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 replacement of genetically deficient enzymes in patients with inherited metabolic disorders by infusion of purified enzymes or by organ transplantation has had very limited success, although good results with bone marrow transplantation have been obtained in some patients with mucopolysaccharidosis, Gaucher disease and inherited immunodeficiency diseases. Genetic engineering of the patient's lymphocytes may ultimately render these approaches redundant, at least for some of these diseases. Treatment of chronic pancreatic insufficiency and of disaccharidase deficiency with oral enzymes can be very effective; therapy can be monitored in the latter by measuring the breath hydrogen excretion and in the former by a range of tests of which stool chymotrypsin assay is the most convenient. Treatment of acute myocardial infarction by intracoronary perfusion of thrombolytic enzymes can improve both cardiac function and long-term survival if given early enough. Successful reperfusion can be identified by changes in the kinetics of serum enzyme release and clearance, especially for the isoenzymes and isoforms of creatine kinase. In cancer chemotherapy, L-asparaginase has long been a useful adjunct in the treatment of acute lymphoblastic leukemia, but recent experience suggests a role in acute nonlymphoblastic leukemia as well.
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PMID:Enzymes as agents for the treatment of disease. 157 79

A 19-year-old woman died suddenly 30 months after allogeneic bone marrow transplantation for refractory leukemia. On postmortem examination severe coronary artery disease and acute myocardial infarction were found. The patient had previously been given chemotherapy including daunorubicin for treatment of her leukemia. She received high dose cyclophosphamide and total body irradiation (1260 cGy) for her transplant. Diffuse chronic graft-versus-host disease, mainly affecting skin, subsequently developed, and was resistant to various therapies. The possible association of coronary artery disease and allogeneic bone marrow transplantation is discussed.
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PMID:Coronary artery disease following bone marrow transplantation. 265 18

Plasma D-dimer was measured and compared with serum fibrinogen/fibrin degradation product levels (FDPs) in patients with disseminated intravascular coagulation (DIC) and other conditions associated with a hypercoagulable state. D-dimer (N less than 200 ng/ml) was elevated in all 43 patients with DIC, in 48 of 59 patients with liver disease, in 22 of 27 patients with acute leukaemia at presentation, in 17 of 23 patients with malignant disease, in 29 of 39 women in the third trimester of a complicated pregnancy, in 17 of 18 patients with deep venous thrombosis and in only four of 27 patients with acute myocardial infarction. There was a significant correlation between plasma D-dimer and serum FDP levels (P less than 0.01) as follows; DIC: r = 0.58, liver disease: r = 0.57, acute leukaemia: r = 0.84, malignancy: r = 0.87. The frequent elevation of D-dimer observed in liver disease, acute leukaemia, malignancy and complicated pregnancy indicates that a hypercoagulable state is a common occurrence in these conditions although in liver disease elevated levels resulting from a failure of normal clearance mechanisms cannot be excluded. The close relationship between D-dimer and FDP levels suggests that serum FDPs predominantly arise from the interaction of plasmin with crosslinked fibrin rather than with fibrinogen in the conditions in which these were compared.
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PMID:Plasma D-dimer levels and their relationship to serum fibrinogen/fibrin degradation products in hypercoagulable states. 291 30

In a case of acute promyelocytic leukaemia presenting with an acute myocardial infarction a fibrin-platelet thrombus was demonstrated postmortem in the anterior descending branch of the left coronary artery. The possible pathogenesis of thrombus formation in the face of disseminated intravascular coagulation and thrombocytopenia is discussed.
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PMID:Acute promyelocytic leukaemia associated with acute myocardial infarction. A case report. 346 Jan 82

A case of a 46 year old man in whom acute myocardial infarction was the earliest outstanding clinical manifestation of an acute promyelocytic leukemia is reported. Reinfarction occurred a few days after, causing death of the patient. autopsy and histologic findings are reported and pathogenetic hypothesis are discussed. The Authors point out the role of an ipercoagulable state created by leukemia itself.
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PMID:[Acute myocardial infarct as the first manifestation of acute myeloid leukemia. Description of an anatomo-clinical case]. 694 Aug 11

The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.
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PMID:Magnesium protects against anaphylactic shock and cardiac myolysis in guinea-pigs. 873 70

Creatine kinase (CK)-MB subunit has been recognized as a useful marker for acute myocardial infarction (AMI). However, we recently experienced one case of osteopetrosis with moderately high CK-MB and an abnormal (more than 100%) CK-MB/total (T)-CK ratio without evidence of AMI in a medical examination. We have already experienced 17 cases with an abnormal CK-MB/T-CK ratios in addition to the present case. Those cases were patients with malignant tumor with metastasis (n = 13), leukemia (2), liver cirrhosis (1), and cerebral death (1), and thereby the band of macro-CK was found in the electrophoresis. However, we detected neither the band of macro-CK nor the abnormal levels of tumor markers such as CEA, alpha-fetoprotein, CA-19-9 in the present case. Instead of the macro CK, the high level of CK-BB was detected in electrophoresis. In the medical examination, especially in screening tests, the CK-MB was generally assayed with use of the immunoinhibition method in automated analyzers. The method principle was based on the absence of CK-BB in the patient serum. Since the patient had the past history of pathological fracture in his boyhood, this patient was diagnosed as osteopetrosis. These results suggest that we must consider the possibility of osteopetrosis when an abnormal CK-MB and CK-MB/T-CK ratio without evidence of serious diseases were found. This is simply because of the assay method of immunoinhibition for CK-MB activity.
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PMID:[A case of osteopetrosis with an abnormal CK-MB/T-CK ratio]. 943 4

This article reviews various studies on effects of electric and magnetic fields of extremely low frequencies on human health and gives an overview of residential and occupational exposure to different sources, currently established exposure limitations, and protection measures. Throughout the evolution biological systems adapted to natural electric and magnetic fields. Only hundred years ago human exposure to radiation was limited to electric and magnetic fields arising either from extraterrestrial or terrestrial sources, yet both natural. For the past fifty years there has been large growth of artificial sources of electric and magnetic fields, especially with frequencies of 50 and 60 Hz (power generating and distribution systems). The concern about long-term exposure to artificial fields and possible adverse effects on human health has been entirely justified and led to numerous intensive epidemiological and laboratory studies. Results of several epidemiological studies confirm the connection between exposure to electric and magnetic fields of extremely low frequencies (up to 300 Hz) and increased risk of leukemia and brain tumor in children and adults. In addition, the risk of breast cancer in occupationally exposed population has increased. Laboratory studies on animal models, in vitro systems, and human volunteers did not confirm this connection. There is a growing interest in investigation of other possible adverse health effects such as neurodegenerative diseases (Alzheimer's disease and other forms of dementia, amyotrophic lateral sclerosis), cardiovascular disorders (arrhythmias and acute myocardial infarction), psychiatric disorders, and electrosensitivity.
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PMID:[Biological effects of nonionizing radiation: low frequency electromagnetic fields]. 1105 71

A 71-year-old man with acute myelogenous leukemia (AML, M2) developed signs of chest oppression, and was diagnosed as having acute myocardial infarction (AMI). At the same time, his leukemia relapsed in association with disseminated intravascular coagulation (DIC). The patient's risk factors for AMI were hyperlipidemia, hyperglycemia, and a history of smoking. Coronary angiography showed occlusion of the circumflex branch. Percutaneous transluminal angioplasty (PTCA) was performed successfully, followed by administration of heparin. After chemotherapy, the patient's DIC improved and a second remission was attained. When elderly patients with AML show evidence of DIC, we should be aware of AMI as a possible complication. PTCA is a safe operation for such patients.
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PMID:[Acute myelogenous leukemia associated with disseminated intravascular coagulation and acute myocardial infarction at relapse]. 1168 Sep 86

This case report deals with an unusual leukostatic complication in a 56-year-old woman with acute myeloblastic leukemia (AML) and extreme hyperleukocytosis (316 x 10(9)/L) who presented with acute myocardial infarction (MI). After leukopheresis the patient achieved hemodynamic stabilization and rapid neurologic recovery of encephalopathy that had also developed after the infarction. Considering the central role of WBC in the remodeling of post MI myocardial tissue, it was obvious that administration of chemotherapy with its subsequent inevitable pancytopenia could impose an increased risk for further cardiac complications including myocardial rupture. Nevertheless, cytarabine-based induction chemotherapy was initiated 3 days after admission, and she achieved prolonged complete remission. Coronary angiography disclosed segmental atherosclerosis, but the only significant obstruction was in the right coronary artery. The patient died with relapsed leukemia 7 years later without recurrence of any cardiac symptoms or signs. Autopsy disclosed segmental coronary atherosclerosis involving the LAD (60% obstruction), suggesting that atherosclerosis was a predisposing risk factor. Additional compromise to blood perfusion due to leukostasis had led to this unusual complication of AML involving a major vessel. This is the first documented case of leukostasis causing coronary artery occlusion as well as the first report of successful induction chemotherapy for AML during a myocardial infarction.
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PMID:Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis. 1222 75


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