Duodenal and gastric contents do reflux into the oesophagus and acid alone certainly causes oesophageal damage which will be worsened by pepsin. In the patient who has undergone gastrectomy duodenal secretions may also be harmful. There is evidence that when the two mix there may be a toxic synergism, leading to mucosal disruption and intracellular damage to oesophageal cells which produces the clinical picture of reflux oesophagitis, with or without symptoms. Clear evidence of the toxicity of duodenal refluxate in humans is lacking, but the ability to measure bile and acid reflux continuously, together with a method of detecting oesophageal damage at a cellular level should help to solve this long debated problem.

A consensus development approach was used to assess the extent to which doctors in the UK agreed about the appropriate indications for cholecystectomy. Two panels, one composed entirely of surgeons and one containing a mix of relevant specialists, were asked to rate a series of possible indications. A consensus was achieved for 61% (surgical panel) and 67% (mixed panel) of indications considered. The surgical panel considered more indications as being appropriate for cholecystectomy (29% v 13%) and fewer indications as being inappropriate (27% v 50%) than the mixed panel. For between one third and a half of all indications, the panels were unable to reach agreement, partly as a result of differences in views as to the role of endoscopic sphincterotomy.

The hydrophilic bile acid ursodeoxycholic acid has recently been shown to reduce biochemical markers of both cholestasis and hepatocellular damage in patients with chronic liver diseases. The most compelling evidence available is for chronic cholestatic liver diseases, in particular primary biliary cirrhosis, primary sclerosing cholangitis, and cholestasis associated with cystic fibrosis. The effects may be less beneficial in patients with advanced liver disease from these conditions. Data from placebo controlled trials are now available in support of earlier uncontrolled observations, but it is not yet clear whether short term benefit results in an improvement in longterm prognosis. The mechanism of action of the compound seems to reside in its displacement of toxic hydrophobic bile acids from both the bile acid pool and hepatocellular membranes. There may be an independent effect on bile flow, which could be of particular importance in cystic fibrosis, and possibly an effect on the immune system. Ursodeoxycholic acid should now be regarded as occupying a central place in the medical management of chronic cholestatic liver diseases, in particular primary biliary cirrhosis, because it improves cholestasis and reduces hepatocellular damage and it is not toxic. Research should now be targeted on whether treatment with ursodeoxycholic acid, initiated early in cholestatic liver conditions, improves the long-term outcome.

The widespread availability of ultrasound imaging has led to more frequent recognition of cystic disease affecting the liver and biliary tract. There is a wide range of possible causes. Cystic disease of infective origin is usually caused by an Echinococcal species, or as the sequel of a treated amoebic or pyogenic abscess. The clinical and radiological features are often then distinctive and will not be dwelt upon in this review, except in respect of their contribution to the differential diagnosis of non-infective disorders. The principal non-infective cysts can be conveniently divided between the simple cyst, the polycystic syndromes (usually with coexistent renal disease), Caroli's syndrome, and choledochal cysts. The overlap between constituent members of these groups, and the association of cystic disease with hepatic fibrosis (especially with congenital hepatic fibrosis) has attracted considerable attention, and it has been suggested that they may all be considered to belong to a hepatobiliary fibrocystic continuum. In addition there are a variety of cystic neoplasms and a miscellany of unusual forms.