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)

Thirty-one patients with a diagnosis of refractory acute myelogenous leukemia received homoharringtonine as their first (15 patients) or second (16 patients) salvage therapy. Homoharringtonine was given as a continuous infusion of 2.5 mg/m2 daily for 15 to 21 days to 13 patients (schedule 1), and of 3.0 mg/m2 daily for 15 days in 18 patients (schedule 2). Overall, one patient achieved complete remission (3%), and three (10%) had a hematologic improvement with normalization of the marrow and peripheral blood picture except for persistent thrombocytopenia. Six patients (19%) demonstrated prolonged myelosuppression, three (23%) on schedule 1 and three (17%) on schedule 2. Cardiovascular complications were minimal consisting of hypotension in one patient (3%) and supraventricular arrhythmias in two patients (6%). Hyperglycemia was observed in 42% of patients and was significant in 10%. The authors conclude that homoharringtonine, at the dose schedule investigated, has definite but low antileukemic efficacy. The low-dose continuous infusion schedule was associated with prolonged myelosuppression but no serious cardiovascular complications. The role of such therapy in myeloproliferative disorders, especially chronic myelogenous leukemia, deserves consideration.
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PMID:Phase II study of low-dose continuous infusion homoharringtonine in refractory acute myelogenous leukemia. 291 87

A 72-year-old man originally seen for anemia and thrombocytopenia was determined to have chronic lymphocytic leukemia (CLL). Bone marrow examination at the time of CLL diagnosis revealed a small but significant population of atypical blasts. Cytogenetic analysis of the bone marrow aspirate disclosed chromosomal abnormalities (-7, +8) suggestive of a myelodysplastic syndrome. Shortly after treatment of the CLL, there was proliferation of the previously noted blast population, which cytochemical studies demonstrated to be of the myeloid series thus indicating acute myeloid leukemia superimposed on CLL. This report presents microscopic, cytogenetic, immunophenotypic, and cytochemical evidence to document the evolution of acute myeloid leukemia in the bone marrow of a patient with CLL after one course of chemotherapy.
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PMID:Coexistence of myelodysplastic syndrome and untreated chronic lymphocytic leukemia with development of acute myeloid leukemia immediately after treatment of chronic lymphocytic leukemia. 291 61

In 45 cases of primary myelodysplastic syndrome; 16 refractory anaemia (RA), 11 RA with ring sideroblasts (RA+), 13 RA with excess of blasts (RAEB), 5 chronic myelomonocytic leukaemia (CMML), the relations between myeloperoxidase (MPO) activity in polymorphonuclear leucocytes (PMN), neutrophil alkaline phosphatase (NAP) activity, absolute number of PMN and thrombocytopenia were investigated. 11 patients (26%) showed abnormal numbers (greater than 4%) of MPO-deficient PMN and 27 (75%) showed abnormal NAP activity (NAP score; greater than 134.0, less than 15.0), mostly decreased. No significant correlations between MPO activity and NAP activity were demonstrated, nor were any significant correlations found with the other parameters investigated. The FAB-subtypes, RAEB and CMML, showed a significant correlation to thrombocytopenia (p = 0.028) and to pancytopenia (p = 0.024). The findings may support the view that at least some of the myelodysplastic syndromes may be fundamentally the same disease as acute myeloid leukaemia.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes. (V): Relation to FAB-classification and neutrophil alkaline phosphatase activity in primary myelodysplastic syndromes. 299 23

One hundred ninety-five adult patients with refractory or first relapse acute myelogenous leukemia (AML) were randomly assigned to receive high-dose cytarabine (HiDAC), 3 g/m2 as a three-hour intravenous (IV) infusion every 12 hours for four doses, followed by 6,000 IU/m2 asparaginase (ASNase) administered at hour 42, or HiDAC without ASNase. Treatment was repeated on day 8. The median patient age was 52 years. There was an overall superior complete remission (CR) rate for HiDAC/ASNase (40%) v HiDAC (24%), P = .02. Subset analysis according to prior response and age showed the following CR rates: 54% from HiDAC/ASNase treatment of refractory AML in patients less than 60 years, and 31% in patients greater than 60 years; CR from HiDAC in the same refractory groups were 18% (less than 60) and 0% (greater than 60); 37% from HiDAC/ASNase treatment of relapsed AML in patients less than 60 years, and 43% in patients greater than 60 years; CRs from HiDAC in the same relapsed groups were 33% (less than 60) and 21% (greater than 60). Toxicity in the two treatment arms was comparable and consisted primarily of leukopenia, thrombocytopenia, mild hepatic dysfunction, diarrhea, conjunctivitis and serositis, and hyperglycemia. There was only one case of transient cerebellar toxicity and no cutaneous toxicity. Median time to full hematologic recovery was 5 weeks. There was an overall survival benefit for patients treated with HiDAC/ASNase (19.6 weeks) compared with HiDAC (15.9 weeks), P = .046, primarily attributable to effects in refractory patients. Median time to failure for refractory patients who achieved CR was 38.5 weeks with HiDAC/ASNase, and 13.3 weeks for those treated with HiDAC. For relapsed patients in CR from HiDAC/ASNase the median time to failure was 17.7 weeks and 18.3 weeks for HiDAC. The overall 42% CR rate from HiDAC/ASNase v 12% from HiDAC in patients with refractory AML indicates that HiDAC/ASNase is not cross-resistant with standard-dose cytarabine (SDAC) and anthracyclines. We conclude that HiDAC/ASNase has substantial activity in poor-prognosis AML and that this combination warrants further trials in earlier stage disease.
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PMID:Synergy between high-dose cytarabine and asparaginase in the treatment of adults with refractory and relapsed acute myelogenous leukemia--a Cancer and Leukemia Group B Study. 316 15

Forty-four patients with a diagnosis of refractory or relapsed acute myelogenous leukemia received salvage chemotherapy with high-dose cytosine arabinosine 3 g/m2 intravenously over 2 hours every 12 hours for six doses and mitoxantrone 5 mg/m2 intravenously daily for 5 days. Overall 16 patients (36%) had a complete remission; 16 patients (36%) had resistant disease; and 12 (27%) died during induction therapy. The most significant predictive factor for remission was the duration of first remission: the response rate was 17% for patients whose first remission duration was shorter than 12 months (including those who did not achieve a first remission), 45% for those with a first remission lasting between 12 to 18 months, and 69% for those with longer remission durations (P = 0.008). Other predictive factors for higher response rates were a younger age group, a good performance status, and a favorable or diploid karyotype. The median survival from start of therapy was 4 months for the total population and 10 months for patients with remission. Serious side effects including pulmonary toxicity and neurotoxicity occurred in less than 10% of patients. This incidence was significantly lower than previous high-dose cytosine arabinoside schedules of 3 g/m2 for nine to 12 doses (total dose, 27 to 36 g per course). Significant granulocytopenia and thrombocytopenia were universal resulting in fever or documented infections in 98% of patients. We conclude that the combination of high-dose cytosine arabinoside and mitoxantrone is an effective antileukemic regimen with acceptable toxicity. Future studies should incorporate it as part of the frontline induction or maintenance strategies in newly diagnosed patients with acute myelogenous leukemia.
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PMID:Mitoxantrone and high-dose cytosine arabinoside in refractory acute myelogenous leukemia. 316 47

Using bone marrow smears of the type prepared routinely in clinical practice, we determined megakaryocyte ploidy distributions in five normal persons, eight patients with both normal platelet counts and normal bone marrow morphology, and 18 patients with quantitative platelet disorders. To include 2N and 4N megakaryocytes in the ploidy distribution histograms, all megakaryocytes were identified by serial immunologic labelling with rabbit antiserum to human platelet glycoproteins and rhodamine-conjugated goat anti-rabbit igG. Cell nuclei were concurrently Feulgen stained with bis-aminophenyl-oxdiazole, and the nuclear fluorescent signals were quantified photometrically. A modal megakaryocyte ploidy value of 32N was seen in 10 of the 13 persons with normal platelet counts, and geometric mean megakaryocyte ploidy values averaged 24.9N +/- 7.0N (arithmetic mean +/- SD). In these normal control individuals, 2N and 4N megakaryocytes accounted for 11.1% of all megakaryocytes, and 2.6% of the megakaryocytes were 128N. Shifts to a higher mean ploidy were observed in five of seven patients with idiopathic thrombocytopenic purpura, resulting from increased percentages of 64N and 128N megakaryocytes at the expense of 4N, 8N, and 16N cells. Shifts to lower ploidy were demonstrated in two patients with acute myelogenous leukemia and one patient each with thrombotic thrombocytopenic purpura and isoimmune thrombocytopenia. Four of five patients with essential thrombocythemia had strikingly abnormal megakaryocyte ploidy histograms characterized by the presence of unusually high ploidy 256N and 512N megakaryocytes. These 256N and 512N cells were virtually unique to the patients with essential thrombocythemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of bone marrow megakaryocyte ploidy distributions in persons with normal and abnormal platelet counts. 327 1

We determined in 35 patients with severe thrombocytopenia (AML n = 10; ALL n = 4; CML = 1; idiopathic myelofibrosis n = 1, aplastic anemia n = 1; undergoing bone-marrow transplantation n = 17) factors influencing the corrected count increment (CCI) after platelet transfusions. Out of 195 transfusions 86 (44%) failed to increased platelet counts (CCI less than 5 X 10(9) platelets/l). A significant percentage of transfusion failures occurred in patients with splenomegaly and/or fever (54% vs. 29%; p less than 0.002). Antibodies directed against donor platelets were found only twice. No correlation between reactivities demonstrable by the lymphocytotoxic test (n = 144) or the radioimmune antiglobulin test (n = 67) and the CCI was obvious. HLA antigen identity was also not predictive. Thus, transfusion failures in patients with low alloimmunization will not be predicted by in vitro antibody screenings. The patients' clinical condition has the most important influence on posttransfusion increment.
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PMID:[Thrombocyte transfusion: increase in platelets in relation to clinical and immunologic prerequisites]. 329 59

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

An anaplastic vaginal tumour was diagnosed in a 29-year-old woman. Before the planned operation leukocytosis and thrombocytopenia developed and further diagnostic tests revealed malignant histiocytosis with bone-marrow infiltration, leukaemic wash-out and tumour formation in the lower pelvis. Intensive chemotherapy, as for acute myeloid leukaemia, achieved full remission. The case demonstrates that, although rare, tumorous organ infiltration may be the initial manifestation of malignant histiocytosis. Its early diagnosis and treatment decisively affects the prognosis.
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PMID:[Vaginal tumor--an initial manifestation of malignant histiocytosis]. 335 34

Between 1980 and 1986, we diagnosed refractory anaemia (RA), according to the FAB classification, in 69 patients, who constituted 22% of the 312 cases of myelodysplastic syndromes (MDS) seen over that period. The haematological features were variable, with pancytopenia in 14 cases (20%), bicytopenia in 24 (36%) and mono-cytopenia in the remaining patients, including 21 (30%) cases of anemia alone, 8 (12%) cases of refractory neutropenia and 2 (3%) cases of refractory thrombocytopenia. Myelodysplastic features were also quite variable, involving one, two or all three lineages. In patients with a single cytopenia or only one dysplastic lineage, FAB criteria appeared insufficient for adequate inclusion among RA and we suggest more precise diagnostic criteria, resulting from the utilization of cytogenetics, ferrokinetics, progenitor cultures and perhaps molecular biology, in such cases. Median survival was 42 months. 12 patients (17%) progressed to RAEB (of whom 7 finally developed ANLL) and 4 patients (6%) to CMML. In spite of the heterogeneity of haematological features, only two factors were associated with poor prognosis, namely age greater than 70 yr at diagnosis and haemoglobin less than 10 g/dl, whereas, to a lesser extent, neutropenia was associated with progression to RAEB.
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PMID:Refractory anaemia according to the FAB classification: a report on 69 cases. 336 22


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