Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego · 2002
[Helicobacter pylori CagA(+) infection in gastric cancer patients].
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Ławniczak MaŁgorzata, Starzyńska Teresa
Аннотация
STUDY AIM: The aim of the study was to evaluate the role of Helicobacter pylori CagA(+) infection in gastric cancer.
MATERIAL AND METHODS: 475 patients were included into the study (270 gastric cancer patients and 205 control subjects). Helicobacter pylori CagA status was determined by enzyme-linked immunoabsorbent assay (ELISA). The frequency of H. pylori CagA infection in gastric cancer patients and control group was compared. The relationship between presence of anti-H. pylori CagA antibodies and selected clinical and pathomorphological parameters was analysed.
RESULTS: Gastric cancer patients and controls had the same prevalence of H. pylori CagA antibodies (54.4 vs 52.5%; p = 0.078). The persons with H. pylori CagA(+) and CagA(-) were at the same risk for developing gastric cancer (OR = 1.08; 95%CI = 0.66-1.49). However subgroup analysis showed that the risk of gastric cancer development in H. pylori CagA(+) depended on age being 2 times higher for young people (15-40 years) (OR = 2.0; 95% CI = 0-4.25) and four times higher for those under the age of 30 years (OR = 4.0; 95%CI = 0-15.9). There was a positive relationship between H. pylori CagA(+) infection and age (p = 0.043). H. pylori CagA(+) infection was independent of sex, family history of cancers, duration of symptoms, ABO blood group, tumour site, stage, histology and p53 accumulation in cancer gastric tissue.
CONCLUSION: Our study shows that H. pylori CagA(+) infection increases the risk for developing gastric cancer in young persons and does not protect the host against cardia cancer. The results suggest also that infection by H. pylori CagA(+) in gastric cancer has no influence on p53 gene mutation development.
MATERIAL AND METHODS: 475 patients were included into the study (270 gastric cancer patients and 205 control subjects). Helicobacter pylori CagA status was determined by enzyme-linked immunoabsorbent assay (ELISA). The frequency of H. pylori CagA infection in gastric cancer patients and control group was compared. The relationship between presence of anti-H. pylori CagA antibodies and selected clinical and pathomorphological parameters was analysed.
RESULTS: Gastric cancer patients and controls had the same prevalence of H. pylori CagA antibodies (54.4 vs 52.5%; p = 0.078). The persons with H. pylori CagA(+) and CagA(-) were at the same risk for developing gastric cancer (OR = 1.08; 95%CI = 0.66-1.49). However subgroup analysis showed that the risk of gastric cancer development in H. pylori CagA(+) depended on age being 2 times higher for young people (15-40 years) (OR = 2.0; 95% CI = 0-4.25) and four times higher for those under the age of 30 years (OR = 4.0; 95%CI = 0-15.9). There was a positive relationship between H. pylori CagA(+) infection and age (p = 0.043). H. pylori CagA(+) infection was independent of sex, family history of cancers, duration of symptoms, ABO blood group, tumour site, stage, histology and p53 accumulation in cancer gastric tissue.
CONCLUSION: Our study shows that H. pylori CagA(+) infection increases the risk for developing gastric cancer in young persons and does not protect the host against cardia cancer. The results suggest also that infection by H. pylori CagA(+) in gastric cancer has no influence on p53 gene mutation development.