Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A twelve-years-old boy developed fever, pharyngitis and acute migrant polyarthralgia. An increasing ASO titre was observed, so that rheumatic fever was firstly diagnosed. Finally splenomegaly and positive IgG and IgM against Epstein Barr virus led to the diagnosis of acute EBV infection with polyarthritis. EBV infection should be considered into the differential diagnosis of migrant polyarthritis.
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PMID:[Migrant polyarthritis and EBV infection]. 931 50

To determine whether Epstein-Barr virus (EBV) constitutes a contributing factor in AIDS and, conversely, whether the human immunodeficiency virus (HIV) alters the course of primary EBV infection in a pediatric population, 62 children born to HIV-infected mothers and prospectively followed were evaluated. EBV infection was documented by EBV-specific serology and polymerase chain reaction and by clinical history. HIV infection status was determined according to the Centers for Disease Control and Prevention pediatric classification system. Demographics from HIV-infected and HIV-uninfected children were comparable. The data suggest that HIV-infected children may acquire primary EBV infection earlier in life. The incidence of accompanying splenomegaly or hepatomegaly (or both) around the time of EBV seroconversion was higher among HIV-infected children than among HIV-uninfected children. In contrast, HIV disease progression and HIV-1 RNA load did not seem to be influenced by primary EBV infection.
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PMID:Natural history of Epstein-Barr virus infection in a prospective pediatric cohort born to human immunodeficiency virus-infected mothers. 953 89

A 49-year-old man was admitted to our hospital for investigation of splenomegaly and lymphocytosis. He had no significant past history and was not a smoker. Physical examination revealed massive splenomegaly and no palpable superficial lymph nodes. Hematological examination showed a hemoglobin concentration of 10.5g/dl, a platelet count of 9.8 x 10(4)/microliter, and a leukocyte count of 21.2 x 10(3)/microliter with 70% abnormal lymphocytes. In May-Giemsa stained blood films, the abnormal lymphocytes had round nuclei, abundant, pale cytoplasm, and slightly serrated edges. Phase-contrast microscopic and scanning electron microscopic examinations revealed many long surface villi. Tartrate-resistant acid phosphatase activity in these cells was negative. The abnormal lymphocytes had a CD5-, CD10-, CD11a+, CD11c+, CD19+, CD20+, CD22+ phenotype. These features were similar to those described for a variant form of hairy cell leukemia (HCL-Japanese variant). However, studies of Ig gene rearrangement and expression of sIg revealed a polyclonal proliferation of B cells. On the basis of these findings, this case was diagnosed as hairy B-cell lymphoproliferative disorder, a recently described condition characterized by polyclonal B-cell lymphocytosis and features resembling HCL-Japanese variant. Serological assays for antibodies against Epstein-Barr virus suggested a past infection. Splenectomy alleviated the anemia and thrombocytopenia, but not the lymphocytosis.
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PMID:[Polyclonal B-cell lymphocytosis with clinical and hematological features resembling hairy cell leukemia]. 975 Apr 56

We have followed the effect of murine gammaherpesvirus strain 72 (MHV-72) infection and immunosuppression on the differential white blood cell count of Balb/c mice. In both the acute and chronic phase of infection, abnormal lymphocytes resembling human B lymphocytes infected with Epstein-Barr virus (EBV) were detected. Immunosuppression had no significant effect on the haematological changes during the infection. Some of mice, which had developed tumours as a consequence of infection, showed splenomegaly, lymphadenopathy, leukocytosis and high percentage of immature blastic forms of leukocytes.
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PMID:Detection of abnormal lymphocytes in the blood of Balb/c mice infected with murine gammaherpesvirus strain 72: the analogy with Epstein-Barr virus infection. 977 74

A 20-year-old man presented with fever, bilateral swelling of the cervical and inguinal lymph nodes, and splenomegaly. Later he noted diplopia. CSF was unremarkable. High serum antibodies to Epstein-Barr virus (EBV) were discovered. MRI revealed an abnormal lesion in the right third cranial nerve, which was considered to be the pathological lesion associated with his clinically apparent oculomotor nerve dysfunction.
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PMID:MR findings in isolated oculomotor nerve palsy associated with infectious mononucleosis caused by Epstein-Barr virus infection. 984 47

The natural history of Epstein-Barr virus (EBV) infection in 556 infants born to 517 human immunodeficiency virus (HIV) type 1-infected mothers was studied in a prospective, multicenter, cohort study. HIV-1-infected children had a cumulative EBV infection rate similar to HIV-1-uninfected children at age 3 years (77.8% vs. 84. 9%) but had more frequent oropharyngeal EBV shedding (50.4% vs. 28. 2%; P<.001). The probability of shedding decreased with longer time from EBV seroconversion and was similar to that of HIV-1-uninfected children 3 years after seroconversion. HIV-1-infected children identified as rapid progressors shed EBV more frequently than nonrapid progressors (69.4% vs.41.0%; P=.01). HIV-1-infected children with EBV infection had higher mean CD8 cell counts. EBV infection did not have an independent effect on mean CD4 cell counts, percent CD4, IgG levels, HIV-1 RNA levels, lymphadenopathy, hepatomegaly, or splenomegaly. Early EBV infection is common in children born to HIV-1-infected mothers. Children with rapidly progressive HIV-1 disease have more frequent EBV shedding.
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PMID:Natural history of primary Epstein-Barr virus infection in children of mothers infected with human immunodeficiency virus type 1. 1022 60

Malignant lymphoma infiltrating the abdominal aorta and resulting in an aortic aneurysm has never been documented. We report here a case of angiocentric T-cell lymphoma in a 33-year-old man who for months presented intermittent fever, splenomegaly, and an abdominal pulsatile mass. Angiography revealed extensive aneurysmal dilatation of the infrarenal abdominal aorta, bilateral iliac artery, and right common femoral artery. Splenic abscess and infected abdominal aortic aneurysm were initially suspected. An urgent splenectomy and aneurysmectomy with an aortic bifemoral bypass were performed. Pathological examination of the aortic aneurysm showed extensive necrosis, severe atherosclerosis, and lymphoma cell infiltration of the aortic wall. The lymphoid cells in the aorta and spleen were stained positive for CD45RO, CD56, and CD8, but negative for CD4 and CD19. Double-labeling immunohistochemistry and in situ hybridization using EBER1 for Epstein-Barr virus (EBV) revealed positive nuclear staining in the atypical T-lymphoid cells. This is the first definitive proof of peripheral T-cell lymphoma involving the abdominal aorta. Our evidence also supports that the EBV infection of T cells could be responsible for the atherosclerosis and hypertriglyceridemia, and the angiocentricity of the tumor cells apparently results in the presenting atherosclerotic aortic wall destruction, providing an additional causative concept for abdominal aortic aneurysm.
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PMID:Epstein-Barr virus-containing T-cell lymphoma and atherosclerotic abdominal aortic aneurysm in a young adult. 1049 49

Primary infection with murine gammaherpesvirus-68 (MHV-68), as with other members of the gammaherpesvirus subfamily, is characterized by a lymphoproliferative phase. MHV-68 causes acute splenomegaly and an infectious mononucleosis-like syndrome in which there is expansion of the CD8+ T cell subset. In long-term infections, MHV-68 is associated with lymphoma development. In order to elucidate the mechanisms underlying the proliferative processes, the events following infection of murine splenocytes or purified murine B lymphocytes in vitro have been examined. MHV-68 infection prolonged the viability of murine splenocytes and stimulated cellular proliferation. Unlike Epstein-Barr virus and herpesvirus saimiri, MHV-68 did not cause growth transformation. Growth transformation did not occur even when cells with a predisposition to transformation were infected or when culture conditions were selected to enhance the viability of the cells. Following MHV-68 infection, the latency-associated viral tRNAs were transcribed. However, transcription of the other known latency-associated gene, M2, was not observed. In addition, there was no evidence of productive virus replication either by staining with antibodies specific for late virus antigens or by in situ hybridization for early and late mRNAs. In contrast to Epstein-Barr virus- and herpesvirus saimiri-infected lymphocytes, where episomal genomes are seen, Gardella gel analysis indicated that the primary lymphocytes infected by MHV-68 in vitro contained only linear virus DNA. This DNA was nuclease sensitive, indicating that, while MHV-68 was efficiently uncoated, its circularization in vitro was extremely inefficient. These results are discussed in terms of the host-virus interaction.
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PMID:Kinetic and phenotypic changes in murine lymphocytes infected with murine gammaherpesvirus-68 in vitro. 1057 67

Inbred athymic nude mice (BALB/c) were injected subcutaneously with the wild-type murine gammaherpesvirus 72 (MHV-72), which has been shown to induce the infectious mononucleosis (IM)-like syndrome in immunocompetent mice. The mice were also injected with UV-irradiated MHV-72. We studied the pattern of acute and chronic infection in the blood cells of the nude mice and detected viral DNA sequences in the infected leukocytes by polymerase chain reaction (PCR) technique up to when the animal died, close to 1 month postinfection. Using the UV-irradiated virus that induces an increase in mouse survival time, the viral sequences were present in the blood up to 3 months postinfection, then disappeared. We detected atypical lymphocytes in the blood of mice infected with both wt and UV-irradiated viruses. These atypical cells were similar in shape to those present in the blood of patients with IM induced by Epstein-Barr virus (EBV). Via Unscheduled DNA Synthesis (UDS), DNA synthesis was demonstrated in the atypical cells whose phenotype is identical to that of B cells, as shown with a panel of monoclonal antibodies. By double immunofluorescence staining, using an hyperimmune anti-MHV-72 serum and an anti-IgG + IgM + IgA monoclonal antibody, we demonstrated that these atypical B cells express some viral antigens. Contrary to the immunocompetent mice, the nude mice did not develop splenomegaly after infection with wt virus, probably due to the lack of T cell subsets. However, we observed an increase of nude mice B cells in the spleen. The nude mice died 1 month postinfection showing a high frequency (40%) of atypical lymphoblast-like B-cells in the blood; the increase in natural killer (NK) cell number was not detected after infection. Such findings suggest that NK cells probably did not play an important role in immune response to the MHV infection in nude mice. Finally, this mouse model could play an important role in antigammaherpesviral therapy of immunocompromised patients.
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PMID:Immunophenotypic study of atypical lymphocytes. Generated in peripheral blood and spleen of nude mice After MHV-72 infection. 1101 96

Hemophagocytic lymphohistiocytosis (HLH) is an unusual syndrome characterized by fever, splenomegaly, jaundice, and the pathologic finding of hemophagocytosis (phagocytosis by macrophages of erythrocytes, leukocytes, platelets, and their precursors) in bone marrow and other tissues. HLH may be diagnosed in association with malignant, genetic, or autoimmune diseases but is also prominently linked with Epstein-Barr (EBV) virus infection. Hyperproduction of cytokines, including interferon-gamma and tumor necrosis factor-alpha, by EBV- infected T lymphocytes may play a role in the pathogenesis of HLH. EBV-associated HLH may mimic T-cell lymphoma and is treated with cytotoxic chemotherapy, while hemophagocytic syndromes associated with nonviral pathogens often respond to treatment of the underlying infection.
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PMID:Hemophagocytic syndromes and infection. 1107 18


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