Serum or Plasma Pepsinogen II (P/S-PGII)
Pepsinogen II (PGII) is secreted from glands covering the whole stomach mucosa, and to some extent also from Brunner glands. As for PGI, the level of PGII in the blood reflects its level in the stomach. The concentration of P/S-PGI in a healthy person is approximately 6-fold higher than the concentration of S/P-PGII. In corpus atrophic gastritis, PGI/PGII ratio decreases significantly more than P/S-PGII level. Therefore PGI/PGII ratio decreases in corpus atrophy (1). PGI/PGII ratio less than 3.0 indicates corpus atrophy. The risk of gastric cancer is increased in corpus atrophy.

Pepsinogen I

Pepsinogen II

Serum or Plasma Gastrin-17 (P/S-G-17)
Secreted exclusively by the G-cells of the antrum of the stomach, G-17 will be depressed in cases of atrophy in this area. Fasting G-17 level can decrease also due to high stomach acid secretion. Protein stimulation increases G-17 secretion from 4 to 5 -fold compared to fasting (basal) level if there is no antrum atrophy. As for PGI and PGII, the level of P/S-G-17 level reflects its level in the stomach. healthy individuals elicit a response of 4 to 5 times higher than that of baseline levels. Measurement of P/S-G-17 following protein stimulation will tell whether low basal G-17 is caused by antrum atrophy or acid. Antrum atrophy is always linked with Helicobacter pylori infection. For unknown reasons, atrophic antrum gastritis increases the risk of gastric cancer, the risk being even 18-fold in patients with advanced atrophic antrum gastritis compared to the cancer risk in persons with a normal antrum mucosa (2).

Gastrin-17

Helicobacter pylori (H. pylori) (IgG) (P/S HpAbG)
Serological presence of antibodies to H. pylori is indicative of the presence of chronic gastritis. H. pylori has been linked with peptic ulceration and gastric cancer (3,4).

Helicobacter pylori