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)

The morphologic and clinical features of four patients who developed significant bone marrow and blood dyspoiesis after successful chemotherapy for acute nonlymphocytic leukemia (ANLL) are described. This postleukemic dyspoiesis developed 1-6 months after leukemia induction therapy and persisted for 5-20 months in a relatively stable state. This period of prolonged dyspoiesis was not associated with rising myeloblast counts or clinical evidence of relapse. Dyspoietic abnormalities developed while two patients were receiving maintenance chemotherapy; the other two patients received no maintenance therapy. The dyspoietic changes in these four patients greatly exceeded those noted in a control group of ANLL patients on maintenance chemotherapy. The morphologic features of postleukemic dysmyelopoiesis were similar to those described in preleukemic dysmyelopoietic disorders. Erythroid abnormalities included hyperplasia with ring sideroblasts, megaloblastic changes, and cytoplasmic PAS reactivity. Myeloid abnormalities consisted of left-shifted granulopoiesis with hyper- and hyposegmentation; megakaryocytic abnormalities included hyperplasia with a predominance of hypolobulated forms. Three of the four patients eventually suffered relapse and have died. The fourth patient died of sepsis after 20 months of pancytopenia and dysmyelopoiesis. Theories to explain the development of postleukemic dysmyelopoiesis are presented which emphasize the possibility of drug-induced leukemia cell differentiation. Cytogenetic studies will be necessary to establish any relationship between ANLL and the subsequent postleukemic dysmyelopoiesis.
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PMID:Postleukemic dysmyelopoiesis. 665 Apr 93

A 52-year-old female presented with Philadelphia chromosome-positive acute nonlymphocytic leukemia and a morphologically benign-appearing histiocytosis with intramedullary cytophagocytosis of formed blood elements. No cause of the reactive histiocytosis could be found. Despite initial successful therapy of the acute nonlymphocytic leukemia with induction of a cytological remission, pancytopenia with marked cytophagocytosis persisted. Therapy aimed at reducing the degree of cytophagocytosis by the histiocytes, in the form of vinblastine-treated platelets and, subsequently, prednisone, was instituted. There was no significant clinical response to either therapeutic maneuver. Cytophagocytosis persisted until leukemic relapse and death ensued.
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PMID:Acute nonlymphocytic leukemia complicated by severe cytophagocytosis of formed blood elements by nonmalignant histiocytes: cause of significant clinical morbidity. 683 72

Thirty-seven patients with acute leukemia in relapse were treated with a three-drug combination that included a 3- or 4-day course of AMSA with total doses ranging from 600 mg/m2 to 740 mg/m2 I.V., cytosine arabinoside 25 mg/m2 I.V. followed by 200 mg/m2 by continuous infusion daily for 5 days, and thioguanine 100 mg/m2 p.o. q 12h for 5 days. Eight of the 25 patients with acute nonlymphoblastic leukemia achieved a complete remission and 3 a partial remission. None of the five patients with acute lymphoblastic leukemia achieved a response and there was one partial remission in the seven patients with myelodysplastic syndrome or blastic CML. Reversible toxicity included nausea and vomiting (78%), alopecia (100%), pancytopenia (100%), mild stomatitis (63%), and hepatic dysfunction (24%). One patient developed seizures and cardiac arrhythmias. The activity of this combination in heavily treated patients with ANLL is comparable to that of the anthracycline-containing regimens, and its use in previously untreated patients with ANLL should now be explored.
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PMID:Treatment of acute leukemia in relapse with 4'(9-acridinylamino) methanesulfon-m-anisidide (AMSA) in combination with cytosine arabinoside and thioguanine. 689 90

Preleukemia refers to the syndrome of hematopoietic dysfunction seen in some patients before typical features of acute myelogenous leukemia develop. Clinically, preleukemia is characterized by variable degrees of pancytopenia, with associated symptoms due to decreased circulating blood elements. The bone marrow is usually hypercellular, and there are prominent morphologic abnormalities in erythroid precursors and more subtle changes in megakaryocytes and granulocyte progenitors. During this phase of the leukemic process, the neoplastic clone is usually already established and predominant. A clear distinction should be made between the preleukemic syndrome and diseases that predispose to development of acute myelogenous leukemia. Preleukemia, like acute myelogenous leukemia, is a clonal hematopoietic stem cell neoplasm manifested functionally by abnormal hematopoietic cell maturation and ineffective hematopoiesis. During the course of preleukemia, precursor cell maturation becomes progressively impaired with termination in the severe maturational block characteristic of acute myelogenous leukemia. We favor the concept that preleukemia is an early phase of acute myelogenous leukemia.
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PMID:Human preleukemia. 693 7

In a family with ataxia and pancytopenia, the proband had cerebellar ataxia, developed hypoplastic anemia at age 3 years, and died of acute myelomonocytic leukemia at age 7. Serial cytogenetic studies of the proband's hypoplastic bone marrow over a 25-month period revealed progressive expansion of a clone of cells with C(6 - 12 + X) monosomy from 33% to 94% of metaphases. The missing chromosome by banding was deduced to be No.7. No increased sensitivity of the patient's cells was found in response to ultraviolet or ionizing radiation or to mitomycin C. Cerebellar atrophy was confirmed at autopsy. Family studies revealed cerebellar ataxia in the proband's father and all four siblings. Two brothers, including one with C-monosomy, died with hypoplastic anemia and another brother died with acute myelocytic leukemia. The only surviving sibling is a 19-year-old sister who has unexplained anemia, decreased mitotic activity in bone marrow, and slow progressive cerebellar ataxia. The name ataxia-pancytopenia syndrome is proposed to encourage study of additional patients with this disorder, which predisposes to pancytopenia and acute leukemia.
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PMID:Ataxia-pancytopenia: syndrome of cerebellar ataxia, hypoplastic anemia, monosomy 7, and acute myelogenous leukemia. 694 57

1-beta-D-Arabinofuranosylcytosine (ara-C), 2 or 3 g/sq m, was administered as a 1-hr i.v. infusion every 12 hr for 10 or 12 doses to patients with acute leukemia and refractory lymphoma. Four of seven patients with relapsed or refractory acute myelocytic leukemia and two of four patients with previously untreated acute myelocytic leukemia achieved complete remission. Of five treatment failures, two patients had leukemia which was clearly resistant to high-dose ara-C, and three patients died of infections or hemorrhagic complications during periods of pancytopenia. Three patients with acute myelocytic leukemia in remission received high-dose ara-C as consolidation therapy following previous courses of intensive, multiagent consolidation chemotherapy. Two of these three patients had prolonged thrombocytopenia following high-dose ara-C. Five patients with refractory acute lymphocytic leukemia were treated. Three patients achieved partial remission, and two patients had drug-resistant disease. Complete or partial disappearance of measurable disease parameters was seen in three of three patients with refractory lymphoma. Response was seen in five of five patients with meningeal leukemia, including complete response in one patient with extensive meningeal infiltration. Toxicity of this regimen was generally moderate and limited to pancytopenia and mild nausea. Patients who had received prior multiagent consolidation chemotherapy appeared to be at greater risk for hematopoietic toxicity. Patients who had received prior cranial irradiation or intrathecal chemotherapy appeared to be at greater risk for neurological toxicity. Plasma levels of ara-C immediately after completion of the infusion were 17.96 +/- 8.02 (S.D.) and 35.0 +/- 2.8 micrograms/ml for doses of 2 and 3 g/sq m, respectively. From 160 to 720 min following completion of the infusion, the plasma levels of drug were comparable to steady-state levels achieved with a continuous infusion of ara-C at 100 mg/sq m over 24 hr. A high degree of penetration into the central nervous system was demonstrated. High-dose ara-C has substantial activity against leukemic and lymphomatous cell populations, including cell populations resistant to conventional doses of the drug, and is an effective treatment modality for patients with these diseases. The high degree of penetration into the central nervous system suggests that this drug regimen may be useful as consolidation therapy for patients at high risk for central nervous system disease.
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PMID:A pilot study of high-dose 1-beta-D-arabinofuranosylcytosine for acute leukemia and refractory lymphoma: clinical response and pharmacology. 694 42

Risk factors were analyzed and searched for possible predictive parameters for the development of acute myeloid leukemia in 216 reported patients previously treated for Hodgkin's disease. The distribution of histologic subtypes and the stage at diagnosis were similar to that of all patients with Hodgkin's disease. Seventy-five percent of the 216 patients in whom acute myeloid leukemia developed had received both radiotherapy and chemotherapy, 15% chemotherapy only, and 10% radiotherapy only. Of those receiving radiotherapy, 66% were given multiple courses or total nodal irradiation. Of the patients receiving chemotherapy, 77% had received more than eight months of single or combination drug therapy; only 4% had not been exposed to alkylating agents. When acute leukemia developed, 78% of the patients showed no clinical or pathologic evidence of residual Hodgkin's disease. A period of pancytopenia preceded the onset of overt leukemia in at least one-third of the patients. Complete or partial remission of the acute leukemia was achieved in 25% of the patients treated with antileukemic chemotherapy. On the basis of these findings, it is deemed advisable to reexamine the intensity of treatment presently being administered to achieve cure of Hodgkin's disease. Unnecessary or unproved programs of combined radiation therapy and chemotherapy should be avoided. An optimal balance between the risks and benefits of treatment needs to be applied.
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PMID:Acute myeloid leukemia following treatment of Hodgkin's disease: a review. 695 91

Four cases of acute myelogenous leukemia and six cases of chronic myelogenous leukemia after treatment with azathioprine and prednisone for renal allotransplantation have been described in the literature. We report another two cases of acute leukemia 10 and 5 years after successful renal allotransplantation. Patient 1, a 29-year-old farmer, exhibited the signs of acute lymphatic leukemia resistent to treatment with cytostatic agens. Death was due to pneumonia. Patient 2, a 47-year-old salesman, developed pancytopenia together with splenomegaly. After splenectomy an atypical subacute myeloid leukemia became apparent which was not treated due to withdrawal of the patient. He died 2 months after diagnosis. Both patients received long-term immunosuppressive therapy with azathiopine and prednisone until the leukemia was diagnosed. A relationship between long-term immunosuppression and the occurrence of leukemia is postulated.
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PMID:[Acute leukemia after kidney allotransplantation (author's transl)]. 699 44

Twenty-one patients with acute nonlymphocytic leukemia were treated with a regimen including daunorubicin, cytosine arabinoside, and 6-thioguanine and 15 patients (71%) achieved a complete remission. Thirteen of the 15 remissions occurred after a single course of therapy and two after two courses of treatment resulting in a rapid time to complete remission. The time from treatment initiation to complete remission was 21-82 days with a median of 29 days. Nine of the 15 patients who gained a complete remission were then treated with two cycles of consolidation therapy utilizing the three induction drugs in modified dosages to determine the toxicity of a consolidation program. With the doses used in consolidation, pancytopenia regularly occurred but only 5/15 courses were associated with complications of bleeding or infection that required hospitalization. No patient died as a result of consolidation therapy. This study confirms the rapid effectiveness of the induction program which provided equivalent complete remission rates for adults at any age (up to 66 years). The consolidation regimen is now being used in a randomized study to determine whether it contributes to the duration of complete remission.
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PMID:Induction therapy and intensive consolidation with daunorubicin, cytosine arabinoside, and 6-thioguanine in adult acute nonlymphoblastic leukemia. 724 50

We describe a 68-year-old Japanese male with hypoplastic acute myelogenous leukemia (AML) who achieved complete hematological reconstitution following granulocyte colony-stimulating factor (G-CSF) administration. The patient had pancytopenia and the bone marrow was hypocellular with 19 to 36% peroxidase-positive blasts without morphological abnormalities suggestive of myelodysplasia. After receiving G-CSF as a supportive therapy for pneumonia, the blood count became normal and the bone marrow was normocellular with less than 5% of blasts. Without subsequent chemotherapy, he relapsed as a form of overt leukemia and died of pneumonia. Chemotherapy may be necessary to maintain remission in hypoplastic AML after hematopoietic reconstitution by G-CSF.
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PMID:Successful hematopoietic reconstitution with granulocyte colony-stimulating factor in a patient with hypoplastic acute myelogenous leukemia. 749 88


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