Screening for atrophic gastritis and gastric cancer – is a blood test okay?
Testing serum pepsinogen (PG), gastrin 17 (G-17) and Helicobacter pylori (HP) IgG antibody levels can effectively pre-screen for atrophic gastritis and gastric cancer.
Clinically relevant study
The study included 458 patients, who were divided into 5 groups based on endoscopic and pathological findings: atrophic gastritis group (92 patients), gastric ulcer group (58 patients), duodenal ulcer group (90 patients), gastric cancer group (141 patients, including 40 patients with early gastric cancer and 101 patients with advanced gastric cancer), and control group (77 patients, including patients with mild non-atrophic gastritis). The levels of PGⅠ, PGⅡ, G-17 and HP IgG antibodies in serum specimens of patients were measured.
The results showed that PGⅠ and serum pepsinogen I/II ratio (PGR) were significantly decreased in patients with atrophic gastritis and gastric cancer (p<0.01). pg, pgr and g-17 levels were significantly correlated with the location and grade of atrophic gastritis (p<0.01)< span="">; PGⅠ and PGR levels were low and G-17 levels were high in patients with atrophic gastric somatitis, while atrophic G-17 was at a low level in patients with gastric sinusitis. G-17 levels were significantly higher in patients with gastric cancer (P<0.01). Pg and pgr levels were significantly lower in patients with advanced gastric cancer than in patients with early stage < span="">, while there was no difference in G-17 levels between them. The HP positive rate in the control group was 54.55%, while the HP positive rate in the other four groups was higher than 85%. pgⅠlevels in HP-positive patients were significantly higher than those in HP-negative patients, while there was no difference in G-17 levels between the two.
The study suggests that low levels of PGⅠ, PGR and G-17 are biomarkers of atrophic gastritis, and gastric cancer screening can be determined by low levels of PGⅠ, PGR and high levels of G-17. HP infection is associated with altered PG levels.
Clinical significance of pepsin I (PGⅠ)
Normal reference value: 70 to 240 ng/ml
Serum PG levels reflect the morphology and function of gastric mucosa at different sites: PGI is a pointer to detect the function of gastric acid-secreting gland cells; PGI increases with increased gastric acid secretion and decreases with decreased secretion or atrophy of gastric mucosal glands; PGII correlates more with fundic mucosal lesions (relative to sinus mucosa), and its elevation is associated with fundic glandular duct atrophy, gastric epithelial hyperplasia or pseudopyloric gland hyperplasia, and heterotypic value-added. Progressive decrease in PGI/II ratio was associated with progression of gastric mucosal atrophy. Therefore, the combined determination of PGI and PGII ratios can serve as a “serological biopsy” of the fundic gland mucosa.
The progression of gastric diseases can be expressed as follows: superficial gastritis – gastric mucosal erosions and ulcers – atrophic gastritis – gastric cancer, and other diseases. It has good diagnostic and screening effects. Pepsinogen I/II test kit is used to detect the content of pepsinogen I/II in serum or plasma, which has the advantages of simplicity and rapidity and avoids the inconvenience of X-ray on human body and gastroscopy.
Clinical significance of Helicobacter pylori antibody (HP-IgG)
Normal reference value: Negative
Used for the diagnosis of H. pylori infection and for monitoring the status of the disease during treatment. H. pylori is closely associated with a variety of gastrointestinal disorders, including non-ulcer dyspepsia, gastric and duodenal ulcers, and active chronic gastritis. The rate of H. pylori infection can exceed 90% in patients with single or compound gastric and duodenal ulcers or non-ulcerative dyspepsia.
Clinical significance of gastrin
Hypergastrinemia: Among them, there are two categories: hyperacidic hypergastrinemia and hypogastrinemic or acid-free hypergastrinemia.
Hypergastrinemic hypergastrinemia: It is seen in gastrinoma, excessive formation of gastric sinus mucosa, and chronic renal failure. After recovery of renal function, gastrin levels mostly return to normal, if not, it often suggests the possibility of atrophic gastritis.
Hypogastrinemic or acid-free hypergastrinemia: seen in gastric ulcer, type A atrophic gastritis, post vagotomy, hyperthyroidism.
Hypogastrinemia: seen in type B atrophic gastritis, gastroesophageal reflux.
Increased gastrin responsiveness is seen in cardia incontinentia, duodenal ulcer disease.
Decreased responsiveness of gastrin is seen in dermatosclerosis.
In gastric cancer, changes in gastrin are related to the site of the lesion. In gastric body cancer, serum gastrin is significantly elevated, while in gastric sinus cancer, gastrin secretion is reduced.