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Current concepts in intrahepatic cholestasis.

L R Schwarz, M Schwenk, H Greim

    Acta Hepato-Gastroenterologica
    |June 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

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    Experimental intrahepatic cholestasis research highlights various functional alterations. High doses of compounds used in studies may not reflect clinical cholestasis at lower doses, obscuring primary causes.

    Area of Science:

    • Hepatology
    • Cell Biology
    • Toxicology

    Background:

    • Experimental intrahepatic cholestasis research has identified multiple potential functional alterations.
    • Many studies utilize high doses of cholestatic compounds, questioning relevance to clinical scenarios at lower doses.

    Purpose of the Study:

    • To review recent findings on experimental intrahepatic cholestasis.
    • To explore potential cellular targets of cholestatic compounds and identify knowledge gaps.

    Main Methods:

    • Review of experimental investigations on intrahepatic cholestasis over the past decade.
    • Analysis of proposed molecular and cellular targets of cholestatic agents.

    Main Results:

    • Cholestatic compounds may target the lipid phase of cellular membranes (sinusoidal, canalicular, endoplasmic reticulum, mitochondria).

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  • Impairment of carrier proteins, hydroxylating systems, and energy supply are potential consequences.
  • Other targets may include cytoplasmic binding proteins and microfilaments.
  • The primary event in drug-induced intrahepatic cholestasis remains undetermined.

    • Conclusions:

    • The precise initiating event in drug-induced intrahepatic cholestasis is unknown.
    • The role of elevated bile acid levels (cause or consequence) in cholestasis requires further clarification.
    • Future research may focus on cellular regulatory processes and lower-dose compound effects.