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)

The results of immunological and purine enzyme investigations in an adult male patient with common variable immunodeficiency, recurrent lymph node granuloma and splenomegaly are presented. Serum immunoglobulins were present in trace amounts only and a progressive loss of Ig-bearing peripheral lymphocytes were demonstrated. Furthermore, the mitogenic responses to PHA. ConA and PWM were markedly reduced and the ratio of T.m/T.g cells was decreased. Finally, a combined deficiency of lymphocyte purine 5-nucleoside phosphorylase was demonstrated in the patient.
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PMID:Common variable immunodeficiency and purine nucleotidase and nucleoside phosphorylase deficiency. A case report. 626 34

A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.
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PMID:Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys. 632 13

Intravenous transfer of BALB/c spleen cells (1-10 X 10(6] immunized against semi-allogeneic hybrid cells bearing H-2k antigens into BALB/c mice resulted in splenomegaly (2- to 6-fold). As few as 2 X 10(4) spleen cells could transfer splenomegaly. A significant spleen enlargement was seen from 2 weeks after cell transfer and reached the peak level at 3 weeks. Those mice with splenomegaly displayed markedly reduced levels of proliferative responses to concanavalin A and lipopolysaccharide. However, the levels of the major Ig classes (i.e., IgG, IgM, and IgA) in the immunodeficient mice were significantly elevated. Such induction of immunodeficiency in mice may help further to understand the acquired immunodeficiency syndrome of humans.
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PMID:Induction of immunodeficiency in mice by injection with syngeneic splenocytes immune to semi-allogeneic hybrid cells. 647 14

A 2 year old girl presented with fever, malaise, a maculopapular rash and lymphadenopathy followed by the onset of haemolytic anaemia and massive splenomegaly. Serology was consistent with acquired toxoplasmosis. A 6 week course of pyrimethamine resulted in a rise in the haemoglobin and reduction of the splenomegaly. During the subsequent 10 years, pyrimethamine treatment of three similar acute episodes resulted in similar clinical responses. There was no spontaneous improvement in the haemolytic anaemia or splenomegaly when pyrimethamine was initially withheld for 6, 1, and 1.5 months respectively during three of these episodes. Investigations did not reveal an immunodeficiency state. This case suggests the possibility of a previously unreported causal association between acquired toxoplasmosis and haemolytic anaemia in a child.
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PMID:Haemolytic anaemia associated with acquired toxoplasmosis. 652 93

A syndrome of acquired immunodeficiency within a group of outdoor-housed rhesus macaques (Macaca mulatta) with unusually high mortality has been identified at the California Primate Research Center. The cause of death for most of the affected animals included septicemia and/or chronic diarrhea with wasting, often complicated by other problems. In many cases, multiple or unusual infectious agents were isolated or recognized, including cytomegalovirus, Cryptosporidium spp., and Candida albicans. Septicemias due to usually innocuous agents such as Staphylococcus epidermidis and Alcaligenes faecalis were seen. Two animals developed cutaneous fibrosarcomas. Affected animals had generalized lymphadenopathy and splenomegaly, with depletion of T-cell populations, initially follicular hyperplasia followed by depletion, and absence of plasma cells. This spontaneous disease syndrome in nonhuman primates has similarities to acquired immune deficiency syndrome (AIDS) in humans, providing an animal model for the study of the complex factors modulating the immune system.
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PMID:The pathology of an epizootic of acquired immunodeficiency in rhesus macaques. 669 18

AKR mice were protected from lethal irradiation and established as long-lived chimeras by transplanting allogeneic C57BL/6 (B6) bone marrow that had been treated in vitro with anti-Thy-1 antiserum without complement. In these chimeras, which were designated [B6 {arrow} AKR], virtually all the thymus and spleen cells were shown to be derived from the B6 donor; several immune functions studied in these chimeras were as follows: (a) The chimeric mice were tolerant of histocompatibility antigens of both donor and recipient strain and nearly fully reactive to antigens of third party, as revealed by Simonsen's splenomegaly assay. The tolerance of these chimeras could not be attributed to suppressor cells but was compatible with clonal depletion. (b) Proliferative responses to concanavalin A, phytohemagglutinin, and lipopolysaccharide as well as natural killer and antibody-dependent cell- mediated cytotoxicity activity of the chimeric mice was normal. (c) Plaque- forming cell (PFC) assays of antibody responses to sheep erythrocytes (SRBC) showed gross deficiency in the primary response of the [B6 {arrow} AKR] and [AKR {arrow} B6] chimeras. By contrast, [B6-H-2(k)(E(k)) {arrow} AKR] H-2-compatible chimeras and [AKR {arrow} AKR] syngeneic marrow transplanted mice had normal primary PFC responses. PFC responses after secondary stimulation with SRBC, however, revealed vigorous direct plaque formation and substantial but somewhat smaller indirect plaque formation in the [B6 {arrow} AKR] chimeras. This observation favors operationally the concept of adaptive differentiation proposed by Katz et al. (44). (d) Analysis of ability of the chimeras to develop and express delayed-type hypersensitivity responses to contact sensitizer (2,4-dinitro-l-fluorobenzene [DNFB]) showed no apparent immunodeficiency of either chimeras to this form of immunization. Development of immunologic tolerance to DNFB, however, was grossly deficient in [B6 {arrow} AKR] chimeras but normal in [AKR {arrow} AKR], [B6 {arrow} B6], and [E(k) {arrow} AKR] chimeras. These findings indicate that full chimeras across major histocompatibility complex have considerable immunologic vigor even though primary immune responses that require histocompatibility between interacting cell types are initially defective.
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PMID:Humoral and cell-mediated immune responses in fully allogeneic bone marrow chimera in mice. 698 46

We examined the changes in the lymphocyte subpopulations in the spleen and peripheral blood of turkeys and the effects of experimental immunodeficiency in the B and T cell compartments on the pathogenesis of hemorrhagic enteritis (HE) in turkeys. Inoculation of turkeys with hemorrhagic enteritis virus (HEV) induced a drop in the relative proportions of IgM bearing cells on Day 2, 3, and 9 post-infection and an elevation in the relative proportions of CD4+ cells on Day 4 and 6 post-infection. Elevated levels of CD8+ cells were observed in the infected turkeys only on Day 16 after infection. Marked depletion of IgM+ cells may play a role in immunodepression caused by HEV. Cyclophosphamide (CY) treatment induced B cell deficiency in turkeys severely impaired HEV replication in the spleen suggesting that B lymphocytes are important for viral replication. Cyclosporin A (CsA) selectively impaired T cell mitogenesis and protected the turkeys against HEV-induced intestinal hemorrhages. CsA did not prevent viral replication in the spleen or the associated splenomegaly. This result suggested that T cell immunity may be important for intestinal hemorrhaging induced by HEV.
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PMID:Hemorrhagic enteritis virus induced changes in the lymphocyte subpopulations in turkeys and the effect of experimental immunodeficiency on viral pathogenesis. 760 31

Lithium salts have been demonstrated to induce the production of hematopoietic cells following administration in vivo and to minimize the reduction of these cells following treatment with either radiation, chemotherapeutic or antiviral drugs. We have previously demonstrated that lithium, when administered in vivo to immunodeficient mice infected with LP-BM5 MuLV (MAIDS) significantly reduced the development of lymphadenopathy, splenomegaly, and the lymphoma associated with late-stage immunodeficiency disease in this model, and increased the survival of these animals compared to virus-infected controls not receiving lithium. We report here the results of in vivo studies in the MAIDS model that determined the effect of lithium on peripheral blood indices and the number of myeloid (CFU-GM), erythroid (BFU-E) and megakaryocyte (CFU-Meg) hematopoietic progenitors from bone marrow and spleen harvested from immunodeficient mice receiving lithium carbonate (1 mM) placed in their drinking water compared to virus-infected controls not receiving lithium. Time-points evaluated were at weeks 1, 5, 9, 13, 17, and 21 postviral infection. Virus-control mice not receiving lithium demonstrated all the signs that are characteristic of MAIDS, i.e., splenomegaly, lymphadenopathy, hypergammaglobulinemia, reduced hematopoiesis, and death. Infected mice receiving lithium demonstrated diminished presence of splenomegaly, lymphadenopathy, hypergammaglobulinemia, no suppression of hematopoiesis nor mortality. Enhanced hematopoiesis was demonstrated by neutrophilia, lymphocytosis, thrombocytosis, and erythrocytosis that was evident by increased myeloid, erythroid, and megakaryocyte progenitor cells cultured from bone marrow and spleen. These studies further demonstrate that lithium influences the disease process in the MAIDS model and restricts the development of hematopoietic suppression that develops in this retroviral animal model of immunodeficiency.
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PMID:Effect of lithium in immunodeficiency: improved blood cell formation in mice with decreased hematopoiesis as the result of LP-BM5 MuLV infection. 760 15

We have previously shown chronic immune activation and enhanced generation of reactive oxygen species in common variable immunodeficiency (CVI). In the present study, we examined levels of glutathione, the dominant intracellular thiol, that play an important protective role against oxidative and inflammatory stress in plasma and in monocytes and lymphocyte subsets in 20 CVI patients and in 16 healthy controls. CD4+ lymphocytes from CVI patients had significantly lower levels of both total and reduced glutathione as well as a lower ratio of reduced to total glutathione compared with healthy controls. This decrease in glutathione levels in CD4+ lymphocytes was most pronounced in the CD45RA+ subset. Plasma levels of total glutathione were also significantly decreased in CVI. In contrast, monocytes from CVI patients exhibited increased levels of both total and reduced glutathione compared with blood donor monocytes. CVI patients had significantly raised serum levels of tumor necrosis factor alpha (TNF alpha) and TNF alpha concentration was strongly associated with glutathione depletion in CD4+ lymphocytes. Furthermore, the lowest levels of both total and reduced glutathione were found in a subgroup of CVI patients characterized by persistent immune activation in vivo, decreased numbers of CD4+ lymphocytes in peripheral blood, and splenomegaly. Finally, supplementation of cell cultures with glutathione-monoethyl ester did significantly enhance interleukin-2 production from peripheral blood mononuclear cells in CVI patients. These glutathione abnormalities in CVI indicate increased oxidative stress, particularly in CD4+ lymphocytes, and intracellular depletion of reduced glutathione of the demonstrated magnitude may have profound implications for CD4+ lymphocyte function and the immunodeficiency in CVI.
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PMID:Decreased levels of total and reduced glutathione in CD4+ lymphocytes in common variable immunodeficiency are associated with activation of the tumor necrosis factor system: possible immunopathogenic role of oxidative stress. 763 46

Rare cases of low-grade lymphomas have been described in patients with human immunodeficiency virus (HIV) infection. However, this is the first reported case of mantle-cell lymphoma, a type of low-grade lymphoma, in a patient who also had HIV infection. Salient clinical features included lymphocytosis, lymphadenopathy, splenomegaly, and involvement of the bone marrow and meninges. The disease proved to be unusually aggressive and response to chemotherapy was insignificant. The patient survived only 4 months.
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PMID:Mantle-cell lymphoma in a patient with human immunodeficiency viral infection. 763 49


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