Correlation of Helicobacter pylori and gastric carcinoma.AK Khanna, P Seth, G Nath, VK Dixit, M Kumar
Department of Surgery, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221005, India. , India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 12082323
Source of Support: None, Conflict of Interest: None
BACKGROUND: Difference of opinion about the prevalence of H. pylori association with gastric cancer exists in the literature. AIMS: To study the correlation of Helicobacter pylori (H. pylori) to gastric carcinoma. METHODS: 50 proved cases of gastric cancer were studied by rapid urease test, culture, histopathology and ELISA test for H. pylori IgG. RESULTS: 68% of cases of gastric cancer were found to be positive for H. pylori infection as compared to 74% of healthy controls. CONCLUSIONS: The prevalence rate of H. pylori infection in our patients of gastric cancer was lower than in the control population though statistically not significant, suggesting that H. pylori may not be responsible for gastric carcinogenesis in this population.
Keywords: Adult, Case-Control Studies, Enzyme-Linked Immunosorbent Assay, Female, Helicobacter Infections, complications,epidemiology,Helicobacter pylori, isolation &purification,Human, Male, Middle Age, Prevalence, Stomach Neoplasms, microbiology,pathology,
Gastric carcinoma, by far is one of the leading killers in the arena of oncology despite worldwide efforts to meet the challenges posed by the disease. Since the discovery of H. pylori in 1983 by Warren and Marshall,  it has been the topic of immense research leading to its proven association with peptic ulcer disease. Several western studies have also shown a definite association between gastric neoplasia and H. pylori infection but the results of various studies is conflicting. Not many Indian studies have been done to look into its role in carcinoma of stomach. This study intends to determine the overall prevalence of H. pylori infection in patients with gastric carcinoma in our setup.
The study was carried out on 50 consecutive patients with histologically proved gastric carcinoma from 1997-99. The patientís blood and gastric mucosa (endoscopic and resected specimen) were obtained. The six biopsy specimens were obtained, five from gastric mucosa from antrum and one bit from corpus. All the specimens were subjected for rapid urease test, culture, histopathological examination and ELISA for detection of anti H. pylori IgG. The culture were done on Campy-BAP plate and studied after 48-72 hrs. ELISA test was done by UBI MagiwelTM H. pylori IgG Kit and the results were interpreted as negative (<30 Eu/ml), equivocal (30-40 Eu/ml) and positive (>40 Eu/ml).
Of 50 patients with gastric cancer, H. pylori was detected by one or other method in 33 cases (66%). Patients less than 45 years had positive results in 75% (9/12) while more than 45 years had 63.1% (24/38) positive results. (Z= 0.76, not significant) As per the site distribution of Gastric cancer, antral lesions comprised 66% with cardiac and body cancers at 16% and 18% respectively. H. pylori was positive in 50% (4/8) cases of lesion in cardia, 66.6% (6/9) in body of stomach and 69.7% (23/33) in antral lesions. In age matched healthy historical controls, the prevalence of H. pylori is 74% studied by ELISA from serum of controls (Z=1.29, not significant)
Though the incidence of gastric carcinogenesis has decreased markedly in the western world it remains one of the common malignancies in many parts of the globe. The role of H. pylori in gastric carcinogenesis is a subject of increasing interest. Reports regarding relationship of H. pylori infection to gastric carcinogenesis are conflicting. Some epidemiological data point to this association although several unresolved issues still cast doubts on the real weight of the association. These issues are that male to female ratio of gastric cancer range from 1.5-4:1 in all studies but prevalence of H. pylori is same in both sexes; the prevalence of H. pylori is as high as 90% in several developing countries whereas frequency of gastric cancer is very low.
Atrophic gastritis and intestinal metaplasia are well-accepted pre-cancerous conditions for gastric cancers. 80% of gastric cancers are related to H. pylori gastritis. H. pylori is not necessarily important for the development of gastric malignancy in atrophic gastritis although H. pylori is the key phenomenon in the triggering of gastritis related processes and the subsequent carcinogenic events.
In our study younger patients of less than 45 years had the prevalence of 75% as compared to 63% in older patients though it was not statistically significant. This falls in concordance with the observation of others that younger patients with H. pylori are at higher risk for developing gastric cancer., H. pylori infection was present in 66% of our cases against 74% in the control group. Many authors have documented a higher overall H. pylori positivity rate. The highest rates are from Shibata et al  in Japan with value up to 90%.
H. pylori has been associated with location of the tumour as tumour of the body and antrum has been associated with H. pylori while cardiac tumours is unrelated. The site distribution of gastric cancer was different in our study.
Antral lesions comprised 66% of the study group with cardiac and body cancers at 16% and 18% respectively. Shibata et al found maximum incidence of gastric cancer in body (52%) followed by antrum and cardia at 38% and 10% respectively. The prevalence of H. pylori lori in our study was 50% in cardia, 66.6% in body and 69.7% in antrum though there was no statistically significant difference between the various locations. Shibata et al found the positivity to be 60-80%, 69-96.2% and 78.9-84.2% in the three sites respectively. Though our findings are somewhat different in respect to maximum incidence, they corroborate the hypothesis of Huang et al that H. pylori infection is more associated with non-cardiac gastric cancer when compared to lesions near cardia.
From the review of various studies it was concluded that H. pylori infection is a risk factor for gastric cancer and the heterogeneity of reported results is caused by the difference in the selection of controls, patient age, site and stage of
gastric cancer.  H. pylori appears to play a role in the initial step as a causative agent for chronic inflammation but development of gastric carcinoma is multi-factorial. The seroprevalence of H. pylori was studied in a population from two areas of Croatia with significantly different average gastric cancer cumulative incidence and mortality rates and revealed no association between prevalence of H. pylori and the level of incidence and mortality from gastric cancer.
An index of identifying patient with H. pylori and carrying a higher risk of gastric carcinoma has been proposed based on the infiltration with lymphocytes, plasma cells, neutrophil infiltration and intestinal metaplasia in antrum and corpus and was suggested that this index might be a simple method of identifying patients infected with H. pylori and carrying a higher risk for gastric carcinoma.
Further testing in studies with larger sample sizes would be required to corroborate our data for use of clinicians in our country as it is amply clear that the expression of H. pylori in Indian subjects is different from that of the West.  It has been shown that H. pylori infection in India is associated with lesser degrees of metaplasia in the stomach mucosa than in the West. This suggests that probably Indians have some protective factors present Intrinsically or extrinsically (diet, environment, etc.) that prevent the inevitable progression of H. pylori infected cases to chronic atrophic gastritis and then metaplasia. This hypothesis can possibly offer a plausible reason for the relatively lower incidence of gastric cancer in our country.