The influence of cholecystectomy on the development of carcinoma of the colon is investigated. The experimental results show a significantly increased rate of carcinoma of the colon induced by subcutaneous injection of 1,2-Dimethylhydrazin (DMH) in the mouse after cholecystectomy. After 10 weekly injections of 15 mg/kg DMH, 70% of the animals with cholecystectomy developed carcinoma. Only 16% of the mice with similar treatment but without cholecystectomy had carcinoma. The cocarcinogenic effect of cholecystectomy is assumed to be due to the increased production of secondary bile salts by the colonic bacteria and the lacking of the resorptive function of the gallbladder for some carcinogenic substances passing through the liver. The background of this experimental studies are the clinical findings that 10% of patients with carcinoma of the large bowel had previous cholecystectomy.

No abstract

No abstract

Endoscopic and biopsy studies were undertaken in 92 patients who had undergone partial gastric resection (end-to-end gastroduodenostomy, Billroth I) one to seven years previously. In addition, the amound of duodeno-gastric reflux was evaluated by measuring bromsulphalein excretion in gastric juice. Atrophic gastritis occurred in 36%, while superficial gastritis was noted in 49% of patients. The degree and severity of the inflammatory changes was most marked near the anastomosis. The severity of the duodenal gastric reflux was decisive in the development of the atrophic mucosal changes. There was no demonstrable relationship between the degree of mucosal changes and the interval since the operation.

The major urinary metabolite of 14C-epichlorohydrin, after oral administration to rats, was identified previously (Gingell et al. 1985) to be N-acetyl-S-(3-chloro-2-hydroxypropyl)-L-cysteine (ACPC) at 36% of the administered dose. In a similar study reported here, 1,2-dibromo-3-chloropropane (DBCP) was metabolized to at least 20 radioactive urinary metabolites. ACPC was only a minor metabolite (4%) of DBCP. Epichlorohydrin was metabolized in vitro by rat liver microsomes to alpha-chlorohydrin, but DBCP was not metabolized to epichlorohydrin or alpha-chlorohydrin under similar conditions. Covalent binding of radioactivity to liver microsomal proteins occurred for both substrates, but was less for 14C-epichlorohydrin than for 14C-DBCP. Addition of 3,3,3-trichloropropylene oxide, an inhibitor of epoxide hydrolase, increased the extent of protein binding of epichlorohydrin, but decreased the amount of 14C-DBCP which was bound. The data indicate the epichlorohydrin is not a significant in vivo nor in vitro metabolite of DBCP in the rat, and is unlikely to be responsible for the toxicity of DBCP.