Gastritis and Peptic Ulcer Disease: Diagnosis and Treatement

Diagnosis

Upper gastrointestinal endoscopy is diagnostic for gastritis and peptic ulcer disease (PUD). This test permits direct visualization of the mucosa and biopsy to evaluate for H pylori infection and rule out carcinoma.

Barium swallow with upper gastrointestinal x–ray series may also be used for diagnosis. This test is less invasive and cheaper than endoscopy, but has lower sensitivity and does not allow for biopsy.

Patients with known PUD should be tested for H pylori infection. However, despite the high prevalence of H pylori infection in PUD patients, routine screening in asymptomatic patients is not advised. Immunoglobin G (IgG) and immunoglobin A (IgA) serologies may be used in patients who have not previously been treated for H pylori. Because IgG remains positive after therapy, it is not a useful test to follow the effectiveness of treatment. Patients who have previously been treated require urease breath testing or endoscopic biopsy to evaluate for active infection.

Depending on the patient’s history, laboratory procedures may include complete blood count, amylase and lipase, liver function tests, electrocardiogram, cardiac enzymes to rule out cardiac ischemia, and a urine pregnancy test.

If perforation is suspected, an upright chest x–ray will reveal free air under the diaphragm; however, CT scan may also be necessary to diagnose a perforation. Endoscopy and barium swallow are contraindicated if perforation is suspected.

Treatment

Patients should avoid agents known to exacerbate gastritis or PUD. These include tobacco, alcohol, NSAIDs, aspirin, and steroids.

Antacid therapy to reduce acid production includes histamine–2 (H2) receptor blockers (eg, cimetidine, ranitidine) and proton pump inhibitors (eg, omeprazole). Oral antacids (eg, Maalox, Mylanta, Rolaids, Tums) and sucralfate, a mucosal protective agent, that binds to ulcers and forms a protective barrier against acid, may also be used.

It is important to treat H pylori infection, if present. Eradication of H pylori decreases the annual ulcer recurrence risk from 50% to 80% to less than 10%, and also reduces the likelihood of complications, such as bleeding. Several “triple therapy” regimens, which are usually administered for 2 weeks, are available (eg, omeprazole, clarithromycin, and amoxicillin; bismuth, metronidazole, and tetracycline).

Ulcer disease tends to be more severe in the absence of H pylori infection. These patients are treated with high–dose proton pump inhibitor therapy. Further, H pylori–negative ulcers appear to have a worse outcome when treated empirically with antibiotics.¹ Thus, H pylori infection should be documented prior to antibiotic treatment, except in settings where the prevalence of H pylori is greater than 90%.²

Emergent surgical intervention is necessary for perforated ulcers and intractable bleeding.

Exercise has been hypothesized to influence the risk for ulcer disease or gastritis through reductions in basal or meal–stimulated acid secretion. Some evidence suggests that exercise significantly decreases the risk of duodenal ulcer³ and of severe gastrointestinal hemorrhage in persons with gastritis or duodenal ulcer.⁴ However, controlled clinical studies have not confirmed the ability of exercise to prevent or ameliorate gastritis. In fact, some have shown that certain kinds of exercise (eg, long–distance running) actually increase the risk for this condition.⁵