hEALTH

INTESTINAL TRACT

Infection with Helicobacter pylori

The bacterium Helicobacter pylori which lives in human stomachs is a chief cause for gastritis and ulcer. It can be eradicated with a medication combining two antibiotics and an antacid. Many people harboring Helicobacter do not show any symptoms.

Why do some people have symptoms caused by H. pylori, and others do not?

While many people are infected with Helicobacter pylori, only some of them show clinical disorders, e.g. inflammation of the gastric mucosa. One possible explanation for this surprising fact may be the occurrence of different strains of this pathogen: only some strains have a kind of pin that they use to inject molecules into stomach cells, thereby triggering an inflammatory response of the host. In detail, H. pylori delivers a peptidoglycan called cag pathogenicity island (cagPAI) into epithelial cells. There it is recognized by an intracellular pathogen recognition molecule called Nod1. However, the researchers assume that this is not the only mechanism leading to the inflammation, but likely the most important. And one remaining question is: why does Helicobacter do this?

Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island.
Viala J, Chaput C, Boneca IG, Cardona A, Girardin SE, Moran AP, Athman R, Memet S, Huerre MR, Coyle AJ, DiStefano PS, Sansonetti PJ, Labigne A, Bertin J, Philpott DJ, Ferrero RL.
Nat Immunol. 5: 1166-74 (2004).

Use of gastric acid-suppressive drugs may augment risk of pneumonia

Many people use drugs such as proton pump inhibitors (PPIs, e.g. Omeprazole) and H2-receptor antagonists (e.g. Ranitidine) to suppress excessive gastric acid. In a study comprising more than 360,000 people, an association between an increased risk of pneumonia (about 27 %) and use of these drugs has been observed. This could be due to the elevated pH in the stomach, resulting in an incomplete killing of pathogens - stomach acidity is a major defense mechanism against ingested pathogens. Because the respiratory tracts are close to the esophagus, the risk increases; however the risk is relatively small.

Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs.
Laheij RJ, Sturkenboom MC, Hassing RJ, Dieleman J, Stricker BH, Jansen JB.
JAMA 292: 1955-60 (2004).

Helicobacter may also trigger stomach cancer

Blood samples of more than 2,000 people were investigated. 70 % of the samples from people suffering from stomach cancer also possess antibodies against Helicobacter. This raises evidence for a causal effect of Helicobacter infections and cancer. However, for ischaemic heart disease, no correlation was found.

Helicobacter pylori infection and mortality from ischaemic heart disease: negative result from a large, prospective study.
Wald NJ, Law MR, Morris JK, Bagnall AM.
BMJ 315:1199-201 (1997).

Breath test as a safe diagnosis method

The diagnosis of a Helicobacter infection is done by gastroscopy. A non-invasive breath test may be a more convenient examination. Researcher found that both test methods show comparable results in detecting Helicobacter.
More than 700 patients with stomach problems were examined by either a breath test, or a breath test followed by gastroscopy. One year later, the diagnosis was revised. The breath test was as effective and safe as endoscopy and less uncomfortable and distressing for the patient.

Randomised trial of endoscopy with testing for Helicobacter pylori compared with non-invasive H pylori testing alone in the management of dyspepsia.
McColl KE, Murray LS, Gillen D, Walker A, Wirz A, Fletcher J, Mowat C, Henry E, Kelman A, Dickson A.
BMJ 324: 999-1002 (2002).

New active substance against Helicobacter

An ingredient from broccoli may act as a useful drug against Helicobacter. The substance sulforaphane displays antibiotic-like characteristics even against bacteria hiding in cells, which are hardly reached by drugs. In addition, Helicobacter shows an increasing resistance against antibiotics. As a consequence, only 80 % of Helicobacter infections could be eradicated by the standard antibiotics therapy.
If sulforaphane will be also convincing in clinical trials, it may be applied as an additional weapon for the treatment of the stomach bacterium.

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors.
Fahey JW, Haristoy X, Dolan PM, Kensler TW, Scholtus I, Stephenson KK, Talalay P, Lozniewski A.
Proc Natl Acad Sci U S A 99: 7610-7615 (2002).

Gastritis caused by other bacteria than Helicobacter - use antibiotics!

When the acid production of the stomach is abolished, other bacteria than Helicobacter may also lead to gastritis and stomach ulcer. In the normal case, the high acidity of the gastric juice kills bacteria which are ingested by food. The hormone gastrin regulates the acid production of the stomach mucosa. Knock-out mice lacking the gene for gastrin developed gastritis, caused by a bacterial overgrowth and subsequent inflammation of the stomach. The same happened when the proton pump inhibitor (PPI) Omeprazole was applied, which switches off the acid production completely.
The researcher conclude that it is preferred to medicate (non-Helicobacter) gastritis with antibiotics instead of PPI to remove the real cause, the bacterial infection. This also reconstitutes the normal regulation of acid production.
Treatment with other antacids like Ranitidine is less problematic than with PPI, because these do not suppress acid production completely.

Genetic or chemical hypochlorhydria is associated with inflammation that modulates parietal and G-cell populations in mice.
Zavros Y, Rieder G, Ferguson A, Samuelson LC, Merchant JL.
Gastroenterology 122: 119-33 (2002).

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