Activin A and follistatin in acute liver failure

Background Liver regeneration may be impaired in acute liver failure due to either inhibition of the proliferative response or ongoing liver cell death. Activin A, a member of the TGFbeta superfamily, inhibits hepatocyte DNA synthesis and induces apoptosis. Methods Levels of activin A and its binding protein follistatin in the serum of 23 patients with acute liver failure were determined by enzyme-linked immunosorbent assay. Results Serum activin A was significantly increased in acute liver failure patients (median 2.15 ng/ml, range 0.28-6.87 ng/ml) compared to normal controls (median 0.25 ng/ml, range 0.19-0.53 ng/ml; n = 10; P< 0.001). However, this was not linked to the final disease outcome. Higher levels of activin A were found in the serum of patients with acute liver failure due to paracetamol overdose (median 2.87 ng/ml, range 0.72-6.87 ng/ml; n = 17) than in patients with acute liver failure due to non-A to E hepatitis (median 1.10 ng/ml, range 0.28-2.70 ng/ml; n = 6; P< 0.05). Serum follistatin was also increased in acute liver failure patients (median 2.84 ng/ml, range 0.57-13.24 ng/ml) compared to normal controls (median 0.68 ng/ml, range 0.32-3.70 ng/ml; P < 0.01). Conclusion Serum activin A is increased in acute liver failure and could be a factor in the inhibition of liver regeneration.