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)

A 71-year-old man was hospitalized in November, 1983 for a back pain and a diagnosis of multiple myeloma was made, based on the Bence Jones proteinuria, The serum M-component of a IgG-kappa type (3.3 g/dl), and plasmacytosis in the bone marrow (37%). Treatment consisted of melphalan and prednisolone. A blood count in March, 1986 revealed 6000/microliters of WBC with 30% of a blast form and 8% plasma cells, and 20,000/microliters of platelets. A bone marrow aspirate revealed that 14% were myeloblasts and 26% were plasma cells. Distinguishing the myeloblasts from the immature plasma cells in the peripheral blood proved difficult. Studies by electron microscopy and an immunological inspection of phenotypes were helpful in achieving a determination. A karyotypic analysis of the bone marrow cells indicated a hypodiploid cell population, a marker chromosome, and a karyotypic instability. These findings indicate that his multiple myeloma had undergone a leukemic change associated with acute myelogenous leukemia.
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PMID:[A myeloma (IgG-kappa) terminating in acute myelogenous leukemia]. 210 37

Three patients with acute myelogenous leukemia (AML) in relapse were treated with intravenous infusions of one or more purified murine monoclonal antibodies (MoAbs) specific for differentiation antigens on normal and malignant myeloid cells. Three of the MoAbs used were IgM immunoglobulins that react with glycolipids, while the fourth, an IgG2b, reacts with a protein antigen. Peripheral blood leukemia cell counts decreased significantly, but transiently, during treatment. Evidence of in vivo binding of each MoAb to leukemia cells was obtained, although two of the four MoAbs could not be detected in the plasma following infusion, perhaps due to circulating blocking factors. Antigenic modulation was not encountered in these studies. However, the induction of human antibody to murine MoAb was observed in one patient who was treated over a 70-day period. Toxicities encountered were minimal and included fever (3 patients), back pain (1 patient), and arthralgias and myalgias (1 patient). This is the first reported clinical trial of (1) IgM MoAbs, (2) MoAb therapy in patients with AML, (3) combinations of MoAbs directed toward different myeloid differentiation antigens, and (4) MoAbs directed to glycolipids. The relative lack of toxicity and the positive effects of MoAb treatment in the reduction of leukemia cell counts permit the continued study of more innovative approaches to the treatment of AML with MoAbs.
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PMID:Monoclonal antibodies to myeloid differentiation antigens: in vivo studies of three patients with acute myelogenous leukemia. 660 73

Hypercalcemia in adult T-cell leukemia has been attributed to increased levels of 1,25-dihydroxyvitamin D (1,25(OH)2D), whereas in other types of leukemia, hypercalcemia has been blamed on direct skeletal invasion by malignant cells, ectopic parathyroid hormone (PTH) production or bone-resorbing cytokines. A 51-year-old man was studied who presented with back pain, circulating myeloblasts, and hypercalcemia. The bone marrow revealed acute myeloblastic leukemia. While the ionized calcium concentration was 8.17 mg/dL (normal, 4.73 to 5.21 mg/dL), the levels of PTH, PTH-related peptide, vitamin D, and thyroxine were normal or subnormal. Bone histomorphometry showed a decreased cortical width with intracortical erosion cavities dissecting into the marrow space. In cancellous bone, the osteoid area, osteoblast perimeter, and tetracycline fluorescence were sparse, whereas the osteoclast perimeter was increased. Persistent marrow fat, the general absence of trabecular narrowing, and the prompt response to calcitonin suggest that the osteoclasts caused the hypercalcemia and lytic lesions, rather than pressure atrophy or osteolysis by leukemic infiltration. Osteoclast activation and subsequent hypercalcemia may have been due to a locally produced cytokine, such as interleukin-1 beta or tumor necrosis factor.
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PMID:Case report: hypercalcemia in acute myeloblastic leukemia is caused by osteoclast activation. 812 79

Bone marrow necrosis is rarely diagnosed during life but is more often seen at autopsy by accident. The prognosis of patients with bone marrow necrosis secondary to neoplastic disease is extremely poor. We described a 53-year-old man with bone marrow necrosis preceding acute monoblastic leukemia. He was admitted in June, 1994, for continuous back pain and marked elevation of serum lactate dehydrogenase. After admission, a hematologic examination showed progressive pancytopenia in peripheral blood and bone marrow necrosis. He was diagnosed as AML (M5) from the sudden appearance of leukemic blasts in the peripheral blood two months later. Induction therapy was immediately administered according to JALSG-92 protocol. The patient suffered from tumor lysis syndrome after chemotherapy, but complete remission was achieved by dialysis.
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PMID:[Marked bone marrow necrosis preceding acute monoblastic leukemia]. 860 24

Four patients with systemic mastocytosis, two men and two women, are presented. Three of them (patients 1, 2, and 4) developed portal hypertension and ascites without histological evidence of cirrhosis in liver biopsy. The remaining patient (patient 3) had severe bone lesions with multiple vertebral fractures. None of the patients had skin or lymph node involvement. Two patients (patients 1 and 2) died 12 and 9 months after diagnosis with acute nonlymphocytic leukemia and overt mastocytic leukemia, respectively, while the other two (patients 3 and 4) are alive 58 and 14 months after diagnosis. Treatment with hydroxyurea or cytosine arabinoside had not any beneficial effect in two patients, while a substantial amelioration of back pain had been obtained by local irradiation and recombinant human interferon-alpha-2b administration in one patient (patient 3). All patients had laboratory findings compatible with autoimmune cholangitis. We concluded that systemic mastocytosis is a rare cause of noncirrhotic portal hypertension often simulating autoimmune cholangitis and leading to the erroneous diagnosis of liver cirrhosis. Diagnosis is based on the presence of mast cells in Giemsa-stained liver histological sections, and it may be confirmed by immunohistochemical detection of tryptase in the cytoplasm of these abnormally proliferating cells.
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PMID:Systemic mastocytosis: a rare cause of noncirrhotic portal hypertension simulating autoimmune cholangitis--report of four cases. 944 86

A 16-year-old girl was hospitalized because of anemia and thrombocytopenia in April 1998, and was diagnosed as having AML (FAB:M2). After failure of initial remission induction therapy, she was successfully treated with the MEC regimen as a second-line chemotherapy. On June 22, the first consolidation therapy was started. One week later, the patient developed a high fever with backache. Chest computed tomography (CT) on July 8 showed a 3cm mass lesion adjacent to the thoracic descending aorta in the left upper lobe. She was given fluconazole and antibiotics, and remained in remission. On July 24, the mass lesion changed to a cavitary lesion on chest CT, suggesting a fungal infection, probably aspergillosis. With recovery from neutropenia, the patient became asymptomatic, and fluconazole was changed to itraconazole. On July 27, she suffered sudden, massive hemoptysis and died. Autopsy revealed a localized adhesion between the cavitary lesion and the thoracic descending aorta, and the aortic wall was ruptured at this site. Microscopic examination revealed invasion of mucormycotic hyphae into the wall of the aorta with infiltration of inflammatory cells. The vasa vasorum were occluded by thrombi, in which mucormycotic hyphae were detected.
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PMID:[An autopsy case of pulmonary mucormycosis with fatal hemoptysis from a rupture of the thoracic descending aorta during remission from acute myelocytic leukemia]. 1119 40

Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML). They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder. Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia. Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia. This is the first case report of paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed CML. A 53-year-old woman reported back pain for 6 days, rapidly progressing to paraplegia. Physical examination noted a large abdominal mass and flaccid paralysis in both lower extremities. Spinal MRI revealed a T4-T6 vertebral mass causing spinal stenosis and cord compression. Tumor debulking and laminectomy were performed emergently. The tumor consisted of noncohesive blast cells. The CBC revealed a leukocyte count of 238,300/microl and a differential consistent with CML. Reexamination of the patient found that the abdominal mass was a giant spleen. Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML. Although extramedullary blast crises herald the accelerated phases in approximately 10% of CML cases, megakaryoblastic blast transformation of CML accounts for less than 3% of these cases. The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.
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PMID:Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia. 1701 92

Pyogenic spondylitis is regarded as a rare infectious disease. The incidence of this disease has been increasing recently due to an increase in the ratio of elderly people in the population as well as an increase in immunocompromised hosts complicated by cancer, diabetes mellitus and liver cirrhosis. Allogeneic hematopoietic stem cell transplantation (HSCT) is now performed widely as a curative treatment for various malignant hematological diseases. However, allogeneic HSCT causes chronic immunocompromise. There is no case report describing infectious spondylitis after HSCT. Here we describe a case of infectious spondylitis after HSCT and discuss risk factors and treatment. The patient was a 56-year-old female with AML-M1 who underwent allogeneic HSCT in our hospital. She developed back pain and fever about 150 days after HSCT and became unable to walk due to the severity of back pain. MRI T1 images showed a low intensity area, T2 images showed a high intensity area and Gd-DTPA-enhanced images showed a high intensity area at the S1-2 disk space. Clinical findings and MRI findings suggested pyogenic spondylitis. Back pain improved gradually after conservative treatment with meropenem (MEPM) for two weeks. After 4 weeks of MEPM administration, she had fully recovered and there has not been any recurrence of back pain to date. In conclusion, pyogenic spondylitis should be considered in the differential diagnoses for HSCT recipients with severe back pain.
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PMID:[Pyogenic spondylitis following unrelated hematopoietic stem cell transplantation]. 2006 78

A 65-year old woman developed progressive, firm, mild to moderately itchy, erythematous, papular and nodular lesions, over cheeks, extensors of limbs, scalp and lower back without any accompanying systemic complaints except for severe backache. Initially clinical diagnosis was cutaneous sarcoidosis. However presence of myeloblasts, monoblasts, myelocytes and metamyelocytes in peripheral blood smear and typical histopathology of nodule with mixed cellular infiltrate more around blood vessels, sweat glands and hair follicles with admixture of larger polymorphonuclears (myeloblasts/myelocytes), eosinophils with double nuclei, and larger phagocytic cells confirmed the diagnosis of acute myelogenous leukemia (AML).
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PMID:Skin changes in acute myelogenous leukemia. 2087 99

One case of acute panmyelosis with myelofibrosis (APMF) is here reported. A 45 year old male presented with abrupt onset of rapidly progressing low backache, weakness and pancytopenia. On examination there was no organomegaly. Peripheral blood examination revealed normocytic normochromic red blood cells with 10% circulating blasts. Flowcytometric examination of peripheral blood revealed blasts which were positive for CD34, HLA- DR and myeloid associated antigens (i.e. CD13 and CD33). Blasts were negative for anti MPO. Bone marrow aspirate resulted in a dry tap. Bone marrow biopsy revealed panmyeloid proliferation with scattered blasts which were CD34 positive on imunohistochemistry and negative for anti MPO. Reticulin stain showed grade III myelofibrosis (WHO). Differential diagnosis considered included AML-M7, MDS-RAEB II and AML with myelodysplasia. He was started on chemotherapy [idarubicin and cytarabine; 3+7 induction regimen followed by three cycles of HIDAC (High dose cytosine arabinoside)] after which patient was in complete morphological remission with markedly reduced bone marrow fibrosis. He is now being worked up for allogeneic stem cell transplantation. Patient is asymptomatic at eight months of diagnosis. In conclusion these patients should be managed aggressively with AML therapy and this case report reaffirms the fact that APMF is subtype of AML.
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PMID:Acute panmyelosis with myelofibrosis - a rare subtype of acute myeloid leukemia. 2379 80


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