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Look Up > Conditions > Peptic Ulcer
Peptic Ulcer
Overview
Definition
Etiology
Risk Factors
Signs and Symptoms
Differential Diagnosis
Diagnosis
Physical Examination
Laboratory Tests
Pathology/Pathophysiology
Imaging
Other Diagnostic Procedures
Treatment Options
Treatment Strategy
Drug Therapies
Complementary and Alternative Therapies
Patient Monitoring
Other Considerations
Prevention
Complications/Sequelae
Prognosis
Pregnancy
References

Overview
Definition

Peptic ulcers are lesions of the mucosal lining of the stomach and the duodenum which penetrate the muscularis mucosae, and are called gastric ulcers (GU) and duodenal ulcers (DU), respectively. They may also affect the distal esophagus as a result of chronic gastrointestinal reflux. Duodenal ulcers are the most common. Often a chronic disorder, peptic ulcers affect about 10% of the population. They are declining in Western countries as a whole but are increasing in the elderly population. Recent work in understanding the pathogenesis of acid-peptic disease, and the role of Helicobacter pylori have resulted in refined and more effective treatments.


Etiology
  • H. pylori damages gastric mucosa; implicated in 90% of duodenal and 70% to 80% of gastric ulcers; unknown concurrent pathogenic factors are present as only 15% to 20% of those infected with H. pylori will actually develop ulcers
  • Nonsteroidal anti-inflammatory drug (NSAID) ingestion causes overproduction of gastric acid unrelated to the presence of H. plyori. It causes up to 25 % of GUs. Acid and pepsin are corrosive agents that overpower the gastroduodenal's defense system's ability to protect the epithelium with adequate mucin and to regenerate the lining quickly.
  • Zollinger–Ellison syndrome—gastric-acid stimulating pancreatic islet cell tumors; causes steatorrhea-type diarrhea and gastric acid hypersecretion.
  • Rarely, gastrinoma.

Risk Factors
  • Age (elderly)
  • Smokers are twice as likely to develop and more likely to die from ulcer, possibly from decreased pancreatic bicarbonate secretion, diminishing mucosal defense.
  • Genetics or higher rate of familial H. pylori infection
  • Blood type O
  • Chronic stress may exacerbate but not cause ulcers. Acute stress in life-threatening and surgical emergencies can cause ulcers.
  • Increased risk with chronic pulmonary disease, renal transplants, chronic renal failure, alcoholism, systemic mastocytosis, and hyperparathyroidism
  • NSAID, alcohol, and caffeine use are loosely associated.

Signs and Symptoms

DUs:

  • Epigastric pain (often burning or gnawing) occurs after eating and lasts from one to three hours; relieved by milk and antacids; episodic with periods of remission.
  • Increased pain, vomiting of blood, tarry or red stools, and significant weight loss are indications of perforation, gastric outlet obstruction, or hemorrhaging.

GUs:

  • Epigastric pain (gnawing, burning) is sometimes relieved by food or antacids and sometimes not.
  • Vomiting and nausea (without obstruction)
  • Antral gastritis from H. pylori
  • NSAID-induced ulcers—sometimes painless

Differential Diagnosis
  • Non-ulcer dyspepsia
  • Crohn's disease
  • Ulcerative colitis
  • Gastric carcinomas
  • Gastritis
  • Pancreatitis
  • Gallbladder disease

Diagnosis
Physical Examination
  • Epigastric tenderness in the midline or slightly to the right of the midline
  • Hyperactive bowel sounds upon auscultation
  • Rigid, board-like abdomen and surrounding tenderness

Laboratory Tests

All antral biopsy specimen tests are accurate for detection of H. pylori. Serological tests are accurate for patients previously untreated for H. pylori.

  • Serum antibodies to IgG and IgA are elevated with H. pylori; enzyme-linked immunosorbent assay (ELISA) test is commonly used.
  • Giemsa and Warthin-Starry stains identify H. pylori.
  • Rapid urease test—antral mucosal biopsy specimens identify H. pylori with 90.2% sensitivity and 100% specificity.

Pathology/Pathophysiology
  • Increase in gastric acid secretion after H. pylori infection, returning to normal within a year
  • Basal levels and serum gastric levels from eating are increased
  • Somatostatin deficiency

Imaging
  • Barium radiographic examination is commonly used for initial diagnosis.

Other Diagnostic Procedures
  • Diagnosis for ulcers typically begins with barium radiographic or endoscopic examination.
  • Urea breath test identifies H. pylori with 100% specificity and sensitivity.
  • Establish location of ulcer, as gastric ulcers develop into malignancies in up to 5% of cases, requiring absolute diagnosis and documented resolution.
  • Endoscopy is more accurate than X ray, detects greater detail, deformities, and hemorrhaging, and is better for carcinoma detection.

Treatment Options
Treatment Strategy

The treatment approach as determined by the National Institutes of Health (NIH) Consensus Development Conference advocates the eradication of H. pylori with concurrent use of antisecretory agents for first occurrences and recurrence. Unless recurrent bleeding is life-threatening, maintenance with antisecretory agents may not be warranted. Gastric ulcers generally take longer and are more difficult to heal than duodenal ulcers.


Drug Therapies
  • For H. pylori "triple therapy" is considered most efficacious, but variations of the regimen are commonly used. H. pylori that is resistant to antibiotics, especially to the macrolides and imidazoles (e.g., metronidazole), is problematic worldwide. Side effects of triple therapy include diarrhea and pseudomembranous colitis. Two-week treatment may be combined with H2-receptor antagonists and proton-pump inhibitors.
  • Amoxicillin 500 mg qid OR tetracycline 500 mg bid
  • Bismuth subsalicylate (Pepto-Bismol) 2 tablets qid
  • Metronidazole 250 mg tid
  • H2-receptor antagonists (e.g., cimetidine 400 mg bid, ranitidine 150 mg bid) inhibit gastric acid secretion; serious side effects are infrequent (e.g., reversible hepatitis with ranitidine).
  • Proton-pump inhibitors (e.g., omeprazole 20 mg/day, lansoprazole 30 mg/day) decrease gastric acid secretion.
  • Antacids are used for relief of symptoms and to aid healing of ulcers.
  • Sucralfate (1,000 mg qid) acts to protect the ulcer crater with an adherent coating; acts only locally (not absorbed); used for up to two months.
  • Colloidal bismuth compounds (e.g., bismuth subcitrate 240 mg bid, bismuth subsalicylate 500 mg qid) can eradicate H. pylori and are also antacids. They increase gastric mucosal secretion of prostaglandins, bicarbonate, and glycoprotein mucus.
  • Surgery is indicated for perforation, gastric outlet obstruction, hemorrhaging, and patients who do not respond to medical treatments. To be considered in the aggressive treatment of GU if other therapies fail.

Complementary and Alternative Therapies

Nutritional and herbal support help to heal gastric mucosa, fight infection, and reduce recurrence. In addition, mind-body techniques such as meditation, progressive muscle relaxation, tai chi, yoga, and stress management may alleviate symptoms and enhance healing.


Nutrition
  • Avoid dairy, caffeine, alcohol, and sugar. Coffee, even decaffeinated, should be eliminated because of irritating oils.
  • Eliminate any known food allergens. Food allergies can be tested for using an IgG ELISA food allergy panel, or by an elimination diet.
  • Include sulfur-containing foods such as garlic, onions, broccoli, cabbage, brussels sprouts, and cauliflower in the diet. Sulfur is a precursor to glutathione that provides antioxidant protection to the gastric mucosa. N-acetylcysteine (200 mg bid) is also a precursor to glutathione.
  • Bananas contain potassium and plantain, both of which yield benefits.
  • Acidophilus (one capsule with meals) can help normalize bowel flora and inhibit H. pylori.
  • Essential fatty acids (1,000 to 1,500 mg bid to tid) reduce inflammation and inhibit the growth of H. pylori.
  • Vitamin C (1,000 mg tid) decreases nitrosamines which are linked to stomach cancer and inhibits H. pylori.
  • Zinc (30 to 50 mg/day) enhances healing.
  • Vitamin E (400 IU/day) enhances healing and provides antioxidant protection.
  • Vitamin A (50,000 IU/day for two weeks followed by 10,000 to 25,000 IU/day) for longer term maintenance.
  • Glutamine (500 to 3,000 mg tid) promotes healing of ulcers. Cabbage juice (1 quart/day) is high in glutamine, although it may initially be irritating.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

  • DGL (deglycyrrhizinated licorice), 250 mg qid 15 to 20 minutes before meals and one to two hours after last meal, increases local circulation and facilitates healing of the gastric mucosa. This preparation has most of the hypertensive factor of licorice root removed and is therefore safe to take long-term and in cases of hypertension.
  • Quercetin (250 to 500 mg before meals) or catechin (500 to 1,000 mg before meals) are flavonoids that reduce gastric inflammation and reactions to irritants and allergies.
  • Powders of slippery elm (Ulmus fulva) and marshmallow root (Althaea officinalis) may be taken singly or together, 1 tsp. bid to tid to decrease inflammation and encourage healing.
  • A soothing carminative tea taken before meals can reduce spasm and normalize digestion. Combine equal parts of three to six of the following herbs in a tea and sip before meals. Chamomile (Matricaria recutita), lemon balm (Melissa officinalis), catnip (Nepeta cateria), passionflower (Passiflora incarnata), meadowsweet (Filipendula ulmaria), peppermint (Mentha piperita), and valerian (Valeriana officinalis).

For H. pylori:

  • Bismuth subcitrate (120 mg qid for eight weeks) may be helpful in eradicating H. pylori and reducing recurrence of peptic ulcer disease. It is poorly absorbed, which decreases the likelihood of side effects; however, it is associated with neurotoxicity if used long-term. Combining it with barberry (Berberis vulgaris), goldenseal (Hydrastis canadensis), and/or Oregon grape (Berberis aquifolium) may potentiate its antimicrobial effects. Take one or more in tincture form, 30 to 60 drops tid.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

  • Argentum nitricum for abdominal distention with belching and violent splinter-like pains that radiate across abdomen. May crave sweets.
  • Arsenicum album for ulcers with intense burning pains and nausea. Patient cannot bear the sight or smell of food and is thirsty but only drinks in small sips.
  • Lycopodium for bloating after eating with burning that lasts for hours. Patient is hungry soon after eating and wakes hungry and irritable in the morning.

Acupuncture

Acupuncture may be helpful in reducing the effects of stress and improving overall digestive function.


Massage

Therapeutic massage can alleviate stress and increase sense of well-being.


Patient Monitoring
  • Patient compliance with triple therapy is often problematic.
  • GUs that do not heal in two to three months are potentially signs of malignancy, requiring endoscopic examination.

Other Considerations
Prevention
  • Smoking increases the risk of developing ulcers and delays ulcer healing.
  • Eliminate food allergies or foods that continually produce dyspeptic symptoms.
  • Eat a fiber-rich diet.
  • If symptomatic, avoid milk and caffeine, as they stimulate gastric acid secretion.
  • Limit use of NSAIDs, aspirin, and cortisone drugs.
  • Alcohol damages the gastric mucosal barrier.

Complications/Sequelae
  • Increased pain, vomiting of blood, tarry or red stools, and significant weight loss are indications of perforation, gastric outlet obstruction, or hemorrhaging, usually requiring surgery.
  • 2% to 5% of suspected GUs are actually ulcerated adenocarcinomas, or GUs that will develop into malignancies.

Prognosis
  • Mortality rates for ulcers complicated by perforation, gastric outlet obstruction, or hemorrhaging can be as high as 23%, especially in the elderly.
  • DUs—60% recur in a year, 80% to 90% within two years; but only 5% to 15% recur after treatment that eradicates H. pylori

Pregnancy
  • Amoxicillin—preferred drug
  • Tetracycline—U.S. FDA rating D, drug to be avoided during pregnancy; positive evidence of fetal risk for pregnancy and lactation
  • Bismuth compounds—no FDA rating but has warnings; high doses and prolonged use contraindicated
  • Metronidazole—contraindicated in first trimester; with caution after first trimester; carcinogenic and adverse effects for lactation
  • Nutritional guidelines and herbal support are safe in pregnancy. The effects of high doses of flavonoids in pregnancy are unknown. Do not use bismuth subcitrate in pregnancy.

References

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:427, 432.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Kruzel T. The Homeopathic Emergency Guide. Berkeley, Calif: North Atlantic Books; 1992:134-137.

Murray M, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:522-523.

Sabiston DC, ed. Textbook of Surgery. 15th ed. Philadelphia, Pa: WB Saunders Co; 1998.


Copyright © 2000 Integrative Medicine Communications

This publication contains information relating to general principles of medical care that should not in any event be construed as specific instructions for individual patients. The publisher does not accept any responsibility for the accuracy of the information or the consequences arising from the application, use, or misuse of any of the information contained herein, including any injury and/or damage to any person or property as a matter of product liability, negligence, or otherwise. No warranty, expressed or implied, is made in regard to the contents of this material. No claims or endorsements are made for any drugs or compounds currently marketed or in investigative use. The reader is advised to check product information (including package inserts) for changes and new information regarding dosage, precautions, warnings, interactions, and contraindications before administering any drug, herb, or supplement discussed herein.