Defective biliary secretion during total parenteral nutrition: probable mechanisms and possible solutions.

Cholestasis associated with TPN is now diminishing in frequency. One factor is likely to be the early initiation of oral feeding. One of the effects of oral intake is to restore the enterohepatic circulation of bile acids. This in turn promotes lipid absorption, which leads to improved nutrition and a decreased in mucosal atrophy. The role of the enterohepatic cycling of bile acids has been explored in this review. In infants or children on TPN who have bile acid malabsorption, UDCA can be used to correct decreased secretion of endogenous bile acids. However, controlled studies showing that UDCA actually decreases moribidity and mortality in infants on prolonged TPN have not yet been performed and they are sorely needed. UDCA is nontoxic and acts as a natural bile acid after conjugation. An improved formulation of UDCA with rapid and efficient intestinal absorption has been developed, but the optimal formulation of UDCA is still not available. Cholylsarcosine, a new conjugated bile acid analogue that has been developed as a bile acid replacement agent, improves lipid absorption in animals with steatorrhea caused by bile acid malabsorption and intestinal resection. However, this compound has not been tested clinically.