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Definition
Reactive gastropathy develops when the stomach lining comes into contact with irritating substances over a period of time. Some types of pain relief medicines called nonsteroidal anti-inflammatory drugs (NSAIDs) and alcohol are among the most common irritating substances. Bile exposure due to the production of nitrous compounds from helicobactor infection is an increasing cause for reactive gastropathy. Bile exposure post gastric surgery (Bilroth 2 gastrectomy) is on the decline as a cause for gastropathy.
Classification
Reactive gastropathy can be classified as mild, moderate or severe, as acute or chronic, and as erosive or non-erosive.
Diagnosis
The diagnosis is by examination of tissue, e.g. a stomach biopsy.
It is characterized, histologically, by:
foveolar hyperplasia with gland tortuosity and dilation,
smooth muscle hyperplasia in the lamina propria, and
scant or minimal inflammation, i.e. lack of large numbers of neutrophils and plasma cells
Relation to gastritis
Reactive gastropathy is a morphologically distinct entity that can be separated from gastritis, which by definition has a significant inflammatory component.
As a reactive gastropathy may mimic a (true) gastritis symptomatically and visually in an endoscopic examination, it may incorrectly be referred to as a gastritis. Even aware of the underlying aetiology of the pathologic process, e.g. NSAID use, the label “chemical gastritis” is often incorrectly applied to a chemical gastropathy.
Treatment of gastropathy
The treatment is aimed at removing the inciting irritating chemical exposure, be it excessive alcohol, non-steroidal anti inflammatory medications or excessive bile. If Helicobactor Pylori infection is present, then this will need treatment with 1-2 weeks of antibiotic eradication therapy. The success or otherwise of treatment can then be confirmed by an acid urea breath test performed 6 weeks after completion of eradication therapy.