Extracutaneous B‐cell post‐transplantation lymphoproliferative disorder and cutaneous T‐cell post‐transplantation lymphoproliferative disorder in a child

2019 ◽  
Vol 61 (1) ◽  
pp. 74-75
Author(s):  
Ho Jeong Shin ◽  
Chang Jin Jung ◽  
Kyung Mo Kim ◽  
Mi Woo Lee
Blood ◽  
1998 ◽  
Vol 92 (9) ◽  
pp. 3137-3147 ◽  
Author(s):  
Malika Benkerrou ◽  
Jean-Philippe Jais ◽  
Véronique Leblond ◽  
Anne Durandy ◽  
Laurent Sutton ◽  
...  

Abstract B-lymphoproliferative disorder (BLPD) is a rare but severe complication of organ and bone marrow transplantation (BMT). Profound cytotoxic T-cell deficiency is thought to allow the outgrowth of Epstein-Barr virus–transformed B cells. When possible, reduction of immunosuppressive treatment or surgery for localized disease may cure BLPD. Therapeutic approaches using chemotherapy or antiviral drugs have limited effects on survival. Adoptive immunotherapy with donor T-cell infusions has given promising results in BMT recipients. We previously reported that administration of two monoclonal anti–B-cell antibodies (anti-CD21 and anti-CD24) could contribute to the control of oligoclonal BLPD. Here we report the long-term results of treatment with these monoclonal anti–B-cell antibodies for cases of severe BLPD. In an open multicenter trial, 58 patients in whom aggressive B-cell lymphoproliferative disorder developed after BMT (n = 27) or organ (n = 31) transplantation received 0.2 mg/kg/d of specific anti-CD21 and anti-CD24 murine monoclonal antibodies (MoAbs) for 10 days. The treatment was well tolerated. Thirty-six of the 59 episodes of BLPD in the 58 patients presented complete remission (61%). The relapse rate was low (3 of 36, 8%). Multivariate analysis identified the following risk factors for partial or no response to anti–B-cell MoAb therapy: multivisceral disease (P ≤ .005), central nervous system involvement (P ≤ .05), and late onset of BLPD (P ≤ .005). The overall long-term survival was 46% (median follow-up, 61 months); it was lower among BMT patients (35%) than organ transplant patients (55%). None of the patients who had received BMT for hematological malignancy survived for 1 year. Eight of these 11 patients presented monoclonal BLPD. Tumor burden was the only other variable that contributed significantly to poor survival. Thus, as assessed from this long-term study, the use of anti–B-cell MoAbs therefore appears to be a safe and relatively effective therapy for severe posttransplant BLPD. © 1998 by The American Society of Hematology.


2001 ◽  
Vol 23 (2) ◽  
pp. 139-142 ◽  
Author(s):  
C. Christopoulos ◽  
A. Tassidou ◽  
S. Golfinopoulou ◽  
G. Anastasiadis ◽  
S. Manetas ◽  
...  

2001 ◽  
Vol 42 (5) ◽  
pp. 1023-1031 ◽  
Author(s):  
Rashad Aboul-Nasr ◽  
Susan O'brien ◽  
Emil J. Freireich ◽  
Cheryl F. Ginsberg ◽  
Hagop M. Kantarjian ◽  
...  

Blood ◽  
2002 ◽  
Vol 100 (7) ◽  
pp. 2341-2348 ◽  
Author(s):  
Pierluigi Porcu ◽  
Charles F. Eisenbeis ◽  
Ronald P. Pelletier ◽  
Elizabeth A. Davies ◽  
Robert A. Baiocchi ◽  
...  

Posttransplantation lymphoproliferative disorder (PTLD) is a life-threatening Epstein-Barr virus (EBV)–associated B-cell malignancy occurring in 1% to 2% of renal transplantation patients. Host- and PTLD-related factors determining the likelihood of tumor response following reduction of immune suppression (IS) and antiviral therapy remain largely unknown. Standard therapy for PTLD is not well established. Eleven consecutive renal transplantation patients who developed EBV-positive PTLD 8 to 94 months after allografting were uniformly treated with acyclovir and IS reduction. All PTLDs were EBV-positive diffuse large B-cell lymphomas. Ten patients (91%) obtained a durable complete response (CR), and 9 (82%) have remained in continuous CR with a median follow-up of 29 months. Five patients (45%) lost their allograft. Of these, 4 patients had PTLD affecting the transplanted kidney. Peripheral blood CD8+ T cells increased significantly (P = .0078) from baseline in 8 responders available for analysis. One of 2 patients whose absolute CD8+ T-cell count subsequently dropped to baseline after IS reduction relapsed. The expanded CD8+ T cells from 2 responders specifically recognized an immunodominant peptide from the EBV lytic gene BZLF-1. Another lytic EBV gene, thymidine kinase, was expressed in all 8 PTLDs tested. IS reduction and antiviral therapy for PTLD after renal transplantation is a highly successful therapeutic combination, but the risk of graft rejection is significant, particularly in patients with PTLD involving the renal allograft. A sustained expansion of CD8+ T cells and a cellular immune response to EBV lytic antigens may be important for PTLD clearance in renal transplantation patients.


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