Application of Hemoadsorption in a Case of Liver Cirrhosis and Alcohol-Related Steatohepatitis with Preexisting Hepatitis C Infection.

course, he developed hepatorenal syndrome and subsequent dialysis dependency. Consequently, the patient was treated for more than a month in the intensive care unit to stabilize the cirrhosis and acute kidney injury. During this time, an evaluation as to whether the patient could be listed for a liver transplantation or not was rejected by the Liver Board. Since no transplant option existed, we continued therapy with available treatment options including steroid therapy with 40 mg per day, however, with no significant improvement. Plasma bilirubin concentrations showed a significant increase of up to 24.5 mg/dL; ammonia levels were 130 μg/dL. In addition, transaminases (GOT 259 U/L, GPT 59 U/L) as well as μGT (352 U/L) were markedly elevated and markers for spontaneous coagulation at this time were also poor. He also exhibited highly elevated markers of inflammation (leukocytes 43,000/μL, C-reactive protein 3.46 mg/dL, and interleukin-6 42 pg/mL). Continuous renal replacement therapy (CRRT) was started in the CVVHD mode (Multifiltrate, Fresenius Medical Care). During this phase, the patient received a low-dose norepinephrine infusion (<0.025 μg/kg/min). As a “last resort” therapy, a hemoadsorpDear Editor, Acute-on-chronic liver failure, including decompensated alcoholic steatohepatitis (ASH), represents a distinct type of hepatic decompensation, accompanied by systemic inflammation, extrahepatic organ failure, and susceptibility to infection that can occur in patients with cirrhosis. Short-term mortality from decompensated alcohol-related liver disease is high with up to 10–20% at 1 month [1, 2] . In most cases, corticosteroids are the only available treatment option; however, the proof for their efficacy is missing. Likewise, despite the availability of various techniques for liver organ support (i.e., MARS, SPAD), application is cumbersome and data on their clinical efficiency remain sparse [3] . We report the case of a 36-year-old male patient with a clinical history of chronic viral hepatitis C and longtime chronic alcohol abuse up to the point of admission to hospital and subsequently to ICU with decompensated ethanol toxic liver cirrhosis. At this point, the patient was hypotonic, tachycardic, and oliguric with upper gastrointestinal bleeding, with a MELD score of 40, and progressive hepatic encephalopathy. Initial attempts were made to stabilize the patient using albumin infusion and multiple paracenteses. However, in further Received: December 9, 2016 Accepted: December 12, 2016 Published online: February 25, 2017