What is the role of hypercholemia in the pathophysiology of cholestasis?

Updated: Aug 09, 2017
  • Author: Hisham Nazer, MBBCh, FRCP, DTM&H; Chief Editor: Carmen Cuffari, MD  more...
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Hypercholemia, or increased serum bile salt concentration, is a universal consequence of cholestasis. The transport of bile salts from plasma to bile is the principal driving force for bile formation. Failure to transport bile salts may be a principal mechanism of cholestasis or may be a consequence of the effects of cholestasis on hepatocyte function. In either case, the liver cell retains bile salts, resulting in down-regulation of new bile acid synthesis and in an overall reduction in the total pool size. Bile salts are regurgitated from the hepatocyte, which results in an increase in the concentration of bile salts in the peripheral circulation. Furthermore, the uptake of bile salts entering the liver in portal vein blood is inefficient, which results in spillage of bile salts into the peripheral circulation.

Overall, patients with cholestasis have an increase in serum concentration of bile salts, an increase in hepatocyte concentration of bile salts, a decrease of bile salts in the enterohepatic circulation, and a decrease in the total bile salt pool size.

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