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Gastric cancer is one of the most important gastrointestinal cancers. It is the fourth most common cancer and second leading cause of cancer deaths (700,000 deaths annually) worldwide. With any risk of cancer, there is always emphasis given to methods for earlier detection and for this cancer, the possibility of avoidance of invasive screening.
Serum pepsinogen is classified into two biochemically and immunologically distinct types, namely, Pepsinogen I (PG1) and Pepsinogen II (PGII). Pepsinogen levels reflect the functional and morphologic status of the stomach mucosa. If the fundic gland mucosal area reduces, the PG I levels gradually decrease, while the PG II levels remain fairly constant. From a results point of view, the lower the PG I/II ratio, the greater the progression from normal gastric mucosa to extensive atrophic gastritis.
Atrophic gastritis is a precancerous change, but extensive atrophic gastritis is a high risk factor for gastric cancer. Serum pepsinogen I (PG I) and pepsinogen II (PG II) levels are known to increase in the presence of H. pylori-related non-atrophic chronic gastritis. The eradication of H. pylori provokes a significant change in serum PG values: it reduces both PG I and PG II and elevates the PG I to PG II ratio.
There are various options for non-invasive assessment of the stomach. They can be used alone or in combination to increase diagnostic potential. These, in particular, include Gastrin, Pepsinogen I and II and markers for H. pylori infection (serum IgG antibodies, stool antigen and urease activity determined by urea breath testing).
The diagnostic methods for H. pylori infection are reliable in daily clinical practice, and if positive, indicate the presence of chronic active gastritis, a condition that virtually always accompanies H. pylori colonisation. The actual level of antibody, antigen or urease has no relation to the severity of gastritis, nor the presence of further pathology such as ulcer disease or premalignant changes. For the latter purpose, further testing is needed.
Gastrin is a marker for gastric acid output. A decrease in acid output, either as a result of inflammation or gland loss generally, is associated with an increase in serum gastrin levels.
Serum levels of pepsinogen I and II increase as a result of gastric inflammation, particularly H. pylori gastritis. Gland loss due to long-standing gastritis eventually leads to a decrease of pepsinogens, particularly pepsinogen I. These phenomena can be used for non-invasive assessment of the condition of the gastric mucosa.
Positive H. pylori serology with increased serum pepsinogen I and II levels confirms H. pylori gastritis.
Positive H. pylori serology with decreased Pepsinogen I level and a decreased Pepsinogen I/II ratio is indicative of long-standing H. pylori gastritis that has led to atrophic changes.
Increased serum fasting Gastrin levels reflect reduced acid output as a result of loss of specialised glands.
A markedly decreased Pepsinogen I and I/II ratio, with increased Gastrin and negative H. pylori serology will be found in patients with marked atrophic gastritis either as a result of previous H. pylori infection or autoimmune gastritis.
|Test||Code||Sample Type||Turnaround Time|
|Pepsinogen I/Pepsinogen II with ratio||PEPI||B||5 days|
|Pepsinogen I/Pepsinogen II with Gastrin||PPRG||B||5 days|
|Pepsinogen I/Pepsinogen II with Gastrin and H. pylori Abs||PPGH||B||5 days|