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)

The clinical, hemodynamic and radiologic signs of pericardial effusion are reviewed. From the symptomatic point of view low pressure (lax) pericardial effusion and compressive effusion (tamponade) are to be distinguished. Echocardiography is today the preferred method for study of patients with suspected pericardial effusion. This technique also provides insight into ventricular performance and is therefore helpful in the differential diagnosis of cardiomegaly due to pericardial effusion, heart failure or both. In our material uremic pericarditis, malignant tumors and leukemia were the predominant causes of pericardial effusion.
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PMID:[Diagnosis and differential diagnosis of pericardial effusion]. 13 71

A case of hypereosinophilic syndrome is reported. Investigation failed to reveal any precipitating cause or evidence of leukaemia. Death was due to intractable cardiac failure, and post-mortem examination showed infiltration of the myocardium with sheets of immature cells. The relevance of these cells is discussed and further investigation such as cardiac biopsy is suggested for similar cases.
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PMID:Myocardial infiltration with immature cells in hypereosinophilic syndrome. 43 70

One hundred consecutive patients with hemoglobin concentration less than 3.5 g/dL (hematocrit reading, less than 10%) were admitted to the University of Baghdad Teaching Hospital, Iraq, during a 30-month period. Twenty-eight patients had aplastic anemia, 27 had leukemia or other hemopoietic malignancies, 16 had chronic renal failure, eight had iron-deficiency anemia, eight had hemolytic anemia, seven had thalassemia major, and six had other conditions. Twenty-three patients died within seven days of admission, mostly due to the underlying disease or complications thereof. Heart failure developed in ten patients, and five had retinal exudates and hemorrhages attributed to severe anemia. Arrhythmias and ECG abnormalities were noted in 20 of 68 patients. Blood transfusion was instituted in all but three patients, whose anemia was corrected with specific therapy without blood transfusion. The tolerance of the 100 patients to such severe anemia was remarkable.
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PMID:Severe anemia. Clinical observations in 100 patients with very low hemoglobin levels. 47 23

Sixteen patients who had died with leukemia were studied at autopsy between September 1975 and Februrary 1977. Special attention was given to degenerative changes in the heart. Five of the patients died of cardiac failure, all with no or only slight leukemic infiltration in various organs at autopsy. Five patients showed basophilic necroses in the myocardium, and two of these also showed necroses in the bone marrow. The myocardial lipofuscin was significantly (P less than 0.01) higher in the autopsies of leukemic patients (mean age 45 years) than in autopsies performed at the Department of Forensic Medicine in 18 cases of accidental death (mean age 36 years). No dose-response relationship could be found between the amount of myocardial lipofuscin and the total dose of rubidomycin. Eight of twelve patients with malignant lymphoma (mean age 45 years) also had increased amount of myocardial lipofuscin.
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PMID:Cardiomyopathy in leukemia, with reference to rubidomycin cardiotoxicity. 53 24

A 12 year old boy died after a 3 year course of recurrent and progressive heart failure. His cardiac symptoms began with a marked leukocytosis (white blood cell count 188,500/mm3) due to eosinophilia (90 percent). In 6 months, the leukocytosis and eosinophilia subsided, but the patient's heart failure progressed over the next 2 1/2 years. At autopsy there was no evidence of leukemia, but a severe endocardial fibrosis extending into the myocardium was found. The origin of endomyocardial fibrosis, although unknown, appears to have been related to the eosinophilia in this patient.
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PMID:Eosinophilia and endomyocardial fibrosis. 125 75

We report a case of essential thrombocythemia (ET) that climaxed in acute myeloid leukemia after developing into refractory anemia. The male patient had ET that was stable for 8 years on carboquone therapy. However, at the age of 72 years he developed an acute terminal illness that was characterized by severe pancytopenia, circulating myeloblasts, extensive bone marrow infiltration by myeloblasts, and an abnormal karyotype [46, XY, t(8q-; 20q+)]. He subsequently died of severe bilateral pneumonia and heart failure. This case suggests that ET may be similar to polycythemia vera; progression to leukemia is unusual except after chemotherapy. Therefore, treatment of patients with asymptomatic ET may not be advisable.
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PMID:Essential thrombocythemia developing into refractory anemia and complicated by acute myeloid leukemia. 128 33

Leukaemia and its associated therapy result in pathophysiological peculiarities relevant to anaesthesia. Leukaemic patients suffer from anaemia, coagulation disorders, and the consequences of immunosuppression. In addition, some patients show infiltrations of the oropharynx, potentially resulting in difficult intubation and/or pharyngeal haemorrhage. Mediastinal masses can induce complete airway obstruction during general anaesthesia. Patients with a white blood cell count (WBC) greater than 100,000/mm3 (hyperleukocytosis) can suffer from the leukostasis syndrome with acute respiratory failure as well as cerebral vascular occlusions and bleeding due to increased blood viscosity and disturbed microvascular perfusion. Since this syndrome may be triggered by surgery, the WBC should be reduced prior to general anaesthesia in patients with hyperleukocytosis. To avoid development of the leukostasis syndrome, transfusion of packed red cells should be restricted in these patients. Hyperleukocytosis can simulate in-vitro hypoxaemia due to the excessive oxygen consumption of the mass of leukaemic blood cells during routine blood gas analysis. Therapy of leukaemia can lead to the tumor-lysis syndrome with hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia, and hypoglycaemia, and may induce acute renal failure. Since drug interactions have only been evaluated for the combination of two or three drugs, interactions of cytotoxic agents with anaesthetics can hardly be predicted because of the large number of drugs simultaneously administered to leukaemic patients. The heart and lungs are target organs for the acute or chronic side effects of cytotoxic drugs, resulting in non-cardiogenic pulmonary oedema (e.g., cytosine-arabinoside), lung fibrosis (e.g., bleomycin), or arrhythmias and cardiac failure (e.g., adriamycin). The severity of these side effects depends on pre-existing organ disease and only in part on drug dosage. Only HLA- and CMV-compatible blood components should be administered to leukaemic patients. Hyperleukocytosis and the first days of cytotoxic treatment represent relative contraindications to general anaesthesia.
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PMID:[Pathophysiologic and anesthesiologic characteristics of patients with leukemia]. 152 54

One hundred and nine consecutive patients with de novo acute nonlymphocytic leukemia aged over 56 years were admitted with the intention of administering high-dose cytosine arabinoside (HD Ara-C) intensification. After remission induction, the patients were consolidated with a course of daunorubicin (30 mg/m2/day, days 1-3) and Ara-C (100 mg/m2/day, days 1-7), followed by the intensification (Ara-C, 2 g/m2/12 h, days 1-4). The planned induction course was not started in 13 patients because of cardiac failure or unsatisfactory general status. Remission was achieved in 55% (53/96) of the patients. Twenty-seven patients (28%) had refractory disease, seven died early during induction therapy, five died of hemorrhage and three of infection during the hypoplasia that followed induction treatment. Thirty-nine patients started consolidation and 32 had the planned intensification. In these last patients the 3-year leukemia-free survival (LFS) probability was 29% (SE, 8%). No patient died as a consequence of intensification. The relapse rate of the intensified patients did not differ from the relapse rate of those patients who did not receive the planned intensification (p = 0.12). The only pretreatment variables significantly associated with a better LFS were younger age (p = 0.02) and a low WBC at diagnosis (p = 0.04). For the whole patient group, the 3-year survival probability was 15% (SE, 4%). This study shows that elderly patients can tolerate HD Ara-C. The patients completing consolidation-intensification have a currently acceptable LFS. To what extent HD Ara-C contributed to the length of the remissions remains unclear.
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PMID:High-dose cytosine arabinoside intensification for acute nonlymphocytic leukemia in patients over 56 years of age. 158 6

Monoclonal gammopathy of type IgG-lambda (IgG concentration 27.8 g/l) was discovered by chance in a 66-year-old woman with aortic and mitral valve disease. The patient declined any further diagnostic procedures. Three months later she experienced severe pain in the lumbar spine and developed decompensated cardiac failure with pulmonary and ankle edema. The IgG concentration had risen to 50.5 g/l. Echocardiography showed a large pericardial effusion and 600 ml of bloodstained fluid containing numerous plasma cells was aspirated (total protein 81.8 g/l, gamma-globulin 38.9%). Iliac crest biopsy showed diffuse infiltration with polymorphic plasma cells, but the differential count in peripheral blood was unremarkable. Multiple myeloma of Stage IIa was diagnosed and she was given cytostatic therapy with 17.5 mg melphalan and 112 mg methylprednisolone daily by mouth (for 4 days at intervals of 6 weeks). Though at first the IgG concentration fell, it later rose again. The beta 2-microglobulin level was raised at 30 mg/l. After three cycles of chemotherapy the patient complained of severe pain in the hips and thighs. The blood film now showed numerous, predominantly immature plasma cells. A few days later, having been ill for four months in all, she died, showing all the signs and symptoms of plasma cell leukaemia.
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PMID:[IgG-lambda-type multiple myeloma with plasma-cell pericardial effusion and terminal plasma-cell leukemia]. 142 69

A 14-year-old girl with acute promyelocytic leukemia (APL) developed cardiomyopathy following chemotherapy for remission induction and subsequent consolidation consisting of cumulative doses of 644 mg/m2 of daunorubicin and 31 mg/m2 of mitoxantrone. Six months after the first complete remission, when relapse of APL was recognized an allogeneic bone marrow transplantation (BMT) from her HLA-identical brother was performed. A preconditioning regimen, consisting of cytarabine (Ara-C, 2 g/m2/day x 3 days and 4 g/m2/day x 3 days), total body irradiation (TBI, 1200 cGy) and etoposide (VP-16, 50 mg/kg) caused moderate gastrointestinal symptoms and transient hemorrhagic cystitis, but did not worsen her cardiac function. Both continuous intravenous administration of heparin to control DIC and continuous low dose dopamine infusion to prevent cardiac failure achieved their purpose. The patient is leukemia-free and has no symptoms related to cardiomyopathy at the eight month after BMT. A preconditioning regimen (Ara-C, TBI and VP-16) appeared to be suitable for BMT to a patient with anthracycline-induced cardiomyopathy.
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PMID:[A successful allogeneic bone marrow transplantation for acute promyelocytic leukemia with anthracycline-induced cardiomyopathy at relapse]. 160 7


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