Reactivation of hepatitis B in an HIV-infected patient with antibodies against hepatitis B core antigen as the only serological marker

Chamorro, Antonio-Javier; Casado, José L.; Bellido, Demian; Moreno, Santiago

doi:10.1007/s10096-005-1355-1

Cited by 39 publications

(30 citation statements)

References 16 publications

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“…Among immunocompromised patients, HBV-DNA can be detected in 10% of HBsAg negative/anti-HBc positive patients. Reactivation of HBV is rare [10]; reactivation of HBV has recently been described in an HIV-positive patient who was anti-HBc alone [26].…”

Section: Discussionmentioning

confidence: 99%

Occult hepatitis B virus infection in immunocompromised patients

Jardim¹,

Gonçales²,

Pereira³

et al. 2008

Braz J Infect Dis

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Occult hepatitis B infection is characterized by hepatitis B virus (HBV) DNA in the serum in the absence of hepatitis B surface antigen (HBsAg). We assessed occult HBV infection prevalence in two groups of immunocompromised patients (maintenance hemodialysis patients and HIV-positive patients) presenting HBsAgnegative and anti-HBc positive serological patterns, co-infected or not by HCV. Thirty-four hemodialysis anti-HIV negative patients, 159 HIV-positive patients and 150 blood donors who were anti-HBc positive (control group) were selected. HBV-DNA was detected by nested-PCR. Occult hepatitis B infection was not observed in the hemodialysis patients group but was found in 5% of the HIV-patients and in 4% of the blood donors. Immunosuppression in HIV positive patients was not a determining factor for occult HBV infection. In addition, no significant relationship between HBV-DNA and HCV co-infection in the HIV-positive patient group was found. A lack of significant associations was also observed between positivity for HBV-DNA and CD4 count, viral load and previous lamivudine treatment in these HIV-positive patients.

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Section: Discussionmentioning

confidence: 99%

Occult hepatitis B virus infection in immunocompromised patients

Jardim¹,

Gonçales²,

Pereira³

et al. 2008

Braz J Infect Dis

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“…With the increasing prevalence of HIV infection, HBV reactivation has also been observed in HBV-infected subjects with advanced immune deficiency due to HIV infection [22][23][24][25][26][27]. Hepatitis due to HBV reactivation has not only been reported in HBsAg-positive patients, HBeAg-positive [6,[28][29][30] or HBeAg-negative [31][32][33][34][35][36][37][38][39][40][41] subjects who were treated with chemotherapy and transplantation but also in HBsAg-negative patients who had past HBV infection (hepatitis B surface antibody; antiHBs positive and hepatitis B core antibody; anti-HBc positive) [42][43][44][45][46][47][48][49], especially those treated with rituximab or alemtuzumab-containing chemotherapy [50][51][52][53][54][55].…”

Section: How Important Is the Problem?mentioning

confidence: 99%

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Lau

2008

Hepatol Int

102

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Hepatitis due to hepatitis B virus reactivation after cytotoxic or immunosuppressive therapy is a serious cause of liver-related morbidity and mortality. With the characterization of the underlying pathogenesis, much progress in the management of this important clinical problem has been made in the past 2 decades. By year 2008, it is mandatory to screen for hepatitis B surface antigen status before initiating intensive chemotherapy or immunosuppressive therapy. All those who are hepatitis B surface antigen positive should be started on preemptive nucleos(t)ide analogues. However, there remains important issues, such as the type and duration of nucleos(t)ide analogue therapy, which need to be understood. As not all hepatitis B surface antigen-positive patients will suffer from HBV reactivation, it is therefore useful to identify risk factors related to HBV reactivation so that patients will not be treated unnecessarily with nucleos(t)ide analogues. To date, a high baseline level of viral replication, as reflected by high serum HBV DNA level, positive serum hepatitis B e antigen, and a high intrahepatic covalently closed circular DNA level, is the most important predictor for HBV reactivation. Recently, there has been an increased awareness of reactivation of occult hepatitis B virus, especially in hepatitis B virus endemic area, such as the Asia-Pacific region. Careful epidemiological study will be needed to clarify the impact of occult hepatitis B infection in patients treated with cytotoxic or immunosuppressive therapy. How important is the problem?Over the past 20 years of clinical practice at Queen Mary Hospital, we have seen a lot of progress in the management of hepatitis due to HBV reactivation in hepatitis B surface antigen carriers [1][2][3][4][5]. In the past, we saw patients who died of fulminant hepatic failure after being administered a few courses of cytotoxic therapy to treat their life-threatening lymphoma [6][7][8][9] and breast cancer [10][11][12] if they were also hepatitis B surface antigen positive. At that time, the literature report of this important clinical issue was scanty. The first report in the field was published by Wand et al. [13] who studied the effects of antitumor chemotherapeutic agents on hepatitis antigen (HBAg) and antibody (HBAb) in 25 patients with myeloproliferative and in 60 patients with lymphoproliferative disorders. This elegant study was performed at the time when only antigen and antibody associated with viral hepatitis could be semiquantified [14]. In those patients who had HBAg at the time of initiation of chemotherapy, bone marrow suppression by chemotherapeutic agents was associated with a marked increase in HBAg titer, which was then followed by hepatocellular damage, as manifested by an elevation in serum transaminase enzymes [13]. Since then, this important observation was further confirmed in other studies [8,15,16], with the rate of HBV reactivation ranging from 19% to 48%. Among them, one-quarter to half would be complicated, with severe hepatitis...

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“…Many factors, similar to those demonstrated for overt infection, have been implicated in the recurrence of HBV replication in HIV/OBI-co-infected patients, including the interruption of HAART [37][38][39] , recovery of immune responses after HIV-treatment [14] , development of resistance to lamivudine therapy [13] , and appearance of HBV immune-escape [40] . The overall prevalence of OBI reactivation in HIV patients and the frequency of the specific triggers of reactivation need to be assessed in prospective longitudinal studies [14] .…”

Section: Clinical Significancementioning

confidence: 99%