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)

Spontaneous splenic rupture as a complication of infectious mononucleosis in 17-years old man was described. Clinical manifestations of infectious mononucleosis were typical without any sign of the splenic rupture. At the end of third week of the disease sonographic investigation revealed subcapsular hematoma of the spleen without overt rupture. The patient was observed. Five days later in the next sonographic investigation the second hematoma of the spleen appeared. Patient was treated underwent splenectomy and he remain alive and well. Authors suggest that in cases with subcapsular hematoma of the spleen splenectomy remains the treatment of choice. Mononucleosis patients with significant enlarged spleen should be observed very carefully. Authors propose control sonographic investigation in 3rd or 4th week of the disease in those cases.
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PMID:[Spontaneous splenic rupture as a complication of infectious mononucleosis]. 913 3

The present study investigated 54 pediatric patients with acute Epstein-Barr virus (EBV)-induced infectious mononucleosis (IM) in Japan. Most of the acute cases clustered within the first 5 years of life, and the peak incidence was observed at around 4 years of age. These patients were arbitrarily separated into three age groups (less than 3 years, 3-5 years, and 6-14 years). Fever, pharyngitis, lymphadenopathy and hepatomegaly were detected in more than 80% of all cases. Tonsillitis and splenomegaly were present in about 60% of cases. Skin manifestations and eyelids edema were less often detected in the older age group than in the young age groups. In addition to an increase of total white blood cell and lymphocyte counts in the peripheral blood, a significant increase in the percentage of CD3+ CD8+ HLA-DR+ T cells was always observed. Epstein-Barr virus seropositivity increased soon after birth and reached approximately 70% around 3 years of age. Close to 100% of the adult controls were EBV seropositive. The results suggest that EBV-induced acute IM is a disease of early childhood in Japan.
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PMID:Infectious mononucleosis as a disease of early childhood in Japan caused by primary Epstein-Barr virus infection. 914 Dec 48

Infectious mononucleosis (IM) syndrome is typically caused by EBV, but also by drugs and other organisms such as CMV and HBV. It demonstrates a wide range of clinical and laboratory characteristics, presumably depending on the age of onset. However, associations of laboratory abnormalities with the clinical features have not been well documented. We evaluated here, the associations among patients with IM syndrome using of multiple regression (MR) and multiple logistic regression (MLR) analyses. We examined 90 (40 males, 50 females) patients, who were admitted to our hospital with IM syndrome. The diagnostic criteria were fever and presence of atypical lymphocytes (> 5% of the WBC or the count including monocytes > 5000/microliter), and at least 3 of 7 clinical features: tonsillitis, lymphadenopathy, skin rash, hepato-, spleno-megaly, hepatic dysfunction. The diagnosis of EBV was serologically confirmed in 41 cases. MR revealed that the higher age group tended to have lower platelet counts, and that lower platelet counts were associated with higher ALT levels. In addition, MLR revealed that patients with skin rash tended not to have splenomegaly. The frequency of splenomegaly was not related to age, contrary to the findings of previous reports. These findings are useful to differentiate IM syndrome based on laboratory data.
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PMID:[Multivariate analysis of the associations between laboratory data and clinical features among patients with infectious mononucleosis syndrome]. 981 19

The murine gamma-herpesvirus MHV-68 causes an acute, transient pneumonitis, followed by an infectious mononucleosis (IM)-like illness with splenomegaly, widespread latent infection of B lymphocytes and an expansion of Vbeta4+ CD8+ T cells. CD8+ T cells specific for an H-2Db-restricted epitope were prominent during the acute respiratory infection, but their prevalence declined rapidly during the mononucleosis. In contrast, CD8+ T cells specific for an H-2Kb-restricted epitope, apparently expressed by virus-infected B lymphocytes, were most numerous during the mononucleosis illness and were maintained at relatively high frequencies thereafter. The prevalence of all peptide-specific CD8+ T cells decreased during the expansion of the Vbeta4+ CD8+ population, which did not recognize any peptide epitopes identified and was apparent also in an MHC class I-deficient environment. The CD8+ T cell population recognizing productively infected epithelial cells thus differed substantially from that responding during the IM illness.
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PMID:Changing patterns of dominance in the CD8+ T cell response during acute and persistent murine gamma-herpesvirus infection. 1022 71

To determine whether established CD8(+) T cell memory to an epitope prominent during the replicative phase of a gamma-herpesvirus infection protects against subsequent challenge, mice were primed with a recombinant vaccinia virus expressing the p56 peptide and then boosted by intranasal exposure to an influenza A virus incorporating p56 in the neuraminidase protein. Clonally expanded populations of functional, p56-specific CD8(+) T cells were present at high frequency in both the lung and the lymphoid tissue 1 month later, immediately before respiratory challenge with gammaHV-68. This prime-and-boost regime led to a massive reduction of productive gammaHV-68 infection in the respiratory tract and, initially, to much lower levels of latency in both the regional lymph nodes and the spleen. The CD8(+) T cell response to another epitope (p79) was diminished, there was less evidence of B cell activation, and the onset of the CD4(+) T cell-dependent splenomegaly was delayed. Within 3-4 weeks of the gammaHV-68 challenge, however, the extent of latent infection in the lymph nodes and spleen was equivalent, and both groups developed the prominent infectious mononucleosis-like syndrome that is characteristic of this infection. The reverse protocol (influenza then vaccinia) seemed to be slightly less effective. Even though immune CD8(+) T cells may be present at the time and site of virus challenge, establishing a high level of CD8(+) T cell memory to lytic-phase epitopes alone does not protect against the longer-term consequences of this gammaHV infection.
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PMID:A gamma-herpesvirus sneaks through a CD8(+) T cell response primed to a lytic-phase epitope. 1043 Sep 34

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

Intranasal infection of mice with the murine gamma-herpesvirus MHV-68 results in an acute lytic infection in the lung, followed by the establishment of lifelong latency. Development of an infectious mononucleosis-like syndrome correlates with the establishment of latency and is characterized by splenomegaly and the appearance of activated CD8+ T cells in the peripheral blood. Interestingly, a large population of activated CD8+ T cells in the peripheral blood expresses the V beta 4+ element in their TCR. In this report we show that MHV-68 latency in the spleen after intranasal infection is harbored in three APC types: B cells, macrophages, and dendritic cells. Surprisingly, since latency has not previously been described in dendritic cells, these cells harbored the highest frequency of latent virus. Among B cells, latency was preferentially associated with activated B cells expressing the phenotype of germinal center B cells, thus formally linking the previously reported association of latency gene expression and germinal centers to germinal center B cells. Germinal center formation, however, was not required for the establishment of latency. Significantly, although three cell types were latently infected, the ability to stimulate V beta 4+CD8+ T cell hybridomas was limited to latently infected, activated B cells.
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PMID:Latent murine gamma-herpesvirus infection is established in activated B cells, dendritic cells, and macrophages. 1087 86

Massive splenomegaly is defined as a spleen weighing about 10 times normal weight. We describe a 36-year-old man who had huge splenomegaly and secondary pancytopenia simulating malignant lymphoma for about 3 months. Splenectomy was necessary because of the suspicion of hematologic malignancy, especially isolated lymphoma of the spleen, and pain and mechanical abdominal disturbances. On operation, the spleen was 25 cm long and weighted 250 g. There was florid, reactive follicular lymphoid hyperplasia. Immunohistochemical staining with CD-20(L26), CD-45Ro(UCHL), bcl-2 oncoprotein (Dakopatts), EBV (anti-EBV mol weight 60 KD, Dakopatts) was consistent with reaction to EBV infection and not with follicular lymphoma. Lack of PCR amplification using DNA extracted from paraffin-embedded splenic tissue indicated absence of a monoclonal B cell population carrying rearranged immunoglobulin genes. The lymphocytic population was proven polyclonal by the negative results of PCR for the bcl-2 gene rearrangement. EBV seroconversion from high titer antibodies of anti-EBV-VCA-IgM to negative, and from negative EBNA to positive was consistent with an apparent primary EBV infection. We have not found on computerized search a previous report of reactive follicular splenic hyperplasia to EBV infection causing huge splenomegaly, with or without EBV-induced infectious mononucleosis.
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PMID:[Follicular splenic lymphoid hyperplasia associated with EBV infection]. 1095 41

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

Background: As the role of PET-FDG imaging is being established in the staging and monitoring of response to therapy in children with lymphoma, we encountered a case of an infection common in adolescence that may present with lymphoma-like signs and symptoms.Methods: A 13-year-old previously healthy male presented with a left neck mass associated with weakness, fatigue, intermittent fevers and weight loss. He was then referred to the hematology/oncology department with a working diagnosis of lymphoma. The total wbc count was 5920/cu mm with 75% lymphocytosis without atypical lymphocytes. ESR was 20 mm. Serologic analysis for EBV, CMV, toxoplasmosis and hepatitis was also performed. The chest x-ray was normal. CT scan demonstrated multiple enlarged lymph nodes in both right and left jugulodigastric and spinal accessory chains; the largest mass within the left spinal accessory chain had focal necrosis within it. There were no enlarged mediastinal or axillary nodes. The spleen was massively enlarged and the splenic index was 924 (normal for age = 744).Results: FDG imaging showed intense uptake in both cervical regions, the mediastinum and in the enlarged spleen. The results of the Monospot test and the EBV panel which were both positive, were available 3 & 5 days later. Based on these serologic results, the history, physical findings and the negative chest x-ray, the final diagnosis was infectious mononucleosis.Conclusion: Despite availability, ease of performance and sensitivity of FDG imaging, this case illustrates the importance of clinical, hematologic and serologic assessment of disease prior to FDG imaging.
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PMID:22. FDG Uptake in Infectious Mononucleosis. 1115 Jul 79


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