Considerable advances have been made in the area of peptic ulcer disease, an imbalance between peptic acid secretion and gastroduodenal mucosal defenses.
It is amazing how far we have come in understanding peptic ulcer disease (PUD). Just 30 years ago, prevailing mental health theory postulated peptic ulcers were physical manifestations of stress and unconscious conflicts. Patients with peptic ulcers spent considerable time in psychotherapy. Treatment failures were common, and they were for good reason— research in the 1980s confirmed an association between Helicobacter pylori
bacteria and ulcers. Ironically, many patients spent thousands of dollars in therapy when relief could have been as simple as a short-term drug regimen.
Succinctly stated, PUD is an imbalance between peptic acid secretion and gastroduodenal mucosal defenses, occurring generally in the stomach and proximal duodenum. PUD creates a gastric or duodenal wall defect extending deep through the muscularis mucosae (the lowermost mucosa) into the submucosa or muscularis propria, eventually eroding major blood vessels and leading to lifethreatening hemorrhages.1-3
Exposure to aggressive irritants (H pylori
, nonsteroidal anti-inflammatory drugs [NSAIDs], alcohol, bile, salts, acid, and pepsin) overwhelm mucosal defenses, injuring cells.2
Approximately 500,000 Americans are diagnosed with PUD annually. Lifetime prevalence is 11% to 14% for men and 8% to 11% for women, and incidence increases with age; however, 70% of patients are between 25 and 64 years of age. H pylori
and/or NSAIDs are peptic ulcer’s most frequent etiologies, accounting for 48% and 24% of cases, respectively.1 H pylori
is more often associated with duodenal ulcers, while NSAIDs tend to be associated with gastric ulcers (Table 1).4
Epigastric pain (gnawing or burning sensation), usually relieved with antacids, is the most common symptom of PUD, generally occurring 2 to 3 hours after meals. It may wax and wane. Pain can last from minutes to hours and may radiate to the back. Other PUD symptoms include nausea, vomiting, heartburn, and dyspepsia (belching, bloating, distention, and fatty food intolerance).2
Endoscopic examination, often coupled with biopsy to rule out malignancies, is the gold standard to establish PUD and to assess clinical trial outcomes.4
As an alternative, the American College of Gastroenterology (ACG) considers the urea breath test the most reliable diagnostic/ confirmation noninvasive test.5
Additionally, the monoclonal fecal antigen test can be used for diagnosis and outcome assessment.
ACG guidelines recommend “test and treat” strategies for patients younger than 55 years of age and who present without alarm symptoms: dysphagia (swallowing difficulties), recurrent vomiting, unexplained weight loss, bleeding, and anemia. All patients with alarm symptoms should undergo endoscopic examination, as should patients aged 55 years and older.1,5
Clinicians should order endoscopic examination for patients without alarm symptoms considering PUD history, clinical profile, risk factors, and symptoms that might be attributed to competing etiologies.
Treatment objectives include: (1) H pylori
eradication to promote healing and reduce the risk of gastric and duodenal ulcer recurrence; and (2) acid suppression with a proton pump inhibitor (PPI) to improve healing rates and reduce bleeding and/ or help avoid or minimize hospitalization and surgical interventions.1
First-line treatment for patients with PUD with H pylori
infection consists of triple therapy with a PPI twice daily plus clarithromycin 500 mg twice daily and either amoxicillin 1 g twice daily or metronidazole 500 mg twice daily for 7 to 14 days (Table 2).
Treatment with PPIs twice daily is superior to once-daily dosing.4,5
Approximately 95% of duodenal ulcers heal within 4 weeks, and 80% to 90% of gastric ulcers heal within 8 weeks.1
Triple therapy results in ulcer remission for 12 months in 70% to 90% of cases. When first-line treatment fails to eradicate H pylori
, bacterial culture and microbial sensitivity must guide second- and third-line antibiotic selection.4
Patients with refractory ulcers—inadequate healing 8 to 12 weeks after treatment—require additional diagnostics to determine the presence of hypersecretory diseases and other disorders.
Because up to 70% of patients with NSAID-associated ulcers test positive for H pylori
, guidelines recommend H pylori
eradication in these patients. Ideally, patients without H pylori
should terminate NSAIDs and start an antisecretory agent. Up to 25% of patients with NSAID-related gastric ulcers require long-term PPIs.1
Counseling must emphasize PUD’s gravity, the likelihood of recurrence, adherence, and prevention. The annual risk for a life-threatening, ulcer-related complication (eg, perforations, bleeding) associated with NSAIDs is 1% to 4%, with older patients at high risk for complications.1
Clinicians should have a high index of suspicion for PUD among NSAID users and query patients about symptoms. Because many elders do not experience the full range or intensity of symptoms, mild symptoms require assessment. Recommend avoiding or minimizing NSAID use; acetaminophen or nonacetylated salicylates may be suitable alternatives. Consider switching noncardiovascular disease patients to a cyclooxygenase-2 inhibitor. All patients with NSAID-related ulcers who need daily NSAIDs require long-term PPI prophylaxis.2
Patients often inquire about dietary restrictions. Spicy foods do not increase PUD risk, although they can cause heartburn and indigestion. Patients should only avoid them if they are problematic.6
They should avoid alcohol, especially on an empty stomach.
Three PUD-related issues continue to challenge clinicians: increased failure to eradicate antibiotic-resistant H pylori
, effective treatment approaches for non-H pylori
and non-NSAID peptic ulcers, and effective prevention and recurrence strategies.4
Given PUD’s increased prevalence in elders and the graying of America, clinicians must stay abreast of changing treatment guidelines.
An excellent source for patient education information can be found at eMedicine’s Web site (www. medicine health.com/script/main/art.asp?article key =60166
Dr. Zanni is a psychologist and health systems consultant based in Alexandria, Virginia.
1. Ramakrishnan K, Salinas RC. Peptic ulcer disease. Am Fam Physician
2. Le T, Fantry G. Peptic ulcer disease. www.emedicine.com/med/TOPIC1776.HTM. Accessed June 21, 2010.
3. Yeomans N, Naesdal J. Systematic review: ulcer definition in NSAID ulcer prevention trials. Aliment Pharmacol Ther
4. Yuan Y, Padol IT, Hunt RH. Peptic ulcer disease today. Nat Clin Pract Gastronenterol Hepatol
5. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol.
6. Peptic ulcer disease—what increases your risk. WebMD Web site. www.webmd.com/digestive-disorders/tc/peptic-ulcer-disease-what-increases-your-risk. Accessed June 21, 2010.