scholarly journals An Epstein-Barr Virus-Associated Leukemic Lymphoma in a Patient Treated with Rabbit Antithymocyte Globulin and Cyclosporine for Hepatitis-Associated Aplastic Anemia

2012 ◽  
Vol 127 (2) ◽  
pp. 96-99 ◽  
Author(s):  
Kinya Ohata ◽  
Noriko Iwaki ◽  
Takeharu Kotani ◽  
Yukio Kondo ◽  
Hirohito Yamazaki ◽  
...  
2019 ◽  
Vol 103 (4) ◽  
pp. 433-441 ◽  
Author(s):  
Sung‐Soo Park ◽  
Sung‐Yeon Cho ◽  
Eunhee Han ◽  
Gi June Min ◽  
Silvia Park ◽  
...  

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.


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.


1988 ◽  
Vol 28 (4) ◽  
pp. 273-275 ◽  
Author(s):  
Judy E. Grishaber ◽  
Kenneth L. McClain ◽  
Donald H. Mahoney ◽  
Donald J. Fernbach

2001 ◽  
Vol 67 (4) ◽  
pp. 252-255 ◽  
Author(s):  
Kürşad Kaptan ◽  
Cengiz Beyan ◽  
Ali Uğur Ural ◽  
Celalettin Üstün ◽  
Türker Çetin ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Tohru Takahashi ◽  
Yumiko Maruyama ◽  
Mayuko Saitoh ◽  
Hideto Itoh ◽  
Mitsuru Yoshimoto ◽  
...  

Epstein-Barr virus (EBV) associated lymphoproliferative disorder (LPD) after immunosuppressive therapy for aplastic anemia (AA) is extremely rare in a nontransplant setting and has not been well described. This report describes a severe AA patient in whom fatal EBV-LPD developed after being treated with rabbit antithymocyte globulins (ATG) and cyclosporine A (CsA). An 81-year-old man was diagnosed as having severe AA. He was started on CsA followed by administration of ATG for five consecutive days. One month after the start of ATG, persistent fever which was not responsive to antibiotics or antifungal agents developed and atypical lymphocytes emerged in peripheral blood. Repeated blood cultures were negative. An extremely high level of EBV virus in his peripheral blood plasma was detected by means of a quantitative real-time PCR assay. Even after the cessation of CsA, the fever persisted and the peripheral atypical lymphocytes proliferated rapidly. The patient suffered from respiratory failure, liver dysfunction, and metabolic acidosis. Rituximab was administered without success and he died.


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