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)

Plasmocytoma and Waldenstroem's disease together with some other very rare diseases form the group of paraproteinaemic haemoblastoses. In these cases the plasmocytoma as a neoplasia of the plasma cells is quite likely to define by the sum of the cytomorphological, radiological and immunological findings in form of the plasmocytosis of the bone-marrow, the destructions of the skeleton and the formation of monoclonal immunoglobulins as cardinal symptoms. Waldenstroem's disease, however, becomes more and more a special form of the IgM-forming malignant lymphomas. In its classical expression apart from the formation of lymphomas, hepato-splenomegaly and haemorhages it above all exhibits the excessive formation of a monoclonal, macromolecular immunoglobulin. In this disease the prognosis is in many cases by far more favourable than that one of the plasmocytoma which, apart from its solitary-multiple form of the course, is a disease with high malignity. Cyclophosphamide and sarcolysin are the remedies of choice in the plasmocytoma, procarbazine in waldenstroem's disease. Nowadays, the inclusion of the two diseases into the large spectre of neoplasias of all cells of the immuno-competent system which finally are structurally derived from the immunocyte and are functionally differentiated renders a special way of description unnecessary.
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PMID:[Diagnosis and therapy of plasmacytoma and Waldenstrom's disease]. 82 13

A 20-year old patient is presented with generalized lymphadenopathy, splenomegaly, hyperleukocytosis and a bone marrow biopsy showing panmyelosis with predominance of immature granulocytes. Lymph node biopsy showed a histopathological feature that was diagnosed as a chronic granulocytic leukemia in blast crisis. The cell surface phenotype of these blast cells showed predominance of immature CD1+, CD7+ T lymphocytes. The T cell lineage was confirmed by DNA rearrangement studies. In addition, the patient showed erythrocytosis, arterial O2 saturation of 92% and thrombocytosis, characteristics of polycythemia vera. After chemotherapy, the patient relapsed with similar symptoms and lymph node cells of similar immature T phenotype. With a revised diagnosis of immature T cell lymphoma associated to a myeloproliferative disorder and polyglobulia, the patient received a combined treatment of Cyclophosphamide-Adriamycin-Vincristine-VM26-Prednisone. Two months later, the patient relapsed again. He received the first phase of induction of the BFM protocol, with partial clinical remission. Five months later, the patient returned with fever, polyadenopathy and splenomegaly. Lymph node cells showed again immature T cell phenotype. The patient was next treated with the m-BACOD scheme, with no response and progression of the disease and he died few days later due to massive bleeding and cardiorespiratory failure.
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PMID:[T lymphoma of immature phenotype associated with polycythemia vera]. 182 May 2

A 40-year-old woman presented with splenomegaly, macrocytic anemia, and red cell aplasia. Although lymphocytosis was absent in the peripheral blood, large atypical lymphoid aggregates were present in the bone marrow. Splenectomy resulted in partial remission of red cell aplasia, but a gradual increase in the number of peripheral blood lymphocytes followed during the next 36 months. Flow cytometric analysis demonstrated that the majority of these peripheral blood lymphocytes had suppressor, natural killer T-cell phenotype. No other treatment was given until red cell hypoplasia worsened 42 months after initial presentation. Repeat bone marrow evaluation again demonstrated severe erythroid hypoplasia and large abnormal lymphocytic infiltrates. Cyclophosphamide given for 8 months resulted in complete resolution of the red cell aplasia and complete clinical remission of CLL. However, flow cytometric analysis revealed persistent increase in bone marrow T-cells, and bone marrow co-culture studies demonstrated residual ability of peripheral blood mononuclear cells to inhibit erythropoiesis in vitro, suggesting that residual, clinically undetectable leukemia persists in spite of complete clinical remission.
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PMID:T-cell chronic lymphocytic leukemia with pure red cell aplasia: laboratory demonstration of persistent leukemia in spite of apparent complete clinical remission. 308 88

Murine toxoplasmosis caused by a low virulence, cyst-forming strain of Toxcoplasma gondii (Pe strain) is characterized by splenomegaly, lymphadenopathy, decreased delayed-type hypersensitivity (DTH), and the presence of toxoplasma cysts in brain tissue. Cyclophosphamide (CY) in a single dose of 100 mg/kg injected 3 days before infection, or splenectomy 3 weeks before infection, augmented DTH and decreased the number of toxoplasma brain cysts. CY-induced augmentation of resistance during the first 3 weeks of murine toxoplasmosis was associated with: (1) an increase in mononuclear phagocytes and a decrease in T lymphocytes (including Lyt2+ cells) in spleens and lymph nodes; (2) suppressed toxoplasma antigen induced proliferation of cultured spleen cells: (3) augmentation of antigen induced proliferation of cultured lymph node cells; and (4) low levels of interferon-gamma production in both spleen and lymph node cultures. The best correlate of the enhanced in-vivo effects of CY was proliferation of nylon wool-purified lymph node cells to toxoplasma antigen. The presence of Lyt2+ cells in lymph nodes of toxoplasma infected mice inhibited maximal proliferation.
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PMID:Murine spleen and lymph node cellular composition and function during cyclophosphamide and splenectomy induced resistance to Toxoplasma gondii. 310 64

Immunotherapeutic agents are often reported to induce opposite effects -- inhibitory and stimulatory -- on tumor growth, depending on the dose, timing or route of administration of the drug. The reason underlying these opposite effects is not yet known. The immunomodulatory polysaccharide levan (polyfructose) has been found to exert such opposite effects on the growth of the F10 variant of B16 melanoma. Low doses inhibit and high doses enhance tumor growth. Cyclophosphamide (CY) augment the inhibitory effect of levan. In order to clarify the mechanism of this switch, we tried in the present study to determine the changes induced by levan at inhibitory and stimulatory treatments, alone or with CY, on the morphology of spleens and lymph nodes of the melanoma-bearing mice. The growth of the tumor in non-treated mice was found to induce a moderate splenomegaly. Microscopically, two main changes were observed: a mild extramedullary hematopoiesis and a sharp increase in the number of germinal centers. A parallel increase in germinal center number was found in the lymph nodes. The data presented suggest that the immune system plays a role in both the inhibition and stimulation of tumor growth by levan. Levan induced a dose dependent splenomegaly, even more pronounced in combination with CY, due to an extramedullary hematopoiesis. Levan reduced the B cell activity caused by the tumor, proportionally to its dose. In combination with CY, levan accelerated the recovery of the B cell activity at the low dose, while the high dose prevented it. A similar trend was found in the lymph nodes. The changes involved in the switch inhibition-stimulation could be either the degree of reduction in B cell activity or the degree of extramedullary hematopoiesis or some interplay between the myelocytic and lymphocytic series, which was found to change in an opposite fashion under the influence of various treatments. Since the immune system is a finely equilibrated system, it is possible that immunomodulation rather than immunostimulation should be aimed at in cancer immunotherapy. However, the conditions required for achieving this equilibrium have to be defined.
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PMID:Effect of tumor inhibitory and stimulatory doses of levan, alone and in combination with cyclophosphamide, on spleen and lymph nodes. 374 40

Indomethacin (IN) was administered to untreated or to cyclophosphamide (CY) treated C57B1/6 mice to study the roles of prostaglandins in regulating hematopoiesis. The following hematopoietic parameters were quantitated: peripheral blood leukocyte (PBL) count; total nucleated cells per spleen; total nucleated cells per femur; and spleen weight. Assays were performed in vitro to measure the number of colony forming units (CFU) present in the bone marrow and spleen. Untreated mice administered IN had a transient rise in their PBL count. These animals also developed splenomegaly and had an increased number of nucleated cells in their spleen. All CY treated mice had a marked decrease in PBL count, spleen cellularity, bone marrow cellularity, and spleen size during the first 5 days after CY treatment. These observations were followed by hematopoietic recovery over the next 10 days. Cyclophosphamide treated mice exhibited a more rapid hematopoietic recovery when treated with IN than without IN treatment. Analysis of the CFU capacity of bone marrow and spleen cells in soft agar showed a larger number of CFU in the bone marrow and spleen of IN treated mice or of CY/IN treated mice than in animals not receiving IN. These results indicate that prostaglandins are involved in the regulation of hematopoiesis in untreated mice and that prostaglandins may limit the hematopoietic recovery of CY treated mice.
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PMID:Stimulation of hematopoiesis in untreated and cyclophosphamide treated mice by the inhibition of prostaglandin synthesis. 376 May 91

Cyclophosphamide (Cy; 150 mg/kg) was administered (i.p.) to groups of Sprague-Dawley rats, followed two days later by immunization with ovalbumin (OVA). From that time, cyclosporin A (CsA; 25 mg/kg) or its vehicle was given (p.o.) for a further 13 days. Control animals tested 14 days after immunization, showed strong Arthus-like and modest delayed-type skin reactions to OVA, in contrast to almost total inhibition in animals tested with Cy, CsA or both. Similar effects were observed with respect to serum anti-OVA antibody levels. Despite itself producing lymphopenia, CsA had no additional effect on the lymphocyte depletion caused by Cy. Both drugs, either alone or in combination, caused neutrophilia and monocytosis. An additional eosinophilia due to Cy was prevented by CsA. Cy induced splenomegaly, nodal extramedullary haemopoiesis and increases in both tissue eosinophils and marrow neutrophils. There was also lymphoid depletion in both spleen and lymph nodes which was enhanced by CsA. Thymic lymphoid atrophy was found only when CsA was given. Despite the powerful immunosuppressive properties of both drugs, detailed biochemical and structural analyses showed no other synergistic toxicity, apart from modest hepatic abnormalities. In particular, there was no enhancement of the nephrotoxicity of CsA.
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PMID:Immunosuppressive activity and toxicity of cyclosporin A in rats pretreated with high dose cyclophosphamide. 408 81

40 children (23 males, 17 females) have been diagnosed have ANLL during the period from february 1970 to september 1981. According to FAB classification, 24 cases were M1,-M2, 9 M3, 3 M4, 3 M5 and 1 M6. At diagnosis, 20 patients (50%) had leukocytes less than 10.000/mmc, 6 (15%) had leukocytes greater than 50.000mmc. Hb levels was 7 g% in 16 patients (40%); 10 children had hepatosplenomegaly (25%), 7 splenomegaly (18%) and 5 lymphoadenomegaly (13%). 4 patients had cutaneous or mucous infiltrates. None had meningeal involvement at diagnosis. According to the year of diagnosis, 3 groups can be identified. In the group I (1970-73), 11 patients have been treated with not codified combination chemotherapy as ARA-C, 6-TG, DNR, CTX, Metil-GAG. In the group II (1974-76) and in the group III (1977-81), the patients (respectively 12 and 17) have been treated according to the following protocols: LAM-5 (3), TRAP (5), COAP (1), LAM 80 (2), AIL 7402 (8), AIL 7604, AIL 7801 (6). Immunotherapy has been performed in 7 cases. CNS prophylaxis (MTX i.t. +/-ARA-C +/- RT) was given in 5 patients of group II and in 6 of group III. I patients of group I (45%), 6 of group II (50%) and 13 of group III (76%) achieved CR. Median duration of remission was 5 months in the group I and in 17 in group II and III.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute non-lymphatic leukemia in children]. 654 20

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

A 46-year-old woman was given a diagnosis of primary myelofibrosis (PMF) in 1996. Because of the progression of anemia and splenomegaly, she was scheduled for allogeneic bone marrow transplantation (BMT) from an HLA-matched sibling donor in April 1998. Cyclophosphamide and busulfan were used as the conditioning regimen. Before BMT, the patient was treated with hydroxycarbamide, which did not resolve splenomegaly. She then underwent a splenectomy, which was followed by massive portal vein thrombosis without any significant clinical outcome. After BMT, the patient obtained rapid hematologic engraftment. Moreover, the alleviation of marrow fibrosis was confirmed 4 months after BMT. We concluded that allogenic BMT can cure patients with PMF, but that the issue of splenectomy and the indications for BMT need to be evaluated further.
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PMID:[Allogeneic bone marrow transplantation for primary myelofibrosis after splenectomy]. 1077 49


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