Long-Term Extracorporeal Bilirubin Elimination: A Case Report on Cascade Resin Plasmaperfusion

Abstract

Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR–350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. Bilirubin levels were lowered to a minimum of 225 μmol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.

Cholemic Nephropathy as Cause of Acute and Chronic Kidney Disease. Update on an Under-Diagnosed Disease

“…The causes of sHyb most frequently reported result from drug-induced cholestasis, liver cirrhosis, obstructive jaundice and malignant cholangiocarcinoma [64], alcoholic hepatitis, severely cholestatic liver graft, organ failure secondary to infections, sepsis, all conditions that could be associated with CN [17,21,22,24,46,48,[63][64][65][66]. The majority of cases reported serum bilirubin levels above 20 mg/dL with peaks of 58 mg/dL in one of the first case described in literature, highlighting the severity of hyperbilirubinemia [67].…”

“…The cases of AKI described in the context of sHyb usually correspond to the most severe cases, associated to the higher values of sCr reported or to the need for dialysis [3,16,48,[63][64][65][66][67][68][69][70][71][72][73][74].…”

Sorbents in Acute Renal Failure and the Systemic Inflammatory Response Syndrome

“…For targeting middle molecular weight uremic toxins (MW 4-40 kDa), a large population of pores engineered to fall within a targeted size range permits the entrance of these toxins to the interior of the adsorbent bead, while excluding larger proteins, such as albumin (MW 66 kDa, molecular diameter 22.6 nm), from the adsorptive interior [19]. The introduction of ion exchange groups can also significantly increase the affinity of resin sorbents for bilirubin [20] and endotoxin [21]. The measured surface area of resins and charcoals is often quite high, in excess of 500 m 2 /g of adsorbent.…”

The Next Step from High-Flux Dialysis: Application of Sorbent Technology

“…For targeting middle molecular weight uremic toxins (MW 4-30 kDa), a population of pores between 4 and 10 nm will permit the entrance of these toxins to the adsorbent interior of the bead, while excluding larger proteins, such as albumin (MW 69 kDa, molecular diameter 22.6 nm), from the adsorptive surface [29]. The introduction of ion exchange groups can also significantly increase the affinity of resin sorbents for bilirubin [30] and endotoxin [31].…”