Gastritis, Atrophic

Home / Gastritis, Atrophic

Issues

Gastritis, Atrophic

 

Atrophic Gastritis is characterized histologically by a focal or diffuse reduction in size and depth of gastric glands with associated inflammatory cells.

 

SIGNALMENT

  • Variable, uncommon in young patients.
  • A high prevalence in the Norwegian Lundehund (range 4–13 years old), males are overrepresented.

 

SIGNS

Chronic vomiting, most often intermittent, food or bile.

Anorexia, lethargy, weight loss, edema, or ascites.

 

CAUSES & RISK FACTORS

  • Idiopathic inflammatory gastroenteritis is a potential risk factor.
  • May reflect chronic gastritis of any cause.

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Other forms of chronic gastritis and chronic enteritis

 

CBC/BIOCHEMISTRY/URINALYSIS

Anemia with thrombocytopenia or thrombocytosis may be present if gastric ulceration is present.

Panhypoproteinemia with no proteinuria can be present with primary disease and in animals with concurrent protein-losing enteropathy.

 

OTHER LABORATORY TESTS

  • Achlorhydria has been reported in dogs; may lead to intestinal dysbiosis.
  • Consider diagnostic testing for hepatobiliary and pancreatic disease, as well as for subnormal cobalamin concentration, in cats.
  • Endoscopic biopsies of the small intestines should be performed to evaluate for infiltrative disease.

 

IMAGING

  • Survey radiographs of the thorax and abdomen are typically unremarkable. Stomach may contain ingesta despite adequate fasting, suggesting delayed gastric emptying.
  • Ultrasonography of the abdomen may reveal a thickened or normal gastric wall, gastric masses, the presence or absence of mesenteric lymphadenopathy, thickened or normal intestinal walls, presence or absence of abdominal effusion.
  • Lymphadenopathy and masses may be present with gastric neoplasia.

 

DIAGNOSTIC PROCEDURES

Definitive diagnosis: gastroscopy with biopsy and histopathologic evaluation.

 

PATHOLOGIC FINDINGS

  • Histopathologic examination of gastric biopsy specimens reveals glandular atrophy and inflammatory infiltrates (neutrophils or mononuclear cells). The majority of lesions are located in the fundic region. In non-Lundehunds, lymphocytic plasmacytic gastritis was found with atrophy. Fibrosis may be present.
  • Mucin staining in Lundehunds gives abnormal mucus neck cells and pseudo-pyloric metaplasia. Neoplastic transformation may be associated with linear hyperplasia of neuroendocrine cells (requires special staining, request in suspected cases: chromagrin A, synaptophysin, Sevier-Munger method).
  • The role of Helicobacter infection is controversial. Cats developing atrophic gastritis have been found to have H. pylori infections, but active Helicobacter infections have not been documented in canine cases. Urease activity in gastric biopsies is not diagnostic and poorly correlated with actual infection. Clinical infection is supported by histological documentation of spiral bacteria in gastric mucosa and pits with associated inflammation.

 

TREATMENT

  • Optimal therapy is unknown. Trial therapy for food-responsive gastropathy with an elimination diet can be tried. Tylosin can be administered in the event that the disorder has an antibiotic-responsive component. Treat any underlying etiology identified.
  • Enteral feeding tubes may be indicated in cachexic patients.
  • If gastric emptying is delayed, low residue fat-restricted diets may aid in emptying; elimination diets containing novel, single protein sources may be helpful in select cases.

 

MEDICATIONS

DRUG(S)

  • Histamine type-2 receptor antagonists (e.g., famotidine 0.5–1 mg/kg PO q12h) or proton pump inhibitors (e.g., omeprazole 0.7–1.5 mg/kg PO q12–24h) to inhibit gastric acid secretion and prevent esophagitis. Long-term use of omeprazole should be avoided, if possible, in light of potential adverse effects (hypocalcemia, osteoporosis, intestinal dysbiosis, hypocobalaminemia, and increased risk of diarrhea).
  • If vomiting persists, antiemetics such as maropitant (1–2 mg/kg PO or SC q24h, for 5 days in dogs, 15 days in cats) or ondansetron (0.5 mg/kg PO or SC q24h for 5–7 days) or prokinetics such as metoclopramide (0.2–0.5 mg/kg PO q8h) or cisapride (0.3–0.5 mg/kg PO q8–12h) may be indicated.
  • If infection with Helicobacter spp. is confirmed based upon histopathologic lesions in the stomach consistent with Helicobacter infection, consider triple therapy: amoxicillin at 11–22 mg/kg PO q12h, metronidazole 10-15 mg/kg PO q12h, and famotidine 0.5–1.0 mg/kg PO q12h or omeprazole 0.7–1.5 mg/kg PO q24h for 2 weeks. This infection may recur.

 

CONTRAINDICATIONS/POSSIBLE INTERACTIONS

Be cautious with medications known to exacerbate gastritis, such as corticosteroids and nonsteroidal anti-inflammatory drugs.

 

FOLLOW-UP

  • Long-term intermittent antacid therapy may be required—long-term administration of omeprazole is discouraged.
  • Correlation with progression to gastric cancer (adenocarcinoma or neuroendocrine carcinoma) is suspected but not proven. However, this has been documented in the Norwegian Lundehund breed. If signs persist or recur, monitor for developing gastric tumors (chest radiographs, abdominal ultrasound).

 

MISCELLANEOUS

Hypergastrinemia and hypoacidity are suspected but not proven in veterinary patients.

 

Visit your veterinarian as early recognition, diagnosis, and treatment are essential.

You may also visit – https://www.facebook.com/angkopparasahayop