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Treatment of chronic delta hepatitis with alpha 2 recombinant interferon (IFN)
GS-VI 5
DOES LOSS OF HBsAG REPRESENT THE "TRUE" RESPONSE I'O INTERFERON IN CHRONIC HBV iNFECTiON? G.J.M. Alexander~ H.M. Smith,_E.A. Fagant A.L.W.F. Eddleston and Roger Williams. Liver Unit, King's College Hospital and School of Medicine and Dentistry, London SE5 8PC<.
Differentiation of spontaneous from drug induced HBeAg:anti-HBe seroconversion is fundamental to interpretation of clinical studies of antiviral agents in chronic HBV infection. 42 chronic HBV carriers entered into a trial of 6 months lymphobiastoid interferon (20 patients) versus no therapy (22 patients) have been followed for 6-24 months, white 15 further patients excluded from the trial because serum aminotransferase levels exceeded 4xnor,nal, were also followed. 5 treated patients have lost HBeAg and developed anti-HtBe following an hepatitis like illness during therapy; 4 of these have lost HBsAg, ] developing anti-HBs, in contrast, all of the controls remain HBeAg positive. Of the 13 patients excluded from the trial, 8 have lost HBeAg, 5 developing anti-HBe, but none have lost HBsAg. The tow rate of HBeAg: anti-HBe seroconversion in both treated and control patients (25% and 0% respectively) and the high rate in those excluded because of elevated serum aminotransferases (61.5%), shows the importance of this parameter as an indicator of impending seroconversion. The absence of seroconversion in the control group allows the effect of therapy t,) be seen rnore readily. Loss of HBsAg, which was observed only in those treated, may be a direct effect of interferon.
GS-VI 6
TREATMENT OF CHRONIC DELTA HEPATITIS WITH ALPHA 2 RECOMBINANT INTERFERON (!FN) F. Rosina 7 G. Saraceo~ W. Lattore~ V. Q u a r t a r o n % G.C. Actis, E. Maran~ F. Bonino M. Bmunetto~ A. Smedile% G. Vemme, M. Rizzetto. Division of Gastroenterology, Ospedale Molinette, Torino, Italy. ~,~=eorgetown University, Washington, D.C.
To evaluate the efficacy of Interferon (IFN) in treatment of Chronic Delta Hepatitis, 24 patients entered a controlled therapeutical trial of Alpha 2 Recombinant IFN (Intron, Schering Essex). The patients were randomly allocated to a treated2or control group. The 12 treated patients received Alpha 2 Recombinant IFN: 5 mega-units/m given subcutaneously thrice weekly for twelve weeks. Pretreatment biopsies showed nuclear and/or cytoplasmatic HDAg in all the patients. HDV-RNA was positive in 8 treated patients and in 9 patients in the control group. Durin~ treatment a decrease in liver enzymes was observed 8 cases (4 to normal levels), an increase in 2 and no significant change in 2, HDV-RNA became undetectable in 6 cases. After treatment remission was maintained only in 1 patient, liver enzymes relapsed in the other 7 cases, HDV-RNA remained undetectable in 5 of the 6 patients who had cleared the virus during therapy. A second biopsy was taken in 8 treated patients: resolution of infla,mmtion with minimal residual portal fibrosis and disappearence of HDAg in immunofluorescence was seen in the case who had showed the biochemical remission. The other 7 did not show significant variations, but a decrease in lobular inf]a,vnation in 2 patients. In the control group no significant change in liver enzymes was seen, except for a peak in ALT levels in one patient; HDV-RNA showed minor fluctuations in 8 cases and a rapid decrease to undetectable levels in one. No important change in histology was seen. These results suggest that administration of IFN produces inhibition of HDV replication and decrease of liver disease activity; remission, however, was sustained only in one case.
S34
DOES LOSS OF HBsAG REPRESENT THE "TRUE" RESPONSE I'O INTERFERON IN CHRONIC HBV iNFECTiON? G.J.M. Alexander~ H.M. Smith,_E.A. Fagant A.L.W.F. Eddleston and Roger Williams. Liver Unit, King's College Hospital and School of Medicine and Dentistry, London SE5 8PC<.
Differentiation of spontaneous from drug induced HBeAg:anti-HBe seroconversion is fundamental to interpretation of clinical studies of antiviral agents in chronic HBV infection. 42 chronic HBV carriers entered into a trial of 6 months lymphobiastoid interferon (20 patients) versus no therapy (22 patients) have been followed for 6-24 months, white 15 further patients excluded from the trial because serum aminotransferase levels exceeded 4xnor,nal, were also followed. 5 treated patients have lost HBeAg and developed anti-HtBe following an hepatitis like illness during therapy; 4 of these have lost HBsAg, ] developing anti-HBs, in contrast, all of the controls remain HBeAg positive. Of the 13 patients excluded from the trial, 8 have lost HBeAg, 5 developing anti-HBe, but none have lost HBsAg. The tow rate of HBeAg: anti-HBe seroconversion in both treated and control patients (25% and 0% respectively) and the high rate in those excluded because of elevated serum aminotransferases (61.5%), shows the importance of this parameter as an indicator of impending seroconversion. The absence of seroconversion in the control group allows the effect of therapy t,) be seen rnore readily. Loss of HBsAg, which was observed only in those treated, may be a direct effect of interferon.
GS-VI 6
TREATMENT OF CHRONIC DELTA HEPATITIS WITH ALPHA 2 RECOMBINANT INTERFERON (!FN) F. Rosina 7 G. Saraceo~ W. Lattore~ V. Q u a r t a r o n % G.C. Actis, E. Maran~ F. Bonino M. Bmunetto~ A. Smedile% G. Vemme, M. Rizzetto. Division of Gastroenterology, Ospedale Molinette, Torino, Italy. ~,~=eorgetown University, Washington, D.C.
To evaluate the efficacy of Interferon (IFN) in treatment of Chronic Delta Hepatitis, 24 patients entered a controlled therapeutical trial of Alpha 2 Recombinant IFN (Intron, Schering Essex). The patients were randomly allocated to a treated2or control group. The 12 treated patients received Alpha 2 Recombinant IFN: 5 mega-units/m given subcutaneously thrice weekly for twelve weeks. Pretreatment biopsies showed nuclear and/or cytoplasmatic HDAg in all the patients. HDV-RNA was positive in 8 treated patients and in 9 patients in the control group. Durin~ treatment a decrease in liver enzymes was observed 8 cases (4 to normal levels), an increase in 2 and no significant change in 2, HDV-RNA became undetectable in 6 cases. After treatment remission was maintained only in 1 patient, liver enzymes relapsed in the other 7 cases, HDV-RNA remained undetectable in 5 of the 6 patients who had cleared the virus during therapy. A second biopsy was taken in 8 treated patients: resolution of infla,mmtion with minimal residual portal fibrosis and disappearence of HDAg in immunofluorescence was seen in the case who had showed the biochemical remission. The other 7 did not show significant variations, but a decrease in lobular inf]a,vnation in 2 patients. In the control group no significant change in liver enzymes was seen, except for a peak in ALT levels in one patient; HDV-RNA showed minor fluctuations in 8 cases and a rapid decrease to undetectable levels in one. No important change in histology was seen. These results suggest that administration of IFN produces inhibition of HDV replication and decrease of liver disease activity; remission, however, was sustained only in one case.
S34