Postprandial hypergastrinaemia in patients with colorectal cancer.

Abstract

Gastrin is trophic to colon cancers that possess gastrin receptors. Whether fasting serum gastrin concentrations are high in patients with colon cancer is controversial. We therefore studied the effect of food on serum gastrin concentrations in patients with colon cancer and control subjects. Fasting serum gastrin was greater, though not significantly so, in patients with colon cancer before surgery (mean (SD) 17*4 (3.6) pmoVI, n=16) compared with control subjects (12.6 (1.9) pmol/l, n=14). Postprandial increases in serum gastrin were significantly and persistently higher than normal in the cancer patients. Blood samples were taken while fasting and then at 10, 20, 40, 60, 90, and 120 minutes after a standardised hospital meal. In the patients with cancer, these studies were performed on the day of admission before bowel preparation, and were repeated 10 days after surgery, immediately before hospital discharge. The blood was drawn into EDTA bottles containing 10 units of Trasylol (Bayer UK, Reading) and immediately placed on ice. Plasma was separated by centrifugation (3000 rpm for five minutes) within 30 minutes of collection and was stored at -70°C before gastrin assay.At surgery, samples (1 g) of tumour and healthy colonic mucosa from the distant resection margin were collected and stored dry at -70°C. These specimens were then extracted by mincing and boiling in distilled water for 30 minutes at a volume of 5 ml water/g tissue (1:5 dilution). The supernatant was separated by centrifugation and stored again at -70°C for subsequent analysis. As a positive control for our extraction procedure, samples of normal gastric antrum taken at gastric surgery were also examined for gastrin concentration.Determination of the gastrin concentration in both serum and tissue extracts was by radioimmunoassay using antibody G179 (a gift of Professor S R Bloom) which recognises the large C terminal fragments of gastrin -that is, G-34 and G-17 -with less than 2% cross reactivity to .'3 The data were analysed using a two way analysis of variance (ANOVA), and where the ANOVA showed a significant difference, the groups at each time point were compared using a Student's t test (p<005 considered significant). ResultsThe results of the effect of feeding on serum gastrin are summarised in Figure 1. Fasting serum gastrin values were higher in the colon cancer patients before surgery (mean (SD)

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

“…This result is keeping with findings by Wong et al 20 Other studies have been unable to demonstrate a decrease in plasma gastrin levels after apparently curative resection of colon cancer. 21,26 In our study, however, the postoperative gastrin levels remained persistently elevated and much higher in patients with colorectal cancer than in control (P<0.001).…”

“…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.…”

“…These results are in agreement with findings by some investigators. 9,[16][17][18][19][20] Other investigators have found that patients with colorectal tumors have gastrin levels similar to those in the normal population. [21][22][23] Some reasons may account for these conflicting results.…”

Prognostic significance of gastrin expression in patients undergoing R0 gastrectomy for adenocarcinoma

“…Certainly, studies in colorectal cancer have shown low gastrin levels within the tumor and increased circulating nonamidated gastrin, i.e., only partially processed gastrin, suggesting that the tumor may be secreting gastrin with resulting hypergastrinemia [20]. This theory is supported by reports of reductions in serum gastrin levels after resection of primary colorectal tumors [21,22] although confl icting evidence exists [23,24]. Serum gastrin measurement may be unreliable for two reasons: commercial antisera react with amidated gastrin, and as nonamidated gastrin is the fully active biological entity, the results of such assays are suspect.…”

A Retrospective Analysis of the Role of Proton Pump Inhibitors in Colorectal Cancer Disease Survival

“…In vitro studies have shown that, in turn, hypergastrinemia promotes cell proliferation and cell migration and inhibits apoptosis-several factors that favour the development and progression of neoplasias of the gastrointestinal tract [18][19][20][21][22] . Animal models have demonstrated that ppis induce hypergastrinemia in mice and rats, enhance proliferation of colonic mucosa cells in those organisms, and promote adenoma progression [23][24][25] .…”