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)

During HIV infection, individuals experience multiorgan disorders such as adenopathy, splenomegaly, and lung and brain diseases. There is an increasing body of evidence that the HIV trans-activating tat gene product possesses multiple activities. First, it can activate several cellular genes; second, in its extracellular soluble form, it plays the role of growth factor in some cells such as Kaposi's sarcoma cells. Thus, we introduced the HIV tat gene, under the control of the cellular proteolipoprotein promoter, into the germline of mice and demonstrate that, when expressed, the tat gene product induces lymphoid hyperplasia in spleen, lymph nodes, and lung, as is observed in AIDS patients, but not in the brain or testes. Our findings indicate that HIV, through some of its genes, directly participates in the pathogenesis of AIDS.
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PMID:Development of lymphoid hyperplasia in transgenic mice expressing the HIV tat gene. 753 11

This report describes the clinical spectrum and outcome of the hemophagocytic syndrome (HS) in 5 HIV infected patients. All 5 patients presented with fever, hepatomegaly and/or splenomegaly, confusion or coma and respiratory symptoms. Severe anemia was associated with thrombocytopenia and with neutropenia in 4 cases. Diffuse intravascular coagulopathy was present in 2 cases. Liver function tests were abnormal in three patients. The diagnosis of HS was made 2 to 12 weeks after the onset of symptoms and required in most patients repeated examinations of the bone-marrow, showing infiltration by histiocytes with prominent phagocytosis of blood cells. In one case this infiltration was not seen in the bone-marrow but only in the liver and the spleen. Varicella, mycobacterium infection, oesophageal candidiasis, Kaposi sarcoma were observed in the evolution of 3 patients. Anaplastic large cell Ki-1 lymphoma was present in one case. Four patients died as a result of complications of HS. The one patient with lymphoma survived.
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PMID:[Hemophagocytic syndrome in HIV infection]. 824 41

We report a case of a 33-year-old man, intravenous drugs abuser, HIV-positive, with peripheral lymphadenopathy, hepato-splenomegaly and fever, in which a ganglionic biopsy showed a histology with morphologic features of multicentric Castleman's-like disease, and minute foci of Kaposi's sarcoma ganglion, without cutaneous lesions. Given the interrelationships between this morphology of angiofollicular lymph node hyperplasia, the development of Kaposi's Sarcoma, and the aggressive clinical course seen in our patient and those in the literature, the use of lymph node biopsy may be an important prognostic tool for the patients with the acquired immunodeficiency syndrome.
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PMID:[Generalized lymphadenopathy with morphologic findings of multicentric angiofollicular ganglionic hyperplasia in a patient with AIDS]. 825 54

C57/BL/6 mice infected with LP-BM5 MuLV virus developed an AIDS-like disease (MAIDS) with splenomegaly, leukopenia, thrombocytopenia, anemia, decreased numbers of helper/inducer and suppressor/cytotoxic T-cells and decreased production of interferon alpha. We have shown previously that HIV-associated Kaposi's sarcoma tissue contains high levels of prostaglandin E2 (PgE2), and this inhibits interferon synthesis through a cAMP-dependent second-messenger process. In this study we treated groups of MAIDS-infected mice with combinations of pentoxifylline, an agent which increases cAMP and inhibits phosphodiesterases, and sodium meclofenamic acid, a PgE2 inhibitor. Treated mice showed: 1) significantly higher total leukocyte and platelet counts, 2) higher total L3T4+ (helper/inducer) and Lyt-2+ (suppressor-cytotoxic) T-cell population. Pathologic examination also showed significantly less hepatosplenomegaly and lymphadenopathy in animals treated with pentoxifylline and meclofenamic acid. Partly, PgE2-induced suppression of interferon alpha production may mediate expression of retrovirus infection in this murine model of AIDS.
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PMID:Pentoxifylline and meclofenamic acid treatment reduces clinical manifestations in a murine model of AIDS. 830 44

Multicentric angiofollicular lymph node hyperplasia (MAFH) is an idiopathic systemic disorder that has been reported only rarely in children. Therefore, we reviewed the clinical and pathologic features of eight patients listed in the Angiofollicular Lymph Node Hyperplasia Registry at our institution. The ages of the patients ranged from two to 17 years (median, 10 yr), and the male-to-female ratio was 1:3. The patients presented with constitutional symptoms, multifocal lymphadenopathy, hepatomegaly, and/or splenomegaly. The laboratory findings included peripheral blood cytopenias, polyclonal hypergammaglobulinemia, and renal and hepatic dysfunction. Histologically, we observed the plasma cell variant of MAFH in five patients (62.5%) and the hyaline-vascular variant in three (37.5%). Immunohistochemical stains revealed a polyclonal plasma cell population in all cases. Two of six specimens were positive for Epstein-Barr virus by RNA in situ hybridization. A clonal immunoglobulin heavy gene rearrangement was identified in one of the five specimens studied, but this had no apparent impact on the clinical course of the disease. None of the four specimens analyzed for the presence of Kaposi's sarcoma-associated herpesvirus was positive. Most patients were stable or free of disease after treatment, which included corticosteroids in six of the eight patients. We concluded that the clinical and pathologic features of MAFH in children are similar to those of adults, but MAFH seems to have a more favorable clinical course, i.e., low morbidity and mortality, in children.
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PMID:Multicentric angiofollicular lymph node hyperplasia in children: a clinicopathologic study of eight patients. 897 72

A unique experimental model has been developed for dissecting the integrity of CD8+ T cell-mediated immunity to a persistent gammaherpesvirus under conditions of CD4+ T cell deficiency. Respiratory challenge of major histocompatibility complex class II -/- and +/+ C57BL/6J mice with the murine gammaherpesvirus 68 (MHV-68) leads to productive infection of both lung and adrenal epithelial cells. Virus titers peak within 5-10 d, and are no longer detected after day 15. Persistent, latent infection is established concurrently in splenic and lymph node B cells, with higher numbers of MHV-68+ lymphocytes being found in all lymphoid sites analyzed from the +/+ mice concurrent with the massive, but transient splenomegaly that occurred only in this group. From day 17, however, the numbers of infected B lymphocytes were consistently higher in the -/- group, while the frequency of this population diminished progressively in the +/+ controls. Infectious MHV-68 was again detected in the respiratory tract and the adrenals of the -/- (but not the +/+) mice from day 22 after infection. The titers in these sites rose progressively, with the majority of the -/- mice dying between days 120 and 133. Even so, some CD8+ effectors were still functioning as late as 100 d after infection. Depletion of CD8+ T cells at this stage led to higher virus titers in the -/- lung, and to the development of wasting in some of the -/- mice. Elimination of the CD8+ T cells from the +/+ group (day 80) increased the numbers of MHV-68+ cells in the spleen, but did not reactivate the infection in the respiratory tract. The results are consistent with the interpretation that CD8+ T cell-mediated control of this persistent gammaherpesvirus is progressively lost in the absence of the CD4+ T cell subset. This parallels what may be happening in AIDS patients who develop Kaposi's sarcoma and various Epstein Barr virus associated disease processes.
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PMID:Progressive loss of CD8+ T cell-mediated control of a gamma-herpesvirus in the absence of CD4+ T cells. 906 46

Multicentric Castleman's disease (MCD), also called multicentric angiofollicular lymphoid hyperplasia, is a systemic lymphoproliferative disorder causing fever, lymphadenopathy and splenomegaly. Recently, Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) DNA sequences have been detected in cases of MCD. We examined HHV-8 DNA sequences in the peripheral blood mononuclear cells (PBMCs) of two HIV-negative patients with MCD and in PBMCs and the lymph node of a HIV-negative patient with localized Castleman's disease (LCD) by the polymerase chain reaction. The novel sequences were detected in all DNA samples. Furthermore, the sequences were detected in only the CD19+ B-lymphocyte fraction of the patient with LCD as previously reported. However, the sequences were detected in CD19+ B-lymphocyte and CD2+ T-lymphocyte fractions of two patients with MCD. These results suggest that HHV-8 has tropisms for both B lymphocytes and T lymphocytes in Castleman's disease.
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PMID:Tropism of human herpesvirus 8 for peripheral blood lymphocytes in patients with Castleman's disease. 943 23

This second part of the review looks at change seen in the bone marrow haemostasis and malignancies found in HIV infection. Examination of bone marrow is requested in the presence of cytopaenias, splenomegaly, lymphomas and myelodysplasia. The findings include marrow hypocellularity, myelodysplasia and poor marrow recovery. Dysmegakaryocytpoiesis is found in 88% while dyserythropoeisis in 83% of cases. Mechanisms leading to these pertubations include direct HIV effect on marrow progenitor cells, effect of drugs and other infective diseases. Altered levels and functions of growth modifies IL6 and G-CSF are also to contribute. Haemostatic disorder frequently noted is bleeding due to thrombocytopaenia. Non-Hodgkin's lymphomas with aggressive characteristics and Kaposi's sarcoma are the commonly associated malignancies. Currently IL6 is being linked with the causation of KS and NHL. While standard approaches to the management of these malignancies tend to be the practices, adjustments are usually necessary in most patients.
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PMID:Haematological changes in human immunodeficiency virus infection. Part II. 955 50

To evaluate the diagnostic utility, value and potential risk of fine needle aspiration biopsy of spleen (sFNAB) in patients with splenomegaly in pyrexia of unknown origin (PUO), a retrospective analysis of medical records and cytological material of 31 patients on whom FNAB was performed between April 1994 and October 1997 was done. The patients were HIV- and presented with PUO. All other relevant investigations were negative. The spleen was either palpable or detected to have space-occupying lesions on ultrasonography (USG). The splenic aspirates showed tuberculosis in 11 patients (35.4%) and inconclusive or reactive changes in nine patients (25.8%). One case out of this group proved to be Kaposi's sarcoma on autopsy. The other diseases encountered were leishmaniasis (n = 3), non-Hodgkin's lymphoma (n = 4), fungal infections (n = 2), Hodgkin's lymphoma (n = 1). The patients who were diagnosed as having tuberculosis had epithelioid cells, giant cells, necrosis and inflammatory cells in various combinations. AFB positivity was 63.6%. The other cases which showed granulomas but no AFB were diagnosed on empirical grounds and all responded to the anti-tuberculosis therapy. No complications were encountered with the procedure. Therefore the authors conclude that sFNAB is rewarding in patients where all other non-invasive modalities of diagnosis have failed.
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PMID:Fine needle aspiration biopsy of the spleen in pyrexia of unknown origin. 1039 68

A simian homologue of Kaposi's sarcoma-associated herpesvirus (KSHV), the eighth human herpesvirus (HHV8), was isolated from a simian immunodeficiency virus (SIV)-infected rhesus macaque (Macaca mulatta) that developed a multicentric lymphoproliferative disorder (LPD). This simian rhadinovirus is genetically similar to a recently described rhesus rhadinovirus (RRV) (Desrosiers, R.C., V.G. Sasseville, S.C. Czajak, X. Zhang, K.G. Mansfield, A. Kaur, R.P. Johnson, A.A. Lackner, and J.U. Jung. 1997. J. Virol. 71:9764-9769) and is designated RRV 17577. RRV 17577 was experimentally inoculated into rhesus macaques with and without SIV(mac239) infection to determine if RRV played a role in development of the LPD observed in the index case. In contrast to control animals inoculated with SIV(mac239) or RRV alone, two animals coinfected with SIV(mac239) and RRV 17577 developed hyperplastic LPD resembling the multicentric plasma cell variant of Castleman's disease, characterized by persistent angiofollicular lymphadenopathy, hepatomegaly, splenomegaly, and hypergammaglobulinemia. Hypergammaglobulinemia was associated with severe immune-mediated hemolytic anemia in one RRV/SIV-infected macaque. Both RRV/SIV-infected macaques exhibited persistent RRV viremia with little or no RRV-specific antibody response. The macaques inoculated with RRV alone displayed transient viremia followed by a vigorous anti-RRV antibody response and lacked evidence of LPD in peripheral blood and lymph nodes. Infectious RRV and RRV DNA were present in hyperplastic lymphoid tissues of the RRV/SIV-infected macaques, suggesting that lymphoid hyperplasia is associated with the high levels of replication. Thus, experimental RRV 17577 infection of SIV-infected rhesus macaques induces some of the hyperplastic B cell LPDs manifested in AIDS patients coinfected with KSHV.
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PMID:Induction of B cell hyperplasia in simian immunodeficiency virus-infected rhesus macaques with the simian homologue of Kaposi's sarcoma-associated herpesvirus. 1049 21


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