Hypergastrinemia and H. Pylori Infection as a Risk Factor for Colorectal Cancer

Abstract

AS Al-Mulhim, H Al Hosieny Mohammad, Hypergastrinemia and H. Pylori Infection as a Risk Factor forColorectal Cancer. 2002; 22(3-4): 252-255 Several lines of evidence support an etiological role for gastrin in colon cancer carcinogenesis. The hormone exerts trophic effects on the mucosa of gastrointestinal tract including that of the colon.1 Gastrin has also been shown to be mitogenic for colonic cancer cells in vitro, and stimulate growth of experimental colonic tumors in rodents.3,4 These trophic effects can be inhibited by gastrin receptor antagonists acting on high-affinity gastrin/cholecystokinin B (CCK-B) receptors.5-8 Such receptors have also been shown on colorectal tumor cell lines.9,10 In addition, some authors have reported that patients with conditions that result in hypergastrinemia (such as those with pernicious anemia and those who have undergone truncal vagotomy or Billroth I gastrectomy) are at increased risk of subsequent development of colorectal cancer, 11-13 although others have not confirmed these findings.14,15 In 1989, Smith et al. 9 showed raised fasting serum gastrin (FSG) concentration in patients with adenomatous polyps and colon cancer. Similar findings with fasting and postprandial hypergastrinemia in patients with colon cancer have been shown by others, [16][17][18][19][20] although some other investigators have been unable to verify these results. [21][22][23] The aim of this study was to compare the serum gastrin levels (fasting and meal-stimulated) in patients with colorectal cancer and closely-matched control subjects. In addition, we proposed to assess the role of the presence of Helicobacter pylori infection and the effect of tumor resection on serum gastrin levels. Materials and MethodsA total of 44 patients included in the present study were divided into two groups: the first group of 24 patients represented the colorectal cancer group. These were newly diagnosed, histologically confirmed colorectal carcinoma patients who were in the hospital awaiting elective surgery. After clinical assessment and full investigation, eight of the patients were found to be inoperable because of distal spread of the tumor. The second group comprising 20 inpatients were the control group. Included in this group were patients who were awaiting surgery under general anesthesia for relatively minor conditions (e.g., inguinal hernia, hemorrhoids and hydrocele), and had no history of gastrointestinal disease. Patients with history of malignancy at any other site, treatment with acid-suppressing drugs (H2-antagonists or proton pump inhibitors), previous peptic ulcer anemia, renal failure, hypercalcemia, recent antibiotic therapy (within one week) or any form of bowel preparation in the two days before the tests were excluded from the study. Clinical characteristics of the patients are summarized in Table 1.In the measurement of basal and meal-stimulated serum gastrin levels, blood samples (5 mL) were taken when fasting, and 30 minutes after a standard hospital breakfast. The samples were centrifu...

Cytotoxin-associated gene A increases carcinogenicity of helicobacter pylori in colorectal adenoma

“…22,23 There are recent reports illuminating that an elevated gastrin level promotes CRA tumorigenesis, which could also be seen in our multivariate logistic regression model analysis. 24,25 Considering that Hp stimulates gastrin expression, and that both Hp and gastrin exert the carcinogenic effect of CRA, we therefore hypothesized that Hp might stimulate gastrin expression and then promote tumor progression in CRA patients. However, because the relevant information is still limited, we compared the serum gastrin expression and inter-tumor ki-67 (a well-known biomarker for cancer cell proliferation) expression between Hp + CagA + /Hp + C agA − patients and Hp − patients, and the results disclosed that both of them were increased in Hp + CagA + patients and Hp + CagA − patients compared to Hp − patients, suggesting that Hp might promote CRA progression by advocating gastrin expression, which might be caused by Hp-induced atrophy changes of the gastric body mucosa, leading to increased levels of serum gastrin by negative feedback on antral G cells, and subsequently stimulated tumor cell proliferation of CRA, which caused an elevated ki-67 expression.…”

Predictive Effect of Helicobacter pylori in Gastric Carcinoma Development: Systematic Review and Quantitative Evidence Synthesis

“…This integrative model also helps explain the interest in H. pylori's potential role in carcinogenesis of non-gastric malignancies. Furthermore, studies have shown its associated risk with non-Hodgkin's lymphoma, pancreatic cancer, colorectal cancer, and even lung cancer with varied responses [20][21][22][23].…”