scholarly journals Epstein-Barr Virus-Related Lymphoproliferative Disorder Caused by the Use of Antithymocyte Globulin and Cyclosporine for Aplastic Anemia

2014 ◽  
Author(s):  
Suzuki
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Hiroko Sugimoto-Sekiguchi ◽  
Haruko Tashiro ◽  
Ryosuke Shirasaki ◽  
Tomio Arai ◽  
Tadashi Yamamoto ◽  
...  

Epstein-Barr-virus- (EBV-) associated lymphoproliferative disorder (LPD) after immunosuppressive therapy for aplastic anemia (AA), in a nontransplant setting, has not been well described. We report one case of colonic EBV-LPD after a single course of immunosuppressive therapy for AA. The patient developed multiple colonic tumors 3 months after receiving immunosuppressive therapy, which consisted of rabbit antithymocyte globulin (ATG), cyclosporine, and methyl-predonisolone. The histological findings of biopsy specimens revealed that atypical lymphocytes had infiltrated colonic glands. Immunohistochemical staining for CD20 was positive, andin situhybridization for EBV-encoded small RNAs was also positive. The EBV viral load in peripheral blood was slightly increased to 140/106white blood cells. After the cessation of immunosuppressant, the colonic tumors spontaneously regressed, and the EBV viral load decreased to undetectable levels. This is the first report of the single use of rabbit ATG inducing colonic EBV-LPD. Because a single use of immunosuppressive therapy containing rabbit ATG can cause EBV-LPD, we should carefully observe patients receiving rabbit ATG for AA.


2019 ◽  
Vol 103 (4) ◽  
pp. 433-441 ◽  
Author(s):  
Sung‐Soo Park ◽  
Sung‐Yeon Cho ◽  
Eunhee Han ◽  
Gi June Min ◽  
Silvia Park ◽  
...  

2015 ◽  
Vol 7 (3) ◽  
Author(s):  
Nobuyoshi Hanaoka ◽  
Shogo Murata ◽  
Hiroki Hosoi ◽  
Aiko Shimokado ◽  
Toshiki Mushino ◽  
...  

B-cell lymphoproliferative disorder (B-LPD) is generally characterized by the proliferation of Epstein-Barr virus (EBV-infected B lymphocytes. We here report the development of EBV-negative B-LPD associated with EBV-reactivation following antithymocyte globulin (ATG) therapy in a patient with aplastic anemia. The molecular autopsy study showed the sparse EBV-infected clonal T cells could be critically involved in the pathogenesis of EBV-negative oligoclonal B-LPD through cytokine amplification and escape from T-cell surveillances attributable to ATG-based immunosuppressive therapy, leading to an extremely rare B-cell-rich T-cell lymphoma. This report helps in elucidating the complex pathophysiology of intractable B-LPD refractory to rituximab.


Viruses ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 416
Author(s):  
Hiroaki Inoue ◽  
Shinya Rai ◽  
Hirokazu Tanaka ◽  
J. Luis Espinoza ◽  
Maiko Komori-Inoue ◽  
...  

Aplastic anemia is a rare blood disease characterized by the destruction of the hematopoietic stem cells (HSC) in the bone marrow that, in the majority of cases, is caused by an autoimmune reaction. Patients with aplastic anemia are treated with immunosuppressive drugs and some of them, especially younger individuals with a donor available, can be successfully treated with hematopoietic stem cell transplantation (HSCT). We report here a rare case of post-transplant lymphoproliferative disorder (PTLD) associated with Epstein–Barr virus (EBV) reactivation in a 30-year-old female patient who underwent allogeneic HSCT for severe aplastic anemia. The PTLD, which was diagnosed 230 days after transplantation, was localized exclusively in the central nervous system (specifically in the choroid plexus) and manifested with obvious signs of intracranial hypertension. After receiving three cycles of high dose methotrexate (HD-MTX) combined with rituximab, the patient achieved a complete clinical recovery with normalization of blood cell counts, no evidence of EBV reactivation, and no associated neurotoxicity.


2016 ◽  
Vol 136 (3) ◽  
pp. 174-177
Author(s):  
Hiroaki Shimizu ◽  
Nobuhiko Kobayashi ◽  
Masahiro Mihara ◽  
Hirono Iriuchishima ◽  
Takuma Ishizaki ◽  
...  

Epstein-Barr virus-associated lymphoproliferative disorder (EBV-LPD) is a currently emerging serious complication in immunosuppressed patients, especially in allogeneic transplant recipients. Several fatal cases of EBV-LPD have been reported in aplastic anemia (AA) patients receiving immunosuppressive therapy (IST) with antithymocyte globulin (ATG) plus cyclosporine A (CsA), but no appropriate prophylactic or therapeutic strategy has been established. Herein, we describe a 29-year-old man whose EBV-LPD was successfully treated with rituximab. He received IST with ATG plus CsA for hepatitis-associated AA. EBV-DNA in plasma, which was not detectable before IST, gradually increased after IST initiation. A high fever and systemic lymphadenopathy developed 31 days after IST initiation. An EBV-DNA titer of 5.7 × 105 copies/μl was detected, and a diagnosis of EBV-LPD was made. Although discontinuation of IST was not effective, a single dose of rituximab on day 33 resolved the clinical symptoms and completely eliminated EBV-DNA. Even after restarting CsA administration, no elevation of EBV-DNA was observed, and his complete blood cell count had fully recovered 1 year after IST. This case suggests that this treatment strategy for EBV-LPD with EBV-DNA monitoring and rituximab administration, which has been recommended in allogeneic transplant recipients, may also be useful in the context of AA patients receiving IST.


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