Background Although many studies have found an association betweenHelicobacter pylori infection and the development of gastriccancer, many aspects of this relation remain uncertain.
Methods We prospectively studied 1526 Japanese patients whohad duodenal ulcers, gastric ulcers, gastric hyperplasia, ornonulcer dyspepsia at the time of enrollment; 1246 had H. pyloriinfection and 280 did not. The mean follow-up was 7.8 years(range, 1.0 to 10.6). Patients underwent endoscopy with biopsyat enrollment and then between one and three years after enrollment.H. pylori infection was assessed by histologic examination,serologic testing, and rapid urease tests and was defined bya positive result on any of these tests.
Results Gastric cancers developed in 36 (2.9 percent) of theinfected and none of the uninfected patients. There were 23intestinal-type and 13 diffuse-type cancers. Among the patientswith H. pylori infection, those with severe gastric atrophy,corpus-predominant gastritis, and intestinal metaplasia wereat significantly higher risk for gastric cancer. We detectedgastric cancers in 21 (4.7 percent) of the 445 patients withnonulcer dyspepsia, 10 (3.4 percent) of the 297 with gastriculcers, 5 (2.2 percent) of the 229 with gastric hyperplasticpolyps, and none of the 275 with duodenal ulcers.
Conclusions Gastric cancer develops in persons infected withH. pylori but not in uninfected persons. Those with histologicfindings of severe gastric atrophy, corpus-predominant gastritis,or intestinal metaplasia are at increased risk. Persons withH. pylori infection and nonulcer dyspepsia, gastric ulcers,or gastric hyperplastic polyps are also at risk, but those withduodenal ulcers are not.
Since the discovery of Helicobacter pylori in 1983,1 the diagnosisand treatment of upper gastrointestinal disease have changedgreatly. A higher risk of the development of gastric cancerhas been reported in subjects with positive serologic testsfor H. pylori.2,3,4 The World Health Organization and InternationalAgency for Research on Cancer consensus group5 stated in 1994that there was sufficient epidemiologic and histologic6,7 evidenceto classify H. pylori as a definite carcinogen. Most but notall recent studies8,9 have found H. pylori to be associatedwith gastric cancer. The rates of infection in patients withgastric cancer vary greatly among studies. These variationsmay be attributable to differences in the methods of detectingH. pylori or in the patient groups. Most prospective studies8,9have used control groups "nested" within cohorts of study patientsfrom whom blood samples were taken years before the onset ofclinical gastric cancer. Various diagnostic tests for H. pylori10,11may have false negative results, and the use of multiple testsmay help to provide a more accurate diagnosis of H. pylori infection.12In Japan, where the incidence of gastric cancer is high, endoscopyis performed frequently for the early detection of gastric cancer,even as part of the examination of patients without symptomsof the disease. As a result, early-stage cancers are often discoveredby endoscopy.
We conducted a prospective, long-term study of a large groupof patients who were assessed for H. pylori infection by endoscopyand biopsy, followed by histologic examination, a rapid ureasetest, and serologic testing, to determine the relation betweenH. pylori infection and the development of gastric cancer.
Methods
Patients
Between April 1990 and March 1993, we enrolled 1603 consecutivepatients with active duodenal ulcers, active gastric ulcers,gastric hyperplastic polyps, or nonulcer dyspepsia. They wereassessed for H. pylori infection and underwent endoscopic follow-upfor the early detection of gastric cancer. We had previouslyexcluded patients with severe underlying disease, includinggastric cancer and adenoma, those who had undergone gastricresection, and those taking nonsteroidal antiinflammatory drugs.We then excluded 77 patients who declined a second endoscopicexamination. The remaining 1526 patients (869 men and 657 women;mean age, 52 years; range, 20 to 76) were studied. Endoscopywith biopsy was performed in all patients at enrollment andbetween one and three years after enrollment. Follow-up datawere censored because of deaths from other causes and the useof antibiotic treatment for the eradication of H. pylori. Themean duration of follow-up was 7.8 years (range, 1.0 to 10.6).All patients gave written informed consent. The study protocolwas approved by the ethics committees of Kure Kyosai Hospitaland was reviewed annually.
Endoscopy and Histologic Examination
All endoscopic examinations were performed with only local anesthesia(lidocaine). An Olympus videoscope (model GIF-230, Olympus,Tokyo, Japan) was used. Four biopsy specimens were taken, twofrom the greater curvature of the antrum and two from the upperbody of the stomach (when lesions suspected to be cancerouswere noted, additional biopsies were performed). Of these fourspecimens, two were fixed in formalin and assessed for H. pylori(by Giemsa staining) and the degree of neutrophil infiltrationand intestinal metaplasia (by staining with hematoxylin andeosin). The remaining two were used for a rapid urease test(CLO, Delta West, Bentley, Australia). The degree of neutrophilinfiltration was classified according to four grades (0 denotingno infiltration, 1 mild, 2 moderate, and 3 marked) and expressedas a score by two pathologists according to the updated Sydneysystem.13 Consensus was reached through joint review of allthe slides. Active gastritis was classified into four categories(no gastritis, antrum-predominant gastritis, pangastritis, andcorpus-predominant gastritis). Intestinal metaplasia was classifiedin two grades (absent or present), because the multifocal distributionof metaplasia may lead to misclassification when only two biopsyspecimens are obtained. Gastric mucosal atrophy was evaluatedaccording to the endoscopic-atrophic-border scale describedby Kimura and Takemoto,14 which correlates with the resultsof histologic evaluation.15,16 There were three classifications(1 denoting mild atrophy or none, 2 moderate, and 3 severe).The pathologists were not aware of the clinical or endoscopicdata. The results were scored blindly with the use of patientcodes.
The rapid urease test was monitored for up to 24 hours. Gastriccancer was defined as evident invasion of neoplastic epitheliuminto the lamina propria of the mucosa or beyond (i.e., category5.1 or 5.2 according to the Vienna classification17) and wasclassified according to Laurén18 as intestinal or diffusetype.
Serologic Evaluation
Blood was sampled immediately before endoscopy; serum was immediatelyseparated and cryopreserved at –20°C until it wasassayed for antibodies against H. pylori (HM-CAP, Enteric Products,Westbury, N.Y.). A positive serologic test for H. pylori wasdefined as one with a titer of 1.8 or more.
Detection of H. pylori Infection
H. pylori infection was identified by histologic examination,the rapid urease test, and serologic evaluation. Patients inwhom any of these assays were positive were classified as H.pylori–positive. Those in whom all three were negativewere considered H. pylori–negative.
Statistical Analysis
All statistical analyses were performed with SAS software (SASInstitute, Cary, N.C.).19 The demographic and clinical characteristicsof the patients were compared by Student's t-test (for age,duration of follow-up, and number of endoscopic procedures)or the chi-square test (for sex, diagnosis, grade of gastricmucosal atrophy, distribution of gastritis, and presence orabsence of intestinal metaplasia). We calculated relative risksfor gastric findings — such as the degree of atrophy,the pattern of distribution of gastritis, and the presence ofintestinal metaplasia — using Cox proportional-hazardsmodels. Since gastric cancer has not been demonstrated to developin patients with duodenal ulcers or in those who are H. pylori–negative(with or without eradication therapy), we could not calculatethe difference in the incidence of gastric cancer using theCox proportional-hazards model. For this reason, Kaplan–Meieranalysis and the chi-square test or Fisher's exact test wereused to assess the difference in proportions. All P values aretwo-sided; significance was indicated by a P value of less than0.05.
Results
Of the 1526 patients, 1246 were H. pylori–positive and280 H. pylori–negative. The base-line characteristicsof both groups are shown in Table 1. There were no significantdifferences between the two groups in age, sex, or the meannumber of endoscopic procedures. The H. pylori–positivepatients included 445 with nonulcer dyspepsia (206 men and 239women; mean age, 54 years; range, 22 to 76), 275 with duodenalulcers (198 men and 77 women; mean age, 48 years; range, 20to 76), 297 with gastric ulcers (226 men and 71 women; meanage, 52 years; range, 22 to 75), and 229 with gastric polyps(84 men and 145 women; mean age, 56 years; range, 26 to 76).The H. pylori–negative patients all had nonulcer dyspepsia.Atrophy and intestinal metaplasia of any grade were found in4 percent and 2 percent of H. pylori–negative patients,respectively. Of the H. pylori–negative group, only 2percent had gastritis, all antrum predominant. In the H. pylori–positivegroup, 53 percent had moderate atrophy and 17 percent had severeatrophy. Antrum-predominant gastritis was found in 56 percent,pangastritis in 27 percent, and corpus-predominant gastritisin 17 percent of H. pylori–positive patients. Thirty-sevenpercent had intestinal metaplasia. There were significant differencesin these variables between the groups (P<0.001 by the chi-squaretest). The duration of follow-up in the H. pylori–positivegroup was significantly shorter than in the uninfected group(P<0.001), because 253 of 1246 infected patients receivederadication therapy at an early stage of follow-up.
Table 1. Base-Line Characteristics of the 1526 Patients.
Development of Gastric Cancer
During follow-up, gastric cancer developed in 36 of 1246 H.pylori–infected patients (2.9 percent) but in none ofthe 280 uninfected patients (P<0.001). All cancers were visibleon endoscopy and were identified histologically on biopsy. InFigure 1, the risk of gastric cancer is shown to be 5 percentat 10 years by Kaplan–Meier analysis. There were 23 menand 13 women with gastric cancer (at base line: mean age, 60years; range, 41 to 76; at the time of detection of gastriccancer: mean age, 65; range, 47 to 83). Sixteen men and sevenwomen had intestinal-type cancers (at base line: mean age, 64years; range, 44 to 76; at the time of detection of gastriccancer: mean age, 70; range, 53 to 83), and six men and sevenwomen had diffuse-type cancers (at base line: mean age, 52 years;range, 41 to 68; at the time of detection of gastric cancer:mean age, 58; range, 47 to 75). The mean age at enrollment andat the time of detection of gastric cancer was significantlylower in the patients with diffuse-type cancer than in thosewith intestinal-type cancer (P<0.001 for both comparisons).
Figure 1. Kaplan–Meier Analysis of the Proportion of H. pylori–Positive and H. pylori–Negative Patients Who Remained Free of Gastric Cancer.
During follow-up, gastric cancer developed in 36 of the 1246 H. pylori–infected patients (2.9 percent) but in none of the 280 uninfected patients (P<0.001).
Table 2 shows the abnormalities of the gastric mucosa at baseline in all the H. pylori–infected patients and in the36 patients with gastric cancer, as well as the relative risksof cancer according to the base-line abnormalities. The frequencyof severe atrophy, corpus-predominant gastritis, and intestinalmetaplasia was significantly higher in patients with intestinal-typegastric cancer than in those with diffuse-type cancer (P=0.002,P<0.001, and P=0.008, respectively). Nine of the patientswith diffuse-type gastric cancer had moderate atrophy, and 10had pangastritis.
Table 2. The Development of Gastric Cancer in H. pylori–Positive Patients According to Abnormalities at Base Line.
During follow-up, gastric cancer was detected in 21 of the 445patients with nonulcer dyspepsia (4.7 percent), in 10 of the297 with gastric ulcers (3.4 percent), and in 5 of the 229 withgastric polyps (2.2 percent) at base line (Figure 2). No gastriccancer was detected in patients with duodenal ulcers. The frequencyof gastric cancer in patients with nonulcer dyspepsia, gastriculcers, and gastric polyps was significantly higher than inthose with duodenal ulcers (Table 3). The frequency of diffuse-typecancer in patients with gastric ulcers was significantly higherthan in patients with nonulcer dyspepsia and gastric polyps(P=0.03 by the chi-square test). The mean age at the time ofdiagnosis of gastric cancer in patients with gastric ulcers(53 years) was significantly lower than in those with nonulcerdyspepsia (63 years) (P=0.009 by Student's t-test). Gastriccancer did not develop in any of the 253 patients with H. pyloriinfection who received eradication therapy. The mean (±SD)duration of follow-up after eradication (4.8±1.2 years)was shorter than the mean duration for patients who were nottreated (8.5±1.7 years; P<0.001 by Student's t-test).
Figure 2. Kaplan–Meier Analysis of the Proportion of Patients Who Had Nonulcer Dyspepsia, Duodenal Ulcers, Gastric Ulcers, and Hyperplastic Gastric Polyps at the Time of Enrollment Who Remained Free of Gastric Cancer.
During follow-up, gastric cancer was detected in 21 of the 445 patients with nonulcer dyspepsia (4.7 percent), in 10 of the 297 patients with gastric ulcers (3.4 percent), and in 5 of the 229 patients with gastric polyps (2.2 percent) at base line. The rates of development of gastric cancer in patients with nonulcer dyspepsia, gastric ulcers, and gastric polyps were significantly higher than the rates in those with duodenal ulcers (P<0.001, P=0.002, and P=0.02, respectively, by Fisher's exact test).
Table 3. The Development of Gastric Cancer in H. pylori–Positive Patients According to Endoscopic Findings.
Discussion
We found that gastric cancer developed in patients with H. pyloriinfection but not in uninfected patients. Our findings are consistentwith those of a recent meta-analysis.8 In Japan, it has beenreported that each year, gastric cancer develops in 300,000(0.5 percent) of the 60 million people who are H. pylori–positive,20which means that gastric cancer develops in 5 percent of H.pylori–positive persons over 10 years. Our results supportthis estimate.
In previous epidemiologic studies showing a close relation betweenH. pylori infection and gastric cancer, a large number of patientswith negative serologic results were found to have cancer.8,9Recent studies10,11,12 have shown that false negative resultsoccur with the serum antibody assay, so it is possible thatthe rate of H. pylori infection has been underestimated in patientswith gastric cancer. Tabata et al.12 concluded from their studyof this issue that a biopsy specimen should be taken from thegreater curvature of the upper gastric body because this procedureresults in fewer false negatives. Enomoto et al.21 performedan immunohistologic study of biopsy specimens from the greatercurvature of the upper gastric body and antibodies against H.pylori; they found that 98 percent of patients with gastriccancer were H. pylori–positive. Their results and ourfindings suggest that there are very few patients with gastriccancer who are not infected with H. pylori. It has previouslybeen shown that in H. pylori–negative patients, histologicevidence of gastritis, especially neutrophil infiltration, israre, and little gastric mucosal atrophy occurs.22,23 This iswhat we found as well. Thus, the onset of gastric cancer maybe related to histologic evidence of gastritis or atrophic gastritisassociated with H. pylori infection.
Our findings suggest that patients with H. pylori infectionand severe atrophic gastritis, corpus-predominant gastritis,or both, along with intestinal metaplasia are at high risk forintestinal-type gastric cancer. It has been shown that intestinal-typegastric cancer develops in patients who have severe atrophicgastritis in association with intestinal metaplasia.24 Progressionof atrophic gastritis can be caused by H. pylori infection.25Our results confirm the hypothesis of Correa24 that severe atrophicgastritis accompanying intestinal metaplasia caused by persistentH. pylori infection is closely related to the development ofintestinal-type gastric cancer.
Since atrophic changes are not severe in diffuse-type gastriccancer,25,26 it was previously considered to have little relationto H. pylori infection. However, epidemiologic and histopathologicalstudies27,28 have shown that the development of diffuse-typecancer is also closely related to H. pylori infection. In ourstudy, many of the patients with diffuse-type gastric cancerhad moderate atrophic changes and pangastritis. Our resultssupport the hypothesis of Sipponen et al.25 and Solcia et al.26that diffuse-type gastric cancer develops during the progressionof atrophic gastritis in patients with H. pylori infection andis associated particularly with active gastritis.
In our study, gastric cancer developed in patients with nonulcerdyspepsia, active gastric ulcers, and hyperplastic gastric polyps,but no gastric cancers developed during follow-up in patientswith active duodenal ulcers. Hansson et al.29 have shown thatgastric ulcer is associated with a high risk of gastric cancer,whereas duodenal ulcer is associated with a low risk. Patientswith gastric ulcers typically have atrophic gastritis and corpus-predominantgastritis. Patients with duodenal ulcers have few atrophic changesand have antrum-predominant gastritis.30,31,32 Thus, there shouldbe a higher rate of gastric cancer in patients with gastriculcers than in those with duodenal ulcers. Diffuse-type gastriccancer is predominant in patients with gastric ulcers, manyof whom are relatively young. In young patients with gastriculcers, it is therefore necessary to perform careful follow-upto detect diffuse-type gastric cancer even after ulcers havehealed. No gastric cancer developed after eradication of H.pylori in 253 infected patients in our study, although the durationof follow-up was relatively short. We have previously shownthat in patients with early gastric cancer that is treated byendoscopic mucosal resection, eradication of H. pylori preventsthe development of new cancer or the continued growth of occultcancer (i.e., cancer undetectable by endoscopy at the time ofinitial treatment).33
In conclusion, we found that H. pylori infection is associatedwith the development of both intestinal-type and diffuse-typegastric cancer. Among infected patients, those with severe atrophyaccompanying intestinal metaplasia, corpus-predominant gastritis,or both are at particularly high risk.
Supported in part by a grant-in-aid for cancer research (8-14)from the Ministry of Health and Welfare of Japan.
Presented in part at the annual meeting of the American GastroenterologyAssociation, San Diego, Calif., May 20, 2000.
We are indebted to Professor Anthony Axon (of the Center forDigestive Disease at the General Infirmary at Leeds, UnitedKingdom) and to Professor Manfred Stolte (of the Institute ofPathology, Klinikum Bayreuth, Germany) for their helpful suggestionsand to Ms. Masako Hiramatsu and Ms. Chiyo Maruyama for theirexcellent technical assistance in the endoscopy unit.
Source Information
From the Departments of Gastroenterology (N.U., S.O., S.Y., N.M., S.Y., M.Y.) and Clinical Pathology (K.T., N.S.), Kure Kyosai Hospital, Kure City; and the Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka (R.J.S.) — both in Japan.
Address reprint requests to Dr. Uemura at the Department of Gastroenterology, Kure Kyosai Hospital, 2-3-28 Nishi-chuo, Kure City, Japan, or at n-uemura{at}mua.biglobe.ne.jp.
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