Serum pepsinogens as markers of response to therapy forHelicobacter pylori gastritis

Abstract

We have investigated the effect of therapy for Helicobacter pylori gastritis on serum concentrations of pepsinogen I and II in 43 patients. In the 22 patients in whom therapy resulted in dramatic decrease in gastritis scores and in clearance of the bacteria, there was a highly significant (P = 0.0001) fall in mean serum pepsinogen II from 13.3 +/- 0.8 to 7.9 +/- 0.7 micrograms/liter, and a less pronounced fall in pepsinogen I from 89.0 +/- 5.9 to 78.5 +/- 0.4 micrograms/liter (P = 0.01). These changes resulted in a significant (P = 0.01) increase in the pepsinogen I/II ratio. In contrast, nonsignificant declines of 3.5% and 11.6% were observed in mean pepsinogen I and II levels in the 21 patients whose gastritis failed to resolve histologically and whose infection did not clear. These findings suggest that serum pepsinogen levels, especially pepsinogen II, are a new tool that may be found to be clinically useful in evaluation of treatment outcome in patients with H. pylori-associated gastritis.

Meta-analysis on the validity of pepsinogen test for gastric carcinoma, dysplasia or chronic atrophic gastritis screening

“…57,[61][62][63][64][65][66][67] H. pylori seems to consistently increase pepsinogen I (mean 58.0 ng/mL in H. pylori positive individuals [n=3887] versus 45.4 ng/mL in H. pylori negative individuals [n=3366]) and pepsinogen II (16.8 ng/mL in H. pylori positive individuals versus 9.0 ng/mL in H. pylori negative individuals), and decrease pepsinogen I/II ratio (3.9 versus 5.7). Furthermore, no differences were found when considering the diagnosis of Hp infection diagnosis with the use of histology or serology.…”

Implications of Helicobacter pylori infection for stomach cancer prevention

“…The radioactive exposure of the 14C-urea breath test, although minimal, makes this test inappropriate for studies involving children, pregnant women, or follow-up screening at frequent intervals, whereas the higher cost of the 13C-urea breath test limits its usefulness in population-based research. Serum pepsinogens have been proposed as markers of response to anti-H. pylori therapy (Hunter et al, 1993).…”

Finding out Serologically Active Gastritis Subjects by Conventional Endoscopy and Picking out Subjects Who might be Benefit from Helicobacter pylori Eradication as a Primary Prevention for Gastric Cancer

“…Recent Japanese studies [1,19] uncovered some groups of atrophy free subject showed GC risk equivalent to extensive atrophic gastritis especially diffuse type GC, the main characteristics of these subgroups were elevated PG II. Considering Hunter et al [20] that H.pylori infection contribute more to PG II elevation than to PG I, and Iranian study [21] suggesting that PG II could be good surrogate marker for body morphological change after H.pylori infection, and major portion of PG II was originated from the active gastritis by neutrophil cell infiltration, we could come to conclusion that H.pylori infected active gastritis creating more neutrophil infiltration would cause more PG II elevation. Group B, rapid urease test(+) and chronic atrophic gastritis (CAG) absent; B-α, pepsinogen (PG) I ≤ 70 ng/mL and PG I/II ratio > 3.0; B-β, PG I > 70 ng/mL and PG I/II ratio > 3.0; B-γ, PG I > 70 ng/mL and PG I/II ratio ≤ 3.0; II-30, PG II > 30 ng/mL; Group C, rapid urease test(+) and CAG present; I-0, PG I ≤ 30 ng/mL; I-30, PG I > 30 ng/ml and ≤ 50 ng/mL; I-50, PG I > 50 ng/mL.…”