Liver Stiffness and Cholestasis

Abstract

Mechanic cholestasis is an established important and independent clinical confounder of liver stiffness (LS) elevation. As rule of thumb, during mechanic cholestasis, an elevation of bilirubin by 1 mg/dL corresponds to an increase of LS by 1 kPa. For instance, a patient with a bilirubin of 4 mg/dL and an obstructed common bile duct can develop a LS of 8–10 kPa which will normalize after e.g., removal of the bile stone. This information can be very helpful when looking at patients with a combination of established liver cirrhosis and additional choletasis due to bile duct obstruction.

Moreover, due to the elevated LS, imaging studies will not show dilatation of the bile ducts. Here, comparison of bilirubin with LS can help to dissect cirrhosis from mechanic cholestasis.

Notably, severe hemolysis does not directly increase LS within short-term periods of time but only later due to hepatocellular damage. Although the data of rare genetic cholestatic diseases are still scarce (e.g., Alagille syndrome), all diseases with impaired bile and bilirubin excretion are expected to show elevated LS including DILI (during induced liver injury) of the cholestatic type. In contrast, conjugation problems such as the rather common Gilbert–Meulengracht syndrome are not causing LS elevation. Mechanic cholestasis even of the small canaliculi also contributes to LS elevation in more common etiologies such as PSC/PBC but also alcoholic liver disease.