Peptic Ulcers

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Peptic Ulcers are sores or lesions that form in the lining of the stomach, the duodenum, or, less frequently, the esophagus. Conventional wisdom for half a century has been that stress and diet caused ulcers, which triggered excessive acid secretion in the stomach. Treatment consisted of stress reduction, bland food, drugs to inhibit acid secretion or neutralize acids, or, if all else fails, surgery. Convincing research over the last decade has shown, however, that the majority of peptic ulcers are caused by an infection with the bacterium, Helicobacter pylori. When the treatment focuses on eradicating the infection, the cure rate for ulcers climbs to 80 % or better, compared with a cure rate of as low as 5% by previous methods.

 

Peptic Ulcers: Finally, Real Cures are Available

 

For more than a half a century, the medical community as well as the general public has a good idea what caused ulcers: stress, diet or other lifestyle factors that lead to excessive acid secretion in the stomach. This acid, as well as the digestive enzyme pepsin then irritated the lining of the stomach, the part of the small intestine known as the duodenum, or, less commonly, the esophagus. Treatment centered on reducing stress, eating bland food, and especially, taking drugs that would reduce acid secretion or neutralize the excessive acid that was produced.

 It was apparent; however, that that these treatments only dealt with the symptoms of ulcers, and not the underlying cause. Ulcers returned at the rate of about 50% over 6 months, increasing to as high as 95% over 2 years. Due to the long-term persistence of ulcers, the cost of acid blockers alone could run up to thousands of dollars over decades of care.

 This situation changed in 1984 when two Australian researchers, Barry Marshall, a resident in internal medicine, and Robin Waffin, a pathologist, isolated a spiral shaped bacterium from the tissues of ulcer patients. Dr. Marshall went on to propose the preposterous notion that ulcers was due to an infection by this organism, now known as Helicobacter pylori. At scientific meetings he was subjected to scorn and ridicule, but evidence in support of his hypothesis accumulated to the point that in 1994, a panel of medical experts recommended an antibiotic approach to treating ulcers. Dr. Marshall is know recognized as an eminent authority on the subject, and is a Nobel Prize nominee.

What are peptic ulcers?

 

Peptic ulcers are sores or lesions that form in the lining (mucosa) of the stomach, the part of the small intestine known as the duodenum, or less commonly, the esophagus. The name derives from the fact that these ulcers can occur where acid and pepsin are present. Stomach ulcers are also known as gastric ulcers.

 

How do ulcers develop?

 The stomach must present an environment that facilitates the digestion of food, while providing the means to protect itself from digestion. Lining the interior of the stomach is the mucosa, which consists of a layer of cells, connective tissue and muscle. Interspersed throughout the mucosa are the gastric glands, which contain three specialized types of cells that secrete the components of gastric juice: mucus-secreting cells, chief cells that release digestive enzymes, and parietal cells that produce hydrochloric acid. Acid is required to convert the enzyme pepsin to its active form. The secretion of mucus is the primary means by which the stomach protects itself against damage by acid. It forms a viscous layer over the mucosa, and is alkaline in nature, helping to neutralize the effects of the acid. The same mucus-secreting cells also secrete histamine, which then bind to histamine receptors in the parietal cells, stimulating the release of hydrochloric acid.

 How does Helicobacter pylori fit into this picture?  Other researchers thought that the organism Marshall and Warren found in the stomach was just a contaminant, since conventional wisdom held that bacteria could not survive and become established in the hostile environment of the stomach. However, H. pylori has several unique characteristics that permit it to thrive under such conditions. The organism lives under the mucus layer, often in grooves between cells, but does not actually invade the mucosa. This provides partial protection against attack by acid and pepsin. H. pylori further protects itself against stomach acid by secreting urease, an enzyme that helps break down urea into ammonia and carbon dioxide, the ammonia in turn neutralizes the acid. The spiral shape of the organism allows it to move readily and resist the muscle contractions that regularly empty the stomach. The organism, however, also commonly leaves the stomach to become established in the duodenum as well.

 After H. pylori has been established, it secretes toxins that causes inflammation of the stomach due to the immune response of the person. For 90% of infected people, this low-level inflammation, known as chronic superficial gastritis, can last a lifetime with little or no symptoms. Since the activities of the organism can lead to damage to the mucosa and a thinning and breakdown of the mucosal layer, the stomach lining is now exposed to attack by acids and pepsin. Ulcers can ensue, but in these cases stomach acid is a contributory factor, not a cause of the ulcer.

 There are other causes of ulcers. The use of non-steroidal anti-inflammatory drugs (NSAIDS) such as aspirin, ibuprofin, Toradol, Cytotec and Feldene can be extremely irritating to the stomach. These drugs interfere with the stomach’s ability to produce mucus and bicarbonate (an acid neutralizer), and can slow healing. Less commonly, patients with Zollinger-Ellison syndrome secrete excess acid that could lead to ulcers.

Current expert opinion holds that type of diet has no effect in either causing or curing ulcers. Emotional stress, likewise, is no longer thought to cause ulcers, although some people with ulcers report that stress increases ulcer pain.

Symptoms of Ulcers

 

The symptoms of peptic ulcers occur when the ulcer penetrates the underlying submucosa that is rich in nerves and blood vessels. Pain has been described as a burning, gnawing or aching in a well-defined area of the abdomen. The pain may come in waves, for three or four days at a time, but may subside completely for weeks or months. Sufferers with duodenal ulcers tend to experience a consistent pain pattern. It is absent when the patient awakens but appears by mid-morning. It is relieved by food, but recurs within two or three hours after a meal. Pain that awakens the patient at 1 or 2 AM is common. Patients with gastric ulcers may not exhibit this pattern, and eating may cause rather than relieve the pain. Gastric ulcers may also cause symptoms of obstruction, such as bloating after eating, or nausea and vomiting. Advanced cases of ulcers can lead to bleeding or actual perforations of linings (a medical emergency).

Diagnosis of Ulcers

 

Prior to treatment, it  must be ascertained if the ulcer is due to H. pylori infection or another cause. The common diagnostic procedures are as follows:

1.      Endoscopy – The patient is mildly sedated, and a lighted flexible tube is passed into the esophagus, stomach and duodenum. Tissues suspected of being ulcerous are sampled (biopsied) and cultured in the laboratory. The growth of H. pylori colonies is the definitive diagnosis. The test may overlook as many as 5 to 10 % of ulcers.

2.      Blood – Since infection with H. pylori stimulates the body to produce specific antibodies against the organism, the presence of these antibodies in the blood could indicate infection. However, false positives are possible, since the antibodies can persist in the blood for a month or more after the infection is eradicated.

3.      Breath – This test has a success rate at least as good as endoscopy, but is faster, cheaper, and less stressful to the patient. The patient drinks a solution of the drug Pranactin, which contains carbon-13 enriched urea, a naturally occurring compound. The urea then enters the stomach where the urease enzyme of H. pylori would break it down into by-products (if the organism were present). These by-products (which contain carbon-13) are then absorbed into the blood, and exhaled by the lungs. After a period of time, the patient exhales into a collection kit that is then analyzed for carbon-13. The detection of these by-products is a positive diagnosis, since the body does not produce urease.

 

Treatment of Ulcers

 If the ulcer is due to H. pylori infection, the standard treatment is to prescribe one or two antibiotics to eliminate the infection together with an acid blocker and possibly a mucosal protector (described below) to aid in healing the ulcer. Although this regimen may require taking as many as a dozen pills a day over two weeks, the ulcer is completely cured in 75 to 90 % of the cases. Common antibiotics used are clarithromycin (Biaxin), metronidazole (Flagyl), amoxicillin (Amoxil or Trimox) and tetracycline.

If the ulcer is due to another cause, antibiotic therapy is neither necessary nor desirable, since antibiotics can cause side effects such as diarrhea and stomach upset, and antibiotic resistance can develop. There are several types of drug treatments that can be prescribed in these cases, including H-2 blockers, acid pump inhibitors and mucosal protective agents.

1.      Histamine-2 (H2) receptor antagonists are currently in widespread use. These drugs act by binding to the histamine receptors in place of histamine, thus blocking the stimulus for release of hydrochloric acid. Common drugs in this class include ranitidine (Zantac), cimetidine (Tagamet), famotine (Pepsid), and nizatidine (Axid).

2.      Acid (or proton) inhibitors  act by blocking the enzyme responsible for release of hydrochloric acid by the parietal cells. These drugs, which include omeprazole (Prilosec) and lansoprazole (Prevacid), may be prescribed in situations where the H2 receptor antagonists are ineffective. This class of drugs has been found to be particularly useful in treating ulcers of the esophagus.

3.       Mucosal protective medications protect the stomach’s mucosal lining from acid, but do not inhibit the release of acid. They include:

1.      Sucralfate (Carafate) – This medication adheres to the ulcer, providing a protective barrier that allows the ulcer to heal.

  1. Misprostol (Cytotec) – This drug is approved only for prevention of NSAID-induced ulcers. It counteracts the effect of NSAID drugs by increasing mucus and bicarbonate production and by enhancing blood flow to the stomach.
  2. Bismuth subsalicylate (Pepto-Bismol) – This common non-prescription drug can have a protective effect similar to sucralfate, and can also have an  antibacterial effect against H. pylori.
  3. Antacids – Many non-prescription brands are available that offer temporary relief from ulcer pain by neutralizing stomach acid. They also may have a mucosal protective role.


Further Reading

1.      Kenneth Alper. “Ulcers as an Infectious Disease,” Science, 1993, Volume 260, pages 159-160.

  1. Martin l. Blaser. “The Bacteria behind Ulcers,” Scientific American, February 1996, pages 104-107.
  2. “A Breakthrough in Ulcer Treatment,” Tufts University Diet and Nutrition Letter, 1996.
  3. “Focus on…Peptic Ulcer Disease,” Medical Sciences Bulletin, Pharmaceutical Information Network, http://pharminfo.com
  4. Peptic Ulcer, Disorders of the Stomach and Duodenum, The Merck Manual, 1996

Merck & Co., Warehouse Station, NJ

  1. “Stomach and Duodenal Ulcers,” National Institutes of Health Publication No.

95-38, January 1995.

  1. Terence Monmaney. “Marshall’s Hunch,” The New Yorker, September 20, 1993,

Pages 64-72.

Resource Item

American Digestive Health Foundation

1201 Connecticut Ave., NW, Suite 300

Washington, D.C. 20036

1-800-NO-ULCER

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