CytoSorbents Corporation (CTSO)

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Case of the week 38/2016
Use of CytoSorb in decompensated alcoholic steatohepatitis

Dr. Stefan Büttner#, PD Dr. Harald Fanik*, Dr. Benjamin Koch#, Dr. Helge Weiler#, Prof. Christoph Sarrazin*, Prof. Helmut Geiger# University Hospital Frankfurt # Medical Clinic III, Cardiology, Angiology and Nephrology * Medical Clinic I, Gastroenterology and Hepatology
This case study reports on a 36-year-old patient (chronic viral hepatitis C, longtime chronic alcohol abuse up to the point of admission to hospital), who was transferred an external hospital with decompensated cirrhosis.
Case presentation

Direct admission of the patient to the intensive care unit with an initial diagnosis of decompensated ethanol toxic liver cirrhosis
At this point the patient was hypotonic, tachycardic, in cardiogenic shock, oliguric, with upper gastrointestinal bleeding and a MELD score of 40
Development of hepatic encephalopathy
Attempt to stabilize the patient using albumin infusion and multiple paracenteses
Hepatorenal syndrome due to decompensated cirrhosis and subsequent dialysis dependency
Portal vein thrombosis was excluded
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 due to the ongoing alcohol abuse up to the point of admission to ICU
Since no transplant option existed, physicians continued therapy with available treatment options. The patient received a steroid therapy with 40 mg per day, however this did not result in any significant improvement
Plasma bilirubin concentrations showed a significant increase of up to 24.5 mg/dl, ammonia levels were 130 µg/dl, albumin was 2.4 g/dl
In addition, transaminases (GOT 259 U/L, GPT 59 U/L) as well as µGT (352 U/L) were markedly elevated
Markers for spontaneous coagulation at this time were also poor with a Quick of 26%, Antithrombin III of 49%, PTT 42, INR 2.87
Inflammation markers were: leukocytes 43,000/µl, CRP low at 3.46 mg/dl, and IL-6 42 pg/ml
During this phase, the patient received a low-dose norepinephrine infusion (<0.025 µg/kg/min)
As a „last resort“ therapy, CytoSorb treatment was also started with the rationale to remove inflammation-triggering factors and liver toxins (bile acids, bilirubin, ammonia) in the context of his systemic inflammatory condition as well as his acute-on-chronic liver failure
Subsequent final diagnosis: Liver cirrhosis and alcohol-related steatohepatitis (ASH) with pre-existing hepatitis C infection
Treatment

In total two treatments with CytoSorb were carried out, 1st treatment for 6 hours, followed by a treatment pause for 5 days to wait for the therapy effect due to non-existing evidence in this kind of patients, 2nd treatment for 6 hours
1st CytoSorb was performed in conjunction with CRRT (Multifiltrate, Fresenius Medical Care) performed in CVVHDF mode, 2nd treatment was performed in hemoperfusion mode
Blood flow rate: 200 ml/min
Anticoagulation: heparin
CytoSorb adsorber position: pre-hemofilter
Measurements

Ammonia (pre/post adsorber)
Bilirubin
Bile acids (pre/post adsorber)
Inflammatory parameters (IL-6, CRP, leucocytes)
Results

After the first treatment ammonia reduced to 88 µg/dl. During the 2nd treatment ammonia levels were measured pre and post adsorber: pre-adsorber 89 µg/dl – directly post adsorber 70 µg/dl; two hours later and also during treatment 2 ammonia levels pre-adsorber were 76 µg/dl and directly post adsorber 60 µg/dl, patient significantly improved both during and after the treatment sessions
Reduction of bilirubin in the course of the first treatment from 24.5 mg/dl to 16.3 mg/dl after 4 hours (thereafter no further reduction, probably due to saturation of the adsorber), between the 1st and 2nd treatment bilirubin rose to 31.5 mg/dl. During the 2nd treatment session levels reduced again to 25.9 mg/dl within 4 hours
Measurement of bile acids pre and post adsorber during the 2nd treatment were as follows:
pre-adsorber 145 µmol/l – directly post-adsorber 119.7 µmol/l
Increase of IL-6 during the first hour of the first treatment to 255.7 pg/ml (suspected catheter-associated infection, however with no subsequent successful pathogen detection), in the further course during the first treatment reduction to 33.5 pg/ml, no more valid measurement performed during 2nd treatment
Leucocytes continuously reduced during both treatments to 20,000/µl after the first and 15,000/µl after the second treatment
CRP was continuously low between 2-4 mg/dl during both treatment cycles
During the first treatment, renal function and thus diuresis improved rapidly, so that CVVH could be discontinued after the first treatment
Patienten Follow-Up

Termination of renal replacement therapy directly after the first CytoSorb session with stable diuresis and stable creatinine
Patient initial clinical recovering with planned discharge to his home environment due to the lack of a transplant option
Subsequent development of a nosocomial pneumonia, after which the patient went into another episode of fulminant pneumogenic sepsis and died on IMC three weeks after the last CytoSorb treatment
CONCLUSIONS

CytoSorb represents a good and viable treatment option for patients with alcoholic steatohepatitis (ASH) and may be especially effective in young patients with severe inflammatory response in the context of their ASH
CytoSorb worked extremely well and effectively as a liver replacement in this case, hepatic encephalopathy improved significantly due to removal of liver toxins
In addition, measurement of pre/post adsorber values indicates that the removal of ammonia and bile acids is directly attributable to the adsorber
According to the medical team, the impressive course of the patient has led to the initiation of a specific study project for such patients
The installation of the absorber into the CVVH circuit and the application of CytoSorb itself was easy and safe
http://cytosorb-therapy.com/the-studies/case-of-the-week/