Hepatitis B Virus Infection and B‐Cell Non‐Hodgkin's Lymphoma in a Hepatitis B Endemic Area: A Case‐control Study

Kim, Jee Hyun; Bang, Yung‐Jue; Park, Byung Joo; Yoo, Taiwoo; Kim, Chul Woo; Kim, Tae-You; Heo, Dae Seog; Lee, Hyo‐Suk; Kim, Noe Kyeong

doi:10.1111/j.1349-7006.2002.tb01280.x

Cited by 95 publications

(91 citation statements)

References 24 publications

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“…[1][2][3][4][5][6] The high incidence (34.3%) of past HBV infection in patients with lymphoma supports the hypothesis that HBV may play a role in the epidemiology and pathogenesis of malignant lymphoma, at least in endemic areas, particularly because a proportion of these patients are viremic. Testing of HBV surface antigen alone may in fact underestimate the true prevalence of chronic HBV infection in lymphoma patients.…”

Section: Discussionmentioning

confidence: 92%

Hepatitis B virus reactivation and role of antiviral prophylaxis in lymphoma patients with past hepatitis B virus infection who are receiving chemoimmunotherapy

Koo

Tan

et al. 2009

Cancer

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BACKGROUND: Individuals who had past hepatitis B virus (HBV) infection appeared to clear their serum hepatitis B surface antigen (HBsAg) while producing antibody to the hepatitis B core antigen (HBcAb), which is detectable in their serum. Currently, it is uncertain whether patients with past HBV infection require routine antiviral prophylaxis during chemotherapy, although some cancer agencies recommend its routine use. The objective of the current study was to determine the prevalence of past HBV infection in patients with lymphoma and its relevance in terms of HBVrelated complications. METHODS: The authors reviewed 430 patients with lymphoma from May 2006 to May 2008. RESULTS: Among the 430 patients, 233 had both the HBsAg and HBcAb tests performed, whereas 197 had only the HBsAg test performed. Among those with both tests performed, 34.3% (80 of 233) were HBcAb positive only. Of these 80 patients, 58 had a concomitant HBV DNA level test, which was positive in 3 (5.2%). Of the 67 patients with past and 26 with chronic HBV infection who received chemotherapy, HBV reactivation occurred in 1.5% and 42.3% of patients, respectively (P<.0001). Prophylactic lamivudine was administered in 7 (10.4%) patients with past HBV infection and in 18 (69.2%) with chronic HBV infection. CONCLUSIONS: The low rate of HBV reactivation reported in our study coupled with the high prevalence of past HBV infection in an endemic area suggests that routine usage of antiviral prophylaxis may not be required for all patients with past HBV infection. Close surveillance remains a reasonable and viable option for the majority of patients. Cancer 2010;116:115-21.

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Section: Discussionmentioning

confidence: 92%

Hepatitis B virus reactivation and role of antiviral prophylaxis in lymphoma patients with past hepatitis B virus infection who are receiving chemoimmunotherapy

Koo

Tan

et al. 2009

Cancer

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“…22 More recently, several case-control studies with large numbers of patients have been published. 23,24 These studies have been recently reviewed in a meta-analysis 25 that included 12 studies. The pooled odds ratio, which, given the rarity of the disorder, is a good estimation of the RR, was found to be consistent with a significant association (odds ratio, 2.56; 95% CI, 2.24-2.92).…”

Section: Association Of Hbv and Nhlmentioning

confidence: 99%

Hepatitis viruses and non-Hodgkin lymphoma: epidemiology, mechanisms of tumorigenesis, and therapeutic opportunities

Marcucci

Mele

2011

Blood

217

200

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Over the past 2 decades considerable evidence has accumulated on the association between hepatitis C virus (HCV) and hepatitis B virus (HBV) and several hematologic malignancies, most notably B-cell non-Hodgkin lymphoma (NHL). In this review we summarize this evidence, address possible mechanisms whereby hepatitis viruses may contribute to lymphomagenesis, and discuss the therapeutic fallouts from this knowledge. Most of this evidence is on HCV, and this is the main focus of the review. Moreover, we mainly address the association with NHL, the most prevalent hematologic malignancy, and the most extensively investigated with regard to an association with hepatitis viruses. Available evidence on the association with other hematologic malignancies is also addressed briefly. (Blood. 2011;117(6):1792-1798) Hepatitis C virus and hepatitis B virusHepatitis C virus (HCV) is a positive, single-stranded RNA virus, member of the Flaviviridae family. 1 During its replicative cycle it goes through a negative-stranded RNA, but not DNA, intermediate, so that integration of HCV nucleic acid sequences into the host genome seems unlikely. As such, it lacks a pivotal property of classical oncogenic retroviruses. The HCV genome produces a single polyprotein that is proteolytically processed by viral and cellular proteases to produce structural (nucleocapsid, E1, E2) and nonstructural (NS) proteins (NS2, NS3, NS4A, NS4B, NS5A, and NS5B).Hepatitis B virus (HBV) is a small DNA virus, member of the Hepadnaviridae family. 2 It presents the unusual feature, for a DNA virus, to replicate through a RNA intermediate and can integrate into the host genome. Moreover, during replication, it undergoes transformation into covalently closed circular DNA. Detection of closed circular DNA HBV-, or negative-stranded HCV-intermediates is important because it identifies genuine viral replication instead of more trivial events such as viral absorption. HBV is characterized by a genome consisting of 4 overlapping open-reading frames: the S gene, encoding envelope proteins; the core gene, encoding the core and "e" proteins; the P gene, encoding DNA polymerase; and the X gene, encoding a transcriptional transactivator.Both viruses can induce acute and chronic hepatitis and are strongly associated with hepatocellular carcinoma (HCC). Epidemiology of non-Hodgkin lymphomaNon-Hodgkin lymphoma (NHL) is the hematologic malignancy with the highest prevalence worldwide. Incidence rates have grown fast up to the beginning of the new millennium, with an annual percentage increase of nearly 3%, which is faster than for most cancers. Thus, delay-adjusted Surveillance, Epidemiology and End Results incidence rate for all races was 11.06/100 000 in 1975, and 20.12/100 000 in 2002. Since then, incidence rates have started to level off, at least in some geographic areas, such as the United States (20.89 in 2007). 3 NHL incidence rates are higher in developed countries such as those in western Europe, North America, and Australia and lower in South America and Asia, but th...

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“…Our results are similar to those observed in the study in the UK, which detected an excess of AIDS and Non-Hodgkin's lymphoma (NHL) mortality. 19 There are 2 case-control studies 59,60 that have detected an excess of NHL among HBV carriers. We could not estimate the specific NHL risk because specific data for haematological neoplasms subtype was not available in the RMC.…”

mentioning

confidence: 99%

Cofactors associated with liver disease mortality in an HBsAg‐positive Mediterranean cohort: 20 years of follow‐up

Ribes

Clèries

Rubió

et al. 2006

Intl Journal of Cancer

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The risk of developing liver cancer in hepatitis B virus (HBV) carriers differs across geographical areas, suggesting that exposure to other risk factors may contribute to HBV‐linked cancer risk. Our study estimates the mortality due to liver disease and the role of other risk factors in a Spanish HBV cohort. 2,352 hepatitis B surface antigen (HBsAg)‐positive and 15,504 HBsAg‐negative subjects were identified among blood donors during 1972–1985 and were followed until December 2000 through the Mortality Registry. Clinical examination and an epidemiological questionnaire were performed on 1,000 HBsAg‐positive survivors during 1994–1996. In subjects deceased from liver disease, medical records were revised and relatives were interviewed. A nested case‐control analysis was conducted comparing both groups. In HBsAg‐positive men, an excess mortality from liver cancer [standardized mortality ratio (SMR): 14.1; 7.7–23.6], cirrhosis (SMR: 10.5; 7.0–15.1), haematological neoplasms (SMR: 3.2; 1.2–6.9) and AIDS was detected (SMR: 5.5; 2.2–11.4). In women, an excess was found for cirrhosis (SMR: 7.2; 1.4–21.1). Progression factors to liver disease were alcohol intake [odds ratio (OR): 6.3; 3.1–12.8], diabetes (OR: 3.6; 1.3–9.6), HBV replication (OR: 50.0; 14.9–167.3) and hepatitis C virus (HCV) infection (OR: 27.4; 7.1–107.7). In conclusion, in Spain after 20 years of follow‐up, chronic HBV exposure appears as a major risk factor for liver cancer among men and for cirrhosis in both sexes. The risk of death from liver disease among HBV carriers with the presence of HBV replication, HCV, alcohol consumption and diabetes was significantly increased and suggests synergism among these exposures and HBV. Mortality from haematological neoplasms was detected and could be associated to HIV coinfection. These results support screening and adequate follow‐up among HBsAg‐positive subjects at high risk to develop liver disease, particularly when these risk cofactors are present. © 2006 Wiley‐Liss, Inc.

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Hepatitis B Virus Infection and B‐Cell Non‐Hodgkin's Lymphoma in a Hepatitis B Endemic Area: A Case‐control Study

Cited by 95 publications

References 24 publications

Hepatitis B virus reactivation and role of antiviral prophylaxis in lymphoma patients with past hepatitis B virus infection who are receiving chemoimmunotherapy

Hepatitis B virus reactivation and role of antiviral prophylaxis in lymphoma patients with past hepatitis B virus infection who are receiving chemoimmunotherapy

Hepatitis viruses and non-Hodgkin lymphoma: epidemiology, mechanisms of tumorigenesis, and therapeutic opportunities

Cofactors associated with liver disease mortality in an HBsAg‐positive Mediterranean cohort: 20 years of follow‐up

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