Helicobacter pylori?

A bacterium that appears to be linked to the occurrence of duodenal ulcer and gastritis has been highlighted. It is a spiral germ and flagellate which is causing an increase in gastrin secretion, so peptic acidity. This induces the formation hyperacidity in the stomach duodenum beaches METAPLASIA. The germ can fix and causes chronic duodenitis of which may form an ulcer.

Certainly, other risk factors are obvious (smoking, alcohol, stress), but the bacteria act as a cofactor.

It seems that the poultry is a major source of the infection, but other sources have been identified, cattle, water, milk.

A test has been developed by the Institut Pasteur to detect this bacterium called Helicobacter pylori and Campylobacter pylori. This test is based on the technique of gene amplification from an endoscopic biopsy (see ENDOSCOPY).

In addition, other methods, serological in particular, are especially developed for the diagnosis.

It is to look for Helicobacter pylori IgG antibodies in serum or whole blood, knowing it takes a few weeks after infection for these serological tests become positive

These serological tests are not a good way to highlight reinfestation because then positivity can be a simple "scar" HIV old.

Finally it should be noted that it is possible for the presence of the germ in the air exhaled by a quite peculiar way: it is the breath test urea labeled with carbon 13.

It seems germ responsible for duodenal ulcer and especially relapse. The rate of recurrence of duodenal ulcer is much more common when we find the seed at the pylorus. The virulence of this organism is related to its mobility in the mucus and the existence of a ulcerogenic toxin it secretes.

This germ is found:

- In 90% of patients with duodenal ulcer and stomach ulcer

- In 70% of patients with ulcer induced by anti-inflammatory non-steroidal stomach.

- In 30% of adults over 50 years carrying non-ulcer dyspepsia.

- In 80-90% of patients with chronic gastritis.

- Reach For many patients with gastric cancer and gastric malignant lymphoma.

It seems that the eradication of gastric germ would prevent this type of cancer.

Antibiotic treatment to eradicate Helicobacter pylori is simple and very effective in 90% of cases.

We now know that no gastric cancer can develop in the absence of this organism.

- The germ could be involved in SUDDEN INFANT DEATH SYNDROME (see this term)

This germ is present especially in developing countries where 60% of the population is reached at the age of 10 years. However, the vast majority of carriers of the germ never develop ulcers.

Recent studies have demonstrated the beneficial effects of eradication of the germ on ulcer healing and rebleeding. Moreover, the destruction of significantly reduced the relapse rate ulcerative germ.

TREATMENT

The administration of a tri-antibiotic for 14 days (amoxicillin + macrolide or metronidazole for example) associated with antisecretory treatment (eg an inhibitor of the proton pump: LANZOR, Mopral, Ogast or Zoltum, Pariet) currently seems the therapeutic approach of choice, taking antibiotics to be preferably after meals.

For example:

- Clarithromycin 500 mg morning and evening or amoxicillin 1g morning and evening.

- Omeprazole 20 mg morning and evening or lansoprazole 30 mg morning and evening or pantaprazole 40 mg morning and evening

- Metronidazole 500 mg morning and evening or tinidazole 500 mg morning and evening

This regimen is to respect scruipuleusement for 14 days.

Tobacco is a failure of this drug combination factor.

It also appears that the administration of a tri-antibiotic similar to that used in duodenal ulcer is also beneficial in the treatment of non-ulcer dyspepsia (which would be a factor in gastric carcinogenesis, that is to say, would promote occurrence of cancer of the stomach).

Moreover, it appears that this bacterium is involved in the occurrence of certain cerebrovascular accicents especially those occurring in atheroma.

Indeed this bacteria in the digestive tract is also present in the blood, where it is associated with inflammation of the arterial wall in particular ds carotid level.

The toxicity of the arterial wall is due to the presence of a gene (cyto-toxin-associated gene-A) CagA.

This reinforces the hypothesis of the role of infectious agents in the weakening of the plaque.

PREVENTION

It relies on strict hygiene measures for the contagiousness is generally oral-oral or fecal-oral route. It is also worth noting the possibility of nosocomial infection (see CONDITIONS NOSOCOMIAL), in particular the role of the endoscope inadequately sterilized between each patient.