Epstein-Barr Virus, Immunodeficiency, and B Cell Lymphoproliferation

Hanto, Douglas W.; Frizzerà, Glauco; Gajl‐Peczalska, Kazimiera J.; Simmons, Richard L.

doi:10.1097/00007890-198505000-00001

Cited by 401 publications

(148 citation statements)

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“…The increased incidence in the older population is to be expected based on the natural history of lymphoma in the general population. The increased incidence in children <10 years is evident within 3 months after transplantation and is most likely owing to primary EBV infection of seronegative recipients (16). Antiviral prophylaxis has been advocated for high-risk patients, but its efficacy has not been established (32).…”

Section: Lymphomas After Solid Organ Transplantationmentioning

confidence: 99%

“…Most cases of post-transplant lymphoma have been linked to unrestrained proliferation of Epstein-Barr virus (EBV)-infected B cells caused by suppression of normal immunosurveillance mechanisms by immunosuppressive therapy (16). It has been suggested that continuing immunostimulation by the transplanted organ may also be involved in lymphoma formation (17).…”

Section: Introductionmentioning

confidence: 99%

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Lymphomas After Solid Organ Transplantation: A Collaborative Transplant Study Report

Opelz

Döhler

2004

American Journal of Transplantation

977

787

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We used the Collaborative Transplant Study database to analyze the incidence, risk, and impact of malignant lymphomas in approximately 200 000 organ transplant recipients. Over a 10-year period, the risk in renal transplant recipients was 11.8-fold higher than that in a matched nontransplanted population (p < < 0.0001). The majority of lymphomas were diagnosed after the first post-transplant year. Heart-lung transplants showed the highest relative risk (RR 239.5) among different types of organ transplants. In kidney recipients, immunosuppression with cyclosporine did not confer added risk compared with azathioprine/steroid treatment, whereas treatment with FK506 increased the risk approximately twofold. Induction therapy with OKT3 or ATG, but not with anti-IL2 receptor antibodies, increased the risk of lymphoma during the first year. Antirejection therapy with OKT3 or ATG also increased the risk. First-year mortality in renal and heart transplant patients with lymphoma was approximately 40% and 50%, respectively, and showed no improvement in recent years. A pattern of preferential localization to the vicinity of the transplant was noted, and the prognosis of the patient was related to localization. This study highlights the continuing risk for lymphoma with time post-transplantation, the contribution of immunosuppression to increased risk, and continuing poor outcomes in patients with post-transplant lymphoma.

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Section: Lymphomas After Solid Organ Transplantationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lymphomas After Solid Organ Transplantation: A Collaborative Transplant Study Report

Opelz

Döhler

2004

American Journal of Transplantation

977

787

View full text Add to dashboard Cite

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“…[107][108][109][110][111]244 The patient may have an infectious mononucleosis-like syndrome, usually of exaggerated severity with respiratory compromise or cervical mass. In other cases, isolated organ dysfunction may occur due to infiltrative or tumorous PTLD.…”

Section: General Summary Of Positransplant Lymphoproliferatne Disordermentioning

confidence: 99%

“…1 85 ,193 In the Minnesota series, 14% of patients had disease confined to the eNS and a total of 45% had eNS disease, usually in association with widespread disease. 108 The tonsils, when involved, usually enlarge quite dramatically, often contain prominent necrosis and may cause acute respiratory embarrassment. Involved lymph nodes in the early stages maintain a smooth, circumscribed capsule and on cut sUIface display a uniform, gray-white to tan surface.…”

Section: Pathology Of Posttransplant Lymphoproliferative Disordermentioning

confidence: 99%

The diagnosis and treatment of posttransplant lymphoproliferative disorders

Nalesnik

Makowka

Starzl

1988

Current Problems in Surgery

249

111

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“…[1][2][3][4] The increased risk of EBVassociated BLPD in patients with T cell dysfunction, both primary and secondary, is well-recognized, but the pathogenesis of BLPD in the immunocompromised host has not been fully characterized. [1][2][3][4] EBV, a member of the human herpesvirus family, infects and immortalizes human B lymphocytes in vitro and in vivo, establishing lifelong viral latency in peripheral blood lymphocytes in healthy EBV-seropositive individuals. 5 Following primary infection in the immunocompetent host, proliferation of EBV-infected B cells is controlled by a multitude of immune mechanisms including virus-specific cytotoxic T cells, humoral responses, antibody-dependent cellular cytotoxicity, natural killer activity, and cytokine regulation.…”

mentioning

confidence: 99%

B cell lymphoproliferative disorders following hematopoietic stem cell transplantation: risk factors, treatment and outcome

Gross

Steinbuch

DeFor

et al. 1999

Bone Marrow Transplant

209

170

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Summary:Twenty-six cases of B cell lymphoproliferative disorder (BLPD) were identified among 2395 patients following hematopoietic stem cell transplants (HSCT) for which an overall incidence of BLPD was 1.2%. The true incidence was probably higher, since 9/26 of the diagnoses were made at autopsy. No BLPD was observed following autologous HSCT, so risk factor analyses were confined to the 1542 allogeneic HSCT. Factors assessed were HLA-mismatching (у1 antigen), T cell depletion (TCD), presence of acute GvHD (grades II-IV), donor type (related vs unrelated), age of recipient and donor, and underlying disease. Factors found to be statistically significant included patients transplanted for immune deficiency and CML, donor age у18 years, TCD, and HLA-mismatching, with recipients of combined TCD and HLA-mismatched grafts having the highest incidence. Factors found to be statistically significant in a multiple regression analysis were TCD, donor age and immune deficiency, although 7/8 of the patients with immunodeficiencies and BLPD received a TCD graft from a haploidentical parent. The overall mortality was 92% (24/26). One patient had a spontaneous remission, but subsequently died Ͼ1 year later of chronic GVHD. Thirteen patients received therapy for BLPD. Three patients received lymphocyte infusions without response. The only patients with responses and longterm survival received alpha interferon (␣IFN). Of seven patients treated with ␣IFN there were four responses (one partial and three complete). These data demonstrate that ␣IFN can be an effective agent against BLPD following HSCT, if a timely diagnosis is made.

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Epstein-Barr Virus, Immunodeficiency, and B Cell Lymphoproliferation

Cited by 401 publications

References 0 publications

Lymphomas After Solid Organ Transplantation: A Collaborative Transplant Study Report

Lymphomas After Solid Organ Transplantation: A Collaborative Transplant Study Report

The diagnosis and treatment of posttransplant lymphoproliferative disorders

B cell lymphoproliferative disorders following hematopoietic stem cell transplantation: risk factors, treatment and outcome

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