Hypergastrinemia Is Associated with Increased Risk of Distal Colon Adenomas

Abstract

Background/Aims:Helicobacter pylori infection is a recognized cause of hypergastrinemia, but the association of blood gastrin levels with colonic adenomas (CAs) is controversial. The aim of this study is to investigate if hypergastrinemia, H. pylori infection and/or cagA protein are risk factors for CAs. Methods: In this prospective case-control study, fasting serum samples from 78 consecutive patients with CAs and 78 demographically matched colonoscopy-negative controls were assayed for anti-H. pylori immunoglobulin G, cagA protein and serum gastrin levels. Multivariate analysis was performed to identify risk factors for colon adenomas. Results: Though prevalence of H. pylori antibodies was not significantly different, the prevalence of cagA protein was significantly higher in patients with adenomas (42.3%) as compared with controls (25.6%, p < 0.03). Mediangastrin levels were significantly higher in patients with CAs (55, 20–975 pg/ml) than in controls (45.2, 23–529 pg/ml) (p < 0.001). Hypergastrinemia (>110 pg/ml) was commoner in patients with CAs than in controls (29.5 vs. 11.5%, p = 0.006) and was the only independent risk factor for adenomas (odds ratio 3.2, 95% CI 1.4–7.5) by multivariate analysis, but not H. pylori infection or cagA positivity. There was a significant association of hypergastrinemia and distal distribution of adenomas (p < 0.002). Conclusions: Our study shows that hypergastrinemia is a risk factor for CAs, especially of the distal colon.

Elevated risk of recurrent colorectal neoplasia with Helicobacter pylori-associated chronic atrophic gastritis: A follow-up study of patients with endoscopically resected colorectal neoplasia

“…A limited number of previously conducted epidemiological studies investigating the correlation between colorectal neoplasia and gastrin, demonstrated inconsistent results. More specifically, certain studies indicated positive correlations (32), while others including a recent large-scale nested case-control study, determined no such correlation (25,33). The differences in results reported in these studies might be attributable to the fact that most commercially available assays for gastrin detect the mature, fully-amidated form of the hormone, while gastrin precursors, such as progastrin or glycine-extended gastrin, are considered to act as more important promoters of colorectal carcinogenesis (2)(3)(4)(5).…”

Role of Bacteria in Oncogenesis

“…Because H. pylori increases gastrin levels, an association between H. pylori infection and colorectal neoplasia has frequently been sought. Although the findings are still debated, H. pylori infection appears to increase the risk of colonic adenomas, particularly in the more distal colon (31,36,85,169,223). The postulated mechanism is similar to that derived for gastric cancer: H. pylori-induced hypergastrinemia influences precancerous lesions toward malignant transformation.…”

Clinicopathologic features of gastric cancer with synchronous and metachronous colorectal cancer in Korea: are microsatellite instability and p53 overexpression useful markers for predicting colorectal cancer in gastric cancer patients?

“…There are several speculations about this association. It has been assumed that H. pylori infection of the gastric mucosa leads to increased levels of serum gastrin, which may act as a growth-promoting hormone on the colon mucosa [43,44]. H. pylori could act on the colon mucosa itself and affect polyp growth or promote the development of mucosa dysplasia.…”