Helicobacter pylori (Hp) infection has been considered to play significant roles in pathogenesis of peptic ulcer. Additionally Hp is associated with the development of gastric epithelial hyperplasia and lymphoid malignancies. The International Agency for Research on Cancer has classified Hp as a class I carcinogen and a definite cause of gastric cancer in humans. Hp infection first causes chronic active gastritis and may slowly lead to infection of whole stomach. In the late stages of infection, mucosal atrophy and intestinal metaplasia (IM), and even dysplasia (DYS) occur[1]. Chronic atrophic gastritis (CAG), IM and DYS are considered markers for development of gastric cancer in high-risk individuals. In our study we analyzed Hp infection prevalence in 486 patients with precancerous gastric lesions.

The mucosal biopsy specimens were collected from 486 patients subjected to routine gastroscopy, including 163 cases of CSG, 207 cases of CAG, 71 cases of IM and 45 cases of DYS. Biopsies were taken from five sites in the stomach: one fro m the angel, four from the lesser and greater curvature of gastric body and gastric antrum. Each biopsy was classified according to the presence or absence of CSG, CAG, IM and DYS, and scanned by Warthin-Starry method.

Data analysis was made with Chi-square test. Statistical significance was defined as P < 0.05.

Gastric pathology data was available for 486 cases. As shown in Table 1, there was no significant difference between the two sexes (P > 0.05), but the prevalence rates increased with age, being significantly higher in ≥ 56 age group than ≤ 40 group for IM and DYS (P < 0.05).

The prevalence of Hp increased steadily with increasing severity of gastric histopathology (Table 2). The detection rates of Hp in IM (76.1%) and DYS (88.9%) were significantly higher than that in CSG (23.9%, P < 0.01), and in CAG than in CSG (P < 0.05).

As shown in Table 3, the prevalence of Hp positivity tended to increase from BLC to BGC, Hp positive rates in IM and DYS were significantly higher than that in CSG in both BLC and BGC (P < 0.05).

The first compelling evidence linking Hp infection to gastric carcinoma was generated by seroepidemiologic studies[2,3], bacterial seropositivity was significantly more common in those with gastric adenocarcinoma, with a n odds ratio ranging from 2.8 to 6.0, suggesting a strong association between Hp and gastric malignancy.

Hp infection was related to both the intestinal and diffuse types of cancer as well as the precancerous lesion of IM or DYS[4], and greater than 70% of gastric carcinomas are linked to IM, although DYS may also be seen without neoplastic disease.

Our study demostrated that the prevalence rates of precancerous lesions varied with age, for IM and DYS, it had an upward trend with aging, while for CSG, it ha d a downward trend with aging, but were not different between the two sexes. The prevalence rose steadily with increasing severity of gastric histopathology, the detection rates of Hp in CAG (42.5%), IM(76.1%) and DYS (88.9%) were significantly higher than that in CSG (23.9%), suggesting that Hp may play a role in late as well as early stages of carcinogenesis.

Our study also showed that Hp positive rates in IM and DYS were significantly higher than that in CSG in the lesser and greater curvature of gastric body, suggesting the more serious the gastric histopathdogy, the higher the Hp infection rate, furthermore, the higher level of Hp infection site. The stud y suggests we should take multiple site biopsy for histopathology and Hp examination.