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 thirteen-year-old boy with nominal aphasia caused by simple partial status epilepticus is described. The aphasia disappeared with intravenous diazepam and has improved on oral carbamazepine. His epilepsy is probably secondary to the cranial irradiation and intrathecal methotrexate that he received as treatment for his Acute Lymphoblastic Leukaemia at the age of nine.
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PMID:Cured of acute lymphoblastic leukaemia but lost for words. 855 19

Anti-CD7-dgA, DA7, consists of deglycosylated ricin A chain coupled to a mouse monoclonal anti-human CD7 antibody. This study determined the maximally tolerated dose (MTD) of this immunotoxin administered as a one hour infusion over five days to 11 patients with T-cell lymphoma (>30% CD7+ malignant cells). The MTD was 0.2 mg/kg/day or 1 mg/kg/120 hours (maximal toxicity grade 3) with vascular leak syndrome (VLS) as dose-limiting toxicity (DLT). Predictors of severe VLS included age and absence of circulating lymphoma cells. Two partial responses and one minimal response were seen. Patients with minimal lymphoma burden or T-cell large granular lymphocyte (LGL) leukemia showed the best responses. The mean maximal serum concentration of immunotoxin at the MTD was 2.5 ug/ml. The mean alpha-phase half-life was 1.5 hours and the mean beta-phase half-life was 8 hours. Repeated dosing had minimal effects on either peak serum immunotoxin concentrations or serum half-lives. While human antimouse antibodies were observed, they were low in concentration (<55 ng/ml). Human anti-ricin antibody was elevated in one patient (190 ng/ml). VLS presented with hypoalbuminemia, dyspnea, pulmonary edema, aphasia, and peripheral edema and cleared over a two week period. Serum fibronectin levels were measured in three patients and were very low in one patient who developed VLS. No specific binding of DA7 immunotoxin was seen with vascular endothelium in various human tissues.
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PMID:Therapy of patients with T-cell lymphomas and leukemias using an anti-CD7 monoclonal antibody-ricin A chain immunotoxin. 932 91

We report a case of primitive neuroectodermal tumor (PNET) arising 8 years after chemotherapy and radiotherapy for acute lymphoblastic leukemia. A 15-year-old boy with a history of acute lymphoblastic leukemia, at the age of 7, underwent chemotherapy and 14Gy of radiotherapy to the whole brain. He was admitted to our department due to the development of aphasia, right hemiparesis and generalized convulsive seizure. MRI showed an irregularly enhanced mass in the left frontal lobe. A gross total removal of the tumor was performed and histological examination showed it to be PNET. Postoperatively, the patient underwent 20Gy of radiotherapy to the whole brain and 42Gy of local radiotherapy. Follow-up MRI showed no evidence of recurrent tumor 4 months after the radiotherapy. This tumor was thought to be a secondary brain tumor arising in this survivor of childhood acute lymphoblastic leukemia and it is a rare complication of successful leukemia treatment.
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PMID:[Primitive neuroectodermal tumor arising 8 years after chemotherapy and radiotherapy for acute lymphoblastic leukemia: case report]. 1600 13

We report a 47-year-old woman with progressive multifocal leukoencephalopathy (PML). She was a carrier of HTLV-I virus, and developed subacute right hemiparesis and marked motor aphasia. She had a malignant lymphoma in the left neck and basal cell carcinoma in the right inguinal region. Three months after the onset, she became unable to walk because of the right leg weakness or to speak because of motor aphasia. Magnetic resonance imaging (MRI) revealed multifocal T2-high lesions in the white matter of the left frontal lobe, and a brain biopsy revealed demyelinating pathology. A biopsy of the left parotid gland revealed a diffuse pleomorphic type large B cell lymphoma. Although anti-HTLV-I antibody was positive in the serum and cerebrospinal fluid (CSF), no adult T-cell leukemia (ATL) cells were found in the blood or CSF. The patient was then admitted to our hospital. Neurological examinations revealed severe motor aphasia, mild sensory aphasia/cognitive impairment, right hemiplegia, mild right hemihypesthesia, limb-kinetic apraxia in the left hand, idiomotor apraxia, agraphia, perseveration, marked spasticity and brisk tendon reflex in four extremities, and positive bilateral pathological reflexes. MRI showed multifocal T2-high lesions mainly in the cerebral white matter, predominantly in the left hemisphere, and partly in the cerebral cortex. No gadolinium enhancement was found. In addition, 99mTcECD-SPECT showed a broad decrease in cerebral blood flow (CBF) in the cortex. Anti-HTLV-I antibody was positive but anti-HIV antibody was negative in serum. ATL cells were found in 1-3% of the peripheral white blood cells after admission. CSF examination revealed that the cell count (1/microl), protein level (24 mg/dl), and IgG index (0.4) were all normal. However, the myelin basic protein level (321 pg/ml; normal < 102) was increased, JC virus DNA was detected by PCR, and anti-HTLV-I antibody (x 8) was detected in CSF. The regulatory region of the JC virus DNA in the CSF was partly deleted; immunostaining with anti-JC virus protein antibodies revealed the existence of JC virus in biopsied brain specimens, and these findings were consistent with PML. Her symptoms such as motor aphasia, cognitive dysfunction and left hemiparesis were subacutely progressive, and she developed akinetic mutism two weeks after admission. Since the efficacy of cytosine arabinoside for PML has been reported, she was administered 80 mg/day of the drug for five days. After treatment, her communication function was mildly improved but the efficacy was transient. Since it has been reported that HTLV-I, as well as HIV, activates the JC virus promoter and its proliferation, the latent infection of HTLV-I in the central nervous system (CNS) in this case might have stimulated the JC virus proliferation, promoting lesion extension over the cerebral cortex. There have been only a few reports of broad decreases in CBF by SPECT in PML patients. Further MRI and SPECT studies on PML patients are therefore necessary to evaluate the significance of HTLV-I in promoting the JC virus infiltration into the CNS.
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PMID:[A case of progressive multifocal leukoencephalopathy presenting white matter MRI lesions extending over the cerebral cortex and a marked decrease in cerebral blood flow on SPECT, and associated with HTLV-I infection]. 1602 67

A 58-year-old male with migraine headaches, complex partial epilepsy, and secondary progressive multiple sclerosis treated with mitoxantrone was admitted to our facility in August 2005 with febrile neutropenia, worsening ataxia, aphasia, cough, and declining mental status. Bone marrow aspirate was consistent with acute nonlymphoblastic leukemia. Review of the literature reveals ten reported cases of nonlymphoblastic leukemias following treatment with mitoxantrone. Although de novo leukemia cannot be fully excluded, the likelihood of de novo disease is low given the patient's medical history. This case continues the important discussion of efficacy versus toxicity when selecting mitoxantrone as a therapeutic option for patients with multiple sclerosis. Although leukemia is rarely seen, the potential for this outcome warrants careful consideration before initiating this therapy.
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PMID:Therapy-related acute nonlymphoblastic leukemia following mitoxantrone therapy in a patient with multiple sclerosis. 1793 54

Cerebral toxoplasmosis nearly exclusively affects immunodeficient or immunocompromised patients. Mostly, it is a reactivation of latent toxoplasmosis. The pathogens, persisting in the reticuloendothelial system of heart and skeletal muscle cells, are causing a multifocal necrotizing encephalitis. The characteristic clinical features are organic psychosyndrome and focal neurological signs such as monoparesis, hemiparesis, aphasia, or seizures. Here we describe a 56-years-old patient who developed cerebral toxoplasmosis after receiving stem-cell transplantation treatment for acute myeloic leukemia, and we discuss the clinical features, differential diagnoses and therapeutic strategies.
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PMID:[Female patient with organic psychosyndrome and neurological focal signs after immunosuppressant therapy]. 1806 Mar 32

We report a patient with prolonged monoparesis and parietal periodic lateralised epileptiform discharges (PLEDs). The patient was a 73-year-old man with chronic myelomonocytic leukaemia who developed persisting monoparesis of the right arm, sensory aphasia, and finger agnosia, initially associated with focal clonic seizures. These neurological deficits remained for seven days without subsequent focal clonic seizures. The EEG showed left-sided PLEDs, maximal in the left occipito-parietal area. Ten days later, following phenytoin treatment, these symptoms suddenly improved and parietal PLEDs disappeared. Sustained PLEDs in the left parietal region may have been causally associated with ictal paresis in this patient.
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PMID:Prolonged ictal monoparesis with parietal Periodic Lateralised Epileptiform Discharges (PLEDs). 2377 6

Chimeric antigen receptor T cell therapy has become an important tool in the treatment of relapsed and refractory malignancy; however, it is associated with significant neurological toxicity. We characterized the neurological toxicity associated with chimeric antigen receptor T-cell therapy in a consecutive series of 100 patients up to 2 months post transfusion, 28 of whom were obtained from chart review and the others by prospective observation. The underlying neoplasms were lymphoma (74%), myeloma (14%), leukaemia (10%), and sarcoma (2%). The median age of the cohort was 64.5 years old and 39% of patients were female. The most commonly occurring neurological symptoms were encephalopathy (57%), headache (42%), tremor (38%), aphasia (35%) and focal weakness (11%). Focal neurological deficits are frequently observed after chimeric antigen receptor T-cell therapy and are associated with regional EEG abnormalities, FDG-PET hypometabolism, and elevated velocities on transcranial Doppler ultrasound. In contrast, structural imaging was typically normal. As this form of treatment is more widely adopted, recognition of the frequently encountered symptoms will be of increasing importance for the neurologists and oncologists caring for this growing patient population.
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PMID:Neurological toxicities associated with chimeric antigen receptor T-cell therapy. 3089 90

Sphenoorbital meningiomas require extensive bone removal around the superior and lateral orbital walls, superior orbital fissure, and anterior middle fossa floor. Incomplete resection can lead to recurrence or growth into the cavernous sinus (CS). A 46-year-old woman with a history of childhood leukemia treated with chemotherapy and whole-body radiotherapy had presented to an outside institution in 2004 with headache and vision changes and undergone subtotal resection for right sphenoorbital meningioma. Residual tumor growth caused progressive optic neuropathy, and she underwent multiple orbital decompressions and fractionated radiotherapy. In 2017, she underwent another craniotomy for repeat resection. Additional tumor growth causing neuropathic facial pain syndrome and progressive ophthalmoplegia was treated with orbital enucleation. On referral to our institution, magnetic resonance imaging demonstrated right sphenoorbital and CS meningioma extending into the sella and nearly to the medial border of the contralateral CS. Given her complete ophthalmoplegia and recent orbital enucleation, she underwent revision right frontotemporal craniotomy for radical resection of invasive meningioma, including right internal carotid artery occlusion and CS resection (Video 1). The skull-base defect was repaired with autologous fascia and a free muscle flap. Postoperative transient aphasia and left hemiparesis resolved over several days. At the 1-month follow-up examination, she was neurologically intact, with moderate improvement of facial pain syndrome (preoperative pain score, 9 of 10; postoperative pain score, 6 of 10). Magnetic resonance imaging demonstrated gross total resection. Pathological tissue analysis was consistent with grade 1 meningioma with an increased MIB-1 proliferative index, although, clinically, the tumor behaved more malignantly. The patient provided consent.
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PMID:Resection of Invasive Sphenoorbital and Cavernous Sinus Meningioma via Frontotemporal Craniotomy. 3241 38