Significance of Chronic Atrophic Gastritis in First-Degree Relatives of Patients With Gastric Cancer

Gastric cancer is the fourth most common cancer worldwide with approximately 934,000 new cases in 2002. Also, an estimated over 700,000 annual death make it the second most common cause of death from cancer (1). In Iran, gastric cancer is the first and third most common cause of cancer in males and females, respectively and its overall incidence is above the world average (2). Although the worldwide incidence of the gastric cancer has decreased rapidly over the recent few decades, its incidence in Iran does not show any decrease in the same time period (2-4). Ardabil in northwest of Iran is one of the areas with highest incidence of the gastric cancer, with ASR of 49.1 and 25.4 for males and females, respectively (5). Chronic atrophic gastritis (CAG), as an intermediate step of carcinogenesis cascade of gastric cancer has showed a strong relationship with gastric adenocarcinoma, particularly intestinal subtype (6). Chronic atrophic gastritis is defined as the loss of appropriate mucosal glandular tissue and/or the loss of appropriate mucosal glandular tissue for the biopsy site according to the updated classification and grading of gastritis; the updated Sydney system. There is a high prevalence of CAG in; i.e. Japan with histologic detection rate of 53%, Estonia, in up to 64% of studied population, Finland, between 27% and 44%, and in Columbia with 45% in comparable age groups (7-10). On the other side, lower prevalence of CAG (21%) in Tehran, which is an intermediate risk area for gastric cancer, is not an unexpected finding (11). Results of investigations using histologic methods for diagnosis of CAG in low-risk populations revealed the similar lower prevalence of this precancerous change (e.g. 28% in Sweden and 22% in Aus-tralia) (12, 13). Helicobacter pylori infection induces superficial non-atrophic gastritis which progresses to CAG with loss of acid secretion and then to dysplasia and cancer. A variety of bacterial, host and environmental factors are known to contribute to the progress through these different pre-cancerous stages (14). Traditionally, relationship between CAG and gastric cancer has been defined for noncardia cancer, but recent studies showed that even adenocarci-nomas located at the cardia region may demonstrate a relationship with CAG, particularly those with the least relationship with gastroesophageal reflux disease (15, 16). In fact, simplifying the relationship between H. pylori, CAG and gastric cancer may result in the ignorance of other intermediate risk factors. Diversity in exposure to dietary factors can …