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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atypical lymphadenopathies fail to achieve the morphologic criteria of a malignant neoplasm, but exceed the usual concepts of follicular, lymphoid, or sinus histiocytic hyperplasias. Rich cellular proliferations usually composed of prominent histiocytes, or immunoblasts, or both with or without a vascular scaffolding obscure the nodal architecture. Toxoplasmosis, infectious mononucleosis, zoster, and vaccination-induced lymphadenopathies are caused by infectious agents, dermatopathic lymphadenitis is associated with cutaneous disease, anticonvulsant pseudolymphoma occurs in individuals hypersensitive to anticonvulsants (usually phenytoin), and Chediak-Higashi syndrome is an inherited abnormality of lysosomal microtubule function; the causes of sinus histiocytosis with massive lymphadenopathy, giant lymph node hyperplasia, angioimmunoblastic lymphadenopathy, mucocutaneous lymph node syndrome, and this histiocytoses remain unknown. The clinical course of these abnormalities varies from self-limited acute diseases (viral lymphadenopathies, toxoplasmosis, dermatopathic lymphadenitis, and usually anticonvulsive lymphadenopathy) to protracted, but benign abnormalities (sinus histiocytes with massive lymphadenopathy, giant lymph node hyperplasia, and multifocal eosinophilic granuloma). The diagnosis of angioimmunoblastic lymphadenopathy, Chediak-Higashi syndrome, and mucocutaneous lymph node syndrome necessitates a guarded prognosis, for death or the advent of a malignant lymphoma may interrupt their clinical course. Acute disseminated histiocytosis, even though the proliferated cell lacks the cytologic criteria of malignancy, should be regarded and treated as a malignant neoplasm.
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PMID:Atypical lymphadenopathies of the head and neck. 627 76

In this study we report the cases of 22 pediatric patients with nodal erythema. The predominance of this condition in male patients was clear. Etiological factors were determined in 77% of the patients. In our series, the principal cause was tuberculosis (36%). We would like to point out the etiological diversity in this small series of children: streptococcal infection, gastrointestinal infection with Salmonella enteritidis or Campylobacter jejuni, cat scratch disease, infectious mononucleosis, chronic hepatitis B, Crohn's disease and pharmacological (amoxycillin). In 22% of the cases no cause was found.
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PMID:[Erythema nodosum in pediatric patients. A study of 22 cases]. 825 Apr 29

Epstein-Barr virus (EBV) infects lymphocytes, where it persists indefinitely for the life of the host; whether the virus interacts with p53 to maintain itself in these cells is unknown. Lymphoid biopsy samples from 10 patients with infectious mononucleosis (IM) were examined for expression of p53 by immunohistochemistry. Accumulation of p53 was detected in all 10 cases, primarily in large lymphocytes of the expanded paracortex. The presence of EBV was confirmed in all 10 cases by EBER1 (EBV-encoded RNA) in situ hybridization, whereas 11 non-IM control samples lacked significant EBER1 and did not express p53 in paracortical lymphocytes. Interestingly, EBV infection alone does not cause accumulation of intracellular p53, because many more cells expressed EBER1 than p53 in the IM tissues. To determine whether p53 was confined to the subset of infected cells in which viral replication was occurring, BZLF1 immunostains were performed. Viral BZLF1 was detected in 8 of 10 IM tissues; however, the paucity and small size of the BZLF1-expressing lymphocytes suggests that they are not the same cells overexpressing p53. To further examine the relationship between p53 and EBV gene expression, the tissues were studied for latent membrane protein 1 (LMP1) expression by immunohistochemistry. Viral LMP1 was observed in the large paracortical lymphocytes of all 10 cases of IM, indicating co-localization of p53 and LMP1 in these cells. Our findings confirm that p53 overexpression is not specific for nodal malignancy and that p53 accumulation is characteristic of IM. Because p53 was not coexpressed in the same cells as BZLF1, it appears that BZLF1 is not directly responsible for p53 accumulation. Nevertheless, co-localization of p53 and LMP1 in activated-appearing lymphocytes suggests that EBV infection is responsible for p53 accumulation. HUM PATHOL 31:1397-1403.
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PMID:Accumulation of p53 in infectious mononucleosis tissues. 1111 15

Monocytoid B cells (MBCs) are a subset of B cells that may be recognized in several reactive and tumoral lymph node conditions, including toxoplasmic lymphadenitis, infectious mononucleosis, and Hodgkin's lymphoma. Although this is a commonly observed cell population, which has even given its name to a type of lymphoma, MBC lymphoma, scarcely any information is available about the function and characteristics of this cell type. A relationship with marginal zone (MZ) B lymphocytes has been claimed for MBCs, but this has not yet been fully proven. Indeed, specific markers for MBCs are still lacking, which has made it difficult to analyze their relationship with other B cell subpopulations and confirm the existence of tumors deriving from this B cell subset. We used a panel of cell cycle markers to explore the characteristics of MBCs and their relationship with MZ B cells, nodal MZ lymphoma, and splenic MZ lymphoma. We therefore compared the phenotypic profile of MBCs in different conditions with normal MZ B cells within the spleen and mesenteric lymph nodes, with a group of seven cases of nodal MZ/MBC lymphoma and another group of five cases of splenic MZ lymphoma. MBCs were mainly in the G(0) to G(1) phases, as deduced from the presence of a proportion of between 10 and 35% Ki67-positive cells, whereas very low expression was observed with cyclin A and cyclin B staining. Nests of MBCs were clearly labeled by the expression of p21(WAF1), a cyclin-dependent kinase inhibitor (CKI), rarely detectable in benign lymphocytes, and by cyclin E. Basically all MBCs were bcl-2-negative, and high cyclin D2 and cyclin D3 were also detected in these cells, at proportions and intensities above expected levels, when the percentage of proliferating cells was taken into account. p27(KIP1) expression was characterized by homogeneous reactivity, higher than that observed in other B cell populations with a relatively high-growth fraction. Immunoglobulin staining showed undetectable light and heavy chains. However, splenic MZ cells, nodal MZ lymphoma, and splenic MZ lymphoma showed a distinct expression of IgM and bcl-2, with high p27 (KIP1) nuclear expression and undetectable or low levels of cyclin A, B, E, or D, or p21(WAF1) expression. The data from this study show an unexpected immunophenotype in MBCs, different from the one observed in splenic and lymph node MZ B cells. This suggests that either MBCs are a unique B cell population from a distinct cell lineage, or if related to MZ cells, they would represent a definite differentiation stage characterized by a distinctive immunophenotype. They also show so-called MZ/MBC lymphoma to be more closely related to lymph node and splenic MZ B cells, as they do not share the most distinctive features of MBCs.
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PMID:Unique phenotypic profile of monocytoid B cells: differences in comparison with the phenotypic profile observed in marginal zone B cells and so-called monocytoid B cell lymphoma. 1129 May 54

Post-transplant lymphoproliferative disease (PTLD) is a well recognized complication of solid organ transplantation and therapeutic immunosuppression, first reported in 1968. PTLD incorporates a spectrum of abnormalities ranging from a benign infectious mononucleosis-like illness to non-Hodgkin's lymphoma with nodal and extranodal site involvement. The first liver transplant was performed at our institution in January 1982. This retrospective study examined the incidence of PTLD, reason for the original transplants, presenting symptoms, radiological findings, immunosuppression regimens and outcomes of these patients. From a total of 2005 adult liver transplants, 23 patients (1.1%) were identified with PTLD. The average age of these patients at the time of transplant was 46.5 years, with a ratio of female-to-male of 14:9. Indication for transplant ranged from primary biliary cirrhosis (eight patients) to epitheloid haemangioendothelioma (one patient). The average time interval between transplant and diagnosis of PTLD was 50 months. Imaging abnormalities identified included generalized lymphadenopathy, liver and portal masses, splenic enlargement, bowel, eye, cerebral and neck involvement; and in two patients, no radiological abnormality. The most common histological findings ranged from B-cell non-Hodgkin's lymphoma (five patients) to early PTLD in one patient. Our rate of PTLD is lower compared with published literature and demonstrates a much longer time interval from transplant to occurrence of PTLD than previously appreciated. This could be secondary to a low immunosuppression therapy followed at our institution. From a few months to several years after liver transplantation, the radiologist needs to be alert to the possibility of PTLD and thorough imaging is required to detect the wide variety of potential presentations.
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PMID:Post-transplant lymphoproliferative disease in liver transplantation. 1739 99

Post-transplant lymphoproliferative disorder (PTLD) is one of the most dreaded complications of orthotopic transplantation. It consists of a heterogeneous group of lymphoproliferative disorders of varying clonal composition, occurring in immuno-suppressed organ allograft recipients and is frequently due to EBV infection. It is most common in heart/lung transplants followed by heart, liver, and kidney and rarely in bone marrow transplants. Clinically, PTLD can present in a number of ways ranging from features resembling infectious mononucleosis, lymphoproliferative masses involving both nodal and extranodal locations, to a fulminant form characterized by a combination of peripheral lymphadenopathy, severe metabolic acidosis, organ failure or allograft dysfunction. Pathologically PTLD is characterized by a dense inflammatory infiltrate with a spectrum ranging from that found in infectious mononucleosis to a polymorphous B-cell hyperplasia to that of a monomorphous lymphoma. Analysis of EBV is especially useful for the diagnosis of early cases of PTLD. In addition, immunophenotyping to determine the lymphocyte type (B or T cell type) and monoclonality are most helpful in determining the prognosis.
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PMID:Post-transplant lymphoproliferative disorders. 1847 Jul 27

Posttransplant lymphoproliferative disease was first reported in 1968. Posttransplant lymphoproliferative disease encompasses a range of abnormalities from benign infectious mononucleosis-like illnesses to non-Hodgkin's lymphomas with nodal and extranodal site involvement. We evaluated five children who had posttransplant lymphoproliferative disease after liver transplantation. Since 2001, we have performed 118 liver transplantations in 115 children. Five children (4.6%), including three girls and two boys of overall mean age, 3.9 year, developed posttransplant lymphoproliferative diseases. The indications for liver transplant were hepatoblastoma in one recipient and cholestatic liver disease in the remaining four subjects. Posttransplant lymphoproliferative disease was diagnosed at 6, 11, 17, 22, and 27 months after the liver transplantation. Imaging modalities identified generalized lymphadenopathy in one, multiple liver masses in one, a large portal mass in one, multiple stomach ulcers in one, and a large mediastinal mass in one recipient. At diagnosis, the recipient with the large mediastinal mass displayed cough; the remaining four recipients were asymptomatic. Histological findings showed B-cell lymphomas in three recipients and T-cell lymphomas in two. The results of in situ hybridization for Epstein-Barr virus were negative in one recipient and positive in four. Four recipients were treated with chemotherapy; the remaining recipient was treated with anti-CD20 monoclonal antibodies. The one recipient who had a large mediastinal mass died at 2 months after receiving the diagnosis of chemotherapy-related sepsis; the remaining four children are alive at 9, 11, 18, and 34 months after treatment. Our rate of posttransplant lymphoproliferative disease was similar to that in the literature. From a few months to several years after liver transplantation, radiologists must be alert to the possibility of posttransplant lymphoproliferative disease. Thorough imaging is required to detect the wide variety of potential presentations.
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PMID:Posttransplant lymphoproliferative disease in pediatric liver transplant recipients. 1976 63

This article provides a review of the anatomic classification and staging of nodal disease in the neck through the use of tables, illustrations, and sample imaging cases. The article reinforces knowledge of nodal disease in the neck while reviewing imaging examples of common and uncommon disease entities in this region. We review nodal disease in the neck using American Joint Committee on Cancer staging criteria. We illustrate anatomy of the nodal levels of the neck with accompanying examples of selected cases. These are presented in an integrated manner, highlighting items of importance to radiologists. The accompanying images and clinical scenarios aid recognition with an emphasis on differential diagnosis. Case examples include a broad range of pathologically and clinically proven disease entities involving lymph node disease in the neck accumulated from 1999 to 2008 at a tertiary referral center. The anatomical relationships and major disease processes for this location are reviewed and illustrated with example images from commonly used imaging modalities for this region. Examples of cases discussed include lymphoma, metastatic neoplasms such as head/neck squamous cell carcinoma and esthesioneuroblastoma, and inflammatory and infectious processes such as mononucleosis. The reader will gain or refresh information about the anatomical relationships and demarcations of the nodal levels of the neck as well as disease entities that frequently present with neck adenopathy. This information is useful both in clinical practice and in preparation for certifying examinations. The images provided aid recognition with an emphasis on clinical context and differential diagnosis. A succinct review of patterns of nodal disease of the neck with anatomic orientation using illustrations of typical and atypical disease entities in this region enhance and reinforce understanding of this often complex area of imaging.
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PMID:Illustrated approach to imaging and staging of nodal disease in the neck. 2011 67

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus infecting over 90% of humans and the infection persists for life. Although most people are asymptomatic, EBV infection may cause a continuous range of symptoms from transient to severe and protracted diseases depending on the immunological response of the individuals. EBV infects primarily B lymphocytes and rarely T and natural killer (NK) cells. It is implicated in around 1% of human tumours with the majority being haematological malignancies including Hodgkin lymphoma, B- and T-cell non-Hodgkin lymphomas, and immunodeficiency-associated lymphoproliferative disorders (LPDs). As it is a ubiquitous virus the confirmation of EBV-related LPDs depends on the demonstration of the viral DNA by in situ hybridisation for EBV-encoded mRNA (EBER). In current practice, CD3 and EBER positive cytotoxic extranodal lymphomas in non-immunocompromised patients are generally considered as extranodal NK/T-cell lymphoma and accordingly EBER should be performed for such tumours except for the few clinically typical entities such as mycosis fungoides. This review focuses on the application of EBER in the diagnosis of various types of T- and NK/T-cell lymphomas in non-immunocompromised patients and the diagnostic pitfalls, especially their distinction from infectious mononucleosis-related LPD of T- and NK-cell origins and the diagnostic dilemma between various T-cell lymphoma entities with or without EBV association, including nodal cytotoxic EBV positive peripheral T-cell lymphoma.
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PMID:In situ hybridisation for Epstein-Barr virus as a differential diagnostic tool for T- and natural killer/T-cell lymphomas in non-immunocompromised patients. 2539 47

The head and neck region is a common site for extranodal lymphomas, second only to the gastrointestinal tract; and 12% to 15% of all head and neck tumors are lymphomas. Non-Hodgkin lymphomas are most common, and Hodgkin lymphoma occurs rarely at extranodal sites in the head and neck. Most non-Hodgkin lymphomas of the head and neck region are of B-cell lineage, and the Waldeyer ring is the most common site. Head and neck lymphomas have distinctive epidemiological and clinicopathologic features, including an association with immunosuppression, infectious organisms, or autoimmune disorders; site-specific differences (eg, thyroid gland versus ocular adnexa) for common lymphomas, such as extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue; and genetic differences that provide insights into etiology. Furthermore, the diagnosis of non-Hodgkin lymphomas at extranodal sites implies differences in prognosis and therapeutic implications with lymphomas at nodal sites. In this review, we discuss various types of non-Hodgkin lymphomas and Hodgkin lymphoma, focusing on unique aspects related to the head and neck region. We also discuss a number of newer entities that are clinically indolent as well as mimics of lymphoma that can occur in the head and neck region, including infectious mononucleosis, Kikuchi-Fujimoto disease, Kimura disease, Castleman disease, and immunoglobulin G4-related disease.
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PMID:Extranodal hematopoietic neoplasms and mimics in the head and neck: an update. 2611 62


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