Overview and Risk Factors
Gastritis and peptic ulcers affect up to 50% of adult populations in Westernized countries. Gastritis is a superficial erosion and inflammation of the gastric mucosa. Peptic ulcers are deeper erosions and ulcerations that extend through the muscularis layer of the gastric or duodenal mucosa.
These disorders result from a disrupted balance between formation of caustic gastric acid and maintenance of the protective mucosal barrier that depends on secretion of bicarbonate, prostaglandins, and mucosal growth factors. In general, gastritis and gastric ulcers are associated with insufficient mucosal protection, whereas duodenal ulcers are associated with excess acid secretion.
Helicobacter pylori infection may be responsible for up to 95% of duodenal ulcers and 85% of gastric ulcers, worldwide. The bacteria disrupt the mucosal protective barrier, making it more vulnerable to acid damage and inciting an inflammatory response. In the United States, H pylori is a less prevalent cause of ulcers; nonsteroidal anti-inflammatory drugs (NSAIDs) are the most common cause of gastric ulcers in the United States. Other etiologies include irritants such as aspirin and steroids; severe physiologic stress, including burns, sepsis, trauma, and major surgery; local trauma, such as nasogastric tube placement; and hypersensitivity and autoimmune reactions.
These disorders are often asymptomatic. When symptoms occur, they may include:
- Gnawing epigastric or right-upper-quadrant abdominal pain that may radiate to the back.
- Nausea and vomiting.
- Weight loss/anorexia.
- Gastrointestinal bleeding that may present as hematemesis, melena, guiac-positive stools, and/or anemia.
Whereas eating exacerbates the pain of gastritis and gastric ulcers, duodenal ulcer pain is relieved by eating, but increases 2 to 3 hours after meals.
The sudden onset of severe pain (or significant worsening of existing pain), or peritoneal signs (abdominal rigidity, guarding, rebound tenderness) may signify a perforation, which is a surgical emergency.
Increasing age. Gastric ulcers typically occur in patients over 40 years old, and the incidence of duodenal ulcers peaks at around age 60.
H pylori infection. One in six patients exposed to H pylori will develop an ulcer. Ulcers recur much less often when H pylori is eradicated.
NSAIDS. NSAIDs suppress prostaglandin formation in the mucosa, which is normally a part of the protective mechanism of the mucosal barrier.
Tobacco use. Nicotine increases acid secretion and reduces mucosal blood flow in the stomach and duodenum.
Alcohol use. Alcohol can cause gastritis by stimulating acid secretion and damaging the mucosal barrier. However, no evidence for a role in ulcer formation has been found.
Major surgery or severe illness. Prophylaxis for gastritis and ulcers may be administered in hospitalized patients, especially those on mechanical ventilation or those undergoing major surgery. Although some reports have argued for prophylaxis in all hospitalized patients, this claim is not backed by rigorous data.
Family history. More than 25% of ulcer patients have a family history of ulcers, compared with 5% of nonulcer patients.
Diagnosis and Treatement
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.
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
For decades, doctors have recommended dietary adjustments aimed at preventing or treating symptoms of gastritis and PUD. Common suggestions have included avoiding spicy foods, coffee, and alcohol, and increasing consumption of bland foods and milk. While these suggestions seem reasonable, some have not stood up well in controlled investigations. For example, milk ingestion tends to increase gastric acid secretion.6 Although certain spices (black pepper, chili powder, red pepper) may cause dyspepsia,6 they have not been shown to contribute to either gastritis or peptic ulcer.
Diet may moderate the risk for gastritis or peptic ulcer through acting on H pylori, among other effects.7 The following factors have been associated with reduced risk of gastritis or ulcer disease in epidemiologic studies:
High-fiber diets. A large cohort study at the Harvard School of Public Health found that high-fiber diets were associated with reduced risk for developing duodenal ulcer. Over a 6-year period, the risk was 45% lower for those with the highest fiber intake, compared with those with the lowest. Food sources of soluble fiber (oats, legumes, barley, certain fruits and vegetables) were especially protective, resulting in a 60% lower risk for this group.8 However, supplementation with dietary fiber in the form of wheat bran had no effect on ulcer recurrence.9 Similarly, high-fiber diets did not appear to increase ulcer healing rates, compared with diets low in fiber.10
Diets high in vitamin A. In the same Harvard cohort study, total vitamin A intake (from food and supplements) was associated with lower risk. The risk was 54% lower among persons consuming the most vitamin A, compared with those consuming the least.11
Green tea. Several studies show that regular green tea consumption is associated with a 40% to 50% lower risk for gastritis.12 Cellular tests suggest that the catechins in green tea (eg, epigallocatechin-3-gallate, EGCG) may suppress H pylori-induced gastritis through antioxidant and antibacterial actions.13 However, current evidence is not yet sufficient for recommending green tea for prevention of gastritis.
Avoiding alcohol. The relationship between alcohol and gastritis and peptic ulcer is complex, and may be related to amounts consumed. Chronic alcohol abuse favors H pylori infection, and the ammonia produced by this organism contributes to gastritis.14 Alcohol may also slow the rate of healing in established ulcers,15 although this has not been demonstrated in patients on proton pump inhibitors.
However, studies have also found an inverse association between moderate alcohol consumption and H pylori infection. Alcohol may have bactericidal effects on H pylori,16 and it may prevent infection and associated gastritis through an adaptive cytoprotective response (eg, endogenous release of prostaglandins with protective effects on gastric mucosa).17 But, while moderate consumption was associated with the lowest odds for infection, higher intakes were associated with greater risk.18 The protective effect of moderate alcohol consumption for gastritis and PUD is not evident among smokers; in combination with smoking, alcohol increases the risk for duodenal ulcer.19
In addition, the following are under study for their role in managing gastritis and PUD:
Avoiding coffee. Coffee, either in its caffeinated or decaffeinated forms, stimulates acid secretion,8 and some studies have suggested a correlation between coffee intake and symptoms in patients with duodenal ulcer.20
Coffee consumption may also mediate the relationship between H pylori infection and ulcer, although studies have variously found coffee consumption to be associated with both increased and decreased risk for H pylori infection.21-23 Overall, there is no current evidence implicating coffee consumption in the susceptibility to, treatment of, or recovery from gastritis.
Probiotics. Probiotics (eg, Lactobacillus caseii) interfere with H pylori adhesion to epithelial cells, attenuate H pylori-induced gastritis,24 and inhibit growth of H pylori in humans, in addition to reducing the side effects of eradication treatment.25 Combining probiotic treatment with omeprazole, amoxicillin, and clarithromycin in H pylori-infected children significantly improved the treatment effectiveness, compared with drug treatment alone.26 Further study is needed to determine if probiotic treatment results in the prevention of initial infection, reduction of gastritis symptoms, prevention of ulcer occurrence, and improved healing of gastric lesions.
What to Tell the Family
Bacterial infection plays a significant role in PUD, and testing and treatment for H pylori are important. In addition, the risk for developing gastritis and ulcer disease may be reduced by following a healthy diet and exercise regimen and properly managing stressful life circumstances. In patients with existing disease, these methods should be used along with medications to reduce acid secretion, speed ulcer healing, and eradicate the bacteria that often cause this disease.
1. Bytzer P, Teglbjaerg PS. Helicobacter pylori-negative duodenal ulcers: Prevalence, clinical characteristics, and prognosis-results from a randomized trial with 2-year follow-up. Am J Gastroenterol. 2001;96:1409-1416.
2. Borody TJ, George LL, Brandl S, et al. Helicobacter pylori-negative duodenal ulcer. Am J Gastroenterol. 1991;86:1154-1157.
4. Pahor M, Guralnik JM, Salive ME, et al. Physical activity and risk of gastrointestinal hemorrhage in older persons. JAMA. 1994;272:595-599.
5. Choi SJ, Kim YS, Chae JR, et al. Effects of ranitidine for exercise induced gastric mucosal changes and bleeding. World J Gastroenterol. 2006;12:2579-2583.
7. Levenstein S. Stress and peptic ulcer: life beyond Helicobacter. BMJ. 1998;316:538-541.
13. Lee KM, Yeo M, Choue JS, et al. Protective mechanism of epigallocatechin-3-gallate against Helicobacter pylori-induced gastric epithelial cytotoxicity via the blockage of TLR-4 signaling. Helicobacter. 2004;9:632-642.
14. Lieber CS. Gastric ethanol metabolism and gastritis: interactions with other drugs, Helicobacter pylori, and antibiotic therapy (1957-1997)--a review. Alcohol Clin Exp Res. 1997;21:1360-1366.
16. Bujanda L. The effects of alcohol consumption upon the gastrointestinal tract. Am J Gastroenterol. 2000;95:3374-3382.
18. Brenner H, Bode G, Adler G, Hoffmeister A, Koenig W, Rothenbacher D. Alcohol as a gastric disinfectant? The complex relationship between alcohol consumption and current Helicobacter pylori infection. Epidemiology. 2001;12:209-214.
19. Piper DW, Nasiry R, McIntosh J, et al. Smoking, alcohol, analgesics, and chronic duodenal ulcer. A controlled study of habits before first symptoms and before diagnosis. Scand J Gastroenterol. 1984;19:1015-1021.
23. Bode G, Hoffmeister A, Koenig W, Brenner H, Rothenbacher D. Characteristics of differences in Helicobacter pylori serology and 13C-urea breath-testing in an asymptomatic sample of blood donors. Scand J Clin Lab Invest. 2001;61:603-608.
25. Tursi A, Brandimarte G, Giorgetti GM, Modeo ME. Effect of Lactobacillus casei supplementation on the effectiveness and tolerability of a new second-line 10-day quadruple therapy after failure of a first attempt to cure Helicobacter pylori infection. Med Sci Monit. 2004;10:CR662-CR666.
26. Sykora J, Valeckova K, Amlerova J, et al. Effects of a specially designed fermented milk product containing probiotic Lactobacillus casei DN-114 001 and the eradication of H. pylori in children: a prospective randomized double-blind study. J Clin Gastroenterol. 2005;39:692-698.