- H. Pylori infection represents up to 20% lifetime chance of peptic ulcers and 2% chance of Gastric Cancer
- Stool antigen over 95% sensitive and 94% specific for detecting H. Pylori infection (unlike that of serum antibody which has poor sensitivity)
The awareness of Helicobacter pylori in gastrointestinal diseases has increased greatly since Marshall and Warren described the presence of
Campylobacter-like organisms in the antral mucosa of patients with histological evidence of antrum gastritis and peptic ulcers, especially duodenal ulcers. The strong correlation between the presence of H. pylori and histologically confirmed gastritis, peptic ulcer disease and gastric carcinoma, as well as disease resolution after H. pylori eradication, indicates a causative relationship.
The ecological niche in humans appears to be restricted to the stomach and duodenum. Patients who harbour the organism are divided into two basic groups: a) colonised and b) infected. Patients who test positive for H. pylori yet have no signs or symptoms of gastrointestinal disease are considered “colonised”. Patients who test positive for H. pylori and present with signs or symptoms of gastrointestinal disease are considered “infected”. The process by which a colonised individual becomes infected remains unclear. The process by which patients become colonised is also still under investigation. Direct detection requires that an invasive biopsy be taken from the upper gastrointestinal tract. The presence of H. pylori is then confirmed by direct microscopic examination, rapid urease testing or culturing of the organism from the biopsy material. This strategy has the advantage of being able to detect active infections while being highly specific with a very high positive predictive value. The invasive approach subjects the patient to unnecessary risk and discomfort.
In contrast, Doctor’s Data, Inc. offers the non-invasive HpSA enzyme immunoassay (EIA), an in vitro qualitative procedure for the detection of H. pylori antigens in human stool. Test results can be used to diagnose H. pylori infection, and to monitor patient response during and post-therapy. Current scientific literature indicates that testing to confirm eradication should be performed at least four weeks after the completion of therapy.
- About 20% of Adult Australians are infected with H Pylori. (WGO 2010)
- Over 80% of those infected with H. pylori show no symptoms.
- Acute infections may appear as an acute gastritis with abdominal pain or nausea.
- H. pylori has been proposed to induce inflammation and locally high levels of TNF-? and interleukin 6 (IL-6).
- Those individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer.
- Over 90% of all patients with duodenal ulcer (and approximately 70% of those with gastric ulcer) are infected with H. Pylori.
- A meta-analysis conducted in 2009 concluded that the eradication of H. pylori reduces gastric cancer risk in those previously infected with H. Pylori.
- Colonisation with H. pylori is not a disease in and of itself but more a condition associated with a number of disorders of the upper gastrointestinal tract.
- Testing for H. pylori is recommended in those presenting with persistent dyspepsia, peptic ulcers, early gastric cancer, or any first degree relatives with history of gastric cancer.
H. Pylori Testing Options
The gold-standard method for detecting H. pylori infection is via biopsy during endoscopy with a rapid urease test, histological examination, and a microbial culture. However non-invasive methods for testing for H. pylori infection include blood antibody testing, stool antigen test, or with the carbon labelled urea breath test.
But no tests are completely fail-safe and the reliability of each test varies. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, rely on correct identification and handling by the immune system and due to variances in lab processes for detecting any potential antibodies, sensitivity ranges widely around 78% with an overall positive predictive value of 64% according to the WGO (2010). Finger-stick blood antibody testing has been shown to have little usefulness.
Stool antigen testing however is specified by the WGO (2010) to be 95% sensitive and 94% specific for accurately detecting the presence of H. Pylori cell fragments (rather than blood antibodies which may or may not be present) in all individuals that are unable to receive a endoscopy/biopsy and is therefore the choice of FxMed for accurately and reliably qualifying the presence of H. Pylori.
H. Pylori Treatment/Eradication Strategies
Standard pharmaceutical treatment in those high risk patients confirmed to have H. Pylori infections includes Triple and Quadruple Antibiotic therapy dependant on potential risk of Antibiotic resistance.
Some natural agents shown to be effective for inhibiting H. Pylori populations include:
- Glycine (and assists effectiveness of antibiotics)
- N-Acetyl-Cysteine (reduces H. biofilm resistance)
- SGS (Broccoli Sprout Glycosinolates yield anti H. Pylori Sulphorophane)
- Ascorbic Acid
- Sufficient Iron Status (“iron deficiency enhances H. pylori virulence ”Noto et. al. 2013)
- Manuka Honey
- Mastic Gum