Defective acid base regulation by the gall bladder epithelium and its significance for gall stone formation.

Abstract

Gall stone disease is a common cause of morbidity and cholecystectomy represents the most common elective abdominal operation in Western society. In the United Kingdom alone about 20% of the population may expect to develop cholelithiasis.' Initially most research had been focused on the biochemical changes that occur in bile during gall stone formation. Recent years have seen significant advances in our knowledge and it is now recognised that the gall bladder is not a passive reservoir but has several absorptive, secretory, and motor functions, which are integrated to produce concentrated bile. The interactions between gall bladder bile and mucosa are of paramount importance to maintain the fine balance between concentration and precipitation of the biliary constituents. The gall bladder mucosa has one of the highest rates of water absorption in the body and an 80-90% decrease in the initial volume of bile occurs within the gall bladder. This is achieved by the coupling of active sodium transport and passive water absorption resulting in isotonic fluid absorption.2 Fluid transport is subject to a variety of influences such as chronic inflammation or the presence of pharmacological agents (prostaglandins, prostacyclin, and various gastrointestinal peptides); fluid absorption is higher in daytime and is reversed to net secretion with feeding.3 Electrolyte transport has been extensively investigated; chloride is actively absorbed in exchange for bicarbonate, and potassium moves from the mucosa to the serosa according to electrochemical gradients.4 5 Calcium is also absorbed and its distribution across the gall bladder epithelium is of importance in the formation of gall stones.6