Semiquantitative anti‐HBc IgM detection in children with chronic hepatitis B: A long‐term follow‐up study

Gaeta, G. B.; Nardiello, S; Pizzella, T; Russo, G; Maisto, Antonella; Sardaro, C; Galanti, B; Giusti, G

doi:10.1002/jmv.1890460302

Cited by 4 publications

(4 citation statements)

References 13 publications

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“…In addition, the pre-core mutant type of HBV, that is predominant in many countries, does not respond well to IFN alpha [Hadziyannis et al, 1990;Pastore et al, 1992;Brunetto et al, 1993]. Further, the HBeAg seroconversion induced by IFN alpha is often preceded by an abrupt, transient accentuation of hepatitis activity, as reflected by an increase in serum ALT in patients with severe liver disease [Marinos et al, 1994;Perrillo, 1994;Gaeta et al, 1995;Hassanein et al, 1996]. In patients with cirrhosis, this flare of activity can lead to liver failure and occasional deaths.…”

Section: Ifn and Hbeag Seroconversionmentioning

confidence: 95%

Hepatitis B e antigen seroconversion: Effects of lamivudine alone or in combination with interferon alpha

Farrell

2000

J. Med. Virol.

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Seroconversion of hepatitis B e antigen (HBeAg) is an important marker for resolution of active hepatitis B virus (HBV) infection and for a long-term positive response to treatment. Lamivudine, a nucleoside analogue, is the first effective oral treatment for chronic hepatitis B in patients with evidence of viral replication and liver disease. When appropriate patient groups are compared, treatment with lamivudine for 1 year leads to HBeAg seroconversion in a similar proportion of patients as a standard course of interferon (IFN) alpha therapy. Seroconversion increases during prolonged therapy (up to 3 years), and is sustained post-treatment in more than three-quarters of patients. Response rates are related to the pretreatment level of serum alanine aminotransferase (ALT) and reach 65% in those patients with serum ALT > 5 x upper limit of normal (ULN) after one year. For patients with pretreatment ALT > 2 x ULN, response was seen in 38% after one year, rising to 65% after 3 years. To date, combination with IFN and lamivudine has not been shown to confer additional benefit compared with lamivudine monotherapy. Lamivudine is effective and appropriate for use in a greater proportion of HBV infected patients than IFN alpha, particularly those infected at birth or in early childhood. Furthermore, because seroconversion after lamivudine is not normally associated with a severe flare of liver disease, as seen with IFN, it is more suitable for use in patients with active liver disease and cirrhosis. In conclusion, lamivudine is more suitable than IFN for a broad range of patients, including those with severe liver disease, recurrent flares, pre-core mutant HBV and those who have failed previously IFN treatment or are immunosuppressed. Lamivudine is also better tolerated than IFN.

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Section: Ifn and Hbeag Seroconversionmentioning

confidence: 95%

Hepatitis B e antigen seroconversion: Effects of lamivudine alone or in combination with interferon alpha

Farrell

2000

J. Med. Virol.

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“…This may have been due to the patients' inability to mount the appropriate antibody response in an acute infection during immunosuppression induced by chemotherapy. It is more likely, however, to be due to the sensitivity of the assay used, which has been set to discriminate between acute and non-acute infections [Diment, 1991;Gaeta et al, 1995;Colloredo et al, 1996]. In chronic HBV infection, the mutation at nt 1896 has also been linked to more severe liver disease in chronic carriers in some but not all reports [Carman et al, 1989;Okamoto et al, 1990;Omata et al, 1991;Brunetto et al, 1990;Bonino et al, 1986;Naoumav et al, 1992;Tur-Kaspa et al, 1992;Chan et al, 1998 ].…”

Section: Discussionmentioning

confidence: 95%

Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: Precore/core mutations may play an important role

et al. 2000

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Reactivation of the hepatitis B virus (HBV) is a rare, but well described complication of cytotoxic chemotherapy that may result in hepatic failure. Patients who are chronic carriers of the HBV and who have a G to A mutation at nucleotide 1896 in the precore region may develop more severe liver disease, possibly because of rapid selection and enhanced replication ability of the mutant strain. Such mutant viruses have been implicated occasionally in chemotherapy induced reactivation of hepatitis B virus. In this report, 5 patients with solid tumours were identified to have developed severe hepatitis B virus related liver disease during treatment with cytotoxic agents (with dexamethasone as anti-emetic). All had clinical and serological evidence of reactivation of the HBV. Three patients developed icteric hepatitis; 2 fully recovered, and 1 had died from progressive metastatic disease while recovering from the reactivation. The other two died from progressive liver failure. Direct sequencing of the polymerase chain reaction (PCR) products of the precore (preC) and precore promoter region of the HBV-DNA was carried out on the patients' serum samples taken during the episode of reactivation. In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promoter. The present findings suggest that reactivation involving a mutant hepatitis B virus may lead to liver failure, which is possibly more severe than that caused by wild type HBV, and can be triggered by cytotoxic chemotherapy, or the administration of corticosteroids. In Eastern Asia the HBV carriage rate in adults is high. HBV reactivation and severe liver disease during cytotoxic treatment may become a serious and common problem in this region as cytotoxic chemotherapy is more widely used. Patients should be screened routinely for HBsAg in endemic areas of chronic hepatitis B virus infection prior to receiving cytotoxic treatment. The possibility of HBV reactivation should be considered in patients developing liver dysfunction. Patients who are HBeAg negative/Anti-HBe positive, and are suspected to be having an HBV reactivation, should have HBV-DNA levels measured for confirmation as they may carry a mutant HBV.

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“…Treatment with IFN alpha is sometimes associated with significant increases in serum ALT, that are potentially hazardous [Perrillo, 1994;Marinos et al, 1994;Gaeta et al, 1995;Hassanein et al, 1996;Hoofnagle and Di Bisceglie, 1997]. In contrast, lamivudine was associated with only modest ALT elevations during treatment.…”

Section: Safety Profile Of Lamivudinementioning

confidence: 90%

“…Response to treatment may be a result of either a direct effect of lamivudine on HBV alone or a combined effect with enhanced cell-mediated immune responses that may follow the reduction in viral load and replication [Boni et al, 1998]. Unlike IFN alpha [Perrillo, 1994;Marinos et al, 1994;Gaeta et al, 1995;Hassanein et al, 1996;Hoofnagle and Di Bisceglie, 1997], lamivudine does not seem to cause flares of liver disease, that is, perhaps, surprising in the light of the increased Tcell response. The reason for this is not clear.…”

Section: Lamivudine Suppresses Hbv Replicationmentioning

confidence: 98%

Lamivudine for hepatitis B in clinical practice

Schiff

2000

J. Med. Virol.

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Lamivudine is a potent, once-daily, oral antiviral therapy that is effective and well tolerated in most patient groups with chronic hepatitis B virus infection, including those with pre-core mutant infection. Studies to date show that lamivudine suppresses serum viral replication, causing reductions in serum hepatitis B virus (HBV) DNA and enhancing hepatitis B e antigen (HBeAg) seroconversion (loss of HBeAg plus presence of antibodies to HBeAg [anti-HBe]). Lamivudine also improves liver disease, as shown by normalisation of alanine transaminase (ALT) levels and reduced progression to cirrhosis. Lamivudine is effective in patients who are interferon (IFN) alpha naïve and in those who have failed to respond to IFN alpha, and it suppresses HBV in decompensated liver disease and in liver transplantation. Variants with mutations in the YMDD (tyrosine-methionine-aspartate-aspartate) motif may emerge with prolonged lamivudine therapy, but most patients maintain clinical control. Lamivudine has a safety profile similar to that of placebo and it is better tolerated than IFN alpha. In conclusion, lamivudine represents a major advance in the therapeutic options available for the management of patients with chronic hepatitis B and should now be considered the drug of choice for most patients who require treatment.

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Semiquantitative anti‐HBc IgM detection in children with chronic hepatitis B: A long‐term follow‐up study

Cited by 4 publications

References 13 publications

Hepatitis B e antigen seroconversion: Effects of lamivudine alone or in combination with interferon alpha

Hepatitis B e antigen seroconversion: Effects of lamivudine alone or in combination with interferon alpha

Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: Precore/core mutations may play an important role

Lamivudine for hepatitis B in clinical practice

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