Gastritis and Peptic Ulcer Disease

Gastritis and peptic ulcer disease (PUD) affect up to 50% of adults in Westernized countries. Gastritis is a superficial erosion and inflammation of the gastric mucosa. It can be either acute or chronic. 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 d isrupt the mucosal protective barrier, making it more vulnerable to acid damage and inciting an inflammatory response. The bacteria also reduce somatostatin production, leading to increased gastrin secretion and action. In the United States, H. pylori infection is a less prevalent cause of ulcers; nonsteroidal anti-inflammatory drugs (NSAIDs) being 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.

Approximately 70% of peptic ulcers (and a smaller percentage of gastritis cases) are asymptomatic. When symptoms occur, they may include:

Dyspepsia. Dyspepsia is the most prominent symptom, consisting of upper abdominal pain or discomfort, usually localized in the epigastrium or right upper quadrant and sometimes radiating to the back. Whereas eating may relieve or exacerbate the pain of gastritis and gastric ulcers, duodenal ulcer pain is relieved by eating but usually increases 2-3 hours after meals.

Nausea and vomiting.

Weight loss/anorexia.

Gastrointestinal bleeding. Bleeding may present as hematemesis (either red blood or coffee-ground emesis), melena (black, tarry stool), guaiac-positive stools, and/or anemia in the setting of chronic bleeding.

The sudden onset of severe, diffuse abdominal pain (or significant worsening of existing pain) or peritoneal signs (abdominal rigidity, guarding, and rebound tenderness) may signify a hollow organ perforation, which is a surgical emergency.

Gastric outlet obstruction is a rare complication that occurs in about 2% of patients with peptic ulcer disease.[1] Symptoms include early satiety, bloating, indigestion, nausea, vomiting and weight loss.

Risk Factors

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 6 patients exposed to H. pylori will develop an ulcer. Ulcers recur much less often when H. pylori is eradicated.

Nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs suppress prostaglandin formation in the mucosa, which is normally a part of the protective mechanism of the mucosal barrier. NSAIDs and aspirin are the major causes of PUD. The dose and duration of therapy also play a role, but the risk is highest in the early treatment period when starting NSAIDs for the first time.

Tobacco use. Nicotine increases acid secretion and reduces mucosal blood flow in the stomach and duodenum. Smoking is known to delay healing of gastric ulcers, but its role in the pathogenesis of ulcers is unclear.

Alcohol use. Alcohol can cause gastritis by stimulating acid secretion and damaging the mucosal barrier. No evidence for a role in ulcer formation has been found, but alcohol may delay healing of gastric ulcers.

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.

Extreme psychological stress, especially that associated with traumatic events.[2]

Family history. More than 25% of ulcer patients have a family history of ulcers, compared with 5% of non-ulcer patients.

Diagnosis

The diagnosis is suspected when a patient presents with signs and symptoms suggestive of peptic ulcer disease or gastritis and especially in the setting of NSAID use and/or H. pylori infection.

Upper gastrointestinal endoscopy is the most accurate diagnostic test for gastritis and peptic ulcer disease. This test permits direct visualization of the mucosa and biopsy to evaluate for H. pylori infection. All ulcers suspected of being malignant should be biopsied as well.

Barium swallow with upper gastrointestinal x-ray series may also be used for diagnosis. This test is less invasive and less expensive 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 urea breath testing or endoscopic biopsy to evaluate for active infection. Patients taking proton pump inhibitors (PPI) can have false negative breath tests and stool tests.

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 may 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 the symptoms of gastritis or PUD. These include tobacco, alcohol, NSAIDs, aspirin, and steroids.

Antacid therapy to reduce acid production includes histamine-2 (H2) receptor blockers (e.g., ranitidine) and proton pump inhibitors (e.g., omeprazole). Oral antacids 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 infection decreases the annual ulcer recurrence risk from over 50% to less than 10% and reduces the likelihood of complications such as bleeding. Several “triple therapy” regimens, which are usually administered for 2 weeks, are available. The treatment usually combines PPIs and antibiotics (e.g., omeprazole, clarithromycin, and amoxicillin; bismuth, metronidazole, and tetracycline).

Ulcer disease tends to be more severe in the absence of H. pylori infection. Patients in this situation 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.[3] Thus, H. pylori infection should be documented prior to antibiotic treatment, except in settings where the prevalence of H. pylori is greater than 90%.[4]

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 ulcer[5] and of severe gastrointestinal hemorrhage in persons with gastritis or duodenal ulcer.[6] 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 (e.g., long-distance running) actually increase the risk for this condition.[7] Approximately 20% of long-distance runners experience GI bleeding, confirmed by endoscopy.[8] Exercise-induced ischemia and acid secretion have been postulated as mechanisms by which runners may develop erosive gastritis, hemorrhagic gastritis, or gastric ulcer.[5]

Nutritional Considerations

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.[9] Although certain spices (black pepper, chili powder, red pepper) may cause dyspepsia,[7] 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.[10] In turn, H. pylori infection can affect nutritional status and may specifically interfere with vitamin C, vitamin A, iron, folate, and vitamin B12 absorption. When iron or vitamin B12 supplementation is paired with H. pylori eradication therapy, deficiencies in those nutrients improve.[11]

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 (found in oats, legumes, barley, and certain fruits and vegetables) were especially protective, resulting in a 60% lower risk for this group.[12] However, supplementation with dietary fiber in the form of wheat bran had no effect on ulcer recurrence.[13] Similarly, high-fiber diets did not appear to increase ulcer healing rates, compared with diets low in fiber.[14]

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.[12]

Tea. Several studies show that regular green tea consumption is associated with a 40%-50% lower risk for gastritis.[15] Cellular tests suggest that the catechins (e.g., epigallocatechin-3-gallate (EGCG)) in some tea varieties may suppress H. Pylori-induced gastritis through antioxidant and antibacterial actions.[16] ,[17] However, current evidence is not yet sufficient for recommending 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.[18] Alcohol may also slow the rate of healing in established ulcers,[19] 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,[20] and it may prevent infection and associated gastritis through an adaptive cytoprotective response (e.g., endogenous release of prostaglandins with protective effects on gastric mucosa).[21] But, while moderate consumption is associated with the lowest odds for infection, higher intakes are associated with greater risk.[22] 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.[23]

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,[24] and some studies have suggested a correlation between coffee intake and symptoms in patients with duodenal ulcer.[25]

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.[26] ,[27] ,[28] Overall, there is no current evidence implicating coffee consumption in the susceptibility to, treatment of, or recovery from gastritis. However, when treating peptic ulcer, clinicians should consider individual tolerances to various food and beverages such as coffee.[29]

Probiotics. Probiotics (e.g., Lactobacillus casei) interfere with H. pylori adhesion to epithelial cells, attenuate H. pylori-induced gastritis,[30] and inhibit growth of H. pylori in humans, in addition to reducing the side effects of eradication treatment.[31] Combining probiotic treatment with omeprazole, amoxicillin, and clarithromycin in H. pylori-infected children significantly improved the treatment effectiveness, compared with drug treatment alone.[32] 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. Dosage, species, and treatment duration are not currently established.[33]

Orders

See Basic Diet Orders Chapter

Alcohol restriction.

Smoking cessation.

Stress reduction.

Exercise prescription.

What to Tell the Family

Bacterial infection plays a significant role in peptic ulcer disease, and testing and treatment for H. pylori are important. Family members can help by encouraging a patient who is suffering from symptoms of gastritis or ulcer to get appropriate testing and treatment.

In addition, the risk for developing gastritis and ulcer disease may be reduced by following a healthy diet and exercise regimen, something that family members can support and take part in.

Caution should be used when considering the use of aspirin and NSAIDs. In patients with existing disease, these treatments should be used along with medications to reduce acid secretion, speed ulcer healing, and eradicate the bacteria that often cause this disease. For individuals having difficulty managing their medications, attentive family members can be helpful.

References

  1. DiSario JA et al: Endoscopic balloon dilation for ulcer-induced gastric outlet obstruction. Am J Gastroenterol 89:868, 1994  [PMID:8198096]
  2. Kanno T et al: Peptic ulcers after the Great East Japan earthquake and tsunami: possible existence of psychosocial stress ulcers in humans. J Gastroenterol 48:483, 2013  [PMID:23053423]
  3. Bytzer P, Teglbjaerg PS, Danish Ulcer Study Group: Helicobacter pylori-negative duodenal ulcers: prevalence, clinical characteristics, and prognosis--results from a randomized trial with 2-year follow-up. Am J Gastroenterol 96:1409, 2001  [PMID:11374675]
  4. Borody TJ et al: Helicobacter pylori-negative duodenal ulcer. Am J Gastroenterol 86:1154, 1991  [PMID:1882793]
  5. Cheng Y et al: Does physical activity reduce the risk of developing peptic ulcers? Br J Sports Med 34:116, 2000  [PMID:10786867]
  6. Pahor M et al: Physical activity and risk of severe gastrointestinal hemorrhage in older persons. JAMA 272:595, 1994 Aug 24-31  [PMID:8057514]
  7. Choi SJ et al: Effects of ranitidine for exercise induced gastric mucosal changes and bleeding. World J Gastroenterol 12:2579, 2006  [PMID:16688805]
  8. Schwartz AE, Vanagunas A, Kamel PL: Endoscopy to evaluate gastrointestinal bleeding in marathon runners. Ann Intern Med 113:632, 1990  [PMID:2400170]
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  12. Aldoori WH et al: Prospective study of diet and the risk of duodenal ulcer in men. Am J Epidemiol 145:42, 1997  [PMID:8982021]
  13. Rydning A et al: Effect of wheat fibre supplements on duodenal ulcer recurrence. Scand J Gastroenterol 28:1051, 1993  [PMID:8303206]
  14. Rydning A et al: Healing of benign gastric ulcer with low-dose antacids and fiber diet. Gastroenterology 91:56, 1986  [PMID:3011583]
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  16. Lee KM et al: Protective mechanism of epigallocatechin-3-gallate against Helicobacter pylori-induced gastric epithelial cytotoxicity via the blockage of TLR-4 signaling. Helicobacter 9:632, 2004  [PMID:15610077]
  17. Ankolekar C et al: Inhibitory potential of tea polyphenolics and influence of extraction time against Helicobacter pylori and lack of inhibition of beneficial lactic acid bacteria. J Med Food 14:1321, 2011  [PMID:21663484]
  18. Lieber CS: Gastric ethanol metabolism and gastritis: interactions with other drugs, Helicobacter pylori, and antibiotic therapy (1957-1997)--a review. Alcohol Clin Exp Res 21:1360, 1997  [PMID:9394105]
  19. Battaglia G et al: Markers of slow-healing peptic ulcer in the elderly. A study on 1,052 ranitidine-treated patients. Dig Dis Sci 38:1414, 1993  [PMID:8344096]
  20. Bujanda L: The effects of alcohol consumption upon the gastrointestinal tract. Am J Gastroenterol 95:3374, 2000  [PMID:11151864]
  21. Tursi A et al: Effect of adequate alcohol intake, with or without cigarette smoking, on the risk of Helicobacter pylori infection. Hepatogastroenterology 45:1892, 1998 Sep-Oct  [PMID:9840171]
  22. Brenner H et al: Alcohol as a gastric disinfectant? The complex relationship between alcohol consumption and current Helicobacter pylori infection. Epidemiology 12:209, 2001  [PMID:11246582]
  23. Piper DW et al: Smoking, alcohol, analgesics, and chronic duodenal ulcer. A controlled study of habits before first symptoms and before diagnosis. Scand J Gastroenterol 19:1015, 1984  [PMID:6398504]
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  25. Eisig JN et al: Coffee drinking in patients with duodenal ulcer and a control population. Scand J Gastroenterol 24:796, 1989  [PMID:2799282]
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  27. Moayyedi P et al: Relation of adult lifestyle and socioeconomic factors to the prevalence of Helicobacter pylori infection. Int J Epidemiol 31:624, 2002  [PMID:12055165]
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  29. Shimamoto T et al: No association of coffee consumption with gastric ulcer, duodenal ulcer, reflux esophagitis, and non-erosive reflux disease: a cross-sectional study of 8,013 healthy subjects in Japan. PLoS ONE 8:, 2013  [PMID:23776588]
  30. Felley C, Michetti P: Probiotics and Helicobacter pylori. Best Pract Res Clin Gastroenterol 17:785, 2003  [PMID:14507588]
  31. Tursi A et al: 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 10:CR662, 2004  [PMID:15567983]
  32. Sýkora 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 39:692, 2005  [PMID:16082279]
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Last updated: January 12, 2018

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TY - ELEC T1 - Gastritis and Peptic Ulcer Disease ID - 1342027 Y1 - 2018/01/12/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342027/all/Gastritis_and_Peptic_Ulcer_Disease ER -