BACKGROUND: The long-term effect of Helicobacter pylori eradication in preventing metachronous gastric cancer (GC) development after endoscopic resection (ER) of early gastric cancer (EGC) remains controversial. The aim of this study was to investigate the effect of H. pylori status on the incidence of metachronous GC after ER during long-term follow-up. PATIENTS AND METHODS: We retrospectively reviewed the medical records of 374 patients who underwent ER for EGC. Helicobacter pylori status was assessed by histology, rapid urease test, and serology. According to the H. pylori status after ER, included patients were classified into H. pylori-negative group (n = 218), H. pylori-eradicated group (n = 49), and H. pylori-persistent group (n = 107). Metachronous GC incidence and risk factors according to H. pylori status were analyzed. RESULTS: Median follow-up duration after ER was 4.3 years (range 1.0-11.3 years). During the follow-up period, metachronous GC had developed in 13 patients (6.0% [13/218]) in the H. pylori-negative group, 2 patients (4.1% [2/49]) in the H. pylori-eradicated group, and 16 patients (15.0% [16/107]) in the H. pylori-persistent group. Cumulative incidence of metachronous GC was significantly higher in patients with H. pylori-persistent group than in those with H. pylori-negative (p = .011, log-rank test) and H. pylori-eradicated group (p = .006, log-rank test). In a multivariate Cox proportional hazard model, age ≥65 years (hazard ratio [HR] 2.29, p = .038), family history of GC (HR 2.60, p = .014), and H. pylori-persistent status (HR 2.42, p = .019) were associated with metachronous GC development. CONCLUSIONS: Persistent H. pylori infection after ER may increase risk of metachronous GC development.
BACKGROUND: The long-term effect of Helicobacter pylori eradication in preventing metachronous gastric cancer (GC) development after endoscopic resection (ER) of early gastric cancer (EGC) remains controversial. The aim of this study was to investigate the effect of H. pylori status on the incidence of metachronous GC after ER during long-term follow-up. PATIENTS AND METHODS: We retrospectively reviewed the medical records of 374 patients who underwent ER for EGC. Helicobacter pylori status was assessed by histology, rapid urease test, and serology. According to the H. pylori status after ER, included patients were classified into H. pylori-negative group (n = 218), H. pylori-eradicated group (n = 49), and H. pylori-persistent group (n = 107). Metachronous GC incidence and risk factors according to H. pylori status were analyzed. RESULTS: Median follow-up duration after ER was 4.3 years (range 1.0-11.3 years). During the follow-up period, metachronous GC had developed in 13 patients (6.0% [13/218]) in the H. pylori-negative group, 2 patients (4.1% [2/49]) in the H. pylori-eradicated group, and 16 patients (15.0% [16/107]) in the H. pylori-persistent group. Cumulative incidence of metachronous GC was significantly higher in patients with H. pylori-persistent group than in those with H. pylori-negative (p = .011, log-rank test) and H. pylori-eradicated group (p = .006, log-rank test). In a multivariate Cox proportional hazard model, age ≥65 years (hazard ratio [HR] 2.29, p = .038), family history of GC (HR 2.60, p = .014), and H. pylori-persistent status (HR 2.42, p = .019) were associated with metachronous GC development. CONCLUSIONS: Persistent H. pylori infection after ER may increase risk of metachronous GC development.
Authors: Da Hyun Jung; Jie-Hyun Kim; Hyun Soo Chung; Jun Chul Park; Sung Kwan Shin; Sang Kil Lee; Yong Chan Lee Journal: PLoS One Date: 2015-04-27 Impact factor: 3.240