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)

Two cases of T-cell chronic lymphoid leukaemia in adults were classified by recently developed immunological methods. Clinically there was splenomegaly, hepatomegaly, marked anaemia, para-aortic lymph nodes, cutaneous infiltration, little peripheral lymph-node enlargement and significant marrow infiltration. Immunological tests of membrane antigens revealed T-cell determinants. T-CLL may differ in its course and prognosis from B-CLL and may require different treatment.
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PMID:[T-cell leukaemia in adults: report of two cases (author's transl)]. 30 81

A case of prolymphocytic leukaemia, showing several features not yet reported in this disease, is reported. The majority of lymphocytes in the peripheral blood and bone marrow had markers of both B- and T-lymphocytes. The simultaneous presence of receptors for sheep RBC and surface immunoglobulins on individual cells was demonstrated and the endogenous origin of these markers was established. The lymphocytes had some of the functional characteristics seen in chronic lymphocytic leukaemia (CCL). In vitro cell death in the presence of colchicine (colchicine ultrasensitivity) and polystyrene bead column retention were of the same order as seen in CLL. In contrast with the findings in CLL, these cells were markedly radioresistant in vitro. The dominant clinical features--anaemia and constitutional symptoms--appeared to be related to hypersplenism associated with massive splenomegaly. The relevance of these findings is discussed.
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PMID:Cell studies in prolymphocytic leukaemia. 31 Mar 13

By lymphoid myelofibrosis or hairy cell leukaemia or tricholeukaemia is meant an unusual haemopathic condition known only for the past few years. It is characterized pathognomonically by the presence of lymphocyte type cells with villous extroflexions, hence the name "hairy cell". Clinically the disease presents as an involutive myelopathy associated with splenomegaly, generally without any particular lymph gland involvement. The attention of students today is concentrated on the nature of the hairy cells; while some are inclined to admit their monocyte or histiocyte derivation, others consider that they derive from B lymphocytes. Therapeutically, almost everybody agrees that splenectomy is the only valid step. A case of H.C.L., which was typical from the clinical and laboratory viewpoints is reported. It is probable that certain haemopathic pictures once classified among atypical leucoses and lymphomas, would today be more correctly classed as hairy cell leukaemia.
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PMID:[Lymphoid myelofibrosis or hairy cell leukemia]. 32 48

A 68-yr-old male with chronic lymphocytic leukemia (CLL) presented with splenomegaly and skin infiltration but no lymphadenopathy. The peripheral blood WBC cound was 300 x 10(9)/liter, with 95% small mature-appearing lymphocytes that were E-rosette positive and EAC-rosette negative. Further characterization of the patient's cells was performed using antisera with known lymphoid sub-population specificity. Anti-p23,30, which reacts with normal circulating B cells but not with T cells or thymocytes, was unreactive with the patient's cells. Anti-311, which reacts with both thymocytes and circulating T cells, was reactive with the patient's cells. Anti-Bk, which reacts only with thymocytes and not with circulating T-cells, failed to react with the patient's cells. The enzyme terminal deoxynucleotidyl transferase, present in thymocytes but absent for circulating T-cells, was also absent from the patient's lymphoid cells. Multimarker analysis therefore showed a mature T-lymphocyte phenotype on this patient's leukemia cells. Further functional analysis will probably show that such cells represent clonal expansion of a mature T-cell subpopulation, analogous to the B-cell clonality of common-variant CLL.
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PMID:Multimarker analysis of T-cell chronic lymphocytic leukemia. 34 7

The life history of a transplantable B cell leukemia (BCL1) that arose spontaneously in a BALB/c mouse is described. Animals bearing this tumor live from 2 to 4 months in apparently good health despite massive splenomegaly and leukemia. Antibody to the idiotype or gamma light chain of the tumor IgM was used in conjunction with the fluorescence-activated cell sorter to identify tumor cells in the BCL1-bearing mice. The results suggest that these cells multiply and differentiate in the spleen and subsequently emigrate to the blood. Tumor cells do not recirculate as evidenced by their failure to enter the thoracic duct or to infiltrate lymph nodes to a significant extent. During tumor growth, a population of T cell blasts appears that may be involved with an immune response against the tumor.
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PMID:Murine B cell leukemia (BCL1): organ distribution and kinetics of growth as determined by fluorescence analysis with an anti-idiotypic antibody. 38 72

Leukemic reticuloendotheliosis, or "hairy cell leukemia," is a neoplasm of the reticuloendothelial system. It is characterized by the presence of many "hairy cells" in blood, marrow, lymph nodes, and spleen; by anemia, leukopenia, thrombocytopenia, and often, by massive splenomegaly. Three such patients with spontaneous rupture and one patient with multiple infarctions of the spleen all had spleens which were large, congested, and diffusely infiltrated by "hairy cells." The lacerations in all three ruptured spleens were located in areas of extensive infarction. Indications for splenectomy in this disease include hypersplenism, severe cytopenia, hemodilution, splenomegaly with severe pressure symptoms, massive splenomegaly, rupture, or infarction.
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PMID:Spontaneous rupture of spleen in leukemic reticuloendotheliosis. 42 89

Infection of BALB/c mice with Rauscher leukemia virus (RLV) gives rise to pronounced erythrocytopoiesis manifesting in splenomegaly and is associated with progressive development of anemia. In the spleen erythroid colony forming units (CFU-E) increase exponentially up to 800-fold that of normal levels by the third week of infection. In vitro these CFU-E are dependent on erythropoietin for colony formation, their erythropoietin requirements being higher than that of CFU-E from normal mice. Numbers of CFU-E in spleen and degree of splenomegaly in anemic RLV infected mice were also shown to be modified by red blood cell transfusion, but progression of the disease was not stopped. Erythroid burst forming units (BFU-E) were also responsive to erythropoietin. However, a small proportion of cells also formed BFU-E colonies at concentrations which did not support growth of normal marrow BFU-E. When compared to normal, CFU-E found in RLV-infected spleen have similar velocity sedimentation rates. However, buoyant density separation of leukemic spleen cells indicated that CFU-E were more homogeneous (modal density 1.0695 g/cm3) than CFU-E from normal spleen. Analysis of physical properties of CFU-E and the nonhemoglobinized erythroblast-like cells, which accumulate in the spleen showed that they differed mainly in their distribution of cell diameter. Our findings show that erythroid progenitor cells in RLV infected mice are responsive to erythropoietin in vitro. Also in vivo erythropoiesis appears to be under control of erythropoietin but other factors which lead to progression of RLV disease apparently exist. Most proerythroblast-like cells, which are characteristic of this disease, apparently lack the potential to form colonies and may be more mature than CFU-E.
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PMID:Erythropoietin responses and physical characterization of erythroid progenitor cells in Rauscher virus infected BALB/c mice. 46 21

Mixed Rauscher leukemia virus (RLV) and M. arthritidis infection of (C57BL/6xA/Sn)f1 mice-hybrids, highly resistant to RLV, was accompanied by a progressive inhibition of rosette-forming cells (RFC) and plaque-forming cells (PFC), resulting in the induction of malignant erythroblastosis identical by cytology to Rauscher leukemia. The mice-hybrids infected with A. laidlawii and RLV developed significant splenomegaly on the 21st day of the infection, and their immune response was almost entirely suppressed, but both RFC and PFC populations as well as the spleen weight returned to the initial level by the 62d day the infection. A possible role of mycoplasm in the induction and development of Rauscher leukemia is discussed.
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PMID:[Immune response of (C57BL/6xA/Sn)F1 mice in mycoplasm-virus infection]. 51 25

Four patients with the Tropical Splenomegaly Syndrome, showing marked lymphoid hyperplasia were studied, using immunological techniques. It has not been possible to decide on a definite diagnosis; chronic lymphatic leukaemia could not be excluded. Careful follow-up of similar patients may provide important clues to the pathogenesis of these diseases.
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PMID:Tropical splenomegaly syndrome or chronic lymphatic leukaemia? 52 46

The value of splenectomy is assessed from diagnostic and therapeutic viewpoints in a series of 80 patients with various syndromes marked by hypersplenia. In the congestive type of splenomegaly, splenectomy resulted in complete normalization of the blood picture in all cases but one, and in primary splenic congestion it even proved curative in the majority of the cases. In leukaemia, non-Hodgkin's lymphomas, in myelofibrosis, and first of all in immuncytopenia, splenectomy was also of benefit, and had generally a palliative effect in non-autoimmune hypersplenia as well. In non-haematological syndromes associated with hypersplenia, namely, splenic tuberculosis, Boeck's sarcoid, SLE, haemorchromatosis and splenic vein thrombosis, splenectomy had generally a palliative, and combined with other therapeutic measures, a curative effect, depending on the primary disease. In a number of patients with hypersplenia associated with splenomegaly, it was only with the aid of splenectomy that the primary disease could be diagnosed.
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PMID:Diagnostic and therapeutic aspects of splenectomy in syndromes associated with hypersplenia. 52 25


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