| Age Range | Either Sex |
|---|---|
| All | 8 - 12 |
| Age Range | Either Sex |
|---|---|
| All | < 8[1] |
A positive test is highly predictive of the presence of chronic or active gastritis, but does not discriminate between ulcer and non-ulcer patients. On the other hand, a negative test result has a high predictive value for exclusion of ulcer and H.pylori related gastritis.
| Age Range | Either Sex |
|---|---|
| All | >= 13 |
Test performed 2 - 3 times a week.
Although the presence of antibodies to H.pylori is indicative of H.pylori infection in symptomatic individuals, antibody levels may remain high for some time following eradication of the organism.
A positive test is highly predictive of the presence of chronic or active gastritis but does not distinguish between ulcer and non-ulcer patients. Positive results should be confirmed by other diagnostic testing procedures.
A negative test result has a high predictive value for the exclusion of ulcer and H. pylori related gastritis.
Helicobacters are microaerophilic, spiral, motile, gram negative rods which are well adapted to live in a highly acidic environment. Following infection the bacterium invades the gastric tissue. Approximately 15% of patients infected with H.pylori will go on to develop gastric carcinoma.
H.pylori infection typically starts in childhood as an inflammatory process in the stomach and can exist in the gastric mucosa for decades without apparent symptoms or disease. Essentially all H.pylori colonised persons have gastric inflammation, but this condition in itself is asymptomatic. Although transmission of the organism appears to occur from person-to-person, the mode of transmission (either oral-oral or oral-faecal) is unknown. Symptoms which develop in fewer than 10% of individuals colonised with H.pylori are due to illness such as peptide ulceration or gastric malignancy. A subset of infected individuals go onto develop significant disease manifestations such as duodenal ulcer disease, gastric ulcer disease, gastric adenocarcinoma, and gastric lymphoma.
A number of special attributes ensure successful colonisation and adaptation of the bacterium in the gastric environment, and also stimulates the production of mediators of inflammation, which contribute to the physiological and histological changes observed in the host. These can be grouped into two groups:
Conserved among all strains:
- urease production and
- presence of flagellins and adhesins
Variable factors:
- cag (cyto toxin - associated gene)
- pathogenicity island (PAi)
- vacuclating cytotoxin (VacA) alleles
- iceA variants
- Lewis antigens
Tests for H.pylori can be divided into two groups:
Invasive:
- Biopsy urease test
- Histology
- Culture
Non-invasive:
- Serology
- 13 C of 14 C urea breath test
The simplest tests for H.pylori infection are serologic, involving the assessment of specific IgG levels in serum. In quantitative tests, a defined drop in antibody titre between matched serum samples taken before and 6 months after treatment (no sooner because of the slow decline in antibody titre) accurately indicates that H.pylori infection has been eradicated.
In 1994, the World Health Organisation classified H.pylori as a definite human carcinogen. This was based on a series of studies showing that: chronic gastritis is an important cancer precursor; gastric cancer occurs at an increased rate in regions with a high prevalence of H.pylori infection; people infected with H.pylori have a slightly higher risk of developing cancer than those without infection.
References
1. Kit insert
2. Clinical Laboratory International. Nov 2002 ; Vol 26 #7 . The relationship between Helicobacter pylori infection and adenocarcinoma . Dr Y Davies and Dr J Parsonnet.
3. Harrison?s Online. Helicobacter pylori Infections.
Dr Sally Roberts, Clinical Microbiologist: ext 22705 mobile: 021 674 140