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Reactivation of chronic hepatitis B virus infection
101
IgM ANTI-DELTA (6) IN CHRONIC 6 INFECTION : RELATIONSHIP TO 6 VIRAL REPLICATION AND PRELIMINARY OBSERVATIONS ON THE EFFECT OF INTERFERON. P. Farci~ R. Shein, I. Lindsey, P.J. Scheuer, S. Sherlock, H.C. Thomas Department of Medicine, Royal Free Hospital, London, U.K.
We have studied the relationship of IgM anti-6 to 6 antigen display in the liver, in 16 patierrts observed for 2-8 years. In addition we observed the rate of change of serum transaminase to determine whether this variable might be useful in monitoring the effects of antiviral therapy. At presentation, 7 patients already had established chronic liver disease (CLD) while in the remaining 9 CLD developed after acute delta superinfection of a chronic flBV carrier. Chronic delta infection was diagnosed on the finding of serum IgG antibody (IgG anti-6) in high titer()l:5OO0). IgM anti-6 was initially found in 14 of the 16 cases. The titer did not change during follow-up. Importantly, in 14 of the 16 patients it was persistent~ ly associated with intrahepatic expression of 6 antigen. In contrast, 6 antigen was absent from the livers of 2 patients who were IgM anti-6 negative. IgM anti-6 was associated with active disease and cirrhosis developed in 8 of these patients. Transaminases fluctuated but did not return to normal during the course of the disease. Two patients were given IM lymphoblastoid interferon. After 6 weeks there was a greater than 60% decrease in transaminase. On reducing the dosage or stopping treatment, transaminases r o s e to pre-treatment levels. CONCLUSION: IgM anti-6 is consistently correlated with 6 antigen display in the liver and may be an indirect measure of viral replication. It is associated with elevated transaminases and active liver disease. In 2 patients a short course of interferon produces a fall in Lransaminases and further studies are in progress to determine the effect on IgM anti-6 and 6 an~.i,.gen, di.s.p.l.ay in tka l~vQr,.
102
REACTIVATION OF CHRONIC HEPATITIS B VIRUS INFECTION G. Fattovich, A.Alberti, P.Pontisso, A.M.Rigoli, F.Tremolada, G.Realdi. Istituto di Medicina Clinica, Clinica Medics 2a dell'Universit~ di Padova, Italy
It has been recently suggested that reactivation of virus replication and of chronic hepatitis may frequently occur in HBsAg chronic carriers who have achieved disease remission after anti-HBe seroconversion.We have followed for at least 12 months (range 12-77 months;mean ~ SD, 33 + 19 me.) 31 patients with chronic hepatitis type B after they had seroconverted from HBeAg Lo ~nti-HBe. All patients underwent serial determinations of alanine aminotransferase levels (ALT) and of hepatitis B virus (HBV) markers including HBsAg,HBeAg,anti-HBe,HBV-DNA and HBVDNA polymerase (DNAP). After seroconversion the disease remained active in 4 patients,2 with continuing HBV replication and one with Delta antigen in the liver,while 27 (87%) cases showed ALT normalization with clearance of HBV-DNA and DNAP from serum. During subsequent followup,a new ALT elevation was observed in 4 of these 27 patients (14.8%) and was accompanied by reappearance of serum HBeAg in two cases and of HBV-DNA and/or HBV-DNAP in 3. Reactivation occurred between 6 and 28 months after seroconversion and lasted at least 8 months in all 4 cases,but ALT levels never exceeded 3 times the normal value. None of the 4 patients developed symptoms during reactivation or showed serologic evidence of delta or HAV superinfection. Thus,in our experience,reactivation of chronic hepatitis B after anti-HBe seroconversion is a rare event and is not accompanied by severe liver damage in contrast with recent data obtained mainly in male homosexuals.
$51
IgM ANTI-DELTA (6) IN CHRONIC 6 INFECTION : RELATIONSHIP TO 6 VIRAL REPLICATION AND PRELIMINARY OBSERVATIONS ON THE EFFECT OF INTERFERON. P. Farci~ R. Shein, I. Lindsey, P.J. Scheuer, S. Sherlock, H.C. Thomas Department of Medicine, Royal Free Hospital, London, U.K.
We have studied the relationship of IgM anti-6 to 6 antigen display in the liver, in 16 patierrts observed for 2-8 years. In addition we observed the rate of change of serum transaminase to determine whether this variable might be useful in monitoring the effects of antiviral therapy. At presentation, 7 patients already had established chronic liver disease (CLD) while in the remaining 9 CLD developed after acute delta superinfection of a chronic flBV carrier. Chronic delta infection was diagnosed on the finding of serum IgG antibody (IgG anti-6) in high titer()l:5OO0). IgM anti-6 was initially found in 14 of the 16 cases. The titer did not change during follow-up. Importantly, in 14 of the 16 patients it was persistent~ ly associated with intrahepatic expression of 6 antigen. In contrast, 6 antigen was absent from the livers of 2 patients who were IgM anti-6 negative. IgM anti-6 was associated with active disease and cirrhosis developed in 8 of these patients. Transaminases fluctuated but did not return to normal during the course of the disease. Two patients were given IM lymphoblastoid interferon. After 6 weeks there was a greater than 60% decrease in transaminase. On reducing the dosage or stopping treatment, transaminases r o s e to pre-treatment levels. CONCLUSION: IgM anti-6 is consistently correlated with 6 antigen display in the liver and may be an indirect measure of viral replication. It is associated with elevated transaminases and active liver disease. In 2 patients a short course of interferon produces a fall in Lransaminases and further studies are in progress to determine the effect on IgM anti-6 and 6 an~.i,.gen, di.s.p.l.ay in tka l~vQr,.
102
REACTIVATION OF CHRONIC HEPATITIS B VIRUS INFECTION G. Fattovich, A.Alberti, P.Pontisso, A.M.Rigoli, F.Tremolada, G.Realdi. Istituto di Medicina Clinica, Clinica Medics 2a dell'Universit~ di Padova, Italy
It has been recently suggested that reactivation of virus replication and of chronic hepatitis may frequently occur in HBsAg chronic carriers who have achieved disease remission after anti-HBe seroconversion.We have followed for at least 12 months (range 12-77 months;mean ~ SD, 33 + 19 me.) 31 patients with chronic hepatitis type B after they had seroconverted from HBeAg Lo ~nti-HBe. All patients underwent serial determinations of alanine aminotransferase levels (ALT) and of hepatitis B virus (HBV) markers including HBsAg,HBeAg,anti-HBe,HBV-DNA and HBVDNA polymerase (DNAP). After seroconversion the disease remained active in 4 patients,2 with continuing HBV replication and one with Delta antigen in the liver,while 27 (87%) cases showed ALT normalization with clearance of HBV-DNA and DNAP from serum. During subsequent followup,a new ALT elevation was observed in 4 of these 27 patients (14.8%) and was accompanied by reappearance of serum HBeAg in two cases and of HBV-DNA and/or HBV-DNAP in 3. Reactivation occurred between 6 and 28 months after seroconversion and lasted at least 8 months in all 4 cases,but ALT levels never exceeded 3 times the normal value. None of the 4 patients developed symptoms during reactivation or showed serologic evidence of delta or HAV superinfection. Thus,in our experience,reactivation of chronic hepatitis B after anti-HBe seroconversion is a rare event and is not accompanied by severe liver damage in contrast with recent data obtained mainly in male homosexuals.
$51