Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In both animal models and human studies in leukemia, residual disease on day 8 following myelosuppressive therapy is in a proliferative phase and therefore may be sensitive to the S-phase specific drug cytarabine. Based on this concept, 17 patients with refractory or relapsed leukemia or lymphoma undergoing either autologous or allogeneic bone marrow transplantation (BMT) were treated on a Phase I protocol using high doses of busulfan (16 mg/kg, days -10, -9, -8, -7) and cyclophosphamide (120 mg/kg, days -6, -5) followed by escalating doses of a 48-h continuous infusion of cytarabine (starting dose 1000 mg/m2/48 h, days -3, -2). Ten patients received autologous transplants (two with Hodgkin's disease, seven with non-Hodgkin's lymphoma, one with chronic myelogenous leukemia (CML) in blast phase). Seven received allogeneic BMT (two with refractory acute myelocytic leukemia (AML), one with refractory acute lymphoblastic leukemia (ALL) undergoing a second BMT, one with Burkitt's-type leukemia, one with ALL in fifth relapse and two with CML in accelerated/blast phase). Two of these patients received a T cell-depleted haploidentical transplant. The maximum tolerated dose of cytarabine was 1500 mg/m2/48 h; a pulmonary syndrome including dyspnea, hypoxemia, and interstitial infiltrates which responded to aggressive diuresis was the dose limiting toxicity. Of the 10 patients who received cytarabine doses of 2000 or 2500 mg/m2/48 h, five patients developed adult respiratory distress syndrome (ARDS) with three patients requiring intubation; two recovered. Of the nine patients with lymphoma, seven responded with complete tumor clearance (CTC) with two patients tumor-free 13 and 15 months post-BMT, one remained refractory and one died too early to evaluate (TETE).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of busulfan, cyclophosphamide, and timed sequential escalating doses of cytarabine followed by bone marrow transplantation. 154 48

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

A 35-year-old man was admitted to our hospital because of lumbago on March 25, 1988. On admission white blood count was 1,200/microliters with neutrophils of 9% and lymphocytes of 91%, hemoglobin level was 11.2g/dl and platelet count was 55 x 10(3)/microliters. Bone marrow smear showed 77% leukemic cell including non-specific or specific esterase-positive cells. Chest X-rays showed the presence of mediastinal tumor and diffuse reticular shadows. A diagnosis of ANLL was made and a hematological remission was obtained after one course of combination chemotherapy consisting of BH-AC, daunorubicin and prednisolone, but the enlarged mediastinal tumor and pulmonary infiltration worsened rapidly followed by marked dyspnea. This radiographic abnormal shadow was confirmed to be leukemic infiltration from the finding of transbronchial lung biopsy. We hesitated to give systemic chemotherapy because he also had had liver abscess. Accordingly we performed BAI of ACNU at a dosage of 150 mg which led to a dramatic improvement in dyspnea. 60Co therapy was performed on the mediastinal tumor. On May 30, when he had a relapse, he was unsuccessfully treated with systemic chemotherapy. The leukemic cells invaded most of the organs and the patient died on July 19, 1988. It is likely that BAI of ACNU for leukemic pulmonary infiltration was effective.
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PMID:[Successful bronchial arterial infusion (BAI) of ACNU in the treatment of pulmonary infiltration of acute non-lymphocytic leukemia (ANLL) cells]. 228 71

A patient with acute hyperleukocytotic myelogenous leukemia who presented with acute respiratory distress is reported. Clinical manifestations included dyspnea, tachypnea, hyperventilation, and cyanosis. Blood gas analysis revealed hypoxemia, hypocapnia, and metabolic acidosis. Chest X-ray and perfusion lung scanning were normal. Pulmonary leukostasis syndrome (PLS) was later confirmed at autopsy. In a patient with hyperleukocytosic from acute nonlymphocytic leukemia and respiratory distress, a normal perfusion lung scintigraph should make one consider the PLS.
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PMID:Acute respiratory failure in hyperleukocytotic acute myeloid leukemia: the role of perfusion lung scintigraphy. 316 47

We report a 21-year-old male patient suffering from acute myeloid leukemia and concomitant thrombocytopenia. Following a diagnostic thoracotomy-which revealed Aspergillus pneumonia-he developed respiratory insufficiency and dyspnea. A thoracic epidural catheter was inserted and epidural morphine treatment led to improved ventilation. No clinical signs of pathological epidural processes were noticed during the treatment. The patient died of Aspergillus sepsis 26 days after catheter insertion. Autopsy revealed bacterial growth in the epidural space with slight infectious tissue reactions as well as an epidural hematoma. No evidence of spinal cord compression was found at autopsy. The development of epidural infection or hematoma seems to be a possible complication of epidural analgesia in patients suffering from impaired defense mechanisms or thrombocytopenia. These risk factors should be taken into account when epidural analgesia is considered. We suggest that the platelet count should be determined beforehand in patients suspected of having thrombocytopenia (e.g. cancer, pre-eclampsia).
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PMID:[Epidural hematoma following epidural catheter anesthesia in thrombocytopenia]. 335 26

Four patients with acute nonlymphocytic leukemia and leukocyte counts of more than 200,000/mm3 developed respiratory distress due to pulmonary leukostasis within 10-48 hours after initiation of chemotherapy. Clinically, the patients manifested fever, dyspnea, tachypnea, diffuse pulmonary rales, pleural effusions, and severe hypoxemia. Chest roentgenograms displayed diffuse pulmonary infiltrates, vascular engorgement, cardiomegaly, and pleural effusions. Three patients died from progressive respiratory failure despite ventilatory support. Pulmonary histology revealed thrombi composed of leukemic blast cells which obstructed and distended the lumens of pulmonary arterioles, capillaries, and venules. Electron microscopy studies of lung tissue showed pulmonary alveolar endothelium and basement membrane damage and interstitial edema. The pathophysiologic basis of pulmonary leukostasis and potential treatment modalities are discussed.
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PMID:Respiratory failure due to pulmonary leukostasis following chemotherapy of acute nonlymphocytic leukemia. 683 46

A 46-year-old woman with acute promyelocytic leukemia (APL) was treated with all-trans retinoic acid (ATRA) and chemotherapy according to the AML-92, M3 regimen of the Japan Adult Leukemia Study Group (JALSG). Between days 7 and 18 of therapy, she suffered chest discomfort, fever, cough, dyspnea and general fatigue. A chest roentogenogram showed bilateral interstitial infiltrates. Her leukocyte count began to increase rapidly to 6,400/microliters on day 14. Marked hypoxia (PO2 35.9 mmHg) suggested occurrence of retinoic acid (RA) syndrome. She underwent endotracheal intubation and mechanical ventilation with administration of methyl-prednisolone (m-PSL) pulse therapy. Her symptoms promptly abated. Therapy with ATRA was continued and her leukocyte count reached 44,800/microliters on day 19 of therapy. She achieved complete remission on day 48.
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PMID:[Effective methyl prednisolone pulse therapy for a patient with retinoic acid syndrome in acute promyelocytic leukemia]. 823 Jul 47

For four months a 28-year-old man had been suffering from a sensation of pressure in his head when lying down, swelling of the face, exertional dyspnoea and weight gain of 9 kg. Biochemical tests and chest radiograph were unremarkable. Echocardiography revealed a 3 x 5 cm mass in the right atrium, extending into the superior vena cava whose lumen was narrowed to a few millimetres. Computed tomography and magnetic resonance imaging were suggestive of a malignant tumour. Bone marrow biopsy as well as transvascular and mediastinoscopically obtained biopsies failed to provide a pathological diagnosis. Exploratory thoracotomy uncovered a nonresectable chloroma surrounding both venae cavae. It had penetrated into the right and left atria, as well as the pulmonary veins. A Gore-tex bypass was placed between the innominate vein and right atrial appendage. The tumour was identified as a local manifestation of acute myeloid leukaemia. Treatment with idarubicin (12 mg/m2 daily for 3 days) and adriamycin (1.5 mg/m2 daily for 4 days) followed by radiotherapy with 35 Gy achieved partial remission and 15 months after onset of treatment the patient is in a good general condition.
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PMID:[Mediastinal chloroma with right heart involvement. Unusual cause of a superior vena cava syndrome]. 846 35

A 17-year-old man diagnosed as acute myelogenous leukemia (M5a) underwent allogeneic bone marrow transplantation from his HLA-identical, MLC non-reactive sister on the occasion of the second complete remission. On day 14 engraftment was confirmed by karyotypic expression. The patient had no evidence of acute graft-versus-host disease (GVHD), therefore cyclosporine A was discontinued on day 62. Having complained of cough and dyspnea by day 100, the patient was diagnosed as interstitial pneumonitis (IP) based on chest X-ray findings. However, no other typical signs of chronic GVHD were present except for modest abnormality of liver function. Since there was no evidence of infection on bronchofiberoscopic examination and prednisolone was very effective, it was considered that the IP might be pulmonary disease of chronic GVHD. It has been reported that HLA-DR which is not normally found, is expressed on epithelial tissues of the patient with GVHD. In this case alveolar epithelial cells were positive for LN-3 (anti-HLA-DR). In conclusion, pulmonary disease in this case may represent a possible manifestation of chronic GVHD, thus suggesting that the current case could provide information to ascertain the mechanism of chronic GVHD.
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PMID:[Pulmonary disease as the chief manifestation of chronic graft-versus-host disease after allogeneic bone marrow transplantation]. 849 13

We described two cases of idiopathic interstitial pneumonitis (IP) after allogeneic bone marrow transplantation (BMT), who were successfully treated with prednisolone (PSL). A 40-year-old male with AML (M3) in the first remission (case 1) and a 36-year-old male with CML in chronic phase (case 2) were treated with BMT from HLA genotypically identical female siblings. Both patients were conditioned with busulfan (16mg/kg) and cyclophosphamide (120mg/kg), and given a combination of cyclosporin A and methotrexate to prevent acute GVHD (aGVHD). Engraftment of donor marrow was documented in both cases. Grade I of aGVHE developed in case 1 and no aGVHD in case 2. Both patients had clinical manifestations of chronic GVHD (cGVHD), which were followed by dyspnea and cough without fever 120 days (case 1) or 100 days (case 2) after BMT. Abnormal lung function tests and radiographic infiltrates indicated that patients developed IP, but causative microorganisms could not be detected in the bronchoalveolar lavage (BAL) specimens. Subjective symptoms disappeared in a few days after administering PSL (1mg/kg/day). Laboratory data also improved thereafter. These observations, including the development of radiographic infiltrates along with clinical manifestations of cGVHD, absence of febrile episodes, absence of causative microorganisms in the BAL specimens, and effectiveness of immunosuppressive drugs, suggested that idiopathic IP observed in our cases might be a manifestation of cGVHD.
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PMID:[Idiopathic interstitial pneumonitis possibly associated with chronic graft-versus-host disease]. 849 16


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