Inflammation-induced cholestasis

Abstract

Inflammatory cytokines produced in response to various infectious and non‐infectious stimuli are potent inducers of intrahepatic cholestasis (inflammation‐induced cholestasis). The cholestatic effect of cytokines results mainly from inhibition of expression and function of hepatocellular transport systems which normally mediate hepatic uptake and biliary excretion of bile salts and various non‐bile salt organic anions (e.g. bilirubin). These cytokine effects are reversible and bile secretory function is restored upon disappearance of the inflammatory injury. This review summarizes the clinical, pathophysiological and molecular aspects of inflammation‐induced cholestasis. © 1999 Blackwell Science Asia Pty Ltd

The Use of Biochemical Markers in Complicated and Uncomplicated Acute Diverticulitis

“…(18) Hyperbilirubinemia has been described in case reports of complicated acute diverticulitis (26,27)and has been linked to extra-hepatic bacterial infection inducing cholestasis and hepatic portal vein gas as a cause. (27,28) Our study extends these observations by showing a significant difference in bilirubin levels between uncomplicated and complicated disease.…”

Clinical courses after administration of oral corticosteroids in patients with severely cholestatic acute hepatitis A; three cases

“…Cholestasis accompanied by viral hepatitis A is mainly based on inflammatory responses. It is developed by the systemic and intrahepatic release of endotoxin (lipopolysaccharide) and pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) or interleukin-1 (IL-1) 6. It is therefore conceivable that cholestasis associated with this inflammatory process can be improved by the administration of steroids.…”

Molecular adsorbent recirculating system in patients with early allograft dysfunction after liver transplantation: A pilot study

“…[22][23][24] Our threshold value of 10% per minute corresponds to the values predicting far worse outcome in previous studies. [22][23][24] ICG elimination by the liver reflects liver blood flow and microcirculation, hepatocyte energy status, and the inhibition of expression and function of hepatocellular transport systems 21,25 that mediate hepatic uptake and biliary excretion of bile salts and various nonbile salt organic anions such as bilirubin and ICG. 25 The marked increase in PDR ICG and decrease of serum bilirubin levels in survivors compared with nonsurvivors in our study is most likely caused by the restoration of energy metabolism and disappearance of ischemia-reperfusion-induced inhibition of expression and function of hepatocellular transport systems in survivors.…”

“…[22][23][24] ICG elimination by the liver reflects liver blood flow and microcirculation, hepatocyte energy status, and the inhibition of expression and function of hepatocellular transport systems 21,25 that mediate hepatic uptake and biliary excretion of bile salts and various nonbile salt organic anions such as bilirubin and ICG. 25 The marked increase in PDR ICG and decrease of serum bilirubin levels in survivors compared with nonsurvivors in our study is most likely caused by the restoration of energy metabolism and disappearance of ischemia-reperfusion-induced inhibition of expression and function of hepatocellular transport systems in survivors. Although ICG and bilirubin use the same hepatocellular transmembranous transport systems, the superiority of PDR ICG over bilirubin is thought to be because bilirubin may already be increased before OLT, and may further increase after excessive transfusion of packed red blood cells, or may be increased as a result of the slow excretion of delta-bilirubin that is measured as a part of total bilirubin.…”