The prognosis of fulminant hepatitis due to non-A, non-B virus infecti
on and acute reactivation of hepatitis B virus in HE carriers is gener
ally poor, and the treatment of choice in Western countries is recogni
zed as liver transplantation. In countries such as Japan where liver t
ransplantation is not readily available, however, these intractable ty
pes of fulminant hepatitis have to be treated medically. Based on the
assumption that persistent replication of causal viruses and enhanced
host immune responses, especially cellular immunity, to eradicate the
viruses are the key mechanism in progressive liver cell destruction an
d the poor prognosis, we attempted a combination treatment with interf
eron and cyclosporin A for these types of fulminant viral hepatitis. S
ubjects in the present study consisted of 1 patient with acute severe
hepatitis without coma and 13 patients with coma (13 with fulminant he
patic failure) due to non-A, non-B virus and acute reactivation of hep
atitis B virus. The patients were given interferon-beta, 300 x 10(4) d
aily, and cyclosporin A, at an initial dose of 3 mg/kg, with tapering.
Fourteen patients with coma received artificial liver support that we
devised. The patient with acute severe hepatitis survived, showing hi
stologically remarkable liver regeneration. Eight of the 14 patients w
ith hepatic coma, all of whom were indications for liver transplantati
on according to the criteria of the King's College group, survived. De
creased transaminase level, increased liver volume, and histological l
iver regeneration were observed in all the survivors. The combination
of interferon and cyclosporin A is worth attempting in fulminant hepat
itis caused by non-A, non-B virus and acute reactivation of hepatitis
B virus in HE carriers.