Journal List > Korean J Gastroenterol > v.70(1) > 1007712

Song, Yang, Lim, Choi, and Kim: The Effect of Helicobacter pylori Eradication on the Metachronous Neoplasm after Endoscopic Resection for Gastric Dysplasia

Abstract

Background/Aims

Helicobacter pylori (Hp) infection is an important risk factor for gastric carcinogenesis. Although several studies have investigated the effect of Hp eradication on the development of metachronous neoplasm after endoscopic resection of the gastric dysplasia, the evidence is still insufficient to make a clear conclusion. The aims of this study was to evaluate the risk factors for the development of metachronous neoplasm after endoscopic resection of gastric dysplasia and to investigate the effect of Hp eradication.

Methods

Between 2005 and 2011, a total of 887 patients underwent endoscopic resection for gastric dysplasia. Among them, 521 patients who had undergone tests for Hp infection and been followed-up for at least one year were included in the final analyses. Of the 292 Hp-positive patients, 116 patients were successfully eradicated, while 176 failed or did not undergo eradication.

Results

During a mean follow-up of 59.1 months (range 12–125 months), metachronous neoplasm had developed in 63 patients (12.1%, dysplasia in 38, carcinoma in 25). In multivariate analyses, age ≥65 (hazard ratio [HR]=2.247, 95% confidence interval [CI] 1.297–3.895), tumor size (HR=1.283, 95% CI 1.038–1.585), synchronous lesion (HR=2.341, 95% CI 1.244–4.405), family history of gastric cancer (HR=3.240, 95% CI 1.776–5.912), and smoking (HR=1.016, 95% CI 1.003–1.029) were risk factors for metachronous neoplasm after endoscopic resection of gastric dysplasia. However, Hp eradication was not associated with metachronous neoplasm (HR=0.641, 95% CI 0.297–1.384).

Conclusions

Hp eradication was not shown to be associated with the development of metachronous cancer after endoscopic resection of gastric dysplasia.

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Fig. 1.
Cumulative incidence rate of metachronous tumor (Kaplan-Meier survival curve). There was no significant difference of cumulative incidence rate of metachronous tumor in accordance with the status of Helicobacter pylori (Hp) infection.
kjg-70-27f1.tif
Table 1.
Baseline Characteristics of the Study Population
  Total (n=521)
Age, years 60.96±8.00
 <65 326 (62.6)
 ≥65 195 (37.4)
Sex  
 Female 197 (37.8)
 Male 324 (62.2)
Hp status  
 No infection 229 (44.0)
 Eradicated 116 (22.3)
 Not eradicated 176 (33.8)
Location  
 Upper third 12 (2.3)
 Middle third 215 (41.3)
 Lower third 294 (56.4)
Size (cm) 1.43±1.00
Synchronous lesion  
 No 464 (89.1)
 Yes 57 (10.9)
Histological grade  
 Low grade dysplasia 386 (74.1)
 High grade dysplasia 135 (25.9)
Endoscopic resection  
 EMR 10 (1.9)
 ESD 511 (98.1)
Intestinal metaplasia, initial  
 No 53 (10.3)
 Yes 463 (89.7)
Family history of GC  
 No 438 (85.4)
 Yes 75 (14.6)
Smoking (pack-year) 9.29±16.73
 0 346 (68.9)
 <20 42 (8.4)
 ≥20 114 (22.7)
Alcohol (g/d) 10.16±22.68
Follow up period (months) 59.11±28.98
Metachronous neoplasm 63 (12.1)
 Dysplasia 38 (60.3)
 Carcinoma 25 (39.7)

Data represent means±standard deviations for continuous variables and numbers (%) for categorical variables.

Hp, Helicobacter pylori; EMR, endoscopic mucosal resection; ESD, endoscopic submucosal dissection; GC, gastric cancer.

Table 2.
Associated Factors for Metachronous Neoplasm of Gastric Dysplasia
  Metachronous neoplasm (−)(n=458) Metachronous neoplasm (+)(n=63) p-value HR a 95% CI a
Age     0.004 b    
 <65 297 (64.8) 29 (46.0)   Reference  
 ≥65 161 (35.2) 34 (54.0)   2.425 1.474–3.987
Sex     0.059 b    
 Female 180 (39.3) 17 (27.0)   Reference  
 Male 278 (60.7) 46 (73.0)   1.583 0.907–2.762
Hp status     0.104 b    
 No infection 194 (42.4) 35 (55.6)   Reference  
 Eradicated 107 (23.4) 9 (14.3)   0.498 0.239–1.036
 Not eradicated 157 (34.3) 19 (30.2)   0.709 0.406–1.240
Location     0.230 b    
 Upper third 9 (2.0) 3 (4.8)   Reference  
 Middle third 186 (40.6) 29 (46.0)   0.527 0.160–1.734
 Lower third 263 (57.4) 31 (49.2)   0.388 0.118–1.270
Size (cm) 1.37±0.93 1.88±1.32 <0.001 c 1.430 1.192–1.714
Synchronous lesion(s)     <0.001 b    
 No 416 (90.8) 48 (76.2)   Reference  
 Yes 42 (9.2) 15 (23.8)   2.791 1.562–4.988
Histological grade     0.102 b    
 Low grade dysplasia 334 (72.9) 52 (82.5)   Reference  
 High grade dysplasia 124 (27.1) 11 (17.5)   0.539 0.160–1.734
Intestinal metaplasia     0.017 b    
 No 52 (11.5) 1 (1.6)   Reference  
 Yes 402 (88.5) 61 (98.4)   7.956 1.103–57.401
Family history of GC     0.001 b    
 No 393 (87.3) 45 (71.4)   Reference  
 Yes 57 (12.7) 18 (28.6)   2.755 1.594–4.761
Smoking (pack-year) 8.42±15.69 15.89±22.25 0.001 c 1.017 1.006–1.029
Alcohol (g/d) 9.35±21.38 16.08±30.11 0.031 c 1.006 0.998–1.014
Follow up period (months) 60.66±29.41 47.84±22.80 0.001 c

Data represent means±standard deviations for continuous variables and numbers (%) for categorical variables.

HR, hazard ratio; CI, confidence interval; Hp, Helicobacter pylori; GC, gastric cancer.

a Univariate analyses of risk factors for metachronous neoplasm by Cox regression analysis

b Statistical analysis was performed by Pearson's chi-square

c Statistical analysis was performed by Student's t-test.

Table 3.
Risk Factors for Metachronous Cancer after Endoscopic Resection of Gastric Dysplasia
  HR a 95% CI a
Age ≥65 2.247 1.297–3.895
Male sex 1.047 0.557–1.970
Hp status    
 No infection Reference  
 Eradicated 0.641 0.297–1.384
 Not eradicated 1.103 0.601–2.026
Size (cm) 1.283 1.038–1.585
Synchronous lesion(s) 2.341 1.244–4.405
Intestinal metaplasia 4.884 0.669–35.663
Family history of GC 3.240 1.776–5.912
Smoking (pack-year) 1.016 1.003–1.029

Hp, Helicobacter pylori; GC, gastric cancer.

a Multivariate analyses adjusted for age, sex, Hp status, size, synchronous lesion(s), intestinal metaplasia, family history of gastric cancer, and smoking.

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