scholarly journals The impact of hepatitis B core antibody levels on HBV reactivation after allogeneic hematopoietic SCT: an 11-year experience at a single center

2016 ◽  
Vol 51 (11) ◽  
pp. 1496-1498 ◽  
Author(s):  
S K Bae ◽  
T Gushima ◽  
N Saito ◽  
I Yamanaka ◽  
T Shimokawa ◽  
...  
2016 ◽  
Vol 34 (7_suppl) ◽  
pp. 138-138 ◽  
Author(s):  
Lisa K. Hicks ◽  
Jordan J. Feld ◽  
Ronak Saluja ◽  
Judy Truong ◽  
Adam E. Haynes ◽  
...  

138 Background: Hepatitis B virus (HBV) affects over 250 million people worldwide. Most people with chronic HBV (HBsAg positive) have no signs or symptoms of infection. However, when exposed to immunosuppression they are at risk of HBV reactivation which can cause hepatitis, liver failure and death. The risk of HBV reactivation in patients receiving chemotherapy for solid tumors, the efficacy of antiviral prophylaxis, and the clinical impact of HBV reactivation in this setting are uncertain. Primary Aim: To estimate the risk of clinical HBV reactivation (increased HBV DNA + transaminitis) among HBsAg-positive patients administered chemotherapy for a solid tumor. Secondary Aims: To estimate the efficacy of anti-viral prophylaxis and the risk of death from HBV reactivation in patients receiving chemotherapy for solid tumors. Methods: A systematic review and meta-analysis of the English language literature on HBV reactivation was completed (OVID Medline, 1946 to Aug 2013). All citations were reviewed by two or more authors. Data from patients with hematologic malignancies were excluded. Pooled probabilities of HBV reactivation risk, death from HBV reactivation, and odds ratio for the impact of anti-viral prophylaxis were estimated with a random effects model. Results: 2,667 citations were identified; 19 were eligible for inclusion. The pooled estimate for clinical HBV reactivation in HBsAg-positive patients receiving chemotherapy for a solid tumor was 21.9% (95% CI; 16.5% to 27.3%) in those not receiving anti-viral prophylaxis, and 2.4% (95% CI 0.7% to 4.2%) in those receiving anti-viral prophylaxis. The odds ratio for clinical HBV reactivation with antiviral prophylaxis compared to no prophylaxis was 0.12 (95% CI 0.06 to 0.25). In the absence of viral prophylaxis, the risk of dying from HBV reactivation in HBsAg-positive solid tumor patients was estimated at 1.3% with a 95% CI of 0.3% to 2.3%. Conclusions: Patients with chronic HBV who are administered chemotherapy for a solid tumor appear to be at substantial risk of clinical HBV reactivation; this risk may be mitigated by anti-viral prophylaxis. In the absence of anti-viral therapy, patients may experience a small but important risk of dying from HBV reactivation.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 6592-6592
Author(s):  
Lee Mozessohn ◽  
Kelvin K. Chan ◽  
Jordan J. Feld ◽  
Lisa K Hicks

6592 Background: Patients with hepatitis B virus (HBV) who are HBsAg+ are recognized to be at risk of HBV reactivation if rituximab is administered in the absence of antiviral treatment. Recently, it has been reported that patients with so-called “resolved HBV infection”(HBsAg-/cAb+) may also be at risk; however, the degree of risk is not known. Methods: We performed a systematic review of the English and Chinese language literature in Medline (1996 to July week 2 2012) and Embase (1996 to 2012 week 29) using the MeSH terms “lymphoma” and “hepatitis B”. Eligible studies were limited to those reporting primary data on HBV reactivation rates in HBsAg-/cAb+ patients receiving rituximab. We excluded case series with less than 5 patients. Pooled estimates were calculated for HBV reactivation and the impact of HBsAb status on HBV reactivation rate was explored. Results: Data from 445 patients in 12 studies were included. Using a standardized definition of HBV reactivation, (ALT >3 x upper limit of normal AND either an increase in HBV DNA from baseline OR HBsAg seroreversion), the pooled estimate for the risk of HBV reactivation in HBsAg-/cAb+ patients was 5.4% (I2 = 63%, P = 0.009). Significant heterogeneity was apparent. Exploratory analyses suggested that patients were less likely to reactivate if they were HBsAb+ (OR = 0.32; 95% CI 0.12-0.85, P = 0.0285). Conclusions: Our meta-analysis confirms that there is a measurable risk of HBV reactivation in HBsAg-/cAb+ patients exposed to rituximab HBsAb+ patients may be at lower risk than those who are HBsAb-. However, heterogeneity in the risk estimates limits their generalizability. Large prospective studies are needed to clarify the risk of HBV reactivation in HBsAg-/cAb+ patients and to inform decisions about best practice.


2013 ◽  
Vol 31 (31_suppl) ◽  
pp. 228-228
Author(s):  
Lee Mozessohn ◽  
Kelvin K. Chan ◽  
Jordan J. Feld ◽  
Lisa K. Hicks

228 Background: Patients with hepatitis B virus (HBV) who are HBsAg+ are at risk of HBV reactivation if rituximab is administered in the absence of antiviral treatment. Recently, it has been reported that patients with so-called “resolved HBV infection”(HBsAg-/cAb+) may also be at risk; however, the degree of risk is not known. Methods: We performed a systematic review of the English and Chinese language literature in Medline (1996 to June week 3 2013) and Embase (1996 to 2013 week 26) using the MeSH terms “lymphoma” and “hepatitis B”. Eligible studies were limited to those reporting primary data on HBV reactivation rates in HBsAg-/cAb+ patients receiving rituximab. We excluded case series with less than 5 patients. Pooled estimates were calculated for HBV reactivation and the impact of HBsAb status on HBV reactivation rate was explored. We also examined reactivation in HBsAg+ patients receiving rituximab by performing a systematic review of the English language literature in PubMed (1997 to June 21, 2013) using the terms “hepatitis B virus”, “reactivation” and “lymphoma”. Results: Data from 550 HBsAg-/cAb+ patients in 12 studies were included. Using a standardized definition of HBV reactivation, (increase in HBV DNA from baseline or HBsAg seroreversion +/- ALT >3 x upper limit of normal), the pooled estimate for the risk of HBV reactivation in HBsAg-/cAb+ patients was 8.1% (I2 = 55%, P = 0.007). Significant heterogeneity was apparent. Exploratory analyses suggested that patients were less likely to reactivate if they were HBsAb+ (OR = 0.32; 95% CI 0.12-0.85, P = 0.0285). In HBsAg+ patients we meta-analyzed prospective, controlled studies. Without antiviral prophylaxis, the reactivation rate for HBsAg+ lymphoma patients was 51.0% (I2 = 0%, P = 0.93). Conclusions: Our meta-analyses confirm that there is a risk of HBV reactivation in HBsAg-/cAb+ patients exposed to rituximab. HBsAb+ patients may be at lower risk than those who are HBsAb-. However, heterogeneity in the risk estimates limits their generalizability. Without prophylaxis, significant reactivation in HBsAg+ patients exists. Large prospective studies are needed to clarify the risk of HBV reactivation in HBsAg-/cAb+ patients and to inform decisions about best practice.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3968-3968
Author(s):  
Liang-Tsai Hsiao ◽  
Po-Min Chen ◽  
Yu-Jiun Chan ◽  
Yi-Hsiang Huang ◽  
Yuan-Bin Yu ◽  
...  

Abstract Abstract 3968 Purpose. Anti-CD20 monoclonal antibody - rituximab leads to hepatitis B virus (HBV) reactivation in HBV surface antigen (HBsAg)-negative patients with B-cell non-Hodgkin¡&brkbar;s lymphoma (NHL), with the reported incidence ranged from 2% to 25%. Using a large cohort of HBsAg-negative B-cell NHL patients in one of HBV-endemic areas - Taiwan, we analyzed the clinical and virological features of de novo HBV reactivation following rituximab-contained immuno-chemotherapy. Materials & Methods. Patients with the diagnosis of CD20 positive B-cell NHL who received rituximab-contained immunochemotherapy in Taipei Veterans General Hospital between 2002/1 and 2008/12 were collected. Clinical features, disease status, treatment and serological data of hepatitis virus (HBsAg, Antibody to HBsAg [HBsAb], anti-HBc, antibody to hepatic C virus [anti-HCV] through the period of rituximab administration were collected. The event of reverse seroconverion (RS, defined by the seroconversion from HBsAg negative to positive) was identified, with additional data collection of liver function tests. Serum HBV DNA was examined using nested and real-time PCR for a subset of patients with available sera through rituximab therapy, including those with and without RS. Results. A total of 517 B-cell NHL who once received rituximab were identified, including 71 HBsAg-positive (13.7%). For 446 HBsAg-patients, there were 27 (6%) with RS, which resulted in deaths in two patients (0.45% of total 446 patients; 7% of 27 patients with RS), with the characteristics shown in Table 1. Fifty-two percents of these patients (n=14) were female and fifty one percents have diffuse large B cell lymphoma. They have received a median of 8 doses rituximab (range, 3–20) before the development of RS. All of RS events developed within 6 months since last dose of rituximab alone or contained therapy, including those four (15% of all events) which appeared during rituximab maintenance therapy. Additional factors which also leaded the development of RS included previous transplantation in 4 patients (3 with hematopoietic stem cell transplantation and 1 with organ transplantation) and previous use of radioimmunotherapy in one patient. Among those patients without RS, sixty percents of these 94 patients (88% being anti-HBc positive) with available sera had a detectable level (> 50 copies/ml) of serum HBV-DNA through the period of rituximab-contained therapy, with the level up to 6 × 1,000 copies/ml. Conclusion. In HBV endemic areas, HBV reactivation is common in HBsAg-negative patients with different subtypes of B-cell NHL through the period of rituximab-contained therapy. The degree of reactivation ranged from asymptomatic viremia to reverse sero-conversion, which may be asymptomatic or accompanied by clinical hepatitis. Using anti-viral agents, primary prophylaxis or preempting therapy during regular monitoring of HBV reactivation may decrease these insults. However, the impact is now more complicated by increased duration of rituximab therapy and subsequent use of additional immunosuppressant in these patients. Disclosures: No relevant conflicts of interest to declare.


2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S787-S787
Author(s):  
Amedine Duret ◽  
Emma Thorley ◽  
Ayolola Eni-Olotu ◽  
Oishi Sikdar ◽  
Padmasayee Papineni

Abstract Background North West London has one of the highest tuberculosis (TB) rates in the UK, at 24.8 per 10,000. The UK prevalence of hepatitis B virus (HBV) is 0.1-0.5% and for hepatitis C virus (HCV) is 0.5-1%. Chronic infection with HBV or HCV can lead to an increased risk of adverse treatment outcomes, such as drug-induced liver injury (DILI) in patients with active or latent TB. National guidelines recommend routinely screening for HBV/HCV prior to initiating TB treatment. Our objectives were to 1) evaluate the HBV/HCV screening practice in local TB clinics, 2) establish the prevalence of HBV/HCV in patients receiving TB treatment. Methods Retrospective analysis of laboratory and medical records of patients treated for active or latent TB identified from the London TB register and clinic records from 01/01/2018 to 31/12/2020 from London North West NHS Trust. Results 1409 patients received treatment for TB during the time period of interest; 574 (40.7%) had active disease and 835 (59.3%) had latent infection. 966/1409 patients (68.56%) were screened for HBV and HCV. 55.9% of the active TB group and 77.2% of the latent infection group were tested. 66 (6.8%) patients had isolated anti-HBc positivity, 22 (2.3%) were HBV surface antigen positive and 8 (0.8%) were HCV-antibody positive. HBV surface antigens were more prevalent in active TB patients: 9/321 (2.80%) with active TB versus 13/645 (2.02%) with latent TB. 36/321 (11.21%) active TB patients had HBV core antibodies compared to 30/645 (4.65%) latent TB patients (p < 0.001). Three patients started antiviral treatment following their viral hepatitis diagnosis (one with HBV, two with HCV). Conclusion The prevalence of chronic HBV in the study population was higher than the estimated UK prevalence. Fifteen diagnoses of hepatitis were new, allowing specialist referral for monitoring of fibrosis and development of hepatocellular carcinoma. Three patients required hepatitis treatment. 6.8% of patients were positive for anti-HBc and therefore identified as being at future risk of HBV reactivation if requiring immunosuppressive therapies.TB disproportionately affects marginalised communities; screening for viral hepatitis in TB clinic represents an opportunity to target these hard-to-reach groups to maximise the impact of public health interventions. Disclosures All Authors: No reported disclosures


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1584
Author(s):  
Tobias Moser ◽  
Ciara O’Sullivan ◽  
Christian Puttinger ◽  
Julia Feige ◽  
Georg Pilz ◽  
...  

Cladribine (CLAD) is a lymphodepleting agent approved for active relapsing multiple sclerosis (MS). The impact of CLAD on the adaptive humoral immune system has not sufficiently been studied. This study aimed to assess the influence of CLAD treatment on specific antibody titers to common pathogens. We included 18 MS patients treated with CLAD. Serum IgG antibody levels to measles, mumps, rubella, hepatitis B and varicella zoster virus (VZV), as well as diphtheria and tetanus toxins, were measured prior to the initiation of treatment and at 12 and 24 months after first CLAD administration. Moreover, specimens were longitudinally analyzed regarding absolute blood concentrations of IgG and main lymphocyte subsets. No reduction in antibody levels against measles, mumps, rubella, VZV, hepatitis B, diphtheria toxin and tetanus toxin associated with CLAD treatment was observed. Loss of seroprotection occurred in < 1%. We found no significant impact of CLAD on absolute serum IgG levels. Absolute lymphocyte counts were significantly reduced at the end of each treatment year (p < 0.00001 and p < 0.000001). This study suggests that CLAD does not interfere with the pre-existing humoral immunologic memory in terms of pathogen-specific antibody titers.


2020 ◽  
Author(s):  
Junko Kuroda ◽  
Shigeru Kusumoto ◽  
Tsukasa Kimata ◽  
Tomomi Kataoka ◽  
Satoshi Hibi ◽  
...  

Abstract Background: There is little evidence regarding the risk of hepatitis B virus (HBV) reactivation in solid tumor patients without hepatitis B surface antigen (HBsAg), but with antibodies against hepatitis B core antigen (anti-HBc) and/or antibodies against HBsAg (anti-HBs) who received systemic chemotherapy. Methods: We conducted two retrospective studies; a single-center retrospective study to measure the incidence of HBV reactivation in 1,376 HBsAg-negative patients with solid tumors who received systemic chemotherapy, and a multicenter retrospective study to clarify the clinical features of HBV reactivation in HBsAg-negative patients with solid tumors who received systemic chemotherapy at 5 institutions. HBV reactivation was defined as reappearance of HBsAg or detection of HBV DNA levels of 1.3 log IU/mL or more in both studies.Results: With a median follow-up time of 607 days, HBV reactivation was confirmed in 2 of 218 patients with resolved HBV infection in the single-center study. Of the 12 patients with HBV reactivation who were diagnosed at a median HBV DNA of 1.3 log IU/mL in the multicenter study, no HBV-related hepatitis was observed. The median time from the first chemotherapy to confirmed HBV reactivation was 141 days. Of the 11 patients in whom both anti-HBc and anti-HBs were measured, all were seropositive for anti-HBc, and 7 were seronegative for anti-HBs at baseline.Conclusions: The risk of HBV reactivation was estimated to be 0.9% in HBsAg-negative patients with solid tumors who received systemic chemotherapy. Seronegativity for anti-HBs at baseline may be an important risk factor for HBV reactivation in these patients.


2008 ◽  
Vol 46 (06) ◽  
Author(s):  
K Rutter ◽  
H Hofer ◽  
M Schöniger-Hekele ◽  
C Müller ◽  
P Munda ◽  
...  

2016 ◽  
pp. 74-80
Author(s):  
Phuong Phung ◽  
Thi Thuy Nguyen

ackground and Objectives: Nowadays, the incidence of cancer is constantly increasing in the world as well as in Vietnam. The treatment of cancer is based on multimodality principle. Among those principal modalities, chemotherapy is widely used for different purposes such as neoadjuvant, andjuvant and palliation. However, chemotherapy can induce activation of latent infections, including hepatitis B. Vietnam is in the endemic region of hepatitis B so the reactivation of hepatitis B on cancer patients with chemotherapy has emerged a concerned problem. However, few interests were gained on this problem in the aspect of clinical setting or researching. Aims: to determine the prevalence of hepatitis B reactivation (HBV) in cancer patients treating with chemotherapy and to detect some risks factors of this situation. Subjects and methods: descriptive prospective. The study included 33 cancer patients with inactive HBV infection who are treating with chemotherapy. We define HBV reactivation by ALT > 3 ULN and HBV DNA copies > 10 positive control limit. Results: We found 6 patients with reactivated HBV, accounting for 18.18 %. Among reactivated HBV patients, age less than 60 accounts 83,33%. Rate of reactivated HBV in males was 25,00% while this rate in females was 14,28%. Rate of reactivated HBV in lymphoma, lung cancer and breast cancer was 33,33%, 25% và 22,22% respectively. Clinial manifestation of reactivated HBV includes jaundice (33,33%), fulminant hepatic failure (6%) and death (5%). The reactivated rate was higher in patients got high dose of corticoid (28,57%) vs low dose (15,38%). This rate was 29,41% in patients treated with anthracyclines which was higher than in group without anthracyclines. The reactivated rate of HBV was dramatically higher in patients treated with rituximab (75%). Conclusion: the reactivation of hepatitis B on cancer patients with chemotherapy is common. We found 6 patients with reactivated HBV of 33 subjects of the study which accounts 18.18 %. We recognized that reactivated HBV rate was higher subgroups of age < 60 years old, males, patients with lymphoma, lung cancer, breast cancer. Reactivated HBV may be more prevalent in patients with high-dose corticotherapy, anthracyclines and Rituximab. Key words: HBV reactivation, chemotherapy, cancer, hepatitis B


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