Z Gastroenterol 2005; 43 - 44
DOI: 10.1055/s-2005-869691

Serum alpha-fetoprotein (AFP) level in non-tumorous chronic liver diseases

A Horváth 1, A Szegedi 1, A Folhoffer 1, T Csak 1, J Osztovits 1, G Bekő 1, P Vargha 1, F Szalay 1
  • 11st Department of Medicine of Semmelweis University, Budapest, Hungary

Introduction: Alpha fetoprotein (AFP) is a glycoprotein, produced by the liver. Serum AFP level decreases below 20 ng/ml after birth. The AFP level is significantly elevated in 70% of patients with hepatocellular carcinoma (HCC). Higher level was also observed in liver regeneration and in chronic HCV infection. Few data known about AFP in non-malignant liver disease with any other etiology.

Aim: To investigate serum AFP level in HCV hepatitis and in chronic liver diseases of other etiology, and to assess its relation with laboratory parameters.

Patients and methods: In a retrospective study we analysed 445 data of 122 tumor free patients with chronic liver disease (43 HCV, 30 PBC, 10 NASH, 11 Wilson disease, 24 alcoholic liver disease, 4 haemochromatosis) from our clinic. We grouped the data of patients with HCV according to GPT level, and the data of cirrhotic patient according to Child scores. For the evaluation of data robustic regression statistical method (STATA) was used, which respects the connection between more different measurement from same patients. No focal lesion in any patients was found by imaging techniques (UH, CT, MRI).

Results: In group of HCV patients elevated AFP level was found in Child B cirrhosis (124.6±74.5 ng/ml) compared to either Child A and Child C stages (53.6±62.3; 23.32±27.8, p<0.0001) or any other group created according to GPT level (normal GPT, <2-fold normal, <3-fold normal, etc: 5.7±5.0;8.7±7.0;8.6±9.1;10.9±12.7;17.5±25.8; 10.3±6.4). The AFP level was also significantly higher in HCV Child B cirrhosis compared to Child B cirrhosis of other etiology (p<0.001). There was no difference in AFP level in Child C cirrhosis between groups of any etilogy. We did not find difference between patients either with different stages of PBC, or alcoholic cirrhosis. We observed 3 patients with HCV cirrhosis in whom despite of more than 200 ng/ml AFP level, we could not detect any tumor even after long term follow up.

Conclusions: We confirmed that AFP level might exceed the normal range without HCC. The cause of elevated AFP level observed in Child B cirrhosis could be the consequence of increased liver regeneration following HCV induced cell death.