Transforming growth factor a (TGFa) is supposed to chain polypeptide of 50 amino acids that is expressed in act as a mitogen for hepatocytes in an autocrine manner cultured hepatocytes and secreted into culture medium in vitro and in vivo. Retarded liver regeneration is a after stimulation with mitogens and provokes DNA possible reason for poor prognosis of fulminant hepatitis synthesis in hepatocytes themselves. [4][5][6][7][8][9] TGFa messen-(FH). We analyzed serum TGFa levels in patients with ger RNA is shown to increase in hepatocytes before FH and patients with acute nonfulminant hepatitis (AH). DNA synthesis after partial hepatectomy in rats. 9,10 Also, the relation of those levels to serum hepatocyte TGFa transgenic mice can produce hypertrophy of the growth factor (HGF) levels and their changes after gluliver with increased TGFa expression in hepatocytes cagon-insulin (G-I) therapy were studied. Maximal seand increased TGFa levels in blood and urine. 11 With rum TGFa levels achieved in each case after admission an enzyme-linked immunosorbent assay for TGFa, we until recovery from disease or death were correlated positively with maximal serum alanine transaminase found that its serum levels vary depending on the re-(ALT) and total bilirubin levels in patients with AH, but generative stimulus, reflecting the degree of liver renegatively with maximal total bilirubin levels in pageneration in patients after partial hepatectomy. 12 tients with FH. Maximal serum TGFa levels in patients Thus, TGFa is supposed to stimulate hepatocyte prolifwith FH were significantly higher in survivors than in eration in an autocrine manner in vitro and in vivo. 13
nonsurvivors. Maximal serum HGF levels were posi-
The liver suffering acute hepatitis can usually regentively correlated with maximal serum TGFa levels in erate actively depending on the extent of hepatic necropatients with AH, but not in patients with FH. Multiple sis. 14 Fulminant hepatitis (FH) refers to a variant of regression analysis indicated that G-I therapy was reacute hepatitis, which shows extensive hepatic necrosis lated to the increment of serum TGFa levels in patients with poor prognosis. [15][16][17][18][19] Retarded liver regeneration, if with FH. These results suggest that serum TGFa levels are increased in accordance with liver regeneration any, might be one reason for this poor prognosis.
after necrosis in patients with AH, but such liver regen-We analyzed serum TGFa levels in patients with FH eration may be retarded, depending on the extent of and compared them with the levels in patients with liver damage in patients with FH. G-I therapy seems to acute nonfulminant hepatitis (AH) to elucidate liver stimulate liver regeneration after liver damage. The posregeneration after necrosis in both pathological condisible contribution of TGFa and HGF to liver regenerations. Also, we studied the relation of serum TGFa levtion merits consideration for recovery from AH. (HEPAels to serum levels of hepatocyte growth factor (HGF)