Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain tissue sections from control male and female Fischer 344 (F344) rats from ten National Toxicology Program (NTP) Bioassays were histomorphologically reviewed for non-neoplastic lesions of the hippocampus. Unilateral segmental hippocampal neuronal necrosis, which has not been reported in normal rats, was observed in 9 of 433 (2.1 per cent) males and 1 of 454 (0.2 per cent) females. Significant coexisting lesions were left-sided atrial and/or valvular thrombosis, metastatic mesothelioma, and large lymphocyte leukaemia. These data suggest that this naturally occurring lesion of predominantly aged male rats may result from an impairment of cerebral perfusion secondary to vascular obstruction by thrombotic emboli or leukaemic cells and haemolytic anaemia concomitant with large lymphocyte leukaemia, which commonly occurs in F344 rats.
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PMID:Hippocampal neuronal necrosis in control Fischer 344 rats. 225 71

A spontaneous large granular lymphocyte (LGL) leukemia was serially transplanted in 92 male F344 rats kept under standard laboratory conditions. Serial transplantation into groups of four rats each resulted in a rapid reduction in the latent period of the disease. After 23 serial transplantations, F344 rats in groups that were injected intraperitoneally with 10(7) cells died between 12 and 16 days after transplantation. At necropsy, "transplanted" rats had enlarged mesenteric lymph nodes, thymus, and spleen. Neoplastic cells were detected in the spleen on day 3 and in peripheral blood on day 6. Extreme leukocytosis with leukemia was present on day 9. Severe hemolytic anemia coincided with a sharp increase in osmotic fragility on day 12. Splenic lymphoid depletion was observed histologically and confirmed by differential cell counts of isolated spleen cells. Analysis for surface markers of splenic lymphocytes by monoclonal antibodies and flow cytometry indicated that cells with T helper/inducer phenotypes were disproportionately decreased, while the number of T suppressor cells did not significantly change. The T helper/T suppressor lymphocyte ratio (normal = 2.09 +/- 0.35) was decreased on day 9 (0.76 +/- 0.10) and day 12 (0.25 +/- 0.04). Hemolytic anemia was not related to a decrease in the number of T suppressor cells. The passaged leukemia cell model should provide investigators with an easily maintained neoplasm of short latency with which to study pathogenesis of leukemia-related disorders.
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PMID:Serial syngeneic transplantation of large granular lymphocyte leukemia in F344 rats. 227 28

Two hundred patients with various haematological diseases underwent splenectomy between 1974 and 1986. The diagnoses were: Hodgkin's disease (n = 76), hairy cell leukaemia (n = 25), idiopathic thrombocytopenic purpura (n = 20), chronic lymphatic leukaemia (n = 19), haemolytic anaemia (n = 18), non-Hodgkin lymphoma (n = 16), myelofibrosis (n = 10), chronic myeloid leukaemia (n = 6), spherocytosis (n = 4), and miscellaneous (n = 6). Many of the patients were treated with corticosteroids and in poor general condition, partly as a result of chemotherapy. There were 37 postoperative complications in 29 patients (14.5%); two died, both of septicaemia. Pneumonia, bleeding, and wound infection were the most common complications, occurring in 9, 8, and 6 patients, respectively. Twelve patients required reoperation, eight for bleeding, two for intra-abdominal abscesses, and one each for pancreatitis and bowel perforation. There was no association between the diagnosis and the type of postoperative complication, but patients whose spleens weighed more than 2 kg had an increased incidence of postoperative complications (30%). We conclude that elective splenectomy is a safe treatment for haematological diseases, even in high risk patients.
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PMID:Splenectomy for haematological diseases. 232 42

Splenectomy has a major role in the treatment of hematologic diseases. Although it is rarely curative, splenectomy removes the site of the destruction or sequestration of erythrocytes, leukocytes, and platelets. Destruction occurs in such diseases as hemolytic anemia and ITP, whereas sequestration occurs as an idiopathic disease or secondary to a host of other diseases described above. Splenectomy is also indicated for symptomatic splenomegaly associated with leukemia, lymphoma, or myeloproliferative disorders. It is palliative, increasing the comfort of the patient by removing a massive spleen. Splenectomy also serves as a staging tool in lymphoma, Hodgkin's disease, and NHL, although it is much more beneficial in Hodgkin's disease, owing simply to stage at presentation. Splenectomy can be performed safely with minimal risk in most patients, but certain diseases carry increased risks of fatality and complications. Such diseases include leukemia, lymphoma, and myeloproliferative disorders, but even in these, splenectomy may be indicated in a select group of patients. The decision to perform splenectomy should therefore be made individually in these cases. Because it can be palliative in some cases, splenectomy can play a role in patient management, even though it may not alter survival.
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PMID:Splenectomy for hematologic disease. 264 43

A 19 year old woman presented as a case of haemolytic anaemia due to multi-enzyme deficiency of the erythrocyte. After a transient improvement with folic acid therapy, she developed acute myeloblastic leukaemia. This is the second reported case of a myelodysplastic syndrome presenting with a haemolytic picture and subsequently developing an acute myeloblastic leukaemia.
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PMID:A case of pre-leukaemia masquerading as haemolytic anaemia due to multi-enzymopathy of the red cell. 276 72

Five weeks after re-induction treatment and nine days after discharge from hospital, remittent fever occurred in a 34-year-old woman with promyelocytic leukaemia in full remission. She also had haemolytic anaemia and thrombocytopenia, as well as a reduced creatinine clearance. Findings on physical examination were unremarkable, but Falciparum malaria was found in the blood smear. Infusion of erythrocyte or platelet concentrates, administered in treating the leukaemia, was the probable source of the infection. Ten days after starting the administration of chloroquine and sulfadoxine-pyrimethamine she was discharged from hospital, cured of the malaria.
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PMID:[Transfusion malaria in promyelocytic leukemia]. 305 88

The vast majority of pediatric RBC hypoplastic anemias are accounted for by red blood cell aplasia associated with chronic hemolysis, Diamond-Blackfan anemia, and transient erythroblastopenia of childhood. However, other causes of hypoplastic anemia occur in children, and some of these are similar to what is seen in adult RBC aplasia. For example, it has been reported that a 5-year-old girl with an aregenerative anemia had a thymoma and later developed pancytopenia. RBC aplasia also has been seen in children receiving anticonvulsant drug therapy, children recovering from severe protein malnutrition, children with hepatitis, and in children with leukemia during maintenance therapy. In addition, it is not uncommon for pediatric hematologists to observe children with RBC aplasia where there is no obvious diagnosis, although many are considered to be variants of Diamond-Blackfan anemia. Several important questions about RBC hypoplastic anemias in children need to be resolved; it is hoped that this will be accomplished in the next decade. Do RBC hypoplastic crises associated with hemolytic anemia occur with viral infections other than HPV? What is the cellular pathophysiology in DBA and TEC? Does the apparent heterogeneity of these disorders reflect limitations of laboratory techniques or are we looking at several different diseases? Is acute leukemia a real complication of Diamond-Blackfan anemia? Is TEC a completely benign entity or will we see other long-term problems in these children? Is the incidence of TEC actually increasing? Will TEC-like problems be seen in other aged children? As a case in point, we recently observed a 16-year-old girl who presented with pure RBC aplasia that required RBC transfusion support for 5 months; she also received prednisone therapy. After 7 months, however, this young lady had a spontaneous remission, and now 4 years later she is normal and free of any hematologic abnormalities. This was a most unusual event in our experience and, in view of the apparent increasing incidence of TEC in young children, we queried whether we were observing an adolescent equivalent of this disorder. During the next several years the answer to this and the other questions posed herein should be available.
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PMID:Diagnosis and management of red cell aplasia in children. 312 94

Conventional doses of intravenous immunoglobulin (i.v. Ig) (0.4 g/kg/day for 5 days) commonly produce a remission in immune thrombocytopenia (ITP) but have only rarely been successful in autoimmune haemolytic anaemia (AIHA). There are a few reports of higher doses of i.v. Ig being more effective in AIHA. We have treated two patients with AIHA with high-dose i.v. Ig (0.5 g/kg/day for 5 days). In one patient with an associated ITP a prompt rise in platelet count but no change in Hb concentration occurred. The second patient with AIHA associated with chronic lymphatic leukaemia showed a prompt response, with a rise in Hb concentration and fall in plasma bilirubin. The poor response to i.v. Ig seen in AIHA may be related to the expansion of the reticulo-endothelial system seen in AIHA but not ITP. Clearance of antibody-coated red cells and platelets may occur at different rates and/or sites in the reticulo-endothelial system and this may account for the differential response seen in case 1. Higher doses of i.v. Ig, in the range 0.5-1 g/kg/day for 5 days, are required in AIHA, particularly if significant splenomegaly is present, and may be effective in refractory cases.
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PMID:High-dose intravenous immunoglobulin in the treatment of autoimmune haemolytic anaemia. 325 Jul 87

A 64-year-old man was found to have a hemolytic anemia with a hematocrit of 0.28 (28%) during a routine evaluation. One month before this his hematocrit had been normal. Further studies revealed a myelodysplastic syndrome and acquired hemoglobin H disease. Eighteen months later this transformed into acute megakaryoblastic leukemia with disappearance of hemoglobin H, and shortly thereafter he had myelofibrosis develop. Acquired hemoglobin H disease, which is an alpha-thalassemia-like syndrome, results in the formation of an unstable hemoglobin composed of beta chain tetramers. This condition has been associated with preleukemia, sickle cell anemia, and hematologic malignancies. Although idiopathic myelofibrosis also has been described as a setting in which this thalassemic syndrome occurs, the present case is unusual in that the myelofibrosis was preceded by refractory anemia with leukemic transformation.
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PMID:Myelodysplastic syndrome with acquired hemoglobin H disease. Evolution through megakaryoblastic transformation into myelofibrosis. 327 51

Two different pathogenic effects of the Friend ecotropic murine leukemia virus (F-MuLV) were distinguished by serial examinations of hematocrits and reticulocyte counts of IRW mice inoculated as newborns. F-MuLV induced hemolytic anemia with increased levels of erythropoiesis, which was detectable as early as 13 days of age, whereas blocked erythroid differentiation, associated with erythroleukemia, was apparent only after 30 days of age. Using strains of Friend-MuLV with different virulences, we constructed recombinant viruses that allowed us to map the hemolytic effect and the ability to induce rapid erythroleukemia to different regions of the viral genome. Moreover, the ability of the virus to induce rapid erythroleukemia appeared to be independent of the presence of severe early hemolytic anemia.
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PMID:Hemolytic anemia and erythroleukemia, two distinct pathogenic effects of Friend MuLV: mapping of the effects to different regions of the viral genome. 346 51


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