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)

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97

A 48-year-old Japanese man was admitted to our hospital because of general fatigue, nasal bleeding, and petechiae on his extremities. He was diagnosed with acute myelomonocytic leukemia with trilineage myelodysplasia (T-MDS). Chromosomal analysis of bone marrow cells revealed t(7;11)(p15;p15), which has been rarely reported but known to be characteristic of Japanese patients. Although t(7;11)(p15;p15) has been reported mainly in acute myelogenous leukemia (AML), it can be occasionally found in so-called stem cell diseases such as chronic myelogenous leukemia or chronic myeloproliferative disorders. Therefore, t(7;11)(p15;p15) might affect trilineage progenitors or stem cells as well as myeloid lineage cells, subsequently resulting in AML with T-MDS, as in our case reported here.
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PMID:t(7;11) and trilineage myelodysplasia in acute myelomonocytic leukemia. 861 92

Because chemotherapy alone does not eliminate clonogenic leukemic cells, disease may recur after induction and consolidation chemotherapy. Studies of patients receiving high-dose chemotherapy supported by bone marrow or blood stem-cell transplantation suggest that immune-mediated effects of transplanted cells help control disease. This antileukemic (graft-versus-leukemia) effect represents several immune reactions. Various approaches to introduce or enhance such immune reactivity in patients with acute myeloid leukemia (AML) are being explored. There is some indication, even in older patients, that immunotherapy is better tolerated than chemotherapy, and efforts are underway to find the most effective treatment for maintaining remission after induction chemotherapy. We have developed a strategy that combines myeloablative chemotherapy with transplantation of autologous stem cells that have been cultured for 1 week in interleukin-2. Low-dose interleukin-2 is also administered for the first week after stem cell infusion. Although all patients developed side effects of fever and fatigue, even older patients tolerated this regimen well. The 3-year disease-free survival rate in a high-risk patient group transplanted in early first remission is 41 percent. Several other compounds are being investigated for their ability to enhance immune reactions after induction chemotherapy for AML. Although immunotherapy cannot eliminate overt leukemia and cytoreductive treatment is still needed initially, immunotherapy may find a place in postinduction management of AML to eliminate minimal (residual) disease or control its growth.
Leukemia 1996 Apr
PMID:Role of postinduction immunotherapy in acute myeloid leukemia. 861 64

A 76-year-old man was admitted to our hospital in February, 1994 because of fever and general fatigue. The patient had received radical gastrectomy for gastric cancer in August, 1987 and was subsequently treated with adjuvant chemotherapy using UFT for 25 months. On admission, the leukocyte count was 57,700/microliters with 74% blasts. Bone marrow aspiration revealed proliferation of blasts with marked giant cells and polynucleolar cells. The diagnosis of T-lineage of acute lymphoblastic leukemia (ALL) was then made by analysis of surface markers and T-cell receptor rearrangement. Although combination chemotherapy was initially effective, blasts rapidly reappeared in the peripheral blood, and the patient died of pneumonia in August, 1994. In the presented case, blasts showed marked morphologic abnormalities. It is well known that most cases of therapy-related leukemia deviate from the myeloid lineage, and rarely from the lymphoid lineage. In addition, morphologic abnormalities are rare in de novo ALL. Since such abnormalities were demonstrated in our patient, and UFT was administered for a long period, it is possible that this leukemia occurred as a second malignancy related to UFT treatment.
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PMID:[Acute lymphoblastic leukemia with marked morphologic abnormalities after chemotherapy for gastric cancer]. 868 64

A multi-institutional cooperative group trial was undertaken by the Cancer and Leukemia Group B (CALGB) to evaluate the efficacy of the combination of cisplatin and intravenous etoposide for the treatment of metastatic or recurrent non-small cell lung cancer (NSCLC). The doses used were those previously determined to be the maximally tolerated dose of this drug combination. Forty patients were entered into the trial, 37 of whom were eligible for evaluation. Cisplatin (35 mg/M2/day for 3 days) and etoposide (200 mg/M2/day for 3 days) were administered every 28 days for a planned 6 cycles of therapy. Sixteen of 37 evaluable patients (43%) responded to therapy. Myelosuppression was the dominant toxicity, with 89% of the patients experiencing grade 4 neutropenia, and nearly half grade 3 or 4 thrombocytopenia. Median survival was 8.5 months, with 30% of the patients alive at 1 year and 10% alive at 2 years. Malaise, fatigue, and peripheral neuropathy were the other major toxicities. The combination of etoposide at the dose of 200 mg/M2/day for 3 days and cisplatin at 35 mg/M2/day for 3 days is a highly potent combination against metastatic non-small cell carcinoma.
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PMID:Etoposide (VP-16) and cisplatin at maximum tolerated dose in non-small cell lung carcinoma: a Cancer and Leukemia Group B study. 871 68

A 67-year-old female was admitted with fatigue. Peripheral blood examination showed severe pancytopenia. Bone marrow biopsy revealed hypoplastic marrow. She was diagnosed as having aplastic anemia. Steroid pulse therapy was not effective. After treatment with erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF), blasts which were positive for CD13, CD33, CD34 and HLA-DR and negative for myeloperoxidase appeared in the peripheral blood. At this time, bone marrow biopsy revealed myelofibrosis with increased blasts. Chromosome analysis showed 46XX, add (1) (p36), add (1) (q44), -2, -5, del (7) (q11), -12, +3mar. She died of pneumonia despite chemotherapy with etoposide. Administration of EPO and G-CSF may have led to the rapid development of leukemia and myelofibrosis.
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PMID:[Transformation of aplastic anemia to acute myeloid leukemia with myelofibrosis following treatment with granulocyte colony-stimulating factor and erythropoietin]. 877 84

A 62-year-old Japanese man complained of fever, general fatigue, anorexia and watery diarrhea during remission of adult T-cell leukemia-lymphoma. Laboratory examinations showed severe hypoproteinemia (2.9 g/dl). However, neither intestinal lesions associated with ATL nor findings suggesting protein losing gastroenteropathy were observed. Cytomegalovirus (CMV) antigen detection assay using peripheral blood leukocytes revealed that he had an active CMV infection with hemophagocytic syndrome. Treatment with ganciclovir and methylprednisolone led to an improvement of hypoproteinemia. CMV disease and associated hemophagocytic syndrome should be considered as a cause of hypoproteinemia in an immunocompromised host.
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PMID:[Cytomegalovirus disease accompanied by severe hypoproteinemia in a patient with adult T-cell leukemia-lymphoma]. 884 9

Fifty-four former patients, in remission after acute leukaemia or highly malignant lymphoma, responded to a questionnaire covering their physical problems, their view of the help they received, who was most helpful to them during the treatment phase, and the impact of the disease and treatment on their current life. Energy loss and nutritional problems were most troublesome during the treatment phase, signifying many other physical problems. Patients with acute leukaemia had more problems, and thought the care was worse than did patients with highly malignant lymphoma. Serious physical problems correlated with low satisfaction with practical help received, indicating that the nurses failed to meet the needs of those suffering the most. Reduced psychological and sexual energy persisted in remission, showed no correlation with the extent of physical problems during the treatment phase, but correlated with co-existing problems and sensitivity to infections, with a great need for intimate help and counselling and with a low sense of coherence. Family relationships were said to have improved, while work and finances were negatively affected. The results indicate that nursing care should actively focus on physical problems, especially on energy loss and nutritional problems. The overwhelming fatigue hinders patients in taking physical care of themselves, and may be overlooked by the nurse since their motor capability seems intact. The long-term effect of the illness means a reduced psychological and sexual energy and a high degree of existential problems and sensitivity to infections, which indicates the importance of follow-up care, and perhaps especially of counselling for the long-term reactions and disturbance of equilibrium.
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PMID:Survivors of acute leukaemia and highly malignant lymphoma--retrospective views of daily life problems during treatment and when in remission. 900 13

To determine major presenting features of chronic myeloid leukaemia (CML) in current practice, we have reviewed the records of 430 patients with CML referred to the Hammersmith Hospital for allogeneic bone marrow transplantation since 1981. Approximately 20% of cases were diagnosed incidentally. Symptoms such as fatigue and weight loss were associated with greater degrees of leucocytosis and splenomegaly and lower haemoglobin levels. Most bleeding patients had normal or elevated platelet counts, suggesting that platelet dysfunction was the primary cause of haemorrhage. Although thrombocytosis was common, thrombosis was not seen. Male patients and the relatively young presented with higher WBC counts and larger spleens. The reason that these groups were diagnosed with more advanced leukaemia is not clear. Although retrospective and limited to a select group of relatively young patients, this is the largest series to be reported on CML at diagnosis, and the first such report in modern clinical practice.
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PMID:Clinical features at diagnosis in 430 patients with chronic myeloid leukaemia seen at a referral centre over a 16-year period. 901 96

2-Chlorodeoxyadenosine (2-CdA) is a purine nucleoside analogue with therapeutic activity in low-grade lymphoproliferative disorders. In addition, 2-CdA has a potent myelosuppressive effect, and it has been shown to be toxic to malignant myeloid cells both in vitro and in vivo. In this pilot study we treated nine patients who had advanced myelofibrosis with myeloid metaplasia (MMM) and progressive hepatomegaly or symptomatic thrombocytosis after therapeutic splenectomy. 2-CdA was administered at 0.05-0.1 mg/kg/d for 7 d for one to five treatment cycles. A reduction in liver size associated with marked improvement in fatigue and control of thrombocytosis and leucocytosis was achieved in seven of the nine patients (78% response rate). In four of the seven responding patients the reduction in liver size was durable (4-28 months) and was associated with a decrease in serum alkaline phosphatase levels. However, no patient had improvement in anaemia, and two of the seven initially responding patients have since died of acute leukaemia or progressive disease. Improvement in bone marrow fibrosis was noted in two of five available post-treatment marrow examinations. Toxicity was mainly myelosuppression, which was severe in two patients. 2-CdA may be considered a palliative therapeutic agent after splenectomy in noncytopenic patients with MMM who have progressive hepatomegaly or extreme thrombocytosis.
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PMID:2-Chlorodeoxyadenosine treatment after splenectomy in patients who have myelofibrosis with myeloid metaplasia. 969 87


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