GastroPanel information

Summary of the data provided by the GastroPanel examination and the ¹³C- urea breath – or stool antigen test. The GastroSoft program supplies a patient report. The reports produced by GastroSoft are based on clinical studies comparing the results of GastroPanel examinations with results from gastroscopy and biopsy specimen examinations. The serious medical and ethical problems can be simply and economically corrected by replacing the ¹³C- urea breath- or stool antigen test by the GastroPanel examination.

(1) The 13C- urea breath - and stool antigen tests give 40 – 50 % false negative results if the patient has a) atrophic gastritis and realated risks, b) MALT lymphoma or c) bleeding peptic ulcer disease or d) if the patient is currently receiving antibiotics or PPIs (proton pump inhibitors). The GastroPanel H. pylori IgA & IgG antibody test combination does not have these types of false negative results.

(2) The risk of gastric cancer is very low without atrophic gastritis in corpus, antrum or both. But in some cases, a H. pylori infection without histologically observable atrophic gastritis may be associated with gastric cancer and peptic ulcer disease.

(3) No peptic ulcer disease with corpus atrophy (no acid, no ulcer). The risk of peptic ulcer disease is very low without antrum atrophy.

(4) Normal or high pepsinogen I and / or pepsinogen I and pepsinogen II ratio in association with low gastrin-17 (below 1,0 pmol /l) may indicate high acid (HCl) output and risks for the complications of gastroesophageal reflux disease (GERD).

(5) When the incidence of H. pylori -related atrophic gastritis is monitored, the patient can be offered targeted, safe treatment at the right time. The need for medication and the costs and adverse effects of medication can thus be reduced. If the patient has been diagnosed with peptic ulcer disease (gastric or duodenal ulcer), the H. pylori infection has to be treated (6). It should also be treated if the patient has atrophic gastritis. The patient and the doctor may also agree on eradication treatment for other reasons for example when the patient's close relatives have been diagnosed with gastric cancer.

(6) Press Release: The 2005 Nobel Prize in Physiology or Medicine, 3 October 2005 jointly to Barry Marshall and J. Robin Warren for their discovery of "the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease": - "An indiscriminate use of antibiotics to eradicate Helicobacter pylori also from healthy carriers would lead to severe problems with bacterial resistance against these important drugs. Therefore, treatment against Helicobacter pylori should be used restrictively in patients without documented gastric or duodenal ulcer disease." http://nobelprize.org/medicine/laureates/2005/press.html

(7) Adequate absorption of dietary calcium requires normal acid secretion that is impaired in atrophic gastritis and in long term PPI therapy. Subsequently, calcium is not absorbed normally in the gut, and the subjects are at risk for osteoporosis and hip fracture. Hypochlorhydric states such as atrophic gastritis and partial gastrectomy have long been known to cause iron deficiency anemia.

(8) Pepsinogen II level below 10 µg /l two months after the treatment indicates that the H. pylori eradication is succeeded. Increased level of pepsinogen II (over 10 µg /l) indicates active H. pylori gastritis or inflammation due to the use of non-steroidal anti-inflammatory drugs (e.g. aspirin) or strong alcohol. Dig. Liver Dis. 2005 Jul; 37(7):501-8. Epub 2005 Apr 18.