| Gastritis may be acute or chronic. Several different histologic forms of gastritis have been identified. Most are likely secondary to the ingestion of various substances that cause injury to the gastric mucosa. Continued mucosal damage may initiate an immune-mediated reaction. Other factors, including allergic reactions, immune mechanisms, and hormonal factors, may play a part in the etiology of chronic gastritis. |
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Acute gastritis is usually caused by dietary indiscretion leading to damage of the gastric mucosa. Chronic gastritis is caused by a variety of diseases, including chronic superficial gastritis, chronic atrophic gastritis, chronic hypertrophic gastritis, and eosinophilic gastritis.
Chronic superficial gastritis is characterized histologically by infiltration of the superficial mucosa and lamina propria with lymphocytes, plasma cells, and fibrosis. Caustic agents, including aspirin, may cause these lesions. Dietary factors may also be responsible.
Chronic atrophic gastritis is characterized by a thin mucosa, a variable inflammatory cell infiltrate, and a reduction in the size and depth of gastric glands. The number of chief and parietal cells is decreased, and that of mucus-secreting cells increased. Chronic atrophic gastritis may represent the sequela of long-standing chronic superficial gastritis or immune-mediated disease directed against the gastric mucosa and parietal cells. It is reported more often in the
Norwegian Lundehund breed.
Chronic hypertrophic gastritis is identified by a diffuse or focal thickening of the gastric mucosa and large rugal folds that result from hypertrophy and hyperplasia of mucosal glands. Gastric outflow obstruction (
Gastrointestinal Obstruction) may follow. Inflammatory infiltrate invariably accompanies these changes, and ulceration may be seen as a result of chronic mucosal inflammation. Trophic factors, eg, histamine and gastrin, may also initiate abnormalities.
For example, increased histamine production from dogs with mast cell tumors, and excessive gastrin levels in dogs with renal dysfunction, predispose to hypertrophic gastritis. The disease is more common in Basenjis, Lhasa Apsos, Shih Tzus, Maltese, Miniature Poodles, and other small-breed dogs. Males are predisposed, and older dogs are most often affected.
Eosinophilic gastritis is uncommon. It is characterized by diffuse eosinophilic infiltration and granulation of the gastric wall. Eosinophilia in a vomiting animal is strongly suggestive of eosinophilic gastritis or eosinophilic gastroenteritis. The etiology is unknown but is suspected to be secondary to exposure to dietary allergens or as a consequence of an immune response to other antigens, eg, migrating parasites. |
| Vomiting (
Vomiting: Introduction,
Drugs to Control or Stimulate Vomiting) is the characteristic clinical sign of gastritis. In cases of acute gastritis, the vomitus may contain evidence of whatever substances the pet ingested (eg, grass). Bile, froth, frank blood, or digested blood that appears like “coffee grounds” may also be present. Occasionally, abdominal pain is signaled by the animal displaying a “praying” position (hindquarters raised and chest and forelegs held
close to floor), a position that apparently gives some sense of relief. Polydipsia is often followed by immediate vomiting in dogs with acute gastritis. Acute or sporadic vomiting is generally not associated with other abnormalities. Diarrhea from concurrent intestinal involvement may also be noted. |
| Chronic vomiting may be associated with weakness, lethargy, weight loss, dehydration, and electrolyte imbalance and acid-base disorders. |
| For diagnosis, treatment, and control, see
vomiting,
Vomiting: Introduction,
Drugs to Control or Stimulate Vomiting. In addition to the treatments discussed under vomiting, therapy for chronic atrophic gastritis includes the use of corticosteroids, azathioprine, and H2-blocking agents. Similarly, H2 -blocking agents are indicated in the management of chronic hypertrophic gastritis. Clinical disease associated with focal or discoid areas of hypertrophy
respond well to simple surgical resection. Therapy for eosinophilic gastritis includes elimination of its cause, eg, parasites or dietary hypersensitivity, and the use of corticosteroids and commercial or homemade hypoallergenic diets. |
| Prognosis depends on the nature of the disease and the ability to eradicate or control it. Acute gastritis responds well to fasting and avoiding further dietary indiscretion. The prognosis for chronic gastritis is variable, depending somewhat on the owner’s ongoing cooperation in dietary trials and continued therapy with H2-blocking agents. Response to treatment is better and seen more often in chronic superficial gastritis than in chronic atrophic gastritis.
Dogs with focal hypertrophic lesions respond well to surgical resection. Hypertrophic gastritis associated with hypergastrinemia and hyperchlorhydria have a guarded prognosis and tend to require continued medical therapy. Dogs with eosinophilic gastritis respond to dietary and corticosteroid therapy but often require continued longterm management. Azathioprine has been used in more intractable cases. |
