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)

Genetically anemic SI/SI(d) mice have been shown previously to have a defective hematopoietic environment which prevents extensive erythroid differentiation of normal hematopoietic stem cells and also confers resistance to the erythroleukemia-inducing virus, Friend spleen focus-forming virus (SFFV). In this study, we show that the relative resistance of SI/SI(d) mice to transformation by SFFV is not due to the inability of SFFV to replicate, nor is it because SFFV cannot transform erythroid cells, in the spleens of these mice. Injection of syngeneic +/+ mouse spleen cells, previously infected in vivo with SFFV, into secondary SI/SI(d) recipients resulted in marked splenic enlargement, and the appearance of large numbers of erythropoietin (Epo)-independent erythroid colonies in plasma clot culture. The cellular proliferation observed in these SI/SI(d) secondary recipients appeared to be due to infection and transformation of host SI/SI(d) cells rather than the growth of possible tumor colony-forming units (TCFU) present in the infected +/+ spleens, because preirradiation of the SI/SI(d) recipients abolished the splenomegaly and appearance of Epo- independent erythroid colonies. Furthermore, prior irradiation (1,200 rads) of donor spleen cells from SFFV-infected +/+ mice only slightly reduced spleen focus formation in unirradiated SI/SI(d) recipients. The conclusion that SI/SI(d) target cells could be infected and transformed by SFFV was confirmed directly by injecting a high titered preparation of SFFV into SI/SI(d) mice. SI/SI(d) mice were not absolutely resistant to infection or transformation by SFFV. Nevertheless, cells from the spleens of SFFV-infected mice were unable to form tumor colonies (TCFU) in irradiated SI/SI(d) recipients, suggesting that TCFU are either present at an undetectably low frequency in these spleens, or that they are still subject to the regulatory influences of the Steel locus.
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PMID:Cellular regulation in Friend virus induced erythroleukemia. Studies with anemic mice of genotype Sl/Sld. 28 12

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

A 22-year-old black male presented with erythrocytosis and proteinuria. The erythrocytosis was characterized by increased red cell mass, normal arterial oxygen saturation, and normal hemoglobin electrophoresis and oxygen affinity. There was no splenomegaly, and the white blood cell count, platelet count, serum uric acid concentration, serum B12 levels and leukocyte alkaline phosphatase activity were normal. Tumors of the liver, lung, kidney and cerebellum, which have been associated with erythrocytosis, were not found. The only associated disease was biopsy proven focal glomerulosclerosis. Renal vein thrombosis was excluded by renal venography and arteriography. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis. Other nephrogenic causes of erythrocytosis are mentioned, including renal cysts, tumors, renal artery stenosis and transplantation. The role of the kidney in erythropoietin production and possible mechanisms of nephrogenic erythrocytosis are discussed.
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PMID:Focal glomerulosclerosis and erythrocytosis. 50 18

A case of erythrocytosis with increased plasma erythropoietin level was reported. Peripheral leucocytes and thrombocytes were normal. No splenomegaly was detected. Studies to find underlying disorders causing increased plasma erythropoietin level and erythrocytosis revealed no abnormalities except for the thickened and tortuous interlobular and afferent arteries in the kidney. This change was suggested as the cause of erythrocytosis found in this case.
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PMID:A case of intrarenal artery stenosis associated with erythrocytosis. 72 26

We developed a cell line (IS) that continuously produced both Friend spleen focus-forming virus (SFFV) and XC plaque-forming virus in vitro. The line was derived from the enlarged spleen of an inbred SIM mouse previously infected with a polycythemic strain of Friend leukemia virus in vivo. Friend SFFV titers of 10(4) spleen focus-forming units/ml of culture medium were maintained for more than 200 cell generations. The virus from IS cells induced the splenomegaly and high hematocrit typical of Friend virus-induced erythroid disease in SIM mice. Cells of the IS line were adherent and phagocytic and had a low saturation density. They produced no tumors after being injected sc into normal syngeneic hosts and no spleen colonies after being injected iv into supralethally irradiated hosts. IS cells did not have the character of erythroid cells: They did not contain detectable heme as measured by benzidine-peroxide reagent, did not contain globin mRNA in detectable amounts, and did not produce erythroid colonies in plasma culture in the absence or presence of erythropoietin. According to these criteria, growth in the presence of dimethyl sulfoxide did not stimulate erythroid differentiation of IS cells. We concluded that Friend SFFV can infect nonerythroid spleen cells but that replication of the virus was not obligatorily coupled to expression of genes associated with the erythroid phenotype.
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PMID:Friend spleen focus-forming virus production in vitro by a nonerythroid cell line. 106 58

Splenomegaly accompanied by anaemia, increased reticulocyte and decreased thrombocyte counts, was induced in Wistar rats by a long-term intraperitoneal administration of methylcellulose. Compared to controls, hypersplenic rats showed significantly enhanced utilization of 59-Fe by red cells and increased titre of erythropoietin. After the exposure of rats to hypoxic hypoxia corresponding to an altitude of 7,000 m for 6 h, no difference in the erythropoietin titre was found in either group. The results suggest that experimental hypersplenism alone does not affect the production of erythropoietin and does not stimulate the formation of an inhibitor of erythropoietin or erythropoiesis. The increased titre of erythropoietin and enhanced utilization of radioiron by red cells in rats with hypersplenism were found to be due to haemolytic anaemia leading to the stimulation of erythropoiesis.
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PMID:Erythropoietin formation in rats with experimental hypersplenism. 114 16

Friend murine leukemia virus induces splenic enlargement and an increase in RNA polymerase activity of spleen nuclei. Actinomycin D, administered at 60 mug/kg body weight/day prevents the development os splenomegaly and the elevation of polymerase activity following infection, but it has only a slight effect on the production of virus in spleen tissue. Thus, the alteration of RNA synthesis is not a result of virus proliferation, but instead may be a manifestation of leukemic erythropoiesis. Normal erythropoiesis, stimulated by erythropoietin administration, produces a similar but transient increase in RNA polymerase activity in spleen nuclei. Erythropoietin administered before, but not after, Friend virus infection results in an enhancement of RNA polymerase activity, as measured 9 days after inoculation. This effect is most simply explained by assuming that there is a common target cell pool for both erythropoietin and Friend virus, and that this pool becomes refractory to the influence of the hormone as a result of the leukemic process.
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PMID:Role of cellular RNA polymerases in virus-induced leukemogenesis. 114 21

In mice hypoxic hypoxia (0.5 atm.) results in a severe and persistent thrombocytopenia with a rapid decline in the platelet count between the fifth and ninth days of hypoxia, after which platelet counts level off at about half their normal value. The thrombocytopenia is not due to the associated polycythemia, splenomegaly, or increased blood volume. There is no significant change in platelet counts of mice made polycythemic by daily injections of 6 units of erythropoietin. Fifteen days of hyperbaria (3 atm.) has no effect on the platelet count of otherwise normal mice. Since there is only a slight decline in platelet count during the first 5 days of hypoxia, the persistent thrombocytopenia appears to be due to either a decreased rate of production of platelets or a structural or metabolic defect in platelets produced under conditions of hypoxia.
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PMID:Hypoxia-induced thrombocytopenia in mice. 115 Nov 49

Anemia developing during the course of chronic renal disease is a frequent complication often necessitating periodic transfusion therapy. A number of etiologic factors have been implicated, including decreased production of erythropoietin; decreased erythrocyte life span secondary to uremia and splenomegaly; increased bleeding tendency due to platelet dysfunction; and acquired lack of folic acid and iron. This paper concerns the problem of acquired hypochromic, microcytic anemia secondary to heavy urinary loss of iron and transferrin in a child with the nephrotic syndrome. The patient had microcytic, hypochromic anemia with serum iron, 12 mug. per dl. and a serum iron-binding capacity of 12 mug. per dl. There was no evidence of major bleeding resulting in a chronic hemorrhagic anemia. Urinary iron was 64 mug. per dl., with a urinary iron-binding capacity of 366 mug. per dl. Renal biopsy showed mesangio-proliferative glomerulonephritis. Evaluation of any patient with the nephrotic syndrome should include careful analysis of the various serum and urinary proteins and determination of serum and urinary iron and iron-binding capacity. This information would offer a more precise evaluation of the underlying cause of anemia in the nephrotic patient who may develop urinary loss of iron and transferrin and subsequent hypochromic, microcytic anemia.
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PMID:Transferrin loss into the urine with hypochromic, microcytic anemia. 124 90

We present a case of placental-site trophoblastic tumor associated with erythrocytosis. This 42-year-old woman had persistent amenorrhea and low elevations of her hCG titer after term delivery of a healthy female infant. The woman was noted to have polycythemia of uncertain etiology and was treated with serial phlebotomy. Placental-site trophoblastic tumor was diagnosed and hysterectomy was performed, with subsequent resolution of the polycythemia. Although erythrocytosis has been reported with other gynecologic tumors, this is the first reported association with a placental-site trophoblastic tumor. A role has been suggested for placental lactogen in erythropoiesis during pregnancy based on previous animal studies. Diffuse positive staining for hPL is characteristic of placental-site trophoblastic tumors. We postulate that hPL may have played an ancillary role to erythropoietin in the erythrocytosis demonstrated in this case. Spider angiomata and splenomegaly are interesting clinical features previously described in association with placental-site trophoblastic tumors, and were demonstrated in this patient.
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PMID:Erythrocytosis associated with a placental-site trophoblastic tumor. 131 61


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