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Helicobacter Pylori


Helicobacter pylori (H. pylori) is a spiral bacteria that specifically and selectively resides beneath the mucus layer next to the stomach (gastric cells).


Helicobacter pylori infection has been associated with the occurrence of gastritis and peptic ulcers. Chronic H. pylori gastritis is a strong risk factor for stomach cancer. However, less than one percent of chronically infected individuals will develop stomach cancer.

In the past, one of the strongly held notions is that acid is the primary cause of duodenal ulcers. Indeed, the term acid peptic disease reflects the prevailing concept of cause, so therapy is aimed primarily at blocking acid.

However, it now appears that an even more important factor may be responsible for some ulcers (at least duodenal ulcers) - infestation with Helicobacter pylori.

Two important lines of evidence now support a possible causal role. First, H. pylori is present in the antrums of 9 to 95 percent of persons with a duodenal ulcer who do not use nonsteroidal anti-inflammatory drugs (NSAIDs) or do not have Zollinger-Ellison syndrome as a possible cause of ulcer.

Second, treatment and eradication of H. pylori dramatically reduces the frequency of ulcer recurrence compared with treatment of acute ulcers by histamine blockers alone. Therefore, H. pylori appears to be a necessary cofactor for the overwhelming majority of duodenal and gastric ulcers not associated with NSAIDs.

H. pylori is transmitted from person to person, but nobody knows by what means. In the U.S., the prevalence of infection rises from less than 10 percent in Caucasians under age 30 to over 50 percent in those over age 60. The prevalence is higher in non-Caucasians and immigrants from developing countries. The majority of infections are probably acquired in childhood.


Acute infection with H. pylori may cause a transient clinical illness, characterized by nausea and abdominal pain that may last for several days. After these symptoms resolve, the majority of people progress to chronic infection.

There is no recognizable symptom complex or syndrome that can be ascribed to chronic gastritis, whether or not due to H. pylori.

Peptic ulcers often present with dyspepsia (upper mid-abdominal pain or dull gnawing). There may be pain at night. Some patients report relief of pain with food or antacids and a recurrence of pain in two to four hours.


H. pylori is detected by a variety of means. At endoscopy (viewing the stomach and duodenum via a lighted tube), a biopsy of gastric (stomach) mucosa can be taken and assessed for H. pylori. Antibodies to H. pylori can be detected by blood tests. Non-invasive breath tests also can detect active infection with H. pylori.


Eradication of H. pylori generally requires a combination of antibiotics and an acid-blocker/proton pump inhibitor. One example for active H. pylori-associated ulcers is (1) clarithromycin, (2) amoxicillin or metronidazole, along with (3) omeprazole or lansoprazole.

Another regimen is (1) omeprazole or lansoprazole, (2) bismuth, (3) tetracycline, and (4) metronidazole.

Current regimens should achieve greater than 85 to 90 percent rates of eradication after one to two weeks of treatment. Once cure has been achieved, reinfection rates are less than 0.5 percent per year. Management of peptic ulcers in some patients may require maintenance treatment.


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