[Intrahepatic cholestasis].
Various effects of cholestatic drugs, bile acids, and estrogens on the hepatocyte plasma membranes, as well as their changes in the cholestatic diseases are briefly reviewed. Cyclosporin A inhibits bile salt transporter (BST) on the canalicular membrane (CM). Ethynylestradiol reduces canalicular glutathione excretion. Estradiol-17beta-D-glucuronide interacts with MDR1, and taurochenodeoxycholic acid and lithocholate-3-O-glucuronide may interact with vesicular transport system, each of which may relate with the genesis of cholestasis. In Byler disease, biliary chenodeoxycholic acid excretion is defective. Lipopolysaccharide decreases the function of canalicular multispesific organic anion transporter (MOAT) which seems the first step in septic cholestasis. Obstructive jaundice causes reduced activity of both canalicular BST and MOAT. The mechanisms of choleretic action of S-adenosylmethionine and other drugs are also reviewed.
Adachi
Y
Y
Second Department of Internal Medicine, Kinki University School of Medicine, Japan.
Kamisako
T
T
D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism; D002352:Carrier Proteins; D002779:Cholestasis; D002780:Cholestasis, Intrahepatic / Q000209:etiology*; D016572:Cyclosporine / Q000009:adverse effects; D004731:Endotoxins; D006801:Humans; D008099:Liver / Q000378:metabolism; D012436:S-Adenosylmethionine / Q000627:therapeutic use
D001647:Bile Acids and Salts; D002352:Carrier Proteins; D004731:Endotoxins; D012436:S-Adenosylmethionine; D016572:Cyclosporine