Epstein‐Barr virus associated B‐cell lymphoma after autologous bone marrow transplantation for T‐cell acute lymphoblastic leukaemia

Briz, Montserrat; Forés, Rafael; Regidor, C; Busto, Maria‐José; Cajal, Santiago Ramón y; Cabrera, Rafael; Díez, J de Miguel; Sanjuán, I; Fernández, Manuel‐Nicolás

doi:10.1046/j.1365-2141.1997.2153034.x

Cited by 30 publications

(30 citation statements)

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“…One of the EBVseropositive patients developed a post-transplant lymphoproliferative disease after a T cell depleted CD34 + selected autologous stem cell transplantation for systemic lupus erythematodes. Although the risk of EBV post-transplant lymphoproliferative disease after autologous transplantation is low, case reports of this complication in the autologous setting exist [Chao et al, 1993, Briz et al, 1997, Hauke et al, 1998]. …”

Section: Discussionmentioning

confidence: 99%

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Meerbach

Wutzler

Häfer

et al. 2008

Journal of Medical Virology

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Epstein-Barr virus (EBV)-associated post-transplant lymphoproliferative disease is a lifethreatening complication following hematopoietic stem cell transplantation. A quantitative polymerase chain reaction to evaluate EBV-genome copy numbers based on a nested polymerase chain reaction and an end-point dilution was used. Applying this assay EBV load was prospectively screened weekly in 123 patients after transplantation. The results demonstrate that EBV reactivations with more than 1,000 EBV-genome copies measured in 10(5) peripheral blood mononuclear cells were observed in 31 patients (25.2%). Three patients developed lymphoproliferative disease with extremely high EBV-genome copies in peripheral blood mononuclear cells (>100,000 copies/10(5) cells) and plasma. After combined antiviral and immune therapy two of three patients showed a dramatic decrease of EBV load and survived, while the third patient died of lymphoma. A subclinical EBV reactivation was observed in 24 cases (19.5%) with EBV-genome copies in 10(5) peripheral blood mononuclear cells ranging between 2,500 and mostly 10,000. After reduction of immunosuppression the EBV levels normalized. In four patients, the high copy number of > or =80,000 copies/10(5) peripheral blood mononuclear cells and plasma positivity prompted us to start pre-emptive therapy with rituximab and cidofovir for prevention of lymphoproliferative disease. After drug administration the high EBV load was reduced remarkably. Ninety-two patients (74.8%) who had < or =1,000 copies/10(5) peripheral blood mononuclear cells did not develop EBV-associated lymphoproliferative disease. In conclusion, monitoring of EBV load is a sensitive and useful parameter in the surveillance of EBV reactivation for early intervention in EBV-associated lymphoproliferative disease as well as for follow-up of the efficacy of therapy. Applying this assay EBV load was prospectively screened weekly in 123 patients after transplantation. The results demonstrate that EBV reactivations with more than

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Section: Discussionmentioning

confidence: 99%

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Meerbach

Wutzler

Häfer

et al. 2008

Journal of Medical Virology

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“…[2][3][4][5] However, it should be noted that, although the majority of cases occur in such high-risk patients, there are reports of PTLD even after autologous BMT. [16][17][18] In our eight cases, the pathology was either DLBC lymphoma (five) or PBCH (three). The six patients with disseminated disease were equally grouped between DLBC lymphoma and PBCH.…”

Section: Discussionmentioning

confidence: 99%

Lymphoproliferative disorders following allogeneic bone marrow transplantation: the Vancouver experience

Micallef

Chhanabhai

Gascoyne

et al. 1998

Bone Marrow Transplant

106

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Summary:Between June 1988 and May 1996, 428 patients underwent allogeneic BMT (288 related donor (RD) and 140 unrelated donor (UD)) at the Vancouver General Hospital. Eight patients (UD six and RD two) developed a post-transplant lymphoproliferative disorder (PTLD). Median age at BMT was 38 years (range 22-51). Five of the six UD allografts were T cell depleted. Cyclosporine ± methotrexate was used for GVHD prophylaxis. All eight patients developed GVHD; in six this was refractory to treatment with corticosteroids. Rabbit antithymocyte globulin (ATG) or an anti-CD5-ricin A chain immunotoxin (Xomazyme) was used as second-line therapy for GVHD. Presentation with PTLD occurred at median day 90.5 (range 34-282) post BMT. Five of the eight patients had a rapidly progressive course characterized by fever, lymphadenopathy, lung and liver involvement and died within 3-8 days. PTLD was an incidental finding at post mortem examination in two patients. The remaining patient had localized disease and recovered. Pathological analysis revealed two morphological patterns; diffuse large B cell lymphoma (DLBC lymphoma, five patients) and polymorphous B cell hyperplasia (PBCH, three patients). EBV expression was positive in all eight cases and monoclonality was demonstrated in seven cases. In multivariate analysis, T cell depletion of the allograft (P = 0.0001, relative risk (RR) = 30.5), anti-T cell therapy for GVHD (P = 0.006, RR = 12.7) and acute GVHD grades 3-4 (P = 0.04, RR = 7.7) were the significant factors for development of PTLD. In conclusion, we have identified two forms of PTLD after BMT: one is characterized by disseminated disease with a rapidly progressive and often fulminant course and the other by localized, relatively indolent disease. Morphology, EBV positivity and clonality do not appear to correlate with the clinical course. The major risk factors for development of PTLD after BMT are ex vivo T cell depletion of the allograft and in vivo anti-T cell therapy for GVHD.

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“…The significance of the TCR gene rearrangement is not clear, however, it has been well reported. 8,13 Perhaps the presence of both IgH and TCR gene rearrangements indicate oligoclonality, and therefore a better prognosis than monoclonal changes. In our patients, the early presentation of PTLD post ASCT may partially explain the favorable response to therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Three of the seven reported cases of PTLD after ASCT were treated with corticosteroids and the only patient who survived also had therapy with acyclovir and IFN. 5,8,11 IFN has been shown to reduce EBV-induced B cell proliferation, and has been successfully used in other hematologic malignancies. 17 Shapiro et al 18 reported the first cases of IFN for B cell lymphoproliferative disorders (two post BMT), with dramatic responses to IFN and IVIG.…”

Section: Discussionmentioning

confidence: 99%

“…3,7 In the autologous bone marrow patients with PTLD reported previously, three were in the context of T cell-depleted grafts, and one in a B celldepleted graft. 4,[8][9][10] One patient was also on prednisone as part of his treatment for PCP and CMV pneumonitis. 11 In our case reports, two had MM which is associated with defective humoral immunity, and the case of angioimmunoblastic NHL is associated with defective cell-mediated immunity.…”

Section: Discussionmentioning

confidence: 99%

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Successful treatment of post-transplant lymphoproliferative disorder in autologous blood stem cell transplant recipients

Jenkins

DiFrancesco

Chaudhry

et al. 2002

Bone Marrow Transplant

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Summary:We report three cases of post-transplant lymphoproliferative disorder (PTLD) in the context of autologous stem cell transplantation (ASCT) for multiple myeloma (MM) and non-Hodgkin's lymphoma. The first two cases received ASCT for MM, one with a CD34-selected autograft and the other with an unmanipulated autograft. Both these cases of PTLD achieved a complete response following treatment with IVIG, gancyclovir, solumedrol and interferon (IFN). The third case received ASCT with an unmanipulated autograft for relapsed angioimmunoblastic lymphoma. He also achieved a complete response but only after rituximab was added to IVIG, gancyclovir, solumedrol and IFN. None of these patients experienced a relapse of their PTLD with follow-up ranging from 1.5 to 5 years. These cases highlight the importance of considering PTLD in the differential diagnosis of lymphadenopathy and fever post ASCT. They also demonstrate the possibility of durable complete remission of post-ASCT PTLD following antiviral and immune modulating therapy. Bone Marrow Transplantation (2002) 30, 321-326. doi:10.1038/sj.bmt.1703603 Keywords: post-transplant lymphoproliferative disorder; autologous stem cell transplantation; interferon; gancyclovir; rituximab; Epstein-Barr virus Post-transplant lymphoproliferative disorder (PTLD) is a well recognized complication of solid organ transplant and allogeneic bone marrow transplantation (BMT). 1,2 Prognosis and mortality vary depending on the clinical features, pathological classification and time since transplantation. Even with early diagnosis and treatment, the mortality rate remains high, ranging from 38% with early onset tumors, to greater than 60% for late onset tumors. 1 The only standard treatment recognized at this time is reduction of immunosuppression, and radiotherapy or surgery for anatomically In autologous stem cell transplantation (ASCT), only rare cases have been reported, most of which have recently been summarized by Lones and colleagues. 3 These previously reported patients received ASCT for chronic myelogenous leukemia, T cell acute lymphoblastic leukemia, Hodgkin's disease, non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) and neuroblastoma. Outcomes in general were poor, and the only successful treatments for PTLD were seen in two patients who received interferon (IFN). 4,5 We report three cases of PTLD occurring after ASCT for MM and NHL, who were successfully managed with antiviral and immunomodulating therapy. Case reports Case 1A 41-year-old man was diagnosed with a stage IIA IgG kappa MM in April 1996. He was treated with two cycles of VAD (vincristine 0.4 mg i.v. daily ϫ 4, adriamycin 9 mg/m 2 i.v. daily ϫ 4, and dexamethasone 40 mg p.o. on days 1-4, 9-12 and 17-20). He then underwent stem cell mobilization with dose-intensive cyclophosphamide 5.25 g/m 2 i.v., etoposide 1 g/m 2 i.v., cisplatin 100 mg/m 2 i.v. (DICEP) and s.c. G-CSF, as previously reported. 6 This was uncomplicated except for culture-negative febrile neutropenia. Four months after initial diagnosis he recei...

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Epstein‐Barr virus associated B‐cell lymphoma after autologous bone marrow transplantation for T‐cell acute lymphoblastic leukaemia

Cited by 30 publications

References 10 publications

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Lymphoproliferative disorders following allogeneic bone marrow transplantation: the Vancouver experience

Successful treatment of post-transplant lymphoproliferative disorder in autologous blood stem cell transplant recipients

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