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)

The coexistence of a myeloma and Paget's disease in the same patient is only rarely reported in the published literature. The frequency of such an association was studied when reviewing 3 cases observed by the authors: an IgG myeloma discovered following a spasmodic paraplegia in a patient with Paget's disease; a patient who was found to have a myeloma, a polynuclear neutrophil leukemia, and Paget's disease; and an IgG myeloma in a patient with probable localized Paget's disease. The incidence of the association myeloma-Paget's disease is much lower than that of sarcomatous degeneration. It should be determined precisely, however, as our future conception of the reciprocal relationship between the two diseases is greatly dependent on this information. Furthermore, the very few cases reported, and their lack of homogenicity, are the reasons why most authors feel that the association of myeloma and Paget's disease as pure coincidence. Many new cases, however, have been recently reported. The problem of the significance of the association of Paget's disease and macroglobulinemia or other monoclonal gammapathies has still to be solved.
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PMID:[The association of a myeloma and Paget's disease (author's transl)]. 43 30

Three cases of unusual traumatic spinal cord injuries are reported. The cases were referred to the neurosurgical unit of Nancy, one tetraplegia and one paraplegia caused by transfixing wounds which were overlooked after the injury. The transfixing wound caused an associated meningitis with tetraplegia, and in the second case the initial small plural effusion associated with paraplegia even, in a very short while, evoked a possible diagnosis of leukaemia amongst others, until the knowledge of trauma had been ascertained, the child being then immediately transferred to the neurosurgical unit. Spanking, in the last case, was the cause of an important luxation of T12-L1, at first with a complete paraplegia, and was associated with the fact that the child was only seen a few days after by a doctor and immediately referred. The child made a full recovery from his paraplegia.
Paraplegia 1978 May
PMID:Three unusual cases of spinal cord injury in childhood. 73 82

Twenty-three children surviving more than 5 years from the diagnosis of leukemia, lymphoma, or malignant histiocytosis were evaluated for clinical evidence of central nervous system disease. Severe impairment, consisting of seizures, paraplegia, and dementia was present in 4, all of whom received methotrexate (MTX) and other agents for 2 to 7 years. Brain biopsies in 3 of these children showed white-matter gliosis and no evidence of viral or other infections or leukemic infiltrates. Of the remaining children 10/19 were found to have mild clinical or EEG abnormalities. All had received i.v. MTX with other drugs for 2-6 years; 5 did not receive cranial irradiation. Common to all impaired patients was the administration of intravenous methotrexate in relatively high doses over a prolonged period of time. Impairment in nervous system function may present as a spectrum of deficiencies, with the most severe resulting in death, or as in the 4 patients described here, profound dementia and dependence. Less dramatic changes in functioning, may, however, result from various combinations of chemotherapy and radiation therapy. Methods of assessing their etiology and impact on survivors need now to be devised.
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PMID:Effects of chemotherapy on the central nervous system. A study of parenteral methotrexate in long-term survivors of leukemia and lymphoma in childhood. 76 54

This paper describes the case history of a 43 year-old patient with so-called primary reticulum cell sarcoma of the brain. The CSF contained cells suggestive of leukaemia which in view of an assumed myelofibrosis, initially seemed also possible to originate from a haematopoietic focus. The patient complained of intermittent violent headaches, which were controlled by spinal taps to release highly cellularised CSF under high pressure and by intrathecal MTX injection, every 4-6 weeks over a period of 4.5 years. In the terminal stage the patient developed paraplegia which, partly on the basis of neuropathological findings, was ascribed to the large accumulated dose of MTX. The tumour proved to be localised in the fornix; the localisation adjacent to the ventricular system made the intermittent cell eruptions in the CSF possible. On the basis of an erroneous diagnostic assumption, a therapy was instituted which resulted in a survival of 6.5 years, which is exceptionally long for a patient with 'primary reticulum cell sarcoma' of the brain.
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PMID:A patient with so-called primary reticulum cell sarcoma of the brain with 6.5 years' survival, treated as 'meningeal leukaemia'. 80 Sep 69

A patient who developed paraplegia following the intrathecal instillation of methotrexate is discribed. The ten previously reported cases of this unusual complication are reviewed. The following factors appear to predispose to the development of this complication: abnormal cerebrospinal dynamics related to the presence of central nervous system leukemia, and epidural cerebrospinal leakage; elevated cerebrospinal fluid methothexate concentration related to abnormal cerebrospinal fluid dynamics and to inappropriately high methotrexate doses based on body surface area calculations in older children and adults; the presence of neurotoxic preservatives in commercially available methotrexate preparations and diluents; and the use of methotrexate diluents of unphysiologic pH, ionic content and osmolarity. The role of methotrexate contaminants, local folate deficiency, and cranial irradiation in the pathogenesis of intrathecal methotrexate toxicity is unclear. The incidence of neurotoxicity may be reduced by employing lower doses of methotrexate in the presence of central nervous system leukemia, in older children and adults, and in the presence of epidural leakage. Only preservative-free methotrexate in Elliott's B Solution at a concentration of not more than 1 mg/ml should be used for intrathecal administration. Periodic monitoring of cerebruspinal fluid methotrexate levels may be predictive of the development of serious neurotoxicity.
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PMID:Paraplegia following intrathecal methotrexate: report of a case and review of the literature. 94 93

A highly aggressive subclone of the human CALLA+C mu+ pre-B acute lymphoblastic leukemia (ALL) cell line NALM-6 (designated NALM-6-UM1) caused disseminated and fatal leukemia in CB.17 mice with severe combined immunodeficiency (SCID). An intravenous challenge with 1 x 10(6) (NALM-6-UM1 cells caused 15 of 27 (56%) SCID mice to become paraplegic at 31 +/- 2 days (median = 33 days) and 27 of 27 (100%) mice to die of disseminated leukemia at 38 +/- 1 days (median = 39 days). We used this SCID mouse model of aggressive human pre-B ALL to evaluate the in vivo antileukemic efficacy of B43 (anti-CD19)-pokeweed antiviral protein (PAP) immunotoxin. A 3-day treatment with nontoxic doses of B43-PAP markedly reduced the incidence of paraplegia and improved event-free survival (EFS) in SCID mice challenged with 1 x 10(6) NALM-6-UM1 pre-B ALL cells, as reflected by significantly higher cumulative proportions of mice free of paraplegia or alive at 1 to 7 months, as compared with phosphate-buffered saline (PBS) treated control mice. The Kaplan-Meier estimates and standard errors of the probability of developing paraplegia after inoculation of 1 x 10(6) NALM-6-UM1 cells was 64% +/- 10% for PBS-treated mice (median time to paraplegia = 37 days) (N = 27), 18% +/- 8% for mice treated with 15 micrograms B43-PAP (5 micrograms/mouse/d x 3 days) (N = 23) and 5% +/- 5% for mice treated with 30 micrograms B43-PAP (10 micrograms/mouse/d x 3 days) (N = 21). While 27 of 27 PBS-treated control SCID mice died of leukemia at 38 +/- 1 days (range = 24 to 54 days), only 16 of 44 B43-PAP-treated mice developed leukemia at 74 +/- 12 days (range = 30 to 182 days), consistent with greater than or equal to 6 logs kill of clonogenic NALM-6-UM1 cells in 64% of SCID mice. The Kaplan-Meier estimates and standard errors of the probability of long-term EFS after inoculation of 1 x 10(6) NALM-6-UM1 cells were 65% +/- 10% for mice treated with 15 micrograms B43-PAP and 60% +/- 11% for mice treated with 30 micrograms B43-PAP with a median survival time of greater than 7 months for both groups. In contrast, neither unconjugated B43 monoclonal antibody nor the anti-T-cell immunotoxin G17.2 (anti-CD4)-PAP decreased the incidence of paraplegia or improved EFS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:In vivo efficacy of B43 (anti-CD19)-pokeweed antiviral protein immunotoxin against human pre-B cell acute lymphoblastic leukemia in mice with severe combined immunodeficiency. 137 67

Hairy cell leukemia complicating hemolytic anemia developed in a 46-year-old woman. Morphologically and cytochemically typical hairy cells were found to express both CD20 and CD2 antigens. Expression of surface IgG of kappa-chain type and the rearrangement of Ig but not T-cell receptor beta genes confirmed a B-cell origin of the leukemia. Blood transfusion was followed by disappearance of the hemolysis and a marked improvement of the leukemia. However, the patient developed progressive spastic spinal paraplegia about seven months after transfusion and was diagnosed as having HTLV-I associated myelopathy (HAM) by the demonstration of HTLV-I antibodies in serum and cerebrospinal fluid. HTLV-I infection via the transfusion may have been involved in the hematologic improvement seen in this patient. Autopsy showed demyelination, vacuolar degeneration, gliosis, and perivascular cuffing in the white matter of spinal cord without evidence of leukemic infiltration.
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PMID:HTLV-I associated myelopathy (HAM) after blood transfusion in a patient with CD2+ hairy cell leukemia. 167 Sep 75

A 42-year-old woman was diagnosed as having acute myelogenous leukemia (M 2 of FAB classification) in May, 1985. Complete remission was achieved with the BHAC-DP therapy (BHAC, daunomycin and prednisolone). Whole skull irradiation and intra thecal chemotherapy were performed by way of prevention. In 1986, she developed her visual disturbance and paraplegia. Myelography and metrizamide CT indicate intraspinal and meningeal infiltration of leukemic cells in the upper thoracic spine. Leukemic cells were found in the cerebrospinal fluid but not in the bone marrow. Complete remission was obtained by irradiation and intrathecal chemotherapy. In Dec. 1986, Ommaya tubing was repeated. Hematological and neurological examinations showed no evidence of malignancy for 3 years. In Oct. 1988, she admitted to our hospital for the maintenance of the remission state, and died of sepsis. The result of autopsy revealed no leukemic cells in her CNS. It is said the intraspinal infiltration of leukemic cells is rather rare. As it is said the intrathecal injection of anti-leukemic agents is not effective for the intraspinal infiltration, irradiation should be needed. Therefore it is very important to critically differentiated intraspinal from meningeal infiltration. Furthermore, Ommaya tubing is effective in order to maintain remission in a patient with CNS leukemia.
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PMID:[Acute myelogenous leukemia with recurrence of the meningeal, spinal cord and the optic nerve infiltration with remission induction by Co therapy and maintained by intrathecal chemotherapy with Ommaya reservoir]. 259 57

We describe a case of adult T-cell leukemia (ATL) with vertebral bone invasion, who developed acute paraplegia and responded well to irradiation and combined chemotherapy. A 36-year-old man born in Tsushima Island was admitted to our hospital in May 1987, because of a sudden onset of paraplegia, hypesthesia below the level of 7th thoracic vertebra and vesicorectal disturbance. The white blood cell count was 9,500/microliter with 16% of abnormal lymphocytes showing lobulated nuclei. The surface marker analysis revealed that CD3, CD4, CD8 and CD25 positive cells were 88.1, 83.9, 6.4 and 1.3% of the peripheral mononuclear cells, respectively. Anti-ATLA antibody was positive. Serum calcium level was elevated. Bone scintigraphy showed multiple vertebral bone lesions. Vertebral bone mass and a compressed spinal cord in the 7th thoracic level were confirmed by CT scanning and MR imaging. Cerebral spinal fluid was negative for tumor cells. A diagnosis of ATL was made. Irradiation and combination chemotherapy improved bone lesions and neurological signs and the disease was well controlled by maintenance chemotherapy up to the present (August, 1988).
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PMID:[Adult T-cell leukemia with vertebral bone tumor and acute transverse myelopathy]. 279 86

Transient or permanent paraplegia after the use of intrathecal (IT) methotrexate (MTX) or cytosine arabinoside (Ara-C) for treatment or prophylaxis of patients with meningeal leukemia is an unusual complication, with an incidence of less than 3% among such patients. Only 15 cases involving IT MTX have been documented and even fewer with IT Ara-C. Three patients were studied who developed permanent or ascending myelopathy from treatment of their leukemia or rhabdomyosarcoma with IT chemotherapy. The patients' ages ranged from 7 to 62 years. Two of the three patients had electromyographic examinations. These revealed a primary motor neuron degeneration or a polyradiculopathy, superimposed on a mild axonal peripheral neuropathy associated with vincristine therapy. This is consistent with other electromyographic studies. Two of the patients showed an elevation of the cerebral spinal fluid (CSF) protein before development of paraplegia; one also showed a rise in myelin basic protein associated with his myelopathy. Neuropathologic findings suggest demyelination as the primary process leading to myelopathy. Increasing evidence has shown that total CSF protein, or more specifically, the myelin basic protein, may be elevated before development of paraplegia. Routine serial testing of the CSF for total protein could be used as a screening test during therapy.
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PMID:Paraplegia and quadriplegia after intrathecal chemotherapy. 321 64


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