lymphoproliferative disorders/eпилептички напад

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Intracranial pseudolymphoma presenting with grand mal seizures.

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Primary central nervous system lymphoproliferative disorders comprise a heterogenous group of intracranial disease, predominantly of the high-grade non-Hodgkin's lymphoma type. We report a 56-year-old woman who developed new-onset grand mal seizures and was found to have two small uniformly

Late-Onset Post-transplantation Central Nervous System Lymphoproliferative Disorder: Case Report.

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Post-transplantation lymphoproliferative disorder (PTLD) is a heterogeneous group of conditions that complicate organ transplantation and are due to immunosuppression. Central nervous system (CNS)-PTLD is rare but its incidence is increasing. It often occurs late and is associated with kidney

Hashimoto's encephalopathy after interferon therapy for hepatitis C virus in adult liver transplant recipient accompanied by post-transplant lymphoproliferative disorder related to Epstein-Barr virus infection.

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A 55-year-old woman underwent living-donor liver transplantation (LDLT). She had no history of autoimmune diseases. Spleen was preserved. Steroids were withdrawn at 3 months after LDLT. Epstein-Barr virus (EBV) infection occurred at 3.5 years after LDLT. Recurrent hepatitis C virus infection was

Central nervous system post-transplant lymphoproliferative disorder after allogeneic hematopoietic stem cell transplantation: The Nagasaki transplant group experience.

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A 17-year-old male received allogeneic transplantation for acute lymphoblastic leukemia, and presented with generalized seizures due to a solitary brain lesion with massive necrosis on day +621. Epstein-Barr virus (EBV) DNA copies were below the cut-off value in plasma. Stereotactic biopsy of the

Posttransplant lymphoproliferative disorders in transplant recipients.

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Posttransplant lymphoproliferative disorder (PTLD) is a serious complication of organ transplantation, with a reported incidence between 0.8% and 32%. The incidence of PTLD mainly depends on the transplanted organ, the immunosuppressive drugs, the viral serology, and the age of the recipient. The

Epstein-Barr virus associated post-transplantation lymphoproliferative disorder with hemophagocytosis in a child with Wiskott-Aldrich syndrome.

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A 23-month-old boy with Wiskott-Aldrich syndrome (WAS) received human leukocyte antigen (HLA)-one locus mismatched, unmanipulated allogeneic bone marrow graft from his mother. An Epstein-Barr virus (EBV)-associated post-transplantation lymphoproliferative disorder (PTLD) of donor cell origin and

A Rare Presentation of Isolated CNS Posttransplantation Lymphoproliferative Disorder.

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Posttransplantation lymphoproliferative disorder (PTLD) is a recognized and extremely morbid complication of solid organ transplantation, but central nervous system involvement, particularly in isolation, is rare. There are no standardized treatment strategies for PTLD, though commonly used

Epstein-Barr virus-associated T/NK cell-type central nervous system lymphoma which manifested as a post-transplantation lymphoproliferative disorder in a renal transplant recipient.

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A 31-year-old male, who had received a cadaveric renal allograft in April 2003, consulted a clinic for a transient hemiplegia in August 2004. At that time, a course observation without medication was chosen. In October 2004, he was admitted to our hospital by ambulance with a clonic seizure and a

Epstein-Barr virus-associated post-transplant lymphoproliferative disease after bone marrow transplantation mimicking graft-versus-host disease.

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In contrast to solid organ transplantation (Tx), the incidence of post-transplant lymphoproliferative disease (PTLD) after hematopoietic stem cell Tx (HSCT) is generally low. This risk, however, is significantly elevated in patients receiving human leukocyte antigen (HLA) mis-matched or

A new therapy in Epstein-Barr virus-associated lymphoproliferative disease: a case report and a revision of the literature.

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Systemic chronic active Epstein-Barr virus infection is an extremely rare childhood disease. Since chronic active Epstein-Barr virus infection can trigger the onset of Epstein-Barr virus-associated lymphoproliferative disease. The clinical manifestations of the disease vary according

Primary Central Nervous System Hodgkin Lymphoma-Like Posttransplant Lymphoproliferative Disorder.

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BACKGROUND Posttransplant lymphoproliferative disorder (PTLD) is a rare condition occurring after organ transplantation. PTLD comprises 4 subtypes, of which Hodgkin lymphoma (HL) type and HL-like type (currently included in polymorphic type) account for only about 1%-3% of cases. Primary central

Atypical hydroa vacciniforme-like epstein-barr virus associated T/NK-cell lymphoproliferative disorder.

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Epstein-Barr virus (EBV)-associated T-cell/natural killer (NK)-cell lymphoproliferative disorders (EBV-T/NK-LPDs) accompany severe chronic active EBV infection (CAEBV) or comprise the CAEBV disease entity. The CAEBV disease entity has the common feature of lymphoproliferation of T or NK cells

Fatal outcome in a patient developing Epstein-Barr virus-associated lymphoproliferative disorder (EBV-LPD) without measurable disease.

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A 51-year-old female patient in the first chronic phase of CML received an allogeneic PBSCT from a matched unrelated donor. The transplant was manipulated by CD34+ cell selection. On day +193 after transplantation the patient was readmitted to the hospital with recurrent fever of unknown origin and

Flavopiridol, fludarabine, and rituximab in mantle cell lymphoma and indolent B-cell lymphoproliferative disorders.

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OBJECTIVE Flavopiridol downmodulates antiapoptotic proteins associated with resistance to fludarabine and rituximab and is effective against p53-mutated chronic lymphocytic leukemia (CLL). We conducted a phase I study of flavopiridol, fludarabine, and rituximab (FFR) in patients with mantle-cell

Intracranial extramedullary hematopoiesis associated with multiple myeloma.

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A 77-year-old woman with multiple myeloma for 5 years presented with obtundation, drowsiness, and disorientation over 15 days. Complete blood count revealed thrombocytopenia (25,000/µL). A brain CT disclosed multiple extraaxial hyperdense foci without bone destruction. Differential diagnosis

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