Explores the Relationship Between Serum Pepsinogen Levels and Gastric Mucosal Changes in Relation to Helicobacter pylori Status in the Eastern Province of Sierra Leone

Background: Pepsinogen I and pepsinogen II are widely used as diagnostic markers in gastric mucosal diseases such as gastric atrophy and pangastritis, and in assessing the risk of progression to gastric cancer. This study assesses the relationship between serum pepsinogen levels and changes in the gastric mucosa and stomach lining, stratified by Helicobacter pylori status. We also evaluate the significance of the serum pepsinogen ratio (PGI/PGII ratio) as a biomarker of atrophic gastritis and intestinal metaplasia that may progress to gastric cancer. Methods: A total of 84 patients presenting with dyspeptic symptoms or indigestion were recruited for the study. The hallmark diagnostic criteria for atrophic gastritis are serum PGI < 70 ng/mL, and for pangastritis, serum PGII > 20 ng/mL. The serum Helicobacter pylori antibody is negative when the concentration is < 30 AU/mL (no infection in the gastric mucosa) and positive when the concentration is ≥ 30 AU/mL (presence of infection in the gastric mucosa) using POCT immunoassay. Results: Our findings defined the diagnosis of serum Helicobacter pylori infection optimal cut-off points concentration of > 25 AU/mL with a sensitivity of 100% and specificity of 95%, atrophic gastritis a PGI < 73 ng/mL, with a sensitivity of 100% and specificity of 97%, and pangastritis a PGII > 18.25 ng/mL with a sensitivity of 100% and specificity of 97.8%, respectively. We defined a PGR ratio ≤ 3 As a risk of precancerous conditions, with a sensitivity of 100% and a specificity of 97.8%. We categorize patients with PGR ≤ 3 as low risk, and those patients with a PGI/PGII ratio < 2.5 (high risk) and < 1.5 (very high risk), who may be at risk of developing gastric precancerous lesions that may progress to gastric cancer. Conclusion: A low PGI, high PGII, and a PGI/PGII ratio ≤ 3 Sensitive biomarkers to identify patients at risk of developing pangastritis and gastric precancerous lesions in the absence of endoscopic gastric mucosal biopsy.