A pilot study on the effects of prednisone withdrawal on serum hepatitis B virus DNA and HBeAg in chronic active hepatitis B

Nair, Prem V.; Tong, Myron J.; Stevenson, Douglas; Roskamp, Deborah; Boone, Cissy

doi:10.1002/hep.1840060616

Cited by 61 publications

(26 citation statements)

References 33 publications

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“…The results of our trial, in which 71 % of the patients became DNA-polymerase-negative and 64% lost HBeAg from serum in the follow-up period are similar to the experi ence of Nair et al [3,12]. The reasons for the high rate of clearance of viral replication in our patients may be diverse.…”

Section: Discussionsupporting

confidence: 70%

“…Furthermore, a large proportion of our cases had a very active form of disease on liver histology (bridging necrosis, active cir rhosis), and it was suggested that in such patients withdrawal of corticosteroids is likely to cause an intense T cell response against infected hepatocytes, since these pa tients are already immunologically 'primed' [ 17], Thus, patients with mild forms of CAH are supposed to be less likely to respond to therapy. However, in contrast to the study of Nair et al [3], we did not find difference in rates of viral clearance between patients with CAH type 1 and those with more advanced liver disease (CAH type II or CAH type III), but it should be noted that the groups were relatively small.…”

Section: Discussioncontrasting

confidence: 55%

“…It is therefore generally accepted that those with signs of advanced liver dis ease should be excluded [3,17], However, even such a cautious approach may not elim inate the therapy-related risks altogether, since one of our patients with well-compen sated liver disease and biochemical abnor malities confined to moderately raised activ ities of transaminases had a prolonged exac erbation and died of liver failure after 18 months. He was initially negative for DNA polymerase activity and cleared HBcAg after therapy, but then he reactivated after 4 months to HBC AG and moreover DNA poly merase appeared in his serum.…”

Section: Discussionmentioning

confidence: 99%

“…However, it was reported that withdrawal from long or short courses of corticosteroids may result in decline of viral replication and even success ful treatment due to an immunologic 're bound' that follows [3][4][5][6],…”

mentioning

confidence: 99%

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Short-Term Corticosteroid Therapy for Chronic Active Hepatitis B

Laskus¹,

Cianciara²,

Loch³

et al. 1990

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Seventeen patients with chronic active type B hepatitis were treated with prednisone for 4 weeks. All were initially hepatitis B e antigen (HB_eAg)-positive and 14 were DNA-polymerase-positive as well. In the follow-up period of 1 year, 10 patients became persistently negative for DNA polymerase and 11 cleared HB_eAg from serum, while among 17 matched untreated controls only one lost DNA polymerase and HB_eAg. However, 1 patient who was initially DNA-polymerase-negative and who lost HB_eAg after treatment reactivated to HB_eAg after 4 months and DNA polymerase appeared in his serum. He suffered prolonged exacerbation of liver disease after treatment and died of liver failure. Short-term corticosteroid therapy may be of value in patients with chronic active type B hepatitis, however, in some cases such treatment may be disastrous.

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Section: Discussionsupporting

confidence: 70%

Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Short-Term Corticosteroid Therapy for Chronic Active Hepatitis B

Laskus¹,

Cianciara²,

Loch³

et al. 1990

Digestion

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“…In the same way, a pronounced rebound of immune response to HBV replication with rapid tapering or abrupt discontinuance of immunosupressants such as steroids may precipitate hepatic decompensation in HBsAg-positive patients with chronic liver diseases like our patient (Case No. 5) (Schullard et al 1981;Nair et al 1986). …”

Section: Discussionmentioning

confidence: 99%

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Kanno

Suzuki²,

Miyazaki³

et al. 1988

Tohoku J. Exp. Med.

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In order to examine the clinical features of severe acute exacerbation in chronic hepatitis B virus (HBV) infection, 297 hepatitis B surface antigen (HBsAg) carriers were followed for 35+22 months (mean+s.D.) in Tohoku University Hospital from 1976 to 1987. Of these, 10 experienced severe acute exacerbation with hepatic decompensation. All of these patients had intense subjective symptoms related to the hepatitis. They were all icteric and 8 had ascites. Three developed to fulminant hepatic failure, eventually died. Histology after the exacerbation showed severe hepatic damage such as massive hepatic necrosis and bridging hepatic necrosis in a half of them. Six cases were suspected to result from spontaneous reactivation and 2 from drug-induced reactivation of chronic HBV infection, and the other 2 from superinfection with non-A, non-B hepatitis agent (s). These results suggest that the reactivation of chronic HBV infection is an important factor of severe acute exacerbations in chronic HBV infection in Japan.severe acute exacerbation ; HBsAg carrier ; reactivation of chronic HBV infection Patients with chronic type B hepatitis positive for hepatitis B e antigen (HBeAg) are considered to experience frequent acute exacerbations (Perrilo et al. 1984;Liaw et al. 1987). However, the exacerbations occasionally occur in hepatitis B surface antigen (HBsAg) carriers negative for HBeAg (Liaw et al. 1987). Such exacerbations are considered to be induced by the spontaneous reactivation of chronic hepatitis B virus (HBV) infection and superinfections with hepatitis A virus (HAY) (Zachoval et al. 1983;Davis et al. 1984b), non-A, non-B (NANB) hepatitis agent (s) (Papaevangelou et al. 1984) and hepatitis delta

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