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Background: Intestinal metaplasia (IM), a precursor of gastric cancer (GC), may be amenable to non-invasive assessment. Aims:We evaluated the diagnostic utility of serum PG-I, PG-II, PG-I/PG-II ratio and gastrin-17 (G-17) to detect IM and atrophy. Methods: The study was conducted at a tertiary care center located in a low-incidence area of GC, endemic for H. pylori infection. Patients with GC and dyspepsia were evaluated by endoscopy, histology for IM (H&E, PAS and Alcian blue stains), gastritis and H. pylori (H&E and Giemsa stains) infection, which was considered to be present if two of three tests (rapid urease test, IgG antibody and histology) were positive. Serum levels of PG-I, PG-II and G-17 were estimated using ELISA. Results: Of 98 patients with GC and 62 with dyspepsia, 35 (36%) and 9 (14%) had IM, respectively (p=0.004). Patients with IM (n=44) had lower PG-I/PG-II ratio than those without IM (n=116; median 4.4, 0.37-23.6 vs. 6.3, 0.19-38.6, respectively; p=0.005). A cut-off value of PG-I/PG-II ratio of 6.0 had 64% sensitivity and 52% specificity for detecting IM (area under ROC curve 0.64). 26/44 (60%) patients with IM and 52/98 (53%) with GC had PG-I/PG-II ratio <6. Serum G-17 was comparable among patients with and without IM. Conclusions: Though PG-I/PG-II ratio was lower in patients with IM, only 60% had a lower ratio suggesting that this test and G-17 may not be useful to detect IM in a low-incidence area of GC, endemic for H. pylori infection.
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Background and aim The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori is controversial. We evaluated endoscopic, 24-h gastric and esophageal acid profile among patients with GERD in relation to H. pylori, as the latter might alter gastric acid secretion. Methods Patients with GERD (n=123), who were not on acid-suppressive drugs, and had not received anti-H. pylori therapy, underwent gastroduodenoscopy and tests for H. pylori detection. Esophageal manometry, 24-h pH metry, serum pepsinogen-I (PG-I), PG-II and gastrin-17 ELISA were done in all these patients. Univariate and multivariate analyses were performed to assess independent predictors for erosive esophagitis (EE). Results Of 123 patients (mean age 40.5 [13.1] years, 85 [69.1%] men), 59 (47.9%) had H. pylori infection. EE was more common in H. pylori non-infected than infected (49 vs. 32, p<0.001). Among patients older than 40 years, absence of H. pylori was associated with lower esophageal pH and longer reflux (p=0.02 and p<0.001, respectively). PG-I/PG-II ratio was lower in H. pylori infected subjects (p <0.001). In patients with higher LA grade of esophagitis, elevated PG-I levels and PG-I/PG-II ratio were associated with more acidic stomach (p=0.04 and p=0.01, respectively). Multivariate analyses showed low gastrin-17 (p=0.016), higher age (p=0.013), hiatus hernia (p=0.004) and absence of H. pylori (p=0.03) were independent predictors for risk of EE. Conclusion H. pylori infection is associated with less acidic stomach and less severe GERD. Low gastrin-17, higher age, hiatus hernia and absence of H. pylori were the best predictors for EE risk.
ABSTRACT
BACKGROUND: Atrophic gastritis is a well known risk factor for gastric adenocarcinoma. Its confirmatory diagnosis requires histology via endoscopy, which is an invasive method; therefore, periodic follow up evaluation as a screening method is difficult to perform. We evaluated the clinical utility of serum pepsinogens (PG) as a biomarker for screening of atrophic gastritis. METHODS: The study population consisted of 130 selected dyspeptic patients (M:F=52:78; age, 16-105 yrs; mean age, 50.8 yrs) who had undergone a diagnostic endoscopy. The serum pepsinogen test was performed by a latex turbidimetric immunoassay method (HBI, Korea) using Toshiba-200FR automatic analyzer. The PGI, II level and PGI:PGII ratio of non-atrophic gastritis group were compared with those of atrophic gastritis group, and a correlation with Helicobacter pylori infection was examined. Cut-off points for screening of atrophic gastritis were determined. RESULTS: The mean serum concentration of PGI showed a decline from normal (60.7 ng/mL), nonatrophic gastritis (54.2 ng/mL), and atrophic gastritis (51.8 ng/mL) to gastric adenocarcinoma (32.6 ng/mL). The mean ratio of PGI:PGII was lower in atrophic gastritis (3.2) compared to non-atrophic gastritis (4.7) (P=0.021). In patients with H. pylori infection, the mean serum PGII level was higher and the PGI:PGII ratio was lower than those in patients without H. pylori infection, and the differences were statistically significant. For screening of atrophic gastritis, the best cut-off point of PGI:PGII ratio was 4, with a sensitivity of 82.6% and specificity of 91.7%. CONCLUSIONS: The serum pepsinogen test is a useful biomarker for screening of atrophic gastritis, a well-known precancerous lesion of gastric adenocarcinoma. Measuring both pepsinogen I and II concentrations simultaneously to obtain pepsinogen I/II ratio provides a clinically useful information for the detection of atrophic gastritis.