Hepatitis B or C virus infection and risk of non-Hodgkin lymphoma among solid organ transplant recipients

Morton, Lindsay M.; Gibson, Todd M.; Clarke, Christina A.; Lynch, Charles F.; Weisenburger, Dennis D.; Engels, Eric A.

doi:10.3324/haematol.2013.101600

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…Analysis of the French Registry for PTLD on KT patients did not identify HCV as a predictive factor . In a large US cohort of solid organ transplant recipients, no association was observed between HCV infection and non‐Hodgkin lymphoma . In the present study, 2.4% of our population developed lymphoma after transplantation and no difference was observed between HCV‐positive and HCV‐negative patients.…”

Section: Discussioncontrasting

confidence: 77%

Malignancies in hepatitis C virus‐positive and ‐negative kidney transplant recipients: A case‐controlled study

Dörr

Bello

Abravanel

et al. 2017

Transplant Infectious Dis

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Section: Discussioncontrasting

confidence: 77%

Malignancies in hepatitis C virus‐positive and ‐negative kidney transplant recipients: A case‐controlled study

Dörr

Bello

Abravanel

et al. 2017

Transplant Infectious Dis

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“…Thus, the immune activation and inflammation associated with HIV infection may underlie the increased risks of these subtypes. An elevated prevalence of HCV infection among individuals with HIV may contribute to the elevated risk observed for marginal zone lymphoma, but evidence from prior studies indicates HCV may not be a risk factor for this NHL subtype in the context of immunosuppression [14–16]. We did not see an elevated risk for follicular lymphoma or CLL/SLL, in line with the previous results [17], suggesting that immune perturbation does not play a major role in development of these types of NHLs.…”

Section: Discussionmentioning

confidence: 99%

Risk of non-Hodgkin lymphoma subtypes in HIV-infected people during the HAART era

Gibson¹,

Morton²,

Shiels³

et al. 2014

Aids

164

142

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Objective HIV-infected people have greatly elevated risk of non-Hodgkin lymphoma (NHL), particularly the AIDS-defining NHL subtypes: diffuse large B-cell lymphoma, Burkitt lymphoma and primary lymphomas arising in the central nervous system. The goals of this analysis were to comprehensively describe risks of NHL subtypes, especially those not well studied, among HIV/AIDS patients; examine risks specifically in the HAART era; and distinguish risks in HIV-infected individuals prior to diagnosis with AIDS. Design Population-based registry linkage study. Methods We used data from the US HIV/AIDS Cancer Match Study from 1996 to 2010 (N = 273 705) to calculate standardized incidence ratios (SIRs) comparing subtype specific NHL risks in HIV-infected people to those in the general population, and used Poisson regression to test for differences in SIRs between the HIV-only and AIDS periods. Results NHL risk was elevated 11-fold compared to the general population, but varied substantially by subtype. AIDS-defining NHL subtypes comprised the majority, and risks were high (SIRs ≥ 17), but risks were also increased for some T-cell lymphomas (SIRs = 3.6–14.2), marginal zone lymphoma (SIR = 2.4), lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (SIR = 3.6), and acute lymphoblastic leuke mia/lymphoma (SIR = 2.4). Conclusion HIV-infected people in the HAART era continue to have elevated risk of AIDS-defining NHL subtypes, highlighting the contribution of moderate and severe immunosuppression to their cause. Whereas non-AIDS-defining subtypes are much less common, immunosuppression or other dysregulated immune states likely play a role in the cause of some T-cell lymphomas, marginal zone lymphoma, lymphoplasmacytic lymphoma/Waldenström macroglobulinemia, and acute lymphoblastic leukemia/lym phoma.

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“…A major risk factor specific to SOT is the use of multivisceral or intestinal transplants due to a high volume of donor lymphoid tissue contained in the graft, which is subject to expansion when exposed to EBV and in an immunodeficient environment (Kinch et al , ). Although an intact immune system is essential for chronic viral hepatitis to directly cause a lymphoproliferative disorder, untreated infection with the hepatitis C virus can contribute to PTLD pathogenesis by inducing alterations in the B‐cell receptor immunoglobulin gene and through chronic antigenic stimulation (Morton et al , ; Tucci et al , ). Recipient HLA‐A26 and HLA‐B38 status has also been associated with a higher risk, probably due to altered antigen presentation or immune tolerance (Reshef et al , ).…”

Section: Epidemiologymentioning

confidence: 99%

Management of post‐transplant lymphoproliferative disorders

et al. 2018

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The post-transplant lymphoproliferative disorders (PTLDs) are a heterogeneous group of neoplasms that are one of the most serious complications of bone marrow and solid organ transplants. Because these disorders are rare, there are no randomized trials from which to derive optimal treatment. Management can be challenging and must balance the goal of PTLD eradication with the risks of graft rejection, graft-versus-host disease, further delays in immune reconstitution and life-threatening infections, among others. This paper will provide a comprehensive review of PTLD following solid organ transplant and haematopoietic stem cell transplant with a focus on management. Included is a discussion of novel agents that are being studied in clinical trials and, when combined or sequenced with conventional therapy, have the potential to improve outcomes.

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Hepatitis B or C virus infection and risk of non-Hodgkin lymphoma among solid organ transplant recipients

Cited by 7 publications

References 15 publications

Malignancies in hepatitis C virus‐positive and ‐negative kidney transplant recipients: A case‐controlled study

Malignancies in hepatitis C virus‐positive and ‐negative kidney transplant recipients: A case‐controlled study

Risk of non-Hodgkin lymphoma subtypes in HIV-infected people during the HAART era

Management of post‐transplant lymphoproliferative disorders

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