Primary Effusion Lymphoma

Chen, Yi-Bin; Rahemtullah, Aliyah; Hochberg, Ephraim P.

doi:10.1634/theoncologist.12-5-569

Cited by 238 publications

(214 citation statements)

References 65 publications

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“…4,6 Primary effusion lymphoma is a distinctive type of diffuse large B cell initially recognized in HIVpositive patients, characterized by occurrence in a body cavity unassociated with a contiguous solid mass, immunophenotypic and genetic features corresponding to a late postgerminal center B cell in most cases, 2,7-12 a distinctive gene expression profile 13,14 and a poor prognosis. 2,7,8,12,15 Tumor cells are usually coinfected by EBV, a g herpesvirus closely related to HHV8 (Tables 1 and 2). Nearly all cases of multicentric Castleman's disease in HIVpositive patients and a subset of multicentric Castleman's disease in HIV-negative individuals contain HHV8.…”

Section: Discussionmentioning

confidence: 99%

HHV8-positive, EBV-positive Hodgkin lymphoma-like large B-cell lymphoma and HHV8-positive intravascular large B-cell lymphoma

et al. 2009

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Section: Discussionmentioning

confidence: 99%

HHV8-positive, EBV-positive Hodgkin lymphoma-like large B-cell lymphoma and HHV8-positive intravascular large B-cell lymphoma

et al. 2009

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“…Human tumors have been attributed to both HHV-8 (Kaposi's sarcoma, primary effusion lymphoma [PEL], and multicentric Castleman's disease) and EBV (Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's and non-Hodgkin's lymphomas) [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

EBV-Associated Lymphoproliferative Disorders: Classification and Treatment

2008

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Since its discovery as the first human tumor virus, Epstein-Barr virus (EBV) has been implicated in the development of a wide range of B-cell lymphoproliferative disorders, including Burkitt's lymphoma, classic Hodgkin's lymphoma, and lymphomas arising in immunocompromised individuals (post-transplant and HIV-associated lymphoproliferative disorders). T-cell lymphoproliferative disorders that have been reported to be EBV associated include a subset of peripheral T-cell lymphomas, angioimmunoblastic Tcell lymphoma, extranodal nasal type natural killer/ T-cell lymphoma, and other rare histotypes. EBV encodes a series of products interacting with or exhibiting homology to a wide variety of antiapoptotic molecules, cytokines, and signal transducers, hence promoting EBV infection, immortalization, and transformation. However, the exact mechanism by which EBV promotes oncogenesis is an area of active debate. The focus of this review is on the pathology, diagnosis, classification, and pathogenesis of EBVassociated lymphomas. Recent advances in EBV cellbased immunotherapy, which is beginning to show promise in the treatment of EBV-related disorders, are discussed. The Oncologist 2008;13:577-585

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“…2 The outlook is generally poor even with treatment, with median survival of 6.2 months and few long-term survivors. 4 In our case, the rapid clinical deterioration after years of stable chronic liver disease was a clue to the development of an aggressive lymphoma. Clinicians should be mindful of this rare diagnosis in cases of severe or intractable serous effusions in immunocompromised patients.…”

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confidence: 58%

Constrictive pericarditis and primary effusion lymphoma following allogeneic BMT for CML

Rose

Kulik

Standish

et al. 2012

Bone Marrow Transplant

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Constrictive pericarditis (CP) after allogeneic SCT may develop after infective pericarditis or pericardial GVHD. Primary effusion lymphoma (PEL), also a rare disease, is usually seen in immunocompromised patients and has a poor prognosis.We describe a case of CP and PEL developing in a patient after allo-SCT for CML. We believe it is the first documented case of these complications in this setting, and include rare FDG-PET images of PEL.A 42-year-old Italian-born man underwent a sibling allograft in 1987 for CML in chronic phase. Myeloablative conditioning was given with CY (60 mg/kg on days À6 and À5) and TBI (2 cGy twice daily on days À4, À3 and À2); complete donor engraftment ensued, with complete cytogenetic remission. Moderately severe chronic GVHD involving skin, oral mucosa, eyes and liver was treated with CYA, prednisolone and PUVA treatment before thalidomide was commenced, with good effect.Twenty-four months post allograft there were no other manifestations of GVHD, but he developed symptoms of pericarditis including chest pain, fever, tachycardia, hypotension and raised inflammatory markers. The electrocardiogram showed widespread ST elevation without elevation of creatine kinase MB, and chest X-ray showed a large pericardial effusion. No infective or autoimmune cause was identified and he improved with symptomatic management. Thalidomide was ceased, with no obvious immediate recurrence of GVHD.At subsequent follow --up the patient was hypotensive and complained of lethargy, dizziness and general malaise. After 6 months he developed right upper quadrant pain and abnormal liver function tests (LFTs), with alkaline phosphatase (ALP) 250 U/L (20 --175 U/L), gamma-glutamyl transferase (GGT) 550 U/L (o45 U/L) and normal transaminases and bilirubin. Ultrasound showed no cholelithiasis; liver biopsy demonstrated micronodular cirrhosis with no other specific features. Some months later, he developed ascites and peripheral oedema, managed with diuretic therapy. Symptoms and signs of chronic liver disease persisted for the next 20 years and were attributed to chronic hepatic GVHD. Cortisone acetate 37.5 mg daily caused marked improvement in appetite, energy and well being (although no improvement in LFTs), and was therefore continued despite normal adrenocorticotropic hormone levels.In 2010, 23 years post transplant, the patient deteriorated rapidly over 3 months. He was admitted to hospital with extreme lethargy, nausea, 10-kg weight loss and worsening ascites, peripheral oedema and hypotension, which did not respond to medical management.On examination he was hypotensive (systolic blood pressure 85 mm Hg), with a sinus tachycardia (100 b.p.m.) and elevated jugular venous pressure (9 cm). He had small pleural effusions, marked ascites and peripheral oedema to the groin. He was afebrile without palpable lymphadenopathy or hepatosplenomegaly.He had mild renal impairment, with creatinine level of 167 mmol/L (30 --120 mmol/L) and normal electrolytes.

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Primary Effusion Lymphoma

Abstract: Disclosure of potential conflicts of interest is found at the end of this article.

Cited by 238 publications

References 65 publications

HHV8-positive, EBV-positive Hodgkin lymphoma-like large B-cell lymphoma and HHV8-positive intravascular large B-cell lymphoma

HHV8-positive, EBV-positive Hodgkin lymphoma-like large B-cell lymphoma and HHV8-positive intravascular large B-cell lymphoma

EBV-Associated Lymphoproliferative Disorders: Classification and Treatment

Constrictive pericarditis and primary effusion lymphoma following allogeneic BMT for CML

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