Gallstones: an intestinal disease?

Abstract

Current evidence suggests that impaired intestinal motility may facilitate gallstone formation by influencing biliary deoxycholate levels or by modulating interdigestive gall bladder motility (fig 2), although a primary intestinal defect in gallstone pathogenesis has not yet been demonstrated. In the cold war period, most interesting events, from a political point of view, occurred at the border between capitalist and communist systems, near the iron curtain. Similarly, the gall bladder and biliary tract can be viewed as the border between liver and intestinal tract, where many interesting things occur with profound impact on both systems. Combined efforts by researchers in the field of hepatology and gastrointestinal motility should brake down the Berlin wall of ignorance of one of the most common diseases in the Western world.

Figure 2

Potential mechanisms of cholesterol gallstone formation.

Figure 1

The intestinal migrating motor complex occurs periodically (1-2 hour cycle) during the fasting state and is characterised by three phases: contractile activity is absent during phase I; irregular activity occurs during phase II; and there are intense, regular coordinated contractions during phase III. Significant periodic gall bladder contraction occurs before phase III and is associated with a rise in plasma motilin concentrations.