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LPD Associated with Epstein–Barr Virus Infection
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
It appears that EBV-driven LPD typically presents as B cell lymphoproliferative diseases (e.g., infectious mononucleosis, chronic active EBV of B cell type, EBV–positive DLBCL lymphoma associated with chronic inflammation, lymphomatoid granulomatosis) in European and North American populations (Figure 75.2), and as T cell and NK cell lymphoproliferative diseases (e.g., EBV-positive T cell and NK cell lymphoproliferative diseases of childhood [chronic active EBV infection of T- and NK-cell type, systemic form or cutaneous form—chronic active EBV infection of T- and NK-cell type/severe mosquito bite allergy; systemic EBV-positive T cell lymphoma of childhood], aggressive NK-cell leukemia, nasal type extranodal NK/T cell lymphoma, primary EBV-positive nodal T- or NK-cell lymphoma) in Asian and Lain American populations [5–8].
Epstein–Barr virus and the nervous system
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Alexandros C. Tselis, Kumar Rajamani, Pratik Bhattacharya
B lymphocytes are the main cells infected by EBV, and this results in the proliferation of immortalized, activated B cells, which infiltrate lymphoid and systemic tissues [9]. A small number of the B cells are lytically infected and produce more viruses, which in turn infects other B cells. This further amplifies the burden of latently EBV-infected B cells. A T-cell-mediated immune reaction against EBV antigens is induced, and cytotoxic T cells also proliferate to eliminate the EBV-infected cells. These reactive T cells form the “atypical lymphocytes” that are seen during acute infection [10]. Eventually, a dynamic equilibrium between latently infected B cells and EBV-specific cytotoxic T cells results. In situations during which this equilibrium is upset (i.e., with the suppression of EBV-specific T cells by immunosuppression secondary to transplantation or cancer chemotherapy), the EBV-infected B cells begin to proliferate, resulting in a reactivated chronic active EBV infection such as post-transplant lymphoproliferative disease. The lymphoproliferation is initially polyclonal but then evolves into an oligoclonal and finally, if unopposed, a monoclonal form, resulting in lymphoma. Lymphoblastoid cell lines consisting of EBV-immortalized B cells can be isolated from the blood of EBV-seropositive patients if T-cell activity in the leukocyte fraction is suppressed (e.g., by cyclosporin). B cells from EBV-seronegative patients do not survive very long in vitro.
Pharyngitis
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
The oncological risks following EBV-related IM include the following: Hodgkin diseasegenome-positive Burkitt lymphomalymphoproliferative disorders in immunocompromised patientsEBV is a cofactor for the development of nasopharyngeal carcinoma. Recent developments in molecular and immunological diagnostic approaches have suggested that EBV has a causative role in chronic active EBV infection syndrome, EBV-related haemophagocytic lymphohistiocytosis, EBV genome-positive T-cell lymphoma, natural killer cell leukaemia/lymphoma, Hodgkin disease and gastric carcinoma.
Clinical Profile and Outcomes of Primary Immunodeficiency and Malignancy in Childhood at a Tertiary Oncology Center in Developing Country
Published in Pediatric Hematology and Oncology, 2022
Derya Özyörük, Zeliha Güzelküçük, Ayse Metin, Suna Emir, Arzu Yazal Erdem, Dilek Kacar, Ayca Koca Yozgat, Can Baris Aker, Selma Çakmakçı, Sonay Incesoy Özdemir, Neriman Sari, Meriç Kaymak Cihan, Namık Yasar Özbek, İnci Ergürhan İlhan
All patients (early and late periods) who received chemotherapy experienced with various degree neutropenia (Grade 3/4) and infections. They also experienced moderate to severe mucositis (Grade 2/3/4) and mild hepatotoxicity (grade 1/2) due to treatment. One patient had a seizure after developing inappropriate antidiuretic hormone (ADH) syndrome. One patient had developed toxoplasmosis during remission period. One patient developed Coombs positive autoimmune hemolytic anemia. One patient had chylothorax. One patient experienced recurrent herpes zoster infections and chronic active EBV infection at CSF/blood. Two other patients also had chronic active EBV infection. One patient developed severe heart failure. Two patients had polyneuropathy due to vincristine. The patient with MPO deficiency developed severe diaper rash due to candida.
Aggressive natural killer cell leukemia: diagnosis, treatment recommendations, and emerging therapies
Published in Expert Review of Hematology, 2021
Yumeng Zhang, Dasom Lee, Quinto Gesiotto, Lubomir Sokol
The incidence of ANKL is highest in East Asia [3] and lowest in Europe and North America [9]. It mainly affects young adults, with the exception of ANKL deriving from chronic active EBV infection, which is frequently observed in children and adolescent patients [7]. Both males and females are equally affected. Patients often present with B symptoms, such as high fevers, hepatosplenomegaly, jaundice, lymphadenopathy, and less frequently with malignant ascites. The central nervous system and gastrointestinal tract are commonly involved with malignant cells [3,10,11]. Based on retrospective cohorts, the CNS positive rate was between 5–10% [11–13]. However, if CNS involvement is left untreated, the outcome is usually fatal. Unlike the more common indolent T-cell large granular lymphocytic leukemia, ANKL is not associated with rheumatologic disease. Laboratory evaluation has shown that cytopenias and coagulopathy related to disseminated intravascular coagulopathy (DIC) often require patients to undergo transfusion support. Many patients also develop macrophage activation syndrome (MAS) either at the time of diagnosis or during the disease course [14]. Neoplastic NK cells release a large number of cytokines, causing uncontrolled activation of normal lymphocytes, NK cells, and macrophages, which results in the development of MAS.
Clinical aspects in patients with rheumatoid arthritis complicated with lymphoproliferative disorders without regression after methotrexate withdrawal and treatment for arthritis after regression of lymphoproliferative disorders
Published in Modern Rheumatology, 2021
Kazuhisa Nakano, Kazuyoshi Saito, Aya Nawata, Kentaro Hanami, Satoshi Kubo, Ippei Miyagawa, Yoshihisa Fujino, Shingo Nakayamada, Yoshiya Tanaka
MTX should not be used in the treatment of RA after LPD regression, while disease activity of RA tends to be high, so bDMARDs are often required. In the FIRST registry, high disease activity of RA and the inability to use MTX were extracted as risk factors for failure to continue bDMARDs in non-LPD RA patients. In RA after LPD regression, in addition to the inability to use MTX, high disease activity of RA was considered to be the main impediment to the continuation of bDMARDs. Among TCZ, ABT, and TNFi, TNFi users were more frequently discontinued. It can be considered that TNFi was already used before the onset of LPD in many cases and that the inability to use MTX was likely to cause secondary failure. It was reported that EBV-DNA levels did not increase during treatment with TCZ and ABT [26]. However, a case of recurrence of LPD while using TCZ has also been reported [27]. In addition, in our current study, a patient treated with TCZ after regression of C-LPD was suspected of developing primary hepatic lymphoma, and another patient treated with ABT after regression of classical Hodgkin lymphoma developed chronic active EBV infection (CAEBV). When using bDMARDs after LPD regression, it is necessary to carefully select and accumulate cases and to check the safety profile.