Neurotoxicity of Commonly Used Antineoplastic Agents

Hd, Weiss; Walker,; Ph, Wiernik

doi:10.1056/nejm197407182910305

Cited by 225 publications

(35 citation statements)

References 43 publications

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“…Comparable morphologic changes in central neurons have been described to occur after experimental intrathecal administration of the drug in animals (17,18) and were also observed at autopsy of children with acute lymphoblastic leukemia, previously treated with vincristine (17). A direct neurotoxic effect is therefore most likely to be responsible for CNS toxicity although vincristine does not appear to penetrate the blood-brain barrier to any great extent (5). In our patient, however, the crossing into the cerebrospinal fluid might have been enhanced due to the presence of a disturbance of the blood-brain barrier.…”

Section: Discussionmentioning

confidence: 54%

“…The evidence implicating vincristine sulfate as the cause of the encephalopathy remains indirect, however, clinical manifestations of CNS toxicity have been reported previously as being associated with the use of vincristine (1,(5)(6)(7)(8)(9). In several cases, these symptoms were clearly related to severe hyponatremia and an inappropriate secretion of the antidiuretic hormone, arginine vasopressin (13)(14)(15)(16).…”

Section: Discussionmentioning

confidence: 99%

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Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report

1985

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Neurotoxicity is a well-recognized and commonly observed side effect associated with the use of vincristine sulfate in cancer chemotherapy. The clinical manifestations of vincristine neuropathy cover a wide spectrum of peripheral neurologic dysfunctions that have been described to be reversible and cumulative in most instances (1, 2). Paresthesias, loss of tendon reflexes, and progressive weakness are the most common clinical features (3, 4). Sensory impairment, cranial nerve palsies, gastrointestinal disturbances, and autonomic dysfunctions including atonic bladder, impotence, and orthostatic hypotension may occur (5). Acute CNS complications, usually presenting as generalized seizures, are extremely rare and only a few cases have been reported which were without underlying biochemical or structural abnormalities (1, 5-9). We describe the case of a woman with multiple myeloma, who developed fulminant encephalopathy following 4 days of continuous vincristine, adriamycin, and day 1-4 pulse dexamethasone (VAD) combination therapy.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report

1985

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“…While less disabling than RT, long-term toxicity compromises the survival of children with OPG who are treated with chemotherapy (Burzynski, 2006). Chronic myelosuppression (Perilongo, 2005;De Vita, Carbone, Owens, Gold, Krant & Edmonson, 1965;Kumar & Dua, 1987;Calvert, Newell & Gore, 1992), gonadal dysfunction (Calvert et al, 1992;Rivkees & Crawford, 1988;Roth, Einhorn & Greist, 1988;Clayton, Shalet, Price & Jones, 1989), renal insufficiency (Schilsky, Sherins, Hubbard, Wesley, Young & DeVita, 1981;Goren, Wright & Horowitz, 1986;Schacht & Baldwin, 1978), pulmonary toxicity (Goren et al, 1986;Schacht et al, 1978;Holoye, Jenkins & Greenberg, 1976;Jones, Moore, Blank & Castellino, 1972), neurotoxicity (Jones et al, 1972;Shingleton, Bienfang, Albert, Ensminger, Chandler & Greenberg, 1982;Weiss, Walker & Wiernik, 1974;Grunberg, Sonka, Stevenson & Muggia, 1989) including hearing loss (Grunberg et al, 1989;Hansen, Helwig-Larsen & Trojaborg, 1989;Schaefer, Post, Close & Wright, 1985) can develop. The use of carmustine and lomustine in the treatment of patients with gliomas is associated with myelofibrosis, secondary myelodysplasia and acute leukemia (Greene, Boice & Strike, 1985;Cohen, Wiernik & Walker, 1976).…”

Section: Discussionmentioning

confidence: 99%

Antineoplastons A10 and AS2-1 in the Treatment of Children with Optic Pathway Glioma: Final Report for Protocol BT-23

Burzynski

Janicki

Burzynski

2017

CCO

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Protocol BT-23, a Phase II study, was performed to determine the efficacy and safety of combination Antineoplaston A10 and Antineoplaston AS2-1 (ANP) in children with an optic pathway glioma (OPG). Sixteen patients (12 males, 4 females) ages 1 to 16 years (median age 4.5 years) were treated. The patients received ANP, by intravenous infusion, six times daily (i.e., every four hours). The length of treatment extended from a minimum of 4.1 weeks to a maximum of 210.0 weeks. The median dosage of A10 was 8.07 g/kg/d while for AS2-1 it was 0.39 g/kg/d.Patients' best response to ANP was determined: 12.5% of this patient population achieved a complete response, 18.8% achieved a partial response, and 31.3% maintained stable disease. The median overall survival was 78.5 months (95% CI: 37.6-92.3) while median progression-free survival was 45.4 months (95% CI: 7.1-71.4). ANP was associated with a 12% incidence of Grade 3 and a 12% incidence of Grade 4 adverse drug experiences (ADEs). There were no Grade 5 ADEs. Grade 3 ADEs included somnolence and elevated SGOT; Grade 4 ADEs included hypernatremia and hypokalemia. Long-term quality of life was excellent with no chronic toxicity identified. Children with an OPG respond very well to ANP with good efficacy and toxicity profiles.

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“…Vin cristine usually causes peripheral neuropathy, but has well-documented CNS effects on humans, in animal studies and on neurons in vitro [2][3][4], ¿-Asparaginase has been associated with stroke-like episodes [5]. High doses of Ara-C result in cerebellar ataxia as well as diffuse, global neurological dysfunction [6,7].…”

Section: Discussion: Dr Tz Barammentioning

confidence: 99%