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[Fulminant hepatic failure and hepatitis B virus reactivation: case reports and analyses of the pathological mechanism].

OBJECTIVE
To investigate the clinical features and mechanisms of hepatitis B virus (HBV) reactivation induced by chemotherapy or immunosuppressive therapy and subsequent fulminant hepatic failure (FHF) in patients with autoimmune diseases.


METHODS
Seven cases of FHF related to HBV reactivation were retrospectively assessed. All patients had been confirmed as hepatitis B e antigen (HBeAg) seronegative and had undergone glucocorticoid-based therapy to manage primary diseases, including nephrotic syndrome (2 cases), polycystic kidney disease combined with chronic nephritis (1 case), conditions following kidney transplantation (1 case), lymphadenoma (1 case), idiopathic thrombocytopenic purpura (1 case), and angitis (1 case). Levels of sero-markers of HBV and HBV DNA were recorded. Serum samples from patients were respectively applied to HepG2.2.15 and HepG2 cell lines in order to investigate the effects on cell proliferation (by MTT assay) and apoptosis (by Hoechst 33342 staining assay). Intergroup differences were statistically assessed by the t-test.


RESULTS
For all patients, the initial clinical signs of hepatic failure emerged at 4 to 11 months after receipt of the glucocorticoid treatment. At the time of hepatic failure, HBeAg seropositivity was detected in 4 patients, including one patient who also showed seropositivity for the hepatitis B surface antibody (HBsAb). All 7 patients showed high levels of HBV DNA when the hepatitis condition flared. Neither remedial antiviral treatments nor internal medicine comprehensive treatments, including therapeutic plasma exchange, were effective in any of these cases. The duration from clinical signs onset to death ranged from 24 to 47 days. Treatment of HepG2.2.15 and HepG2 cells with serum samples from patients with FHF showed a dosage-effect relationship of the serum concentration on the cellular proliferation inhibition rate, with the serum of patients with FHF having more severe inhibiting effects on the HepG2.2.15 cells than on the HepG2 cells. The HepG2.2.15 cells showed a greater tendency towards apoptosis upon treatment with serum samples from patients with FHF, compared to the HepG2 cells.


CONCLUSION
HBV reactivation induced by chemotherapy or immunosuppressive therapy is a problem currently encountered in the management of malignancies or rheumatic autoimmune disease patients. It is critical to verify HBV status prior to initiation of these treatment strategies so that appropriate antiviral prophylaxis may be administered, so as to reduce the risk of HBV reactivation and subsequent repression of cell proliferation and apoptosis that can promote development of FHF and increase a patient's risk of death.