Peptic Ulcer Disease

DESCRIPTION

A chronic ulcer in the lining of the gastrointestinal tract.

  • Duodenal ulcer (DU): Most are located in the duodenal bulb. Multiple ulcers, and ulcers distal to the bulb, raise the possibility of Zollinger–Ellison syndrome.
  • Gastric ulcer (GU): Much less common than DU (in the absence of NSAIDs). Most commonly located along the lesser curvature of the antrum near the incisura and in the pre-pyloric area.
  • Esophageal ulcers: A peptic ulcer in the distal esophagus may be part of Barrett’s epithelial change due to chronic reflux of gastroduodenal contents.
  • Ectopic gastric mucosal ulceration: May develop in patients with Meckel’s diverticula or other sites of ectopic gastric mucosa.
  • System(s) affected: Gastrointestinal
  • Genetics: Higher incidence with HLA-B12, B5, Bw35 phenotypes, identical twins
  • Incidence/Prevalence in USA:
    • DU: 4 times more common than GU. Lifetime prevalence = 10% for men; 5% for women (gender gap is closing). 200,000–400,000 new DU cases annually.
    • GU: 87,500 new cases annually. Incidence of new GU in adults: 50 per 100,000.
  • Predominant age:
    • DU: 25–75 years (rare before age 15)
    • GU: peak incidence age 55–65; rare under age 40
  • Predominant sex:
    • DU: Male > Female (slightly)
    • GU: Male = Female (female predominance among NSAID users)
SIGNS AND SYMPTOMS
  • In adults (DU)
    • Gnawing or burning epigastric pain 1–3 hours after meals, relieved by food, antacids, or antisecretory agents
    • Nocturnal pain causing early morning awakening
    • Epigastric pain in 60–90% (often vague discomfort, cramping, hunger pangs). Non-specific dyspeptic complaints (belching, bloating, abdominal distention, food intolerance) in 40–70%.
    • Symptomatic periods occur in clusters lasting a few weeks followed by symptom-free periods for weeks to months. Some seasonal occurrence (spring and fall).
    • Early satiety, anorexia, weight loss, abnormal saline load test, succussion splash, gastric retention of barium, nausea, vomiting suggest pyloric obstruction
    • Heartburn (suggesting reflux disease)
    • Sudden, severe mid-epigastric pain radiating to right shoulder, peritoneal signs, and free peritoneal air may indicate perforation
    • Dizziness, syncope, hematemesis, or melena suggest hemorrhage
  • In adults (GU)
    • Symptom complex similar to DU
    • NSAID-induced ulcers often silent; perforation or bleeding may be initial presentation
    • Epigastric pain following a meal is uncommon; early satiety, nausea, vomiting suggest gastric outlet obstruction
    • Weight loss can occur with either benign or malignant gastric ulcers
  • In children (DU)
    • Positive family history in 50% of early-onset DU patients (under age 20)
    • May account for chronic abdominal pain syndrome in young children
    • Gastric outlet obstruction from ulcer must be distinguished from congenital infantile hypertrophic pyloric stenosis (seen within the first month after birth along with visible peristalses and a palpable pyloric mass)
CAUSES

Etiology of DU and GU is multifactorial. H. pylori gastritis is present in >80% of DU and >60% of GU.

  • Imbalance between aggressive factors (e.g., gastric acid, pepsin, bile salts, pancreatic enzymes) and defensive factors maintaining mucosal integrity (e.g., mucus, bicarbonate, blood flow, prostaglandins, growth factors, cell turnover), which may relate to H. pylori infection
  • Ulcerogenic drugs (e.g., NSAIDs)
  • Zollinger–Ellison syndrome
  • Other hypersecretory syndromes
RISK FACTORS
  • Strongly associated:
    • Drugs (e.g., NSAID use)
    • Family history of ulcer
    • Zollinger–Ellison syndrome (gastrinoma)
    • Cigarettes (> 1/2 pack/day)
  • Possibly associated:
    • Corticosteroids (high dose and/or prolonged therapy)
    • Blood group O
    • HLA-B12, B5, Bw35 phenotypes
    • Stress
    • Lower socioeconomic status
    • Manual labor
  • Poorly or not associated:
    • Dietary spices
    • Alcohol
    • Caffeine
    • Acetaminophen
  • Annual risk of DU developing in H. pylori–positive individuals < 1%
LABORATORY
  • Anemia uncommon in absence of hemorrhage. Fecal occult blood requires colonic evaluation before attributing a positive test to ulcer alone (especially in patients > 40 years).
  • Elevated serum gastrin (to rule out Zollinger–Ellison syndrome)
  • Gastric analysis (to rule out achlorhydria, acid hypersecretion)
  • Secretin stimulation test (paradoxical rise seen in Zollinger–Ellison syndrome)
  • Serum pepsinogen

Drugs that may alter lab results: Antisecretory medications may give falsely low gastric analysis or elevated gastrin
Disorders that may alter lab results: N/A

PATHOLOGICAL FINDINGS
  • Helicobacter pylori gastritis
  • Ulcer crater usually > 5 mm in diameter; extends through the mucosa (in contrast to stress-related ulceration)
SPECIAL TESTS
Serology or urea breath test for H. pylori
IMAGING
  • Endoscopy more accurate than radiography
  • Radiographic features of benign GU include ulcer projecting beyond the lumen, radiolucent band (Hampton line) paralleling ulcer base, radiating folds
DIAGNOSTIC PROCEDURES
  • Endoscopy (accuracy > 95%)
  • Barium meal (accuracy 70–90%)
  • Mucosal biopsy, cytology (excludes malignancy in > 99%)
  • Exploratory laparotomy
  • Histology or urea breath test for H. pylori
APPROPRIATE HEALTH CARE
  • Empiric treatment for young healthy patients with dyspepsia; otherwise endoscopy or barium meal for suspected complications, weight loss, persistent vomiting, etc., or symptom onset after age 50 years
  • Emergency endoscopy and hospitalization for suspected ulcer bleeding
  • ICU care for severe hemorrhage
  • Surgical consult for suspected perforation or obstruction, or uncontrolled bleeding
GENERAL MEASURES
  • Reduce use of NSAIDs and psychic stress
  • Avoid or eliminate cigarette smoking
SURGICAL MEASURES

For bleeding complication, obstruction or perforation

ACTIVITY

Fully active for uncomplicated disease

DIET

3 regular meals daily with avoidance of dietary irritants

PATIENT EDUCATION

National Digestive Diseases Information, Box NDDIC, Bethesda, MD 20892, (301)468-6344

PREVENTION/AVOIDANCE
  • Eradication of H. pylori: recurrence < 10% in the first year, off of all therapies
  • Maintenance therapy (using a proton pump inhibitor or H2 blocker) suppresses ulcer relapse indefinitely while treatment is continued; however, relapses occur in most patients who remain H. pylori positive off therapy
  • Bleeding ulcers require continued maintenance therapy (e.g., H2 blocker or PPI if H. pylori not eradicated)
  • NSAID-related ulcers are best managed by avoiding salicylates and NSAIDs. If NSAIDs are needed, add misoprostol (Cytotec) or a proton pump inhibitor.
  • Selective COX-2 NSAIDs (e.g., celecoxib, rofecoxib) produce significantly fewer GI ulcers; consider use in patients at risk for ulceration
POSSIBLE COMPLICATIONS
  • Hemorrhage in up to 25% of cases (initial presentation in 10%)
  • Perforation occurs in < 5%, usually related to NSAID use
  • Gastric outlet obstruction occurs in up to 5% of patients with duodenal or pyloric channel ulcers. Men predominate.
EXPECTED COURSE AND PROGNOSIS
  • Ulcer relapse rates after H. pylori eradication are low; suspect surreptitious NSAID use
  • Reinfection rates < 1% per year
  • The risk of rebleeding after H. pylori therapy alone remains less well defined
  • NSAID-related ulcers may occur independently of H. pylori status
  • Intractability is now rare; cost effectiveness has been proven for H. pylori eradication
ASSOCIATED CONDITIONS
  • Zollinger–Ellison syndrome (gastrinoma)
  • Systemic mastocytosis
  • MEN Type 1
  • COPD, chronic renal failure, cirrhosis, hyperparathyroidism, carcinoid syndrome, polycythemia rubra vera, basophilic leukemia, porphyria cutanea tarda
AGE-RELATED FACTORS

Pediatric: Uncommon before puberty; hemorrhage and perforation more common
Geriatric: N/A
Others: N/A

PREGNANCY

Unusual in gestation; safety of H2 blockers not established in first 16 wks, but considered reasonably safe later; sucralfate and antacids preferred as initial therapy

OTHER NOTES

N/A

ABBREVIATIONS

HP = Helicobacter pylori

Clinical Investigations

ROLE OF HOMOEOPATHY

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