Bile acids and the increased risk of colorectal tumours after truncal vagotomy

Abstract

An association between colorectal cancer and previous peptic ulcer surgery is reported. In a prospective screening study, 100 asymptomatic patients (80 men and 20 women) who had undergone truncal vagotomy at least 10 years previously were investigated by barium enema, colonoscopy and gallbladder ultrasonography. Control data were obtained from forensic autopsy subjects. The incidence of neoplasms greater than or equal to 1.0 cm in the vagotomized group was 14 per cent (11 adenomas, 3 carcinomas) and 3 per cent in controls (P = 0.01). Duodenal bile obtained at endoscopy from 21 vagotomized patients with normal gallbladders and from 21 control patients undergoing endoscopy was analysed by high performance liquid chromatography. The mean percentage of cholic (CA), chenodeoxycholic (CDCA), deoxycholic (DCA) and lithocholic (LCA) acids in the bile of vagotomized patients was 32.3, 45.6, 20.7 and 1.4 per cent respectively compared with 45.3, 36.2, 17.9 and 0.7 per cent respectively in controls. The increased proportions of CDCA and LCA and decreased proportions of CA in the duodenal bile of vagotomized patients were significant (P less than 0.001; P = 0.02; P = 0.007). Abnormalities in bile acid metabolism may help to explain the increased risk of colorectal neoplasia 10 years after truncal vagotomy.

Low tumour cell proliferation at the invasive margin is associated with a poor prognosis in Dukes’ stage B colorectal cancers

“…Factors such as secondary bile acids (mainly lithocholic acids), other steroid-derived compounds, short-chain fatty acids and the direct influence from the bacterial content are known to affect the proliferation of colorectal cells (Mullan et al, 1990). However, we found no correlation between the depth of tumour invasion and the proliferative activity at the invasive margin.…”

“…Several faecal factors, such as secondary bile acids and short chain fatty acids, are known to have an effect on proliferation in colonic cells (Mullan et al, 1990;Butler et al, 1992), and therefore these factors could be responsible for the systematic differences between separate compartments in colorectal cancer. If this hypothesis is correct, the proliferative activity is expected to decrease as the diffusion distance for faecal factors increases.…”

Occurrence of non‐gastric cancer in the digestive tract after remote partial gastrectomy: Analysis of an Amsterdam cohort

“…Our analysis did not confirm an increase in esophageal cancer, and the risk of colorectal cancer was decreased in postgastrectomy patients, contrary to the observations of others (Shearman et al, 1970;McLean Ross et al, 1982;Bundred et a/., 1985;Caygill et al, 1987;Mullan et al, 1989). Also, we found no increase in small-intestine cancer.…”

“…N-nitroso compounds and bile have been linked to cancer growth at other digestive tract sites (Wynder et al, 1973;Sagar, 1989;Spigelman et al, 1989). Indeed, several studies have reported an increased risk of pancreatic (McLean Ross et ul., 1982;Mack et al, 1986;Caygill et al, 1987;Offerhaus et al, 1987), biliary tract (Caygill et al, 1988), colorectal (Mclean Ross et al, 1982;Watt et al, 1984a,b;Bundred et al, 1985;Caygill et al, 1987;Mullan et al, 1989), and esophageal (Shearman et al, 1970;Caygill et al, 1987) cancer after peptic ulcer surgery, while other reports reveal no increased risk (Maringhini et al, 1987;Thiruvengadam et al, 1988).…”

Systematic heterogeneity and prognostic significance of cell proliferation in colorectal cancer

“…Such proliferative stimulators are, for example, secondary bile acids, mainly lithocholic acid, other steroid-derived compounds, short-chain fatty acids and the direct influence from the bacterial content (Mullan et al, 1990). However, local non-specific regenerative factors from the ulcerative process at the luminal border can also increase the luminal proliferative activity.…”