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)

Compared to leukemia, malignant lymphoma and other hematogenous tumors, multiple myeloma rarely metastasizes to the central nervous system. Intracerebral metastasis without involvement of the cranium itself is rarer. We report a case of Ig-G k-type multiple myeloma with metastasis to the left frontal lobe extending to the right basal ganglia without involvement of the cranium. A 71-year-old male complained of exertional dyspnea and lumbago. His laboratory data revealed hyperproteinemia and an abnormal increase in Ig-G (6117mg/dl) in his serum. Serum protein immunoelectrophoresis revealed an IgG k-type band, and Bence-Jones protein was detected in his urine. MMPP, VMCP, VIPP and MP chemotherapy was given, and serum IgG level decreased to a normal range. 21 months after his first admission, incontinence, disorientation, gait disturbance and apathy developed. CT-scan showed an isodense lesion with massive edema in the left frontal lobe and right basal ganglia. On MRI, a Gd-DTPA enhancing lesion was detected extending from the left frontal to the opposite frontal lobe through the splenium. No abnormal skull punched out lesions were noted. Left frontal lobectomy was performed. Histopathology revealed plasmablastic myeloma cells with clear nucleole and eccentric nucleus in the cerebrum. He was diagnosed as having intracerebral metastasis of multiple myeloma without involvement of the cranium. Unfortunately, he died of pancytopenia and pneumonia. Our case suggests the possibility of metastasis via blood into the cerebrum.
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PMID:[A case of multiple myeloma with intracerebral metastasis]. 140 49

In this report, we described a case of acute lymphoblastic leukemia with leukoencephalopathy that responded to oxygenation under hyperbaric pressure (OHP) therapy. The patient was 6 year-old female who was diagnosed as acute lymphoblastic leukemia (ALL) one year and 9 months earlier. After the first relapse of the central nervous system (CNS) leukemia, intrathecal administration of methotrexate (MTX) and skull irradiation induced CNS remission. The patient was readmitted because of second CNS relapse. After the third administration of weekly intrathecal MTX injection, apathy and finger tremor were observed. Her conscious disturbance continued for two weeks and magnetic resonance imaging (MRI) revealed abnormal findings in the white matter of her brain. Subsequently OHP therapy was commenced, and the conscious disturbance was improved gradually. One month later, neuro-disturbance resolved completely and the findings of MRI were improved. We could not find any case of leukoencephalopathy which was treated with OHP in the literature. But our case suggested that OHP therapy is valuable in patient with leukoencephalopathy in the early stage.
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PMID:[A case report of childhood acute lymphoblastic leukemia with leukoencephalopathy that responded to oxygenation under hyperbaric pressure therapy]. 143 44

Cytostatic long-term treatment for about 36 months was administered to 18 children with acute lymphatic leukaemia who were in long-term remission (43-98 months). Prophylaxis of meningosis involved intrathecal 198Au colloid and methotrexate. Seven recurrences occurred during the long-term remissions: the bone marrow was involved six times, leukaemic meningosis occurred once. Five out of seven recurrences occurred within one year of cessation of treatment. There were no complications induced by intrathecal radio-gold, such as the apathy syndrome or leukoencephalopathy. Intrathecal methotrexate led to side effects before administration of radio-gold: encephalopathy twice, paraplegia once. Symptoms regressed completely in two children, one child with encephalopathy continues to have symptoms. All three children were given 198Au colloid intrathecally thereafter which was tolerated very well. 198Au colloid represents an alternative for prophylaxis of meningosis with 60Co telecobalt irradiation in leukaemias and non-Hodgkin lymphomas in childhood.
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PMID:[Cessation of treatment in childhood acute lymphatic leukemia. Long-term observations after meningosis prevention with intrathecal gold colloid radioisotopes and methotrexate]. 626 99

Since 1972, telecobalt irradiation plus intrathecal methotrexate (ITMTX) has been successfully replaced in Jena by intrathecal colloidal radioactive gold (198Au) plus ITMTX for meningosis prophylaxis in leukemia. Seventy-three children with acute lymphocytic leukemia (ALL) were given 1.24-4.89 mCi (45.8-181 MBq) of colloidal 198Au IT after successful initiation of remission. During cytostatic therapy, the following relapses occurred: meningosis leucaemica, five patients (6.8%); bone-marrow relapse and the meningosis leucaemica, one patient; and bone-marrow relapse, 20 patients (27.4%). In 18 children, combination chemotherapy was terminated after two and a half or three years of treatment. After that time, one meningeal relapse and six bone-marrow relapses occurred. Within the first 24 hours after application of radioactive gold, headaches, vomiting, and fever occurred in less than 10% of the children. An apathy syndrome, leukecephalopathy, or severe infections, were not observed in a single case. Radioactive gold spreads in the subarachnoid space and is phagocytized by the arachnoidea. The tumoricide effect extends selectively over the space of distribution of the latent meningosis leucaemia. The cerebral parenchyma remains unaffected by radiation. Thus, radioactive gold may be preferable to telecobalt irradiation in preventing central nervous system leukemia.
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PMID:Meningosis prophylaxis with intrathecal 198Au-colloid and methotrexate in childhood acute lymphocytic leukemia. 627 5

Groups of six BALB/c mice each were intravenously inoculated with lethal doses of Ba-P210 (B210) or 12B1 cells and examined by autopsy, histology, special staining methods, enzyme histochemistry and immunohistochemistry. Clinical symptoms related to neoplasia consisted of a poor nutritional state, anaemia, mild to moderate dehydration and apathy. Paresis was apparent in three mice inoculated with 12B1 cells. Necropsy revealed splenomegaly in all animals. Sporadic haemorrhages in the lungs and enlargement of some lymph nodes were seen in some of the animals. Histological examination showed neoplastic cells in the spleen, in the bone marrow of the sternum, in the lung interstitium and in sinusoids of the liver in all mice. In six of nine brains examined, mild to moderate infiltration by neoplastic cells was observed. In all but two mice mild infiltration of the kidneys was found. The enlargement of lymph nodes was caused by an accumulation of neoplastic cells. The paresis was due to neoplastic infiltration of the vertebra, epidural space and spinal roots. Staining with Sudan black revealed cytoplasmic granules in neoplastic cells; however, the peroxidase reaction was negative. Numerous neoplastic cells disseminated in the red pulp of the spleen were reactive with CD3, CD79beta, CD11b and with neutrophil antibodies. We classified the disease induced by both of the cell lines as acute myeloid undifferentiated leukaemia (AML MO).
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PMID:Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice. 1618 May 44

A 55-year-old woman developed acute promyelocytic leukaemia during treatment with all-trans-retinoic acid and arsenic trioxide. Initially, she presented with symptoms of epigastric pain, vomiting, and nausea, and she developed acute pancreatitis. She was treated with parenteral nutritional supplementation for 20 days. However, the patient continued to develop refractory hyponatraemia, hypotension, and apathy. Finally, the patient was diagnosed with Wernicke encephalopathy (WE) using head magnetic resonance imaging. The patient underwent high-dose intravenous thiamine administration, and her symptoms were alleviated. WE is a rare adverse event during acute pancreatitis therapy. Acute pancreatitis that is caused by all-trans-retinoic acid and arsenic trioxide is a rare complication of acute promyelocytic leukaemia during chemotherapy. Further study is essential to improve our comprehension of the risk factors for complications in patients with acute promyelocytic leukaemia, considering that the associated complications were potentially caused by multiple etiological factors. A better understanding of these risk factors may help to improve the prognosis of patients with acute promyelocytic leukaemia at an early stage.
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PMID:Severe Wernicke encephalopathy and acute pancreatitis due to all-trans-retinoic acid and arsenic trioxide during treatment of acute promyelocytic leukaemia: a case report. 3299 92