In the GastroPanel® test, the concentrations of four biomarkers are determined from a blood sample. The biomarkers: pepsinogen I (PGI), pepsinogen II (PGII) and gastrin-17 (G17), which are secreted by the cells in gastric mucosa, are measured. Additionally, Helicobacter pylori antibodies are measured.
An overall interpretation of all four biomarker results provides a more reliable and comprehensive understanding of the structure and function of the gastric mucosa than could be achieved using the individual biomarkers separately.
The GastroPanel® report is a written statement that describes the test results and classifies the findings as one of the five diagnostic outcomes: normal (healthy) stomach, H. pylori infection, atrophic antrum gastritis, atrophic corpus gastritis and atrophic pangastritis (antrum and corpus).
Biomarker reference ranges
The reference ranges (=normal values) of the four biomarkers, have been determined on Finnish people, analyzed at the Biohit Laboratory.
Also, multiple published clinical studies on these markers, incorporating endoscopic mucosal biopsy assessment, are consistent with these settings.
GastroPanel report by GastroSoft™
The GastroPanel® report is a tool designed to assist doctors in interpreting GastroPanel® test results. The report contains the biomarker results (including the cut-off values) and a brief interpretation of the results. The interpretation provides information on the structure and function of gastric mucosa, including any changes in acid secretion and associated risks. Where relevant, the report also provides recommendations for helicobacter eradication therapy or gastroscopy.
|Pepsinogen I (PGI)
|30 - 160 µg/l
|Pepsinogen II (PGII)
|3 - 15 µg/l
|3 - 20
|1 - 7 pmol/l
|3 - 30 pmol/l
|H. pylori IgG (HPAbG)
|< 30 EIU
* GastroPanel® reference values may be subject to changes following new clinical trial data. The above values are based on the results at Biohit Laboratory.
Helicobacter IgG antibodies (H. pylori IgG)
Helicobacter pylori nests on gastric mucosa of an infected person. It is usually transmitted in childhood and causes an infection (inflammation, gastritis). If left untreated, the infection becomes chronic and persists for life. The infection is very common in older age groups and it increases the risk of duodenal or gastric ulcers. For some patients, Helicobacter pylori infection causes gastric mucosal atrophy and dysfunction (atrophic gastritis). Atrophic gastritis is usually asymptomatic, and it causes the stomach to become acid-free, where oral microbes are able to live and produce a carcinogenic acetaldehyde from sugars and alcohol. Although Helicobacter pylori infection can be treated, an acid-free stomach rarely recovers, and this poses a significant risk of developing stomach and oesophageal cancer. Acid-free stomachs are associated with malabsorption of vitamin B12, iron, magnesium, calcium, zinc and certain drugs. Calcium deficiency causes osteoporosis and deficiency of vitamin B12 can cause anaemia, dementia, depression and peripheral nervous system damage. Performing Endoscopy on individuals suffering from atrophic gastritis may help to diagnose stomach cancer at an early stage, when the prognosis of gastric cancer significantly improves. Infection with Helicobacter pylori is likely when the antibody level is more than 30 EIU. When eradication therapy of Helicobacter pylori is completed, it may take several months before the antibody levels return to normal after successful eradication therapy.
Pepsinogen I (PGI)
Pepsinogen I concentration in blood reflects the mucosal structure and function of the gastric body (corpus). Infection with Helicobacter pylori or autoimmune disease can cause moderate to severe atrophy of stomach body mucosa (atrophic gastritis of corpus). Then follows a fall in blood pepsinogen I levels below 30 µg/l, and the associated acid-free or low-acid stomach. In contrast, if the patient has inflammation of stomach body mucosa, but no atrophy (gastritis of corpus), the blood pepsinogen I concentration tends to increase to some extent.
Pepsinogen II (PGII)
Pepsinogen II concentration in blood reflects the structure and function of whole stomach mucosa. Its concentration in blood circulation increases in the case of stomach mucosal inflammation (gastritis). In most cases the reason for this is a Helicobacter pylori infection, but sometimes other factors are involved such as some drugs, bacterial, viral or parasitic infections, biliary reflux (rise of bile acids from the intestine to the stomach), strong spices or alcohol. Values more than 10 µg/l often refer to inflammation.
Pepsinogen I/Pepsinogen II (PGI / PGII)
The Pepsinogen I/II ratio is used together with Pepsinogen I value for diagnosis of atrophy of the gastric body mucosa (atrophic gastritis of corpus). In the case of atrophic gastritis of corpus, the ratio decreases below 3.
Basal Gastrin-17 (G-17b)
The Gastrin-17 concentration in blood reflects the integrity and function of the lower part of the stomach (the antrum). Gastrin17 is secreted exclusively from G-cells of the antrum and duodenum. Biohit's monoclonal antibody only measures the biologically active amidated Gastrin-17 peptide (sulphated and non-sulphated), having a specific receptor on the surface of enterochromaffin-like cells (ECL) (cholecystokinin receptor, CCK2R). On the effect of Gastrin-17 stimulates the ECL cells to release histamine into the blood circulation, which seeks the histamine receptor on the surface of the parietal cell, and stimulates secretion of hydrochloric acid from them. The Gastrin-17 concentration in blood (during fasting) will fall when the acidity of the gastric contents rises (pH below 2.5) (less than 1 pmol/l refers to increased secretion of hydrochloric acid). The Gastrin-17 value during fasting also falls in case of the antrum mucosal atrophy, where G-cells disappear. Low gastrin-17 levels in blood during fasting may therefore indicate either an increased secretion of hydrochloric acid or antrum mucosal atrophy (antrum mucosa atrophy, however, is dependent upon infection with Helicobacter pylori). If the Gastrin-17 concentration is above 7 pmol/l, it is usually because of decreased secretion of hydrochloric acid; a slight decrease (7 – 10 pmol/l), hypochlorhydric stomach (10 -20 pmol/l), achlorhydric stomach (over 20 pmol/l) (PPI medication or atrophy limited to corpus mucosa) or inflammation of antrum mucosa (antrum predominant gastritis, see PGII).
Increased secretion of hydrochloric acid may increase the risk of, and complications of gastroesophageal reflux disease. In the case of reflux disease (heartburn), stomach contents are regurgitated into the oesophagus, particularly if muscle of lower oesophageal sphincter (LES) is weak. This could result in ulcerative esophagitis, and so-called Barrett's esophagus, which if untreated are risk factors of oesophageal cancer.
Stimulated Gastrin-17 (G-17s)
The main accelerators of Gastrin-17 secretion are vagal tonus, gastrin-releasing peptide hormone, stretching of gastric antrum and protein-rich food. Distinguishing between antrum mucosal atrophy caused by Helicobacter pylori infection and increased secretion of hydrochloric acid (gastrin17 basal <1 pmol/l) can be performed by gastroscopy (preferred) or by measuring the response of gastrin-17 after protein stimulation. If person has been infected by H.pylori and the gastrin-17 value is still low after protein stimulation (less than 3 pmol/l) it may indicate atrophic gastritis in antrum. However, if H.pylori antibody levels are not elevated, the results indicate increased secretion of hydrochloric acid.
Proton pump inhibitors (PPI) and biomarkers (GastroPanel)
Proton pump inhibitors reduce the secretion of hydrochloric acid from parietal cells. The drug metabolite binds irreversibly to the parietal cell proton pump. When the concentration of hydrochloric acid in the stomach decreases, gastrin-17 secretion increases. It has a trophic effect on the cells secreting pepsinogen in the stomach mucosa, whereas pepsinogens I and II levels in the blood circulation will rise and remain high for a rather long time. The half-life of proton pump inhibitor is about 18 hours, so it will take 4-10 days before the secretion of hydrochloric acid returns to the normal level after treatment. Because of the active feedback system, the gastrin-17 concentration is reduced at the same time (in 4-10 days). Therefore, gastrin-17 is a very good non-invasive marker of acid secretion regulation. Stopping long-term PPI therapy follows with very strong "acid surge", when patients gets very strong heartburn again (gastrin-17 level is generally very low, less than 1 pmol/l).