Serological assessment of gastric intestinal metaplasia and atrophy using pepsinogen-I, pepsinogen-II and gastrin-17 levels in a low incidence area of gastric cancer endemic for H. pylori infection.

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 low-incidence area of GC, endemic for H. pylori. The evaluation was designed as a prospective case-control study. Patients with GC and dyspepsia were evaluated by endoscopy, histology for IM (H&E, PAS and Alcian blue stains) and H. pylori (H&E and Giemsa stains), rapid urease test and IgG antibody (positive results in any two assays). Serum levels of PG-I, PG-II and G-17 were estimated using ELISA.

RESULTS

Of the 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-UPG-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 the 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 low-incidence areas of GC, endemic for H. pylori infection.