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

Twenty cats with a chronic progressive polyarthritis were studied. The disorder occurred exclusively in male cats, and all but six of the cats were between 1.5 and 5.0 years of age. There were two forms of the disease as determined by radiographic changes: joint instability and deformity, and clinical course. The most prevalent form of the disease was characterized by osteopenia and periosteal new bone formation surrounding affected joints. Marginal periarticular erosions and collapse of the joint spaces with fibrous ankylosis occurred with time, but joint instability and deformities were not seen. The second form of the disease was characterized by severe subchondral marginal erosions, joint instability, and deformities. The periosteal proliferative form resembled Reiter's arthritis of man, and the deforming type resembled human rheumatoid arthritis. The disease began as tenosynovitis and synovitis, with subsequent changes in the articular cartilage and periosteal bone. Histopathologic changes in these cats were similar to those occurring in both chronic Reiter's and rheumatoid arthritis of man. Chronic progressive polyarthritis of cats was not caused by identifiable bacteria or mycoplasma, but was etiologically linked to feline leukemia virus (FeLV) and feline syncytia-forming virus (FeSFV) infections. The FeSFV was isolated from the blood or was detected by a serologic test in all of the cats with the disease, whereas FeLV was isolated or identified by immunofluorescence technique in 60% of the cats. The arthritis could not be reproduced by inoculation of cell-free cynovial tissue from diseased cats or with tissue culture fluid containing FeSFV and FeLV isolates. It was postulated that arthritis was an uncommon manifestation of FeSFV infection that occurred in predisposed male cats. Feline leukemia virus may not have been directly involved in the disease, but may have acted in some way to potentiate the pathogenic effects of FeSFV.
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PMID:Feline chronic progressive polyarthritis. 625 Apr 22

Aggregation of the receptor for IgE on mast cells, basophils, and a tumor analog, rat basophilic leukemia (RBL) cells, induces a calcium-dependent degranulation of the cells. We have measured the membrane potential (delta psi) of RBL cells during this reaction by using the tetraphenylphosphonium ion (Ph4P+) equilibration technique. We observed a 20-45% reduction in ionophore-sensitive Ph4P+ accumulation. The phenomenon persisted under conditions expected to collapse the mitochondrial membrane potential, consistent with the effect being due to a change in delta psi of the plasma membrane. We estimated that the change reflects a depolarization of 20 mV (from -90 to -70 mV, interior negative). Whereas degranulation fails to occur in the absence of external Ca2+, this was not true of the depolarization, indicating that the latter was not a consequence of secretion. When aggregation of the receptor is induced by reaction of the cell-bound IgE with a multivalent antigen, the secretory reaction can be halted by adding a univalent hapten. In this case, complete repolarization occurs. Equivalent depolarization was observed in the absence of Na+ but was diminished when both Ca2+ and Na+ were absent. Together, the data suggest that aggregation of the receptor opens ion channels and that the latter disappear promptly when the receptors are disaggregated. It is plausible that formation of these channels leads to the entry of Ca2+ and is an early and critical consequence of the aggregation of the receptors, thereby leading to degranulation.
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PMID:Crosslinking of the receptors for immunoglobulin E depolarizes the plasma membrane of rat basophilic leukemia cells. 631 May 90

A hypercalcemic patient with adult T-cell leukemia was treated with deoxycoformycin (DCF) in a dose of 5 mg/m2 daily for three days. Several days later, severe thrombocytopenia appeared abruptly and then microangiopathic hemolytic anemia ensued. Subsequently, renal failure and hypertension developed, and the patient died seven weeks after DCF therapy. Needle necropsy of the kidney showed glomerular damage including swelling of endothelial cells, mesangiolysis and segmental collapse. This is the second reported case of hemolytic-uremic syndrome due to DCF.
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PMID:Hemolytic-uremic syndrome due to deoxycoformycin: a report of the second case. 754 51

Having noted symptomatic osteoporotic vertebral collapse in young adult survivors of childhood malignancy, bone mineral density (BMD) was examined at three sites by dual-energy X-ray absorptiometry in 64 patients treated in childhood for intracranial malignancy (group 1; n = 21) or acute leukaemia (group 2; n = 43). Patients in group 1 were selected for growth hormone deficiency (GHD) by auxological and biochemical criteria before the end of puberty (Tanner stage V). Seven patients (six men; mean (+/- SEM) age at study, 28.0 +/- 2.9 years; mean age at diagnosis, 8.7 +/- 1.5 years) in this group had been treated with human pituitary growth hormone (GH) for 1-12 years; and 14 patients (nine men; mean age at study, 26.8 +/- 1.0 years; mean age at diagnosis, 10.7 +/- 1.4 years) had not received GH. Bone densities in group 1 were normal in the GH-treated patients at the femoral neck (98.4 +/- 3.8% of control), lumbar spine (100.4 +/- 6.1% of control) and Ward's triangle (101.0 +/- 6.1% of control) but markedly reduced in the untreated group (femoral neck, 81.2 +/- 2.6% of control (p = 0.002); lumbar spine, 79.1 +/- 4.1% of control (p = 0.04); Ward's triangle, 80.1 +/- 3.6% of control (p = 0.01)). The majority of patients in group 2 had been treated for acute lymphoblastic leukaemia (ALL) and were in three subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineralization after treatment of growth hormone deficiency in survivors of childhood malignancy. 794 25

Cytosine arabinoside is usually considered to be lethal by incorporation into DNA followed by chain termination. Recently, we have reported that the radical scavenger N-acetyl-cysteine (NAC) protects cultured clonogenic AML blast cells from the lethal affects of Ara-C if given before the drug. This observation provides indirect evidence that toxic reactive oxygen intermediates (ROI) are generated in AML blast cells following Ara-C-induced damage to DNA. In the present paper we present evidence in support of this hypothesis. Using flow cytometry and multiple fluorescent probes for live cell function, we have mapped a sequence of discrete stages that occur during Ara-C cytotoxicity. An early event was the increased generation of ROI. Initially this oxidative stress was countered by an increase in the cellular content of reduced glutathione (GSH), but cells then underwent an abrupt transition to a state characterized by low GSH and very high ROI generation indicative of collapse of cellular redox balance. Next, the capacity to maintain low intracellular ionized calcium was lost, probably due to lipid peroxidation at membrane sites of calcium regulation. Finally, surface membrane integrity was lost. Concurrent measurements of clonogenic cell survival insured the relevance of these flow cytometry measurements to the stem cell population. We used OCI/AML-2 cells transfected with bcl-2 to look for the place in this sequence where bcl-2 protein protects cells against apoptosis; bcl-2 transfectants showed an increase in ROI generation similar to controls, but were able to maintain GSH levels in the face of this oxidative stress. We conclude that oxidative stress plays a major role in Ara-C toxicity, and that bcl-2 protein protects cells by maintaining cellular redox balance in a reducing state. These studies complement previous work showing how regulators of AML growth affect the sensitivity of blast cells to Ara-C by changing the concentration or stability of bcl-2 protein.
Leukemia 1996 Jul
PMID:Generation of reactive oxygen intermediates after treatment of blasts of acute myeloblastic leukemia with cytosine arabinoside: role of bcl-2. 868 94

Menopause, conventionally defined as the permanent cessation of menstruation as a result of loss of ovarian follicular activity, is biologically expressed by the collapse of plasma estradiol levels and increased plasma levels of the gonadotrophins FSH (follicle stimulating hormone) and LH (luteinizing hormone). At present, estimation of the ovarian follicle reserve is based on endocrine capacity tests of the ovaries, with increased FSH representing the first sign of exocrine ovarian failure. We report the case of one of our amenorrhoeic patients after chemotherapy, total body radiation and allogenic bone marrow transplantation for acute immunoblastic leukaemia. This patient was included in an in vitro fertilization with oocyte donation (IVF-OD) programme for iatrogenic premature ovarian failure with increased FSH levels. Instead of high levels of gonadotrophins, this young woman recovered spontaneous follicular development, benefited from standard IVF with her own oocytes and brought a twin pregnancy to term. This observation shows that a high FSH level is not a definitive prediction of ovarian exocrine capacity. In young women of child-bearing age such as these wanting a child and showing signs of endogenous estrogen impregnation, evaluation of the existence and quality of follicular development is an important factor.
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PMID:[Recovery of ovarian function after radiation-induced menopause. Does follicle-stimulating hormone (FSH) have a definitive prognostic value?]. 897 71

Cryptococcus neoformans typically causes an insidious illness with symptoms related to meningitis or to lung involvement. This is the first reported sudden death due to cryptococcosis, which occurred in a child with leukemia that was in remission. The child had suddenly looked seriously ill and cried with abdominal pain and then died within 25 minutes. Disseminated cryptococcal infection of the lungs, heart, and pancreas was an unexpected finding at autopsy. This clinical experience raises the question whether fungal infections should now be considered in immunosuppressed patients who have an apparent septic collapse.
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PMID:Sudden death due to disseminated cryptococcosis in a child with leukemia in remission. 940 18

Vertebral body collapse and back pain are an unusual presentation for childhood leukemia. This report is intended to promote greater awareness that acute lymphocytic leukemia can cause significant back pain in children without other systemic symptoms. We describe four cases in which patients with acute lymphocytic leukemia presented with back pain and vertebral compression fractures. All of the patients were initially misdiagnosed. No patient had neurologic compromise, despite extensive vertebral body collapse. The back pain was relieved after chemotherapy.
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PMID:Childhood leukemia presenting with back pain and vertebral compression fractures. 1022 99

Acute lymphatic leukemia presenting with bone pain and spine involvement is a recognized clinicopathologic complex that can mimic a wide range of orthopaedic conditions. Bone pain as the presenting complaint is common, with a reported incidence of 27% to 50%. Radiologic abnormalities associated with leukemia in children has been described previously. In the literature, the incidence of spinal involvement is controversial, but there is agreement that the spine is less commonly involved than are the long bones. At the onset of the disease, only 10% of children have normal peripheral blood counts. If the patient has spinal involvement and a normal leukocyte count, the diagnosis is often unclear. Only three of these patients have been described in the literature; this article adds one more patient with acute lymphatic leukemia with back pain as the main symptom, vertebral collapse, and a normal peripheral blood cell count at the time of initial presentation. It illustrates that delay in diagnosis frequently occurs, with the classic features of the disease being uniformly absent.
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PMID:Vertebral collapse and normal peripheral blood cell count at the onset of acute lymphatic leukemia in childhood. 1064 13

Recent studies showed that arsenic trioxide (As2O3) could induce apoptosis and partial differentiation of leukemic promyelocytes. Here, we addressed the possible mechanisms underlying these two different effects. 1.0 microM As2O3-induced apoptosis was associated with condensation of the mitochondrial matrix, disruption of mitochondrial transmembrane potentials (DeltaPsim) and activation of caspase-3 in acute promyelocytic leukemia (APL) cells regardless of their sensitivity to all-trans retinoic acid (ATRA). All these effects were inhibited by dithiothreitol (DTT) and enhanced by buthionine sulfoximine (BSO). Furthermore, BSO could also render HL60 and U937 cells, which had the higher cellular catalase activity, sensitive to As2O3-induced apoptosis. Surprisingly, 1.0 microM As2O3 did not induce the DeltaPsim collapse and apoptosis, while 0.1 microM As2O3 induced partial differentiation of fresh BM cells from a de novo APL patient. In this study, we also showed that 0.2 mM DTT did not block low-dose As2O3-induced NB4 cell differentiation, and 0. 10.5 microM As2O3 did not induce differentiation of ATRA-resistant NB4-derived sublines, which were confirmed by cytomorphology, expression of CD11b, CD33 and CD14 as well as NBT reduction. Another interesting finding was that 0.10.5 microM As2O3 could also induce differentiation-related changes in ATRA-sensitive HL60 cells. However, the differentiation-inducing effect could not be seen in ATRA-resistant HL60 sublines with RARalpha mutation. Moreover, low-dose As2O3 and ATRA yielded similar gene expression profiles in APL cells. These results encouraged us to hypothesize that As2O3 induces APL cell differentiation through direct or indirect activation of retinoic acid receptor-related signaling pathway(s), while DeltaPsim collapse is the common mechanism of As2O3-induced apoptosis.
Leukemia 2000 Feb
PMID:Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia. 1067 43


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