia, perforated ulcer, dysphagia, and constipation¹. Our patient presented with nausea, vomiting, and alarm symptoms like loss of appetite and weight.

In adults, collagenous gastritis may be associated with other autoimmune disorders like Sjogren’s syndrome, lymphocytic gastritis, celiac sprue⁴. Colonoscopy with multiple random biopsies was done in our patient to evaluate the presence of associated colitis. However, she had isolated collagenous gastritis.

Nodularity of the gastric corpus is the most common and characteristic endoscopic finding. Other features are mucosal erythema, erosions, and exudates¹. Uneven inflammation causes glandular atrophy and collagen deposition in the depressed mucosa while the nodular areas show fewer inflammatory infiltrates and atrophic changes¹. This finding is supported by Narrow band imaging (NBI) 5 and histology. NBI imaging of the nodular areas show normal capillary structure while the depressed mucosa shows absent or irregular surface structure with abnormal capillary pattern. This is in contrast to collagenous colitis shows a relatively even distribution of inflammation and atrophic changes, resulting in the homogeneous mucosal changes seen colonoscopy. Nodularity of the gastric mucosa has been more commonly reported with H pylori associated gastritis, atrophic gastritis, intestinal metaplasia⁷.

Histopathology findings clinch the diagnosis and is typically characterized by chronic inflammatory cells (lymphocytes, plasma cells, eosinophils) in the subepithelial layer, especially the lamina propria and deposition of collagen bands thicker than 10 µm⁶. The collagen band can be identified on Masson’s trichome staining and its thickness may increase with time, and vary based on the site of biopsy rather than the severity of disease due to the heterogenous nature of deposition.Collagenous gastritis occurs in three distinctive inflammatory milieus, a lymphocytic gastritis-like pattern, an eosinophil-rich pattern, and an atrophic gastritis pattern⁸. Scleroderma is also be associated with collagen deposition, however collagen deposition is diffuse and is seen around crypts too. Radiation associated gastritis also has diffuse deposition of collagen.

There is no established therapy for collagenous gastritis, with no RCTs or guidelines. Multiple therapeutic options have been explored with varying results including anti-secretary agents including  protonpump inhibitors, H2-receptor antagonists, steroids, iron supplementation, hypoallergenic diets¹. In our case, the patient had some symptomatic relief with budesonide, however endoscopically, disease appeared to have progressed and further need for surgery (partial gastrectomy) may have to be considered in case of gastric outlet obstruction.