Der Klinikarzt 2016; 45(02): 88-91
DOI: 10.1055/s-0042-101600
Schwerpunkt
© Georg Thieme Verlag Stuttgart · New York

Nicht-alkoholische Fettlebererkrankung (NAFLE) – Was leistet die Labordiagnostik?

Non-alcoholic fatty Liver disease (NAFLD) – What does laboratory diagnostics?
Katharina Willuweit
1   Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Essen
,
Ali Canbay
1   Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Essen
› Author Affiliations
Further Information

Publication History

Publication Date:
21 March 2016 (online)

Die nicht-alkoholische Fettkleberkrankung (NAFLE) ist die hepatische Manifestation des metabolischen Syndroms. Diese kann über eine Fibrose zur Leberzirrhose und letztendlich zur Entstehung eines hepatozellulären Karzinoms führen. Die Diagnostik der NAFLE erfolgt durch Anamnese, klinische Symptome und bildgebende Verfahren. Die invasive Leberbiopsie gilt als Goldstandard der Beurteilung von Lebererkrankungen, ist jedoch komplikationsträchtig und kostenintensiv. Als nicht-invasives Verfahren ist die Verwendung von serologischen Biomarkern eine wegweisende Möglichkeit, eine einfache und reproduzierbare Beurteilung der Lebererkrankung zu erlangen. Zytokeratin-18 (CK-18) ist ein Intermediärfilamentprotein, welches während der hepatischen Schädigung von den Zellen sezerniert wird und im Serum nachweisbar ist. Für die NAFLE lässt sich mittels CK-18 zwischen der simplen Steatose und der nicht-alkoholischen Steatohepatitis (NASH) unterscheiden, da NASH-Patienten signifikant höhere Werte aufweisen. Die Bestimmung von CK-18 lässt Aussagen über die Aktivität und das Ausmaß der Lebererkrankung zu und kann zukünftig im klinischen Alltag zur Therapieentscheidung und zum Monitoring beitragen.

Non-alcoholic fatty Liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD may cause liver fibrosis and proceed to cirrhosis that eventually leads to hepatocellular carcinoma. The diagnosis is based on anamnesis (exclusion of extensive alcohol ingestion), clinical symptoms, imaging techniques, and liver biopsy, which is still the gold standard though associated with complications and sampling errors. As a non-invasive method, the use of serological biomarkers seems to be a good opportunity to gain a simple and reproducible assessment of ongoing liver injury. Cytokeratin-18 (CK-18) is an intermediate filament protein which is secreted during hepatic injury and detectable in patients' sera. Recent data indicate that CK-18 levels may differentiate between simple steatosis and non-alcoholic steatohepatitis (NASH). Furthermore the determination of CK-18 allows conclusions about the type and severity of liver disease and can potentially contribute to clinical diagnosis and management in clinical practice.

 
  • Literatur

  • 1 Altinbas A, Sowa JP, Hasenberg T, Canbay A. The diagnosis and treatment of non-alcoholic fatty liver disease. Minerva Gastroenterol Dietol 2015; 61: 159-169
  • 2 Kelly T, Yang W, Chen CS et al. Global burden of obesity in 2005 and projections to 2030. International journal of obesity 2008; 32: 1431-1437
  • 3 Kemmer N, Neff GW, Franco E et al. Nonalcoholic fatty liver disease epidemic and its implications for liver transplantation. Transplantation 2013; 96: 860-862
  • 4 Ertle J, Dechene A, Sowa JP et al. Non-alcoholic fatty liver disease progresses to hepatocellular carcinoma in the absence of apparent cirrhosis. International journal of cancer Journal international du cancer 2011; 128: 2436-2443
  • 5 Angulo P, Lindor KD. Non-alcoholic fatty liver disease. Journal of gastroenterology and hepatology 2002; 17 (Suppl. 01) 186-190
  • 6 Kalsch J, Bechmann LP, Heider D et al. Normal liver enzymes are correlated with severity of metabolic syndrome in a large population based cohort. Scientific reports 2015; 5: 13058-13058
  • 7 Ratziu V, Charlotte F, Heurtier A et al. Sampling variability of liver biopsy in nonalcoholic fatty liver disease. Gastroenterology 2005; 128: 1898-1906
  • 8 Schulze-Osthoff K, Ferrari D, Los M et al. Apoptosis signaling by death receptors. European journal of biochemistry/FEBS 1998; 254: 439-459
  • 9 Bantel H, Lugering A, Poremba C et al. Caspase activation correlates with the degree of inflammatory liver injury in chronic hepatitis C virus infection. Hepatology 2001; 34: 758-767
  • 10 Wahl K, Siegemund M Lehner et al. Increased apoptosis induction in hepatocellular carcinoma by a novel tumor-targeted TRAIL fusion protein combined with bortezomib. Hepatology 2013; 57: 625-636
  • 11 Rutherford AE, Hynan LS, Borges CB et al. Serum apoptosis markers in acute liver failure: a pilot study. Clinical gastroenterology and hepatology. The official clinical practice journal of the American Gastroenterological Association 2007; 5: 1477-1483
  • 12 Bantel H, Schulze-Osthoff K. Mechanisms of cell death in acute liver failure. Frontiers in physiology 2012; 3: 79-79
  • 13 Bantel H, Lugering A, Heidemann J et al. Detection of apoptotic caspase activation in sera from patients with chronic HCV infection is associated with fibrotic liver injury. Hepatology 2004; 40: 1078-1087
  • 14 Wieckowska A, Zein NN, Yerian LM et al. In vivo assessment of liver cell apoptosis as a novel biomarker of disease severity in nonalcoholic fatty liver disease. Hepatology 2006; 44: 27-33
  • 15 Feldstein AE, Wieckowska A, Lopez AR et al. Cytokeratin-18 fragment levels as noninvasive biomarkers for nonalcoholic steatohepatitis: a multicenter validation study. Hepatology 2009; 50: 1072-1078
  • 16 Joka D, Wahl K, Moeller S et al. Prospective biopsy-controlled evaluation of cell death biomarkers for prediction of liver fibrosis and nonalcoholic steatohepatitis. Hepatology 2012; 55: 455-464
  • 17 Bechmann LP, Gieseler RK, Sowa JP et al. Apoptosis is associated with CD36/fatty acid translocase upregulation in non-alcoholic steatohepatitis. Liver international : official journal of the International Association for the Study of the Liver 2010; 30: 850-859
  • 18 Canbay A et al. MicroRNAs as mediators in the pathogenesis of non-alcoholic fatty liver disease and steatohepatitis. Z Gastroenterol 2014; 52: 1-27