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Interpretation of the results

INTERPRETATION OF GASTROPANEL RESULTS

GASTROPANEL AND DIAGNOSIS OF STOMACH CONDITIONS

GastroPanel gives information on the structure and function of the stomach mucosa, and of the risks caused by a possible abnormal mucosa. Based on the GastroPanel results, it is possible to get information to support the diagnosis of:

  • Healthy stomach mucosa.
  • Functional and organic dyspepsia (when GastroPanel results indicate a healthy stomach mucosa, the cause of stomach problems is often functional dyspepsia or a disease outside the stomach).
  • Atrophic gastritis (damaged stomach mucosa that is severly dysfunctional) and likelihoods of the conditions specifically in the corpus and antrum areas of the stomach (normal, gastritis or atrophic gastritis).
  • Helicobacter pylori infection.
  • Acidity of the stomach.

When required, GastroSoft report gives recommendations on:

  • Gastroscopy and biopsy examination
  • Treatment of H. pylori infection 
  • Taking into account risks of acidic stomach (gastroesophageal reflux disease, GERD, and its complications).

GastroPanel examination is also well suitable for the follow-up of the success of H. pylori and/or atrophic gastritis treatment.

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INFORMATION PROVIDED BY TEST RESULTS

The four tests of the GastroPanel examination provide information as follows:

  • Pepsinogen I - provides information on Corpus mucosa 
  • Pepsinogen II - provides information on whole mucosa
  • Gastrin 17 - provides information on Antrum mucosa
  • H.Pylori - provides information on Helicobacter pylori status

The expected range (clinical decision making criteria) in the table below is based on clinical studies on dyspeptic patients. If a measured value falls out of these ranges, it indicates abnormal result; a value which is seldom found from normal healthy stomach not using any drugs such as PPIs and NSAIDs.

 Assay

 Expected range

 Pepsinogen I

 30 - 165 µg/l

 Pepsinogen II

 3 - 15 µg/l

 PGI/PGII-ratio

 3 - 20

 Gastrin-17 stimulated

 5 - 30 pmol/l

 Gastrin-17 basal

 1 - 10 pmol/l

 HPABG  0 - 30 EIU
Table 1. GastroPanel assay expected range. The values are subject to change on new clinical studies and information.
 
In general, the results of the GastroPanel examination tests can be used to conclude the following.
 
Pepsinogen I (PGI) and Pepsinogen II (PGII)
Low PGI or PGI/PGII ratio indicates corpus atrophy. The lower the value, the more probable and more severe is the atrophy. The risk of Vitamin B12 deficiency, and the related risk of increased homocysteine level, must be taken into consideration when atrophy is diagnosed. Corpus atrophy can also cause deficiency of e.g. iron, calcium and zinc. Corpus atrophy means that the stomach has no/ very little acid.

Ongoing PPI (proton pump inhibitor) treatment can cause increased pepsinogen levels, which has not effect on health.

Gastrin-17 (G-17)
Low fasting gastrin-17 value may indicate antrum atrophy and/or high acid secretion from the corpus. The cause of low gastrin-17 can be tested with the aid of protein stimulation. In the case of antrum atrophy, gastrin-17 level will not rise to over 5 pmol/L following the stimulation. In the case of high stomach acid secretion, gastrin-17 level will rise to over 5 pmol/L. Antrum atrophy causes increased risk of gastric cancer and peptic ulcer disease, and it is always linked with Helicobacter pylori infection. High acid secretion, in turn, causes increased risk of gastroesophageal reflux disease (GERD) and its complications (e.g. Barrett’s espophagus).

Elevated gastrin-17 level may confirm diagnosis of corpus atrophy. Stomach acid downregulates gastrin-17 level, and in corpus atrophy, the level of acid is very low.

Ongoing PPI treatment may also increase gastrin-17 value, which has no effect on health.

Helicobacter pylori (H. pylori) antibodies (HpAbG)
A high H. pylori antibody level indicates H. pylori infection. If the patient has recently received H. pylori eradication treatment, the antibody levels may stay up for some time even after a successful treatment. Follow-up of the antibody levels ensures that H. pylori eradication treatment has worked (the titer of H. pylori antibodies will decrease approximately 50% per every half a year).

H. pylori infection increases risk of e.g. atrophic gastritis and peptic ulcer disease.

 

 PGI

PGII

 PGI/II

 G17B

 G17S

 HPABG

 Atrophic gastritis in corpus

 low

 low

 high

 Atrophic gastritis in antrum

 low

 low

 high

 Atrophic gastritis in antrum/corpus

 low

 low

 low

 low

 Non-atrophic gastritis

 high

 Non-atrophic gastritis, H.pylori infection

 high

 high

 Gastroesophageal reflux disease (GERD)

low

Table 2. How GastroPanel paramaters tends to behave in different cases.

Interpretation can be carried out based on the expected range according to the general information provided by table 2, however, Biohit provides a software tool, GastroSoft, to generate a report with interpretation of gastropanel results in selected language. For more information, please contact Biohit sales personnel or email info@biohit.com.

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Recent clinical evaluations at the Jorvi Hospital in Finland comparing the test panel: H. pylori Ab, Pepsinogen I and Gastrin-17 with gastroscopy and biopsy have demonstrated a sensitivity of 89% and a specificity of 93% which is comparable with the results of the histological examination. Additionally, the accuracy of gastroscopy is improved when used in conjunction with the test panel because the clinician  can benefit the information of the type, severity and location (in antrum, corpus or both) of atrophic gastritis.

The diagrams below depict from the results of the biochemical investigations how an assessment of the risk of peptic ulceration and gastric cancer can be determined.

References

  1. Varis K., Samloff I.M., Ihamäki T., Siurala M. An Appraisal of Tests for Severe Atrophic Gastritis in Relatives of Patients with Pernicious Anaemia. Dig Dis Sci 1979; 24:187-191.
  2. Sipponen P., Kekki M., Haapakoski J., Ihamäki T., Siurala M. Gastric cancer risk in chronic atrophic gastritis; statistical calculations of cross-sectional data. Int J Cancer 1985; 35:173-177.
  3. Wadstrom T. (1995). An Update on Helicobacter pylori . Current Opinion in Gastroenterology 11:69-75.
  4. Northfield T.C., Mendall M., Goggin P.C. (1994). H.pylori Infection Pathophysiology, Epidemiology and Management. Kluwer Academic Press Dortrecth.

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