Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with acute lymphocytic leukemia is described who developed meningeal leukemia 14 months after the initial diagnosis was made. As part of his antileukemic therapy, at that time, he received prednisone and vincristine, given prophylactically to maintain a bone marrow remission. He inadvertently received 15 mg of vincristine instead of 1.5 mg. Following this overdosage he developed pancytopaenia, mild neurotoxicity and subsequently a grand mal seizure associated with the delayed onset of hyponatremia. This was presumed to be due to the inappropriate secretion of antidiuretic hormone (ADH) secondary to vincristine toxicity. This responded to fluid restriction and anti-epileptiform therapy.
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PMID:Inappropiate ADH secretion associated with massive vincristine overdosage. 16 81

We describe fatal rhabdomyolysis in a 24-year-old man who had received a bone marrow transplant from a sibling for the treatment of chronic granulocytic leukaemia. The rhabdomyolysis was preceded by a grand mal seizure probably caused by a combination of cyclosporin A and corticosteroids given for the prevention and treatment of acute graft-versus-host disease.
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PMID:Fatal rhabdomyolysis as a complication of bone marrow transplantation. 239 Jun 34

Inorganic arsenic trioxide (As(2)O(3)) induces a high proportion of complete remissions in relapsed patients with acute promyelocytic leukemia (APL). Previously, we have shown that both As(2)O(3 )and melarsoprol, an organic arsenical used for the treatment of trypanosomiasis, exhibit broad antileukemic activity against both chronic and acute myeloid and lymphoid leukemia cell lines. Given the breadth of this activity, we initiated a clinical study to evaluate the pharmacokinetics, safety, and potential efficacy of melarsoprol in patients with refractory or resistant leukemia. Using the antitrypanosomal dose and schedule, patients received escalating intravenous doses daily for 3 days, repeated weekly for 3 weeks. Doses were 1 mg/kg on day 1, 2 mg/kg on day 2, and 3.6 mg/kg on day 3 and on all days thereafter, up to a maximum daily dose of 200 mg. Eight patients [6 AML (2 morphologic APL), 1 CML, 1 CLL] were treated. Mean peak plasma concentrations of the parent drug were obtained immediately after injection, ranged from 1.2 microg/ml on day 1 to 2.4 microg/ml on day 3, were dose proportional, and decayed with a t(1/2) congruent with 15 min. A minor clinical response (regression of splenomegaly and lymphadenopathy) was observed in a patient with chronic lymphocytic leukemia. Central nervous system (CNS) toxicity proved limiting on this dose and schedule. Three patients experienced generalized grand mal seizures during the second week of therapy. We concluded that this dose and schedule of melarsoprol is associated with excessive CNS toxicity and that verification of the striking preclinical activity in patients with leukemia will require developing an alternative dose and schedule.
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PMID:Clinical study of an organic arsenical, melarsoprol, in patients with advanced leukemia. 1050 16

Allogeneic bone marrow transplantation is frequently associated with neurological complications, particularly intracerebral bleeds and infections. Cerebral venous sinus thrombosis has only rarely been reported following allogeneic transplants. We report three cases of cortical venous thrombosis following allografting for acute lymphoblastic leukaemia. Two patients received marrow from HLA-identical siblings and one from an unrelated donor. Two of the patients presented with grand mal seizures and one presented with a headache. No neurological abnormalities were found upon clinical examination and lumbar puncture was normal in all three cases. In two of the patients computed tomography (CT) of the brain was normal and in the third showed non-specific abnormalities. Magnetic resonance imaging (MRI) with MR angiography (MRA) demonstrated cerebral venous sinus thrombosis in all three patients. In conclusion, cerebral venous sinus thrombosis should be considered in the differential diagnosis when neurological symptoms occur following allogeneic bone marrow transplantation. We therefore advocate the use of MRA for unexplained neurological symptoms post-allograft since without it cerebral venous sinus thrombosis may easily be missed.
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PMID:MR angiographic diagnosis of cerebral venous sinus thrombosis following allogeneic bone marrow transplantation. 1074 67