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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of elderly patients, who suffer from leukemia must not be standardized. Impaired bone marrow function, cardiovascular disease and other organopathias require an individually adapted therapy. The aim of treatment should be a good quality of life and not a remission at any price. Aggressive therapy in cases of acute leukemia with little progress should be avoided in favour of symptomatic treatment. CLL are treated in the progressive state of disease. Haemolytic anaemia and recurrent infections may complicate the course of CLL. CML is not a disease of old age but when it occurs intermittent therapy with cautious dosage is preferable to a continuous therapy.
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PMID:[Treatment of leukemia in the elderly (author's transl)]. 3 67

When mated to normal BALB/c partners, male and female NZB mice transmitted auto-immune haemolytic anaemia to three generations of their hybrid progeny. Red cell auto-antibodies (positive Coombs tests) were detected, on average, 11 months later in the F1 hybrids than in the parental strain, and the course of the disease was protracted. In explicably, the auto-immune reactions then appeared progressively earlier in successive generations of both croses. The Coombs reactions of the F1 and F2 hybrids were often weak and inconsistent, while those of F3 offspring showed the strong and stable picture typical of NZB mice. The incidence of auto-immune disease in each generation, although similar in the reciprocal crosses, indicated that the pattern of inheritance was very complex. The hybrids did not develop the lymphoid type B reticulum cell neoplasia which characterizes auto-immune NZB mice. Instead, and irrespective of Coombs status, they had lymphocytic leukaemias, lung adenomas, hepatomas and type A reticulum cell neoplasms of the liver. Murine leukaemia virus was identified electronmicroscopically in F1 embryos, and in all the adults examined. It was also isolated from leukaemic spleen cells passaged briefly in vivo, and from malignant hepatic (reticulum) cells maintained in vitro. These isolated were leukaemogenic in newborn BALB/c, NZB, and F1 hybrid recipients, but did not induce or accelerate positive Coombs reactions. Only a small proportion of the hybrids had significant glomerulonephritis, and overt kidney disease was minimal. The lesions were not confined to Coombs-positive mice. Possible links between auto-immunity, malignancy, and virus infection in NZB mice are discussed in the light of these results.
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PMID:Transmission of auto-immune haemolytic anaemia and murine leukaemia virus in NZB-BALB/c hybrid mice. 18 Nov 87

F1(BALB/c X NZB)hybrid progeny derived by ovum transplantation were used to study the transmission of auto-immune haemolytic anaemia and murine leukaemia virus (MuLV) by male New Zealand black (NZB) mice. Fertilized ova, collected from the normal BALB/c partners 3 1/2 days after mating, were transferred to other, surrogate, BALB/c mothers, which then carried, delivered, and reared the hybrid young. This technical manoeuvre effectively closed the congenital transplacental route theoretically available to any infectious MuLV originating from the NZB father. Nevertheless, such progeny developed exactly the same profile of auto-immune haemolytic disease and the same range of diverse malignancies as their normally-derived F1(BALB/c X NZB) counterparts, and they carried type C MuLV particles readily detectable by electronmicroscopy. We concluded, therefore, that both the auto-immunity and virus were transmitted before placentation, presumably by the NZB male at fertilization, and probably as genetic information.
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PMID:Transmission of auto-immune haemolytic anaemia and murine leukaemia virus in F1 (BALB/c X NZB) hybrid mice derived by ovum transplantation. 18 67

Heterogeneous clinical features of inherited hemolytic anemia due to pyruvate kinase (PK) deficiency were observed in three related homozygous patients. Erythrocytes were separated into old and young cells by means of density-layer centrifugation using a new supporting medium: Stractan-Urografin gradients. Those fractions containing older RBC disclosed defective PK which resulted in an impaired metabolism. Following an intake of chloramphenicol the clinical course of one female family member converted to acute monocytic leukemia. Thus, the report of a PK instability trait, in one family member associated with pancytopenia which converted in leukemia, suggests that inherited red cell enzyme deficiency might be also an expression of the vulnerability of the hematopoietic stem cells.
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PMID:[Inherited hemolytic anemia due to pyruvate kinase deficiency: II. Density-layer centrifugation of erythrocytes (author's transl)]. 28 28

One hundred consecutive patients with hemoglobin concentration less than 3.5 g/dL (hematocrit reading, less than 10%) were admitted to the University of Baghdad Teaching Hospital, Iraq, during a 30-month period. Twenty-eight patients had aplastic anemia, 27 had leukemia or other hemopoietic malignancies, 16 had chronic renal failure, eight had iron-deficiency anemia, eight had hemolytic anemia, seven had thalassemia major, and six had other conditions. Twenty-three patients died within seven days of admission, mostly due to the underlying disease or complications thereof. Heart failure developed in ten patients, and five had retinal exudates and hemorrhages attributed to severe anemia. Arrhythmias and ECG abnormalities were noted in 20 of 68 patients. Blood transfusion was instituted in all but three patients, whose anemia was corrected with specific therapy without blood transfusion. The tolerance of the 100 patients to such severe anemia was remarkable.
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PMID:Severe anemia. Clinical observations in 100 patients with very low hemoglobin levels. 47 23

In cold autoimmune hemolytic anemia, the causative autoantibodies (cold agglutinins) are most reactive at low temperatures. The anti-I type of cold agglutinin is found in cold hemagglutination disease and in hemolytic anemia secondary to malignant lymphoma, leukemia, or atypical pneumonia. The anti-I type of cold agglutinin is found in many patients with infectious mononucleosis and in an occasional patient with other lymphoproliferative disorders. Paroxysmal cold hemoglobinuria, a disorder in which exposure to cold temperatures triggers massive hemolysis, is characterized by a unique biphasic cold autoantibody called the Donath-Landsteiner antibody. By way of summary and review of this and the two previous articles in this series, table 4 presents a practical approach to diagnosis of the autoimmune hemolytic anemias.
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PMID:Autoimmune hemolytic anemia. 3. Cold antibody type. 48 74

Platelet antibodies either bound to the surface of platelets or free in the serum were sought in patients who had low platelet counts for a variety of reasons. They were detected by finding excess IgG on the surface of washed platelets either directly or after incubation of the serum with normal platelets. The technique used was a modification of that described recently (Dixon et al, 1975) in which the greater the amount of anti-IgG consumed by the reaction with platelets the less the subsequent lysis of sheep red cells coated with IgG. This test could be calibrated by adding known quantities of IgG to the antisera and thus the amount of bound IgG could be measured. Platelets from normal donors and those with thrombocytopenia due to non-immunological causes such as aplastic anaemia or acute leukaemia were found to have 15-70 ng IgG/10(7) platelets (mean 53 ng). 37 out of 38 thrombocytopenic patients in whom immune destruction of platelets was suspected were found to have excess IgG on their platelets ranging from 70 to 720 ng/10(7) (mean 297 ng, P less than 0.001) and there was a significant inverse correlation between this amount and the platelet count (r = 0.85, P less than 0.001). Antibody in the serum was found in 14 of 22 patients with 'idiopathic' thrombocytopenic purpura (ITP), three of four patients with underlying lymphoma and in all five cases of systemic lupus erythematosus (SLE). Four non-thrombocytopenic patients with autoimmune haemolytic anaemia (AIHA) due to IgG on the red cells were also studied and were shown to have no increase in platelet-bound IgG. Our results confirm the work of Dixon et al (1975) that platelet antibody as excess IgG can be readily detected on the surface of platelets in patients with immune thrombocytopenia. The clinical implications of these findings are discussed.
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PMID:Platelet antibodies in thrombocytopenic patients. 86 90

The case of a 27-year-old woman with pancytopenia, revealing acute monocytic leukaemia and haemolytic anaemia, is described in detail. The underlying cause for the red cell destruction was found to be a pyruvate kinase (PK) instability. Further investigation into three generations of her family (n = 12) disclosed a hereditary PK instability. This was proven by performing biochemical studies to elucidate mutants representing a structurally defective enzyme. Since conversions of pancytopenia with acquired red cell enzyme deficiency into leukaemia have been described, our observation emphasizes that hereditary red cell enzymopathy might also be associated with adult acute leukaemia.
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PMID:Haemolytic anaemia with hereditary pyruvate kinase instability developing acute leukaemia. 105 38

A 76-year-old man with spontaneous rupture of a hemangiosarcoma of the spleen, together with a review of 49 previously reported patients with splenic hemangiosarcoma are presented. Twenty-three were women and 27 were men. All but 3 were adults. Fiften were 50-59 years of age. The symptomatology was nonspecific. Three patients developed microangiopathic hemolytic anemia. Spontaneous rupture occurred in 17 cases (34%). Metastases occurred in 42 cases; they were primarily hematogenous and most often in the liver. Lymph node involvement, however, was present in 13 cases. The prognosis of untreated splenic hemangiosarcoma is poor. Three of 25 patients survived a year or more after the initial onset of symptoms. Splenectomy before rupture is advisable, since 5 of 19 patients survived at least 1-5 years. It is suggested that hemangiosarcoma be considered in patients with: 1) splenomegaly without evidence of malignant lymphoma or leukemia, 2) splenomegaly with microangiopathic hemolytic anemia, and 3) unexplained intraperitoneal hemorrhage.
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PMID:Hemangiosarcoma of spleen with spontaneous rupture. 116 82

The syndrome of CD8 hyperlymphocytosis with neutropenia is a heterogeneous disorder ranging from reactive benign state to neoplastic pathology. The prognosis for LGL (Large Granular Lymphocyte) leukemia depends likely on its phenotype:-NK phenotype, extremely poor prognosis and rapidly fatal-T phenotype (CD8+), chronic disease with slow progression. Here, we report four cases of CD8+ hyperlymphocytosis with neutropenia, which are CD2+/-, CD3+, CD4-, CD8+, CD16-, CD56+/-, CD57+ phenotype. These lymphocytic proliferations were associated with clonal rearrangement of T-cell receptor b gene. In two cases, characteristic blood hyperlymphocytosis appeared only after splenectomy, but retrospective bone marrow analysis showed that the CD8+, CD57+ lymphocyte proliferation previously existed. These lymphocytes had a low natural killer activity against K562 cell line. HTLV1 proviral sequence was not integrated in leukemic cell DNA. This monoclonal pathology has a chronic clinical course, with a thirteen year evolution in one case. Splenectomy did not correct neutropenia but allowed the control of hemolytic anemia and auto-immune thrombocytopenia in one case.
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PMID:[Lymphoproliferative syndrome with granular lymphocytes of CD8+ phenotype: a clonal pathology with a chronic course]. 128 65


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