Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An unusual neurological syndrome occurred in 4 of 158 patients treated for osteogenic sarcoma with combination chemotherapy. There was an abrupt onset of focal cerebral deficits approximately ten days after chemotherapy with vincristine and high-dose methotrexate plus citrovorum factor rescue. The syndrome was short lived and always occurred early in the course of treatment. Prolonged neurological deficits remained in 2 patients. When similar chemotherapy was reinstituted in the 4 patients, no further neurological complications ensued. Possible causes include a leukoencephalopathy related to methotrexate or an embolic cerebral vasculopathy related to necrotic tumor microemboli emanating from the lungs.
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PMID:Transient cerebral dysfunction following chemotherapy for osteogenic sarcoma. 31 Feb 78

The authors describe the results of five pediatric patients with nonmetastatic osteosarcoma of an extremity, admitted from 1987 to 1989 to the Hospital Infantil del Estado de Sonora. Four patients presented with their primary tumor located at the distal end of the femur, whereas one had a primary lesion of the humerus. All of them received preoperative chemotherapy consisted of two cycles of cisplatin and adriamycin. One of the patients presented immediate complications after first cicle and died due to overwhelming sepsis by Candida albicans. Surgery was an amputation in one patients and block ressection in three cases. Necrosis was good in three cases, fair in one. Postoperative chemotherapy consisted of bleomycin, cyclophosphamide and dactinomycin every four weeks alternated with cisplatin plus adriamycin. One of the three patients, in which block ressection was made, had a local recurrence 12 months after diagnosis, without metastasis. He underwent desarticulation and died four months later of leukoencephalopathy and no tumor was found on necropsy. Three patients have remained continuously free of disease with follow up of 20, 26 and 31 months after diagnosis and are out of chemotherapy since 5, 12 and 17 months, respectively. In two of them the affected extremity still is safe.
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PMID:[Treatment of osteosarcoma in children with pre- and postoperative chemotherapy and block resection of the tumor]. 206 45

During the use of a therapeutic regimen of high-dose methotrexate (HD-MTX) with leucovorin rescue in two cases of osteogenic sarcoma and malignant lymphoma without central nervous system (CNS) involvement, serial EEG monitoring before and after MTX infusion was performed with special reference to occipital basic activity. The EEGs were analyzed as to the power average spectrum using an ATAC-450 (NIHON KOHDEN). At 48 hours after the initiation of MTX, there was a transient but statistically significant slowing, such as a drop in the dominant frequency and a decrease in the alpha/theta ratio. Complete recovery of EEG changes occurred within one week. No clinical symptoms suggestive of CNS impairment were noted in either case. These data suggest that EEG alterations might be a reflection of subclinical CNS impairment. Therefore, serial EEGs might be a good early indicator for the detection of leukoencephalopathy in high-risk patients.
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PMID:[Spectral EEG analysis in children treated with high-dose methotrexate]. 349 31

Osteosarcoma patients free of CNS metastases are at risk for acquiring leukoencephalopathy after receiving multiple courses of high dose intravenous methotrexate followed by oral leucovorin rescue (MTX-LV). A prospective study of the adequacy of CNS rescue of MTX biochemical toxicity by oral leucovorin was undertaken in newly diagnosed neurologically normal osteosarcoma patients. Prior to surgical resection of the primary tumor, ten patients received 4 weekly courses of MTX-LV. During the fourth weekly MTX-LV treatment, 0 and 72 hr serum and CSF determinations of MTX, 5-methyl-tetrahydrofolate (5-MTHF) and LV were made. No CSF MTX was detectable at 0 hr in any patient, but a significant elevation in CSF MTX occurred in 9/9 patients at 72 hr (mean 47.2 +/- 31.8 ng/ml or 1.04 +/- 0.7 X 10(-7) M). There was no significant change in mean CSF 5-MTHF over 72 hr despite a rise in serum 5-MTHF. MTX exceeded 5-MTHF in 6/9 patients in CSF, whereas only 3/8 patients had higher MTX in the serum at 72 hr. No acute systemic or neurotoxicity was seen. The failure of oral leucovorin to consistently elevate CSF 5-MTHF levels at 72 hr in the context of significant levels of CSF MTX may result in intermittent CNS folate deficiency. The clinical and pathological syndrome of leukoencephalopathy may be related to this phenomenon and may evolve after repeated MTX-LV treatments.
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PMID:The inability of oral leucovorin to elevate CSF 5-methyl-tetrahydrofolate following high dose intravenous methotrexate therapy. 661 87

Visual disturbance, hypertension, convulsions, and unconsciousness developed in a 70-year-old man after cisplatin chemotherapy and upper-limb amputation for osteosarcoma. MR imaging revealed bilateral reversible abnormalities in the occipital, parietal, and frontal white matter. Clinical and neuroradiologic features corresponded to reversible posterior leukoencephalopathy syndrome (RPLS), which some immunosuppressive and chemotherapeutic drugs have been reported to trigger. Cisplatin may be among these drugs. Our patient also had hypomagnesemia, which may have figured in the pathophysiology.
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PMID:Cisplatin neurotoxicity presenting as reversible posterior leukoencephalopathy syndrome. 954 27

Methotrexate (MTX) is a common antimetabolite agent that is widely used today in treating leukemia, lymphoma, and osteosarcoma. Its use has been associated with leukoencephalopathy causing seizures, paralysis, and even coma. To achieve the best possible outcome, it is important to be able to make a prompt diagnosis. Studies reported restricted diffusion on diffusion-weighted imaging (DWI) which is a reliable early sign of acute MTX-induced leukoencephalopathy. However, we report here the first case of MTX-induced leukoencephalopathy without typical restricted diffusion on DWI and the utility magnetic resonance spectroscopy to support this diagnosis in the difficult case such as the one being presented here.
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PMID:Methotrexate-induced Leukoencephalopathy without Typical Restricted Diffusion on Diffusion-weighted Imaging and the Utility of Magnetic Resonance Spectroscopy to Support the Diagnosis. 3028 63

Leukoencephalopathy with brain calcifications and cysts (LCC) is a rare cerebral microangiopathy, the cause of which was recently determined to be recessively inherited mutations in the SNORD118 gene. We report the case of a 32-year-old Irish Traveller woman who presented to the emergency department in convulsive status epilepticus with abnormal neuroimaging features characteristic of LCC. Her medical history consisted of epilepsy, intellectual impairment, previous craniotomies for excision of cerebral cysts and resection of a tibial osteogenic sarcoma. Whole exome sequencing identified a previously described homozygous variant, NR_033294.1 n.*5C>G, in the 3' UTR of the SNORD118 gene. Her sister was subsequently found to be homozygous for the same variant but with a significantly milder clinical phenotype consisting of migraine without aura and mild, non-specific, cerebral white matter changes on neuroimaging. Knowledge of the existence of LCC within this population means that targeted genetic testing for this specific mutation should be considered in Irish Traveller patients presenting with the characteristic clinical and radiological features. Given the striking phenotypic variability seen within this family, LCC should also be considered in Irish Traveller patients even in the absence of the complete radiological triad.
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PMID:Phenotypic Variability in Leukoencephalopathy with Brain Calcifications and Cysts: Case Report of Siblings from an Irish Traveller Family with a Homozygous SNORD118 Mutation. 3236 77