Helicobacter ISSN 1523-5378 doi: 10.1111/hel.12116
The Association Between Helicobacter pylori Status and Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer Young-Il Kim, Il Ju Choi, Myeong-Cherl Kook, Soo-Jeong Cho, Jong Yeul Lee, Chan Gyoo Kim, Keun Won Ryu and Young-Woo Kim Center for Gastric Cancer, National Cancer Center, Goyang, Korea
Keywords Helicobacter pylori, Endoscopic resection, Metachronous, Gastric cancer. Reprint requests to: Il Ju Choi, Center for Gastric Cancer, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang, Gyeonggi-do 410-769, Korea. E-mail: [email protected]
Abstract 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.
Endoscopic resection (ER), including endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), has been widely accepted as one of the curative treatment modalities for early gastric cancer (EGC) without concomitant lymph node metastasis [1– 4]. A major problem after ER is that metachronous gastric cancer may develop in the residual gastric mucosa with a rate of 5.1–14% [5–9]. An emerging question is whether Helicobacter pylori eradication could prevent the development of metachronous gastric cancer after the treatment of primary gastric
194
cancer. Currently, eradication of H. pylori after ER of EGC is recommended in guidelines to prevent or reduce the development of metachronous gastric cancer [10,11]. Uemura et al. [12] firstly reported observational study that H. pylori eradication after ER reduced the occurrence of new gastric cancer. However, to date, only one prospective randomized trial showed the preventive effect of H. pylori eradication on the development of metachronous gastric cancer during a short-term followup period of 3 years [13]. Therefore, it remains to be investigated whether this preventive effect of H. pylori
© 2014 John Wiley & Sons Ltd, Helicobacter 19: 194–201
Kim et al.
eradication persists on long-term follow-up. Two recent long-term retrospective studies showed disappointing results of failed gastric cancer prevention by H. pylori eradication. Maehata et al. [7] reported that H. pylori eradication seemed to reduce the incidence of metachronous gastric cancer at the 5-year follow-up point, but such effect disappeared after 5 years of follow-up. Kato et al. [14] also reported that H. pylori eradication did not reduce the development of metachronous gastric cancer throughout the follow-up period. The aim of this study was to investigate the effect of H. pylori status on the development of metachronous gastric cancer in patients who underwent ER for EGC and were properly evaluated for H. pylori status at the time of ER.
Methods Patients Medical records of 823 patients who underwent ER for curative treatment of EGC from June 2001 to December 2009 at the Center for Gastric Cancer in National Cancer Center, Korea, were reviewed. Exclusion criteria were as follows: inclusion in other competing clinical trial, additional gastrectomy after ER due to positive resection margin, history of previous gastrectomy, short-term follow-up duration (
The Association Between Helicobacter pylori Status and Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer Young-Il Kim, Il Ju Choi, Myeong-Cherl Kook, Soo-Jeong Cho, Jong Yeul Lee, Chan Gyoo Kim, Keun Won Ryu and Young-Woo Kim Center for Gastric Cancer, National Cancer Center, Goyang, Korea
Keywords Helicobacter pylori, Endoscopic resection, Metachronous, Gastric cancer. Reprint requests to: Il Ju Choi, Center for Gastric Cancer, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang, Gyeonggi-do 410-769, Korea. E-mail: [email protected]
Abstract 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.
Endoscopic resection (ER), including endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), has been widely accepted as one of the curative treatment modalities for early gastric cancer (EGC) without concomitant lymph node metastasis [1– 4]. A major problem after ER is that metachronous gastric cancer may develop in the residual gastric mucosa with a rate of 5.1–14% [5–9]. An emerging question is whether Helicobacter pylori eradication could prevent the development of metachronous gastric cancer after the treatment of primary gastric
194
cancer. Currently, eradication of H. pylori after ER of EGC is recommended in guidelines to prevent or reduce the development of metachronous gastric cancer [10,11]. Uemura et al. [12] firstly reported observational study that H. pylori eradication after ER reduced the occurrence of new gastric cancer. However, to date, only one prospective randomized trial showed the preventive effect of H. pylori eradication on the development of metachronous gastric cancer during a short-term followup period of 3 years [13]. Therefore, it remains to be investigated whether this preventive effect of H. pylori
© 2014 John Wiley & Sons Ltd, Helicobacter 19: 194–201
Kim et al.
eradication persists on long-term follow-up. Two recent long-term retrospective studies showed disappointing results of failed gastric cancer prevention by H. pylori eradication. Maehata et al. [7] reported that H. pylori eradication seemed to reduce the incidence of metachronous gastric cancer at the 5-year follow-up point, but such effect disappeared after 5 years of follow-up. Kato et al. [14] also reported that H. pylori eradication did not reduce the development of metachronous gastric cancer throughout the follow-up period. The aim of this study was to investigate the effect of H. pylori status on the development of metachronous gastric cancer in patients who underwent ER for EGC and were properly evaluated for H. pylori status at the time of ER.
Methods Patients Medical records of 823 patients who underwent ER for curative treatment of EGC from June 2001 to December 2009 at the Center for Gastric Cancer in National Cancer Center, Korea, were reviewed. Exclusion criteria were as follows: inclusion in other competing clinical trial, additional gastrectomy after ER due to positive resection margin, history of previous gastrectomy, short-term follow-up duration (
