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Liver regeneration in fulminant hepatitis as evaluated by serum transforming growth factor α levels
Author(s) -
Tomiya T,
Fujiwara K
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510230209
Subject(s) - medicine , liver regeneration , endocrinology , fulminant hepatitis , hepatocyte growth factor , hepatology , liver disease , regeneration (biology) , hepatitis , biology , receptor , microbiology and biotechnology
Transforming growth factor α (TGF α) is supposed to act as a mitogen for hepatocytes in an autocrine manner in vitro and in vivo . Retarded liver regeneration is a possible reason for poor prognosis of fulminant hepatitis (FH). We analyzed serum TGF α levels in patients with FH and patients with acute nonfulminant hepatitis (AH). Also, the relation of those levels to serum hepatocyte growth factor (HGF) levels and their changes after glucagon‐insulin (G‐I) therapy were studied. Maximal serum TGF α levels achieved in each case after admission until recovery from disease or death were correlated positively with maximal serum alanine transaminase (ALT) and total bilirubin levels in patients with AH, but negatively with maximal total bilirubin levels in patients with FH. Maximal serum TGF α levels in patients with FH were significantly higher in survivors than in nonsurvivors. Maximal serum HGF levels were positively correlated with maximal serum TGF α levels in patients with AH, but not in patients with FH. Multiple regression analysis indicated that G‐I therapy was related to the increment of serum TGF α levels in patients with FH. These results suggest that serum TGF α levels are increased in accordance with liver regeneration after necrosis in patients with AH, but such liver regeneration may be retarded, depending on the extent of liver damage in patients with FH. G‐I therapy seems to stimulate liver regeneration after liver damage. The possible contribution of TGF α and HGF to liver regeneration merits consideration for recovery from AH.