Пепсиноген I

Pepsinogen I (PGI; PgI) serves as a circulating marker of the structural and functional integrity of the gastric corpus mucosa. The test supports detection of corpus atrophic gastritis and pangastritis in individuals with dyspeptic symptoms, those at increased risk, or patients with concomitant autoimmune disease, and it helps triage whether endoscopy or radiologic evaluation is warranted. In persons receiving long‑term proton pump inhibitor therapy (>1 year), serial PGI measurement assists in assessing mucosal status and guiding treatment decisions. When used alongside pepsinogen II, gastrin‑17, and assays for active Helicobacter pylori infection, the PGI test contributes to early recognition of gastric adenocarcinoma and gastric carcinoid risk.

Pepsinogen is the zymogen precursor of pepsin, which initiates protein digestion in the stomach. Hydrochloric acid converts pepsinogen to active pepsin. Two immunochemically distinct isoforms exist: pepsinogen I and pepsinogen II. Pepsinogen I is produced exclusively by chief cells located in the gastric corpus. A small fraction reaches the circulation and is measurable. The corpus is the sole site of gastric hydrochloric acid and intrinsic factor synthesis; disorders affecting this region reduce pepsinogen I, acid output, and intrinsic factor. Consequently, serum pepsinogen I reflects the severity of corpus mucosal injury and is used for diagnosis and follow‑up of corpus‑predominant disease. Helicobacter pylori is the most common cause of chronic gastritis. This acid‑tolerant, spiral, gram‑negative bacterium colonizes gastric mucus and releases cytotoxins and proteases that progressively damage the mucosa, culminating in atrophic change. Disease often begins in the antrum and pylorus and may extend to the corpus; patterns include antral atrophic gastritis, corpus atrophic gastritis, and pangastritis. Not every patient with atrophic gastritis has active H. pylori, indicating that smoking, alcohol use, and ongoing nonsteroidal anti‑inflammatory drug exposure can perpetuate inflammation. Only about half of infected individuals develop atrophic changes, reflecting variable host susceptibility. Molecular mimicry between H. pylori antigens and the parietal cell H+-K+-ATPase can trigger cross‑reactive antibodies and parietal cell destruction, a hallmark of autoimmune atrophic gastritis. Autoimmune gastritis commonly coexists with type 1 diabetes mellitus, vitiligo, and Hashimoto thyroiditis and is thought to arise in predisposed persons after long‑standing H. pylori infection. Atrophic gastritis typically evolves insidiously with few symptoms; patients may report mild epigastric pain, early satiety, postprandial fullness, nausea, and weakness. Progressive loss of parietal cells produces achlorhydria and intrinsic factor deficiency. Gastric acid is required for protein digestion, release of food‑bound vitamin B12, and oxidation of calcium, iron, zinc, and magnesium to absorbable forms. Achlorhydria therefore leads to vitamin B12 deficiency with hematologic, gastrointestinal, and neurologic sequelae: macrocytic anemia with weakness, dizziness, and tachycardia; maldigestion with diarrhea; and demyelination of spinal cord tracts that may be irreversible, causing paralysis and sensory loss. Severe parietal cell destruction and achlorhydria are most characteristic of autoimmune atrophic gastritis. In corpus atrophic gastritis and pangastritis, chief cells also degenerate, lowering serum pepsinogen I; the magnitude of reduction parallels disease severity. Pepsinogen I can be used to monitor response after antibiotic treatment. Acid normally suppresses ingested pathogens; achlorhydria increases susceptibility to enteric infections, including giardiasis and pseudomembranous colitis. Patients with hyperacid gastritis are often treated with proton pump inhibitors (e.g., omeprazole). Prolonged suppression of acid secretion is associated with gradual parietal cell atrophy; individuals receiving proton pump inhibitors for more than 1 year should have pepsinogen I measured to inform continuation or adjustment of therapy. Atrophic gastritis is a major risk factor for gastric adenocarcinoma. Destruction of normal mucosa is accompanied by foci of intestinal‑type metaplasia that are precancerous. Gastric adenocarcinoma develops in 2.5–5% of patients with moderate to severe atrophic gastritis, and severe atrophic pangastritis is associated with a 90‑fold increase in risk. Additional risk factors include diets rich in nitrates and smoked foods, heavy alcohol intake, smoking, H. pylori infection, radiation therapy, familial predisposition, and other precancerous conditions such as gastric polyps and Ménétrier disease. Because early symptoms are nonspecific (weakness, epigastric discomfort, weight loss) and patients often present late with pain, vomiting, gastrointestinal bleeding, or ascites, regular evaluation of high‑risk groups is recommended. Endoscopy with biopsy or contrast radiography is not used for population screening due to potential complications; pepsinogen I offers a convenient, noninvasive appraisal of corpus mucosal status. A combined biomarker approach—pepsinogen I, pepsinogen II, gastrin‑17, and testing for active H. pylori—provides a comprehensive view of gastric mucosal health. A normal composite profile suggests preserved mucosa and may obviate endoscopy, whereas low pepsinogen I together with a low pepsinogen I/II ratio points to corpus atrophic gastritis, pangastritis, or gastric adenocarcinoma and warrants endoscopic and histologic confirmation. Reported sensitivity for this composite strategy is 71–83% with specificity of 95–98%. In corpus atrophic gastritis, particularly the autoimmune form, the risk of enterochromaffin‑like cell (ECL) carcinoid is approximately 5%. These tumors may secrete excess 5‑hydroxytryptophan, producing flushing and diarrhea; larger lesions can cause gastric bleeding and obstruction.