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; = 10; 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; = 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; = 6; 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; 0.01).

Conclusion: Serum activin A is increased in acute liver failure and could be a factor in the inhibition of liver regeneration.