Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a female patient with chronic myelogenous leukemia who presented, 8 yr after initial diagnosis, with pancytopenia, encephalopathy, and myalgia. The tentative diagnosis was accelerated phase of chronic myelogenous leukemia. However, because the patient had been treated with cimetidine for 7 months we first omitted this drug. When cimetidine was stopped, bone marrow recovered, and myalgia and encephalopathy subsided. Immunological studies showed stimulation of the patient's lymphocyte blastogenesis by cimetidine and a marked increase in the proportion of cytotoxic/suppressor T lymphocytes after incubation of peripheral blood lymphocytes with cimetidine for 6 days. These findings indicate a role for cell-mediated immunity in the pathogenesis of cimetidine-induced pancytopenia in this patient.
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PMID:Immune basis for cimetidine-induced pancytopenia. 347 Oct 83

A 24-year-old man with disseminated herpes zoster, which occurred 9 months after bone marrow transplantation for chronic myeloid leukemia, developed encephalopathy and immobilizing myoclonus after 7 days of vidarabine treatment (10 mg/kg of body weight per day). Only mild hepatic dysfunction was a risk factor for a toxic reaction. After the vidarabine therapy was stopped, the symptoms worsened until treatment with hydration, large doses of chlordiazepoxide, and protective care gave symptomatic relief.
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PMID:Vidarabine-associated encephalopathy and myoclonus. 372 52

We treated 13 adult patients with acute leukemia or chronic myelocytic leukemia (CML) in blast phase using succinylated Acinetobacter glutaminase-asparaginase (SAGA) administered on a daily dose schedule. SAGA reduced the peripheral blast count in two patients with acute lymphoblastic leukemia and two with blastic CML; however, no patient achieved either complete or partial remission. Marked central nervous system toxic effects (encephalopathy and coma) were observed, limiting treatment in patients whose disease appeared responsive; this effect finally prompted early discontinuance of the trial. Other toxic effects observed included nausea, hyperglycemia, and respiratory alkalosis. Hypersensitivity reactions to the enzyme were not seen. Pharmacologic analyses showed that prolonged blood glutamine depletion was achieved only by daily enzyme administration; however, we noted the importance of performing amino acid analysis on blood which was deproteinized immediately following phlebotomy. Our results demonstrate excessive central nervous system toxicity when glutaminase-asparaginase is administered on a daily schedule. Because of this effect, we propose that future trials of similar enzymes be limited to short courses of enzyme therapy, possibly with the addition of antimetabolites or amino acid analogs, which could enhance the antitumor effect without increasing toxicity.
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PMID:Clinical evaluation of succinylated Acinetobacter glutaminase-asparaginase in adult leukemia. 704 29

Idiopathic hyperammonemia (IHA) has been described as a rare complication of intensive chemotherapy, but there is little data regarding its occurrence after bone marrow transplantation (BMT). IHA is defined as elevated plasma ammonia concentrations (> 200 mumol/l) in the absence of significant liver function abnormality. From a 21 year BMT database of 2358 patients, we have identified 12 patients (0.5%) with IHA, ages 19 to 46 years. Diagnoses included ALL (n = 2), AML (n = 4), CLL (n = 1), CML (n = 3) and aplastic anemia (n = 2). Eight received marrow from a matched sibling donor, three from an unrelated donor and one autologous marrow. IHA occurred between 14 and 106 days after transplant (median, 25 days). Most frequently patients presented with symptoms of a metabolic encephalopathy, with lethargy and confusion evolving into unresponsiveness, metabolic coma and in eight cases, seizures. At diagnosis of IHA, liver functions were normal or only modestly abnormal. Ten of the 12 patients died 1 to 9 days (median 3.5 days) after diagnosis of IHA despite treatment with combinations of dialysis and ammonia-trapping therapy. While IHA is a rare complication of BMT, it is associated with a high mortality. Early recognition of the syndrome by measurement of plasma ammonia concentrations in patients with neurological symptoms may improve outcome.
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PMID:Idiopathic hyperammonemia: a frequently lethal complication of bone marrow transplantation. 880 24

A 46-year-old man with chronic myelogenous leukemia received allogeneic bone marrow transplantation (BMT) from a partially human leukocyte antigen (HLA)-mismatched sibling. Cyclosporine (CYA)-related encephalopathy developed on days 10 and 21 following BMT, and CYA-related thrombotic thrombocytopenic purpura (TTP) developed on day 45 following BMT. We measured serum concentrations of thrombomodulin (TM) as a marker of endothelial injury. The concentrations of TM were increased during the encephalopathy or TTP and decreased following recovery. Since CYA can cause endothelial injury, we suggest that CYA-induced endothelial injury is common to the pathogenesis of both the encephalopathy and the TTP. CYA therapy should be reinstituted with extreme caution in patients with a past history of CYA-related encephalopathy, since readministration of a low-dose CYA can evoke the immediate return of the encephalopathy.
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PMID:Cyclosporine-related encephalopathy following allogeneic bone marrow transplantation. 886 27

We present a case of death likely to be directly due to cyclosporine (CsA) neurotoxicity. To date, there have been no reports of deaths directly due to CsA neurotoxicity, nor has an associated histological lesion been described independent of confounding processes. A 54-year-old male received an HLA-matched-unrelated BMT for CML. He developed progressive encephalopathy and on day +79 had a generalized seizure. All CSF studies were negative for infectious causes. MRI revealed diffuse, symmetrical white matter abnormalities located in the occipital sub-cortex, thalamus, mid brain, pons, and cerebellum which were typical of CsA toxicity. The patient died of central respiratory failure within 72 h of discontinuing CsA. Autopsy revealed diffuse patchy white matter edema and astrocytic injury without evidence of axonopathy, demyelination, microvascular injury, or infectious/inflammatory process. This case demonstrates previously undescribed lethal CsA neurotoxicity and may reveal an associated primary pathological lesion.
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PMID:Fatal outcome due to cyclosporine neurotoxicity with associated pathological findings. 1019 8

We prospectively evaluated the neuropathological complications of 180 patients who underwent autopsy studies following bone marrow transplantation (BMT) (177 allogeneic, three autologous). The most frequent underlying disorders included severe aplastic anemia (n = 55), chronic myelogenous leukemia (n = 53), acute myelogenous leukemia (n = 24) and Fanconi anemia (n = 16). There were 114 males and 66 females. Neuropathological findings were detected in 90.55% of the patients. The most frequent findings were subarachnoid hemorrhages (SAH) (n = 57), intraparenchymal hemorrhages (IHP) (n = 49), fungal infections (n = 16), Wernicke's encephalopathy (n = 10), microglial nodular encephalopathy (n = 10) and neurotoxoplasmosis (n = 8). In only 17 patients was the brain within normal limits. Survival time after BMT averaged 5.4 months and the majority of patients died in the first 3 months post BMT (n = 105). Central nervous system (CNS) pathology was the main cause of death in 17% of the patients (n = 31), with a predominance of IHP in this particular group. Furthermore, the survival time of these patients who died of CNS causes (96.3 days) was almost half of the survival time of those who died of extra-cerebral causes (177.8 days) (P = 0.0162). IHP (70. 96 vs27.22%) (P < 0.001), fungal infections (25.8 vs 8.88%) (P < 0. 001) and toxoplasmosis (9.67 vs 4.44%) (P < 0.001) were significantly more frequent in the group of patients who died due to CNS causes than in the control group. The findings of this work provide a possible guide to the possible causes of neurological syndromes following BMT. Bone Marrow Transplantation (2000) 25, 301-307.
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PMID:Neuropathological findings after bone marrow transplantation: an autopsy study of 180 cases. 1067 2

A 23-year-old woman underwent HLA-matched unrelated BMT for CML. She developed cerebral blindness on day 81. Brain magnetic resonance imaging revealed hyperintensity on a T2-weighted image in the white and gray matter of the right frontal and both occipital lobes. Single-photon emission computed tomography (SPECT) was consistent with a decrease in radionuclide uptake in these areas, suggesting a vasoconstrictive mechanism. A diagnosis of CsA-induced encephalopathy was made and CsA was discontinued. Her vision recovered completely after 24 h and abnormal imaging resolved within 2 weeks. This case demonstrates late onset CsA-induced cerebral blindness with the previously unreported abnormalities on SPECT.
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PMID:Late onset cyclosporine-induced cerebral blindness with abnormal SPECT imagings in a patient undergoing unrelated bone marrow transplantation. 1091 13

We studied clinical features of immunosuppressive (cyclosporine, tacrolimus) associated encephalopathy in bone marrow transplant patients. 378 cases of allogeneic bone marrow transplant recipients over fifteen years old of chronic and acute leukemia (CML, ANLL, ALL) (n = 311), myelodysplastic syndrome (MDS) (n = 42) and severe aplastic anemia (SAA) (n = 25) were investigated. Immunosuppressive associated encephalopathy occurred in 12 cases. The rate of incidence was significantly higher in SAA and MDS (7 cases) than in leukemia. The cases which showed typical radiological abnormality in MRI were limited in SAA and hypoplastic MDS. 10 cases died, which revealed worse than an overall survival rate of recipients without immunosupressive-associated encephalopathy. 5 of 7 cases in SAA and MDS had taken cyclosporine as treatment of the disease before bone marrow transplantation and that might influence the incidence of encephalopathy.
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PMID:[Immunosuppressive-associated encephalopathy in bone marrow transplant recipients]. 1527 97

Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia (CML) in blast crisis, accelerated or chronic phase, and also for advanced gastrointestinal stromal tumors. Severe hepatic toxicity and three deaths from hepatic failure have been reported. We report the case of a 51-year-old woman who was admitted to our institution with severe acute hepatitis. She was diagnosed with CML and began treatment with imatinib mesylate at a dose of 400 mg/d. Five months after beginning treatment, she developed severe hepatitis associated with coagulopathy, and was admitted to our institution. She had been consuming acetaminophen 500-1000 mg/d after the onset of symptoms. She had a progressive increase in bilirubin level and a marked decrease of clotting factor V. Five days after admission, grade II encephalopathy developed and she was referred for liver transplantation. Her clinical condition progressively deteriorated, and 48 h after being referred for transplantation she suffered a cardiac arrest and died. This report adds concern about the possibility of imatinib-mesylate-induced hepatotoxicity and liver failure, particularly in the case of concomitant use with acetaminophen. Liver function tests should be carefully monitored during treatment and, with the appearance of any elevation of liver function tests, treatment should be discontinued.
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PMID:Imatinib-induced fatal acute liver failure. 1816 37


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