What is PGⅠ/PGⅡ?

Pepsinogen (PG) is the precursor of pepsin and is classified according to its biochemical and immunochemical properties into pepsinogen I and pepsinogen II. Most of the pepsinogen enters the stomach lumen and is converted into pepsin, which performs the digestive function. Only 1% of pepsinogen enters the blood circulation through the capillaries of the gastric mucosa and remains stable. PG is a good indicator of the exocrine function of the mucosa of the gastric body and sinus, and can be called a "serological biopsy".

Pepsinogen I is secreted by the principal cells of the fundic glands and cervical mucous cells. PGI is a pointer for detecting the function of gastric acid-producing gland cells; PGI increases with increased acid secretion and decreases with decreased secretion or atrophy of gastric mucosal glands.

Pepsinogen II is secreted by the fundic, cardia, pyloric, and duodenal glands. PGII correlates more with fundal mucosal lesions (relative to the mucosa of the gastric antrum), and its elevation is associated with atrophy of the fundal glandular ducts, gastric epithelial metaplasia or pseudo-pyloric glandular metaplasia, and heterogeneous value-addition

There is a significant correlation between the ratio of PGI and PGII (PGR) and the progression of gastric mucosal atrophy. During the development of atrophic gastritis, PGI and PGI/PGII ratios decreased as gastric mucosal atrophy increased. Therefore, the decrease of serum PG can indicate the progress of atrophic gastritis.

Clinical application of PGⅠ/PGⅡ

With the development of gastric diseases, PGI in serum increases and then decreases, PGII increases and then maintains a high level. Abnormalities in PGI, PGII, and PGI/PGII ratios will indicate different gastric diseases, so PG is a primary screening indicator for gastric diseases such as superficial gastritis, erosive gastritis, gastric ulcers, duodenal ulcers, atrophic gastritis, gastric cancer and other gastric diseases, as well as a monitoring indicator for treatment.

Specific clinical applications of NGAL are shown below:

① Inclusion of PG as a marker for chronic atrophic gastritis in early screening for gastric cancer as a "serological gastric biopsy".

② PG is an indicator of the state of the gastric mucosa and is more sensitive to damage to the gastric mucosa. In general, when PGI is higher than normal, the likelihood of having a peptic ulcer is higher; and when PGI and PGI/PGII ratios are lower than normal, they are more specific for chronic atrophic gastritis.

③ PGⅠbelow normal value can diagnose the gastric body, gastric low mucous membrane atrophy or damage, may be related to superficial gastritis, atrophic gastritis, etc.

④ Higher than normal PG II values can diagnose H. pylori infection, gastric ulcers, duodenal ulcers, etc.

⑤ Decreasing PGⅠconcentration and PGⅠ/PGⅡratio are indicative of atrophic gastritis, and PGⅠconcentration≤70 μg /L and PGⅠ/PGⅡ≤3.0 are usually regarded as the threshold values for the diagnosis of atrophic gastritis.

⑥ Low serum PG I levels and low PG I / PG II ratio can be used as markers to identify people at high risk of gastric cancer: gastric cancer screening using PG I concentration ≤70 μg/L and PC I/PG II ≤7.0 as criteria for high gastric cancer populations.

Factors affecting PGⅠ/PGⅡ

1. Increased PGⅠ/PGⅡlevels may be due to:

Peptic ulcer

Vesiculobullous gastritis

Damage to the gastric mucosa

Helicobacter pylori infection

2. Decreased PGⅠ/PGⅡ levels may be due to：

Atrophic gastritis

Gastric cancer

Summary

Screening for gastric cancer in high-risk groups and increasing the rate of early diagnosis will enable a higher proportion of gastric cancer patients to be treated at an early stage, thereby reducing the mortality rate and improving the prognosis of gastric cancer patients.PG, as a simple, cost-effective and efficient serological test suitable for large-scale census and physical examination, can identify and prevent gastric pre-cancerous lesions, assist in the diagnosis of gastric cancer in the early stage of screening and monitor the effectiveness of Hp treatment and long-term prognosis assessment.

The ReLIA PGⅠ/PGⅡ（2 in 1） Immunoassay is CE-marked cleared. For more details on ReLIA PGⅠ/PGⅡ（2 in 1） Immunoassay products and prices please contact us at  marketing@ReLIAchina.com

References

[1] Huang C B,Xu J,Huang J F,Meng X Y.Sulphomucin colonic type intestinal metaplasia and carcinoma in the stomach. A histochemical study of 115 cases obtained by biopsy. Cancer . 1986

[2] Wang J Y,Hsieh J S,Huang C J,Huang Y S,Huang T J.Clinicopathologic study of advanced gastric cancer without serosal invasion in young and old patients. Journal of Surgery . 1996

[3] Chen XZ,Schottker B,Castro FA.Association of Helicobacter pylori infection and chronic atrophic gastritis with risk of colonic,pancreatic and gastric cancer:A ten-year follow-up of the ESTHER cohort study. Oncotarget . 2016

[4] Al-Ezzy A I A.Immunopathological and modulatory effects of cag A+ genotype on gastric mucosa,inflammatory response,pepsinogens,and gastrin-17 secretion in iraqi patients infected with H.pylori. Open Access Macedonian Journal of Medical Sciences . 2018

[5] Santarelli L,Gabrielli M,Santoliquido A,et al.Interaction between helicobacter pylori infection and untreated coeliac disease on gas.tric histological pattern. Gastroenterologia . 2006

[6] Mertz HR,Peterson WL,Walsh JH.Familial hyperpepsinogenemia andHelicobacter pylori infection. The American journal of Gastroenterology . 2000