Collagenous gastritis (CG) is a long-term inflammatory condition affecting the stomach lining, representing an extremely rare form of gastritis. This disorder is characterized by persistent inflammation, which sets it apart from the more common, temporary causes of stomach inflammation. CG belongs to a group of diseases called collagenous gastroenteritides, which also includes collagenous colitis and collagenous sprue.
Defining Collagenous Gastritis
The defining feature of collagenous gastritis is a distinct pathological change in the stomach tissue. The disease involves an abnormal buildup of collagen protein just beneath the epithelial layer, known as the subepithelial layer. This accumulation forms a thickened band of collagen, accompanied by an infiltration of inflammatory cells within the lamina propria.
To confirm the diagnosis, the subepithelial collagen band must be greater than 10 micrometers thick, which is significantly thicker than the layer found in a normal stomach. This characteristic thickening gives the condition its name. The condition is often classified as idiopathic, meaning the precise cause remains unknown, and it represents a chronic inflammatory process.
Common Clinical Symptoms
The symptoms experienced by individuals with collagenous gastritis are often non-specific, which can make initial diagnosis difficult. Upper abdominal pain, particularly in the epigastric area, is a frequently reported complaint, occurring in over half of all patients. Other upper gastrointestinal complaints include nausea and vomiting.
Chronic anemia is a common presentation of the disease, often due to persistent, low-level gastrointestinal blood loss or malabsorption. Anemia is reported in a majority of patients, especially children, and can lead to symptoms like fatigue, pallor, and a general lack of energy. Weight loss is also sometimes noted, particularly in adults.
Theories on Causes
The exact reason collagenous gastritis develops is still unclear, and it is largely considered idiopathic. Research points strongly toward a link with the body’s immune system. The thickening of the collagen band is hypothesized to be a reparative response by subepithelial cells to a chronic inflammatory, autoimmune, or toxic insult.
A primary theory suggests an autoimmune connection, as CG frequently occurs alongside other autoimmune disorders. These co-occurring conditions include Celiac Disease, lymphocytic gastritis, and collagenous colitis. This association suggests a common underlying mechanism of immune dysregulation may be at play.
The disease presents in two general patterns: a pediatric-onset type, which is often limited to the stomach, and an adult-onset type, which is more commonly associated with diffuse involvement of the gastrointestinal tract. Environmental and genetic factors are suspected to play a role, and the inflammatory response may stimulate the fibroblasts responsible for the excessive collagen production.
Diagnostic Procedures
Confirming a diagnosis of collagenous gastritis relies on a specialized procedure called an upper endoscopy, or esophagogastroduodenoscopy (EGD). This procedure allows a doctor to visually inspect the lining of the upper digestive tract, including the stomach. Endoscopic findings in CG often show an abnormal appearance, such as mucosal nodularity, which may look like a cobblestone texture, although the mucosa can also appear normal, erythematous, or eroded.
The definitive diagnosis is made by a histological examination of a tissue sample, or biopsy, taken during the endoscopy. Pathologists examine the biopsy under a microscope, and the hallmark finding is the presence of the abnormally thickened subepithelial collagen band. Special stains, such as Masson’s trichrome, are used to highlight the collagen, confirming the thickness is greater than the diagnostic threshold of 10 micrometers.
A differential diagnosis is necessary to rule out other conditions that might mimic the symptoms or endoscopic appearance. This involves checking for other causes of gastritis, such as Helicobacter pylori infection, and determining if co-existing collagenous colitis or celiac disease is present. The biopsy is the gold standard, providing the specific pathological evidence required to confirm this rare condition.
Treatment and Management
Because collagenous gastritis is rare and its cause is not fully understood, a standardized treatment protocol has not been established. The current therapeutic strategy is empirical, focusing on managing symptoms and reducing inflammation. Treatment typically progresses from less aggressive options to more potent therapies if the initial approach is unsuccessful.
First-line treatments usually involve anti-secretory agents aimed at reducing stomach acid, such as proton pump inhibitors (PPIs) and H2-receptor antagonists. These medications help manage symptoms like abdominal pain and dyspepsia, though they do not address the underlying collagen deposition. For patients presenting with anemia, iron supplementation is necessary. Oral iron can sometimes be poorly tolerated or ineffective due to malabsorption, requiring intravenous iron infusions.
For cases that do not respond to initial therapies, more aggressive treatment involves corticosteroids. Systemic corticosteroids like prednisone or targeted topical corticosteroids, such as budesonide, are used to suppress inflammation in the gastric lining. Budesonide can lead to a clinical response in a high percentage of patients, offering a viable option for refractory cases.
Immunosuppressive drugs like azathioprine may be considered for patients with severe, persistent disease. Dietary modifications, such as a gluten-free diet, are also sometimes attempted, particularly when celiac disease is a co-existing condition. Long-term monitoring is necessary to track the disease’s progression and manage symptom recurrence.