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Helicobacter pylori Genotypes Inf luence Serum Pepsinogen C Levels
Author(s) -
Plebani Mario,
Basso Daniela,
Navaglia Filippo,
DiMario Francesco
Publication year - 1997
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.1997.tb00082.x
Subject(s) - helicobacter pylori , caga , gastroenterology , rapid urease test , medicine , gastritis , genotype , pepsin , biomarker , antrum , atrophic gastritis , stomach , biology , gene , enzyme , biochemistry , virulence
Background. Infection from Helicobacter pylori significantly influences pepsinogen A (PGA) and C (PGC) levels in serum. Increased PGA and PGC serum levels are observed in H. pylori positive patients, while a significant decrease is observed after eradication. Little is known about the relative role of H. pylori cytotoxic strains in this phenomenon. The aim of our study was to assess the influence of cag A genotype on circulating levels of PGA and PGC. Materials and Methods. We studied 81 consecutive H. pylori positive patients, 64 H. pylori negative patients and 18 healthy controls. H. pylori was evaluated histologically in two antral and two body biopsies (Giemsa and/or Warthin Starry staining). Extracted DNA was then submitted for PCR amplification of both the urease A and cag A genes. A serum obtained from each patient before endoscopy was used for specific radioimmunoassay measurement of PGA and PGC. Results. The urease A gene was found in all H. pylori positive patients, the cagA gene was detected in 55 H. pylori positive patients and in none of the H. pylori negative patients. PGA and PGC levels were significantly higher in H. pylori positive than in H. pylori negative patients. A significant association was found between cagA and raised serum PGC levels in patients with antral gastritis but not in patients with peptic ulcer. Serum PGA levels were not affected by cagA. Conclusions. Our results indicate that cagA positivity may influence the circulating PGC levels, probably because it causes a higher grade of mucosal inflammation.