[Barrett's esophagus: Diagnosis, treatment and minimizing of risk]. / Diagnos, behandling, risk och kontroll vid Barretts esofagus.

Gastroesophageal reflux disease (GERD) is characterized by regurgitation of gastric juices into the esophagus. This has an erosive effect on the mucosa with accompanying symptoms, such as heartburn, acid regurgitation and positional-/exertion--induced chest pain. The associated inflammation in the multi-layered squamous epithelium of the esophagus (esophagitis) can usually be seen macroscopically at gastroscopy and is always possible to demonstrate microscopically as well-characterized changes. GERD is abundant in the adult population in the Western world, and the incidence appears to be increasing. Serious manifestations of GERD include the appearance of esophageal injury (esophagitis) and columnar lined esophagus (Barrett's esophagus) and, in rare cases, peptic stricture. The glandular-transformed (metaplastic) mucosa carries its clinical significance by constituting the basis for continued cell transformation (development of dysplasia), which eventually might lead to esophageal adenocarcinoma (EAC). EAC is an aggressive form of cancer whose incidence continues to increase in particular in the Western part of the world. In this article the potential mechanisms for the development of the metaplastic glandular epithelium and its progression to dysplasia and cancer is reviewed. In addition, recommendations are given on how important signals about future risks can be captured and managed and how these risks can be minimized and preferably prevented.

Biliary sphincterotomy does not relate to diarrhoea or major changes in bile acid synthesis or plasma lipids.

OBJECTIVES: Bile acid (BA) malabsorption may occur after cholecystectomy. Bile may flow more freely into the duodenum after endoscopic sphincterotomy (EST), in part resembling the situation after cholecystectomy. The (75)SeCHAT test used to diagnose BA malabsorption correlates inversely with synthesis and faecal excretion of BAs. The BA intermediate 7alpha-hydroxy-4-cholesten-3-one (C4) mirrors BA and lathosterol cholesterol synthesis. The aim was to study whether EST causes BA diarrhoea and alterations in BA synthesis or lipid profiles. MATERIAL AND METHODS: Twelve patients underwent the (75)SeHCAT test prior to and 3 months after undergoing EST and a further 22 only after EST. The Gastrointestinal Symptom Rating Scale (GSRS), 1 week daily stool frequency and consistency, C4, lathosterol, cholesterol and triglycerides were investigated. The (75)SeHCAT values of 29 healthy subjects served as controls. RESULTS: Stool frequency (median 1/day, IQR (interquartile range): 0.7) and consistency (median: 3, IQR: 0.65) were normal and none reported diarrhoea after EST (n=34). The GSRS scores were normal. There was no significant change in (75)SeHCAT (median 22%, IQR 29% versus 19.5%, IQR 25, n=12). There was a trend towards lower (75)SeHCAT after EST compared with the controls (median 26%, IQR 32, n=34 versus median 38%, IQR 19.5, n=29, p=0.075) and higher lathosterol (median 47.1 mg/mole, IQR 32.7 versus median 52.5 mg/mole, IQR 35.6, n=14, p=0.055). The C4 and lipids did not change significantly. CONCLUSIONS: EST did not induce diarrhoea and in line with this BA synthesis and serum lipids are unaltered.