Cells, Cultured ; Comet Assay ; DNA Damage ; drug effects ; Female ; Humans ; Lymphocytes ; drug effects ; Male ; Micronucleus Tests ; Vincristine ; toxicity

When neurological symptoms occur during the treatment of acute lymphoblastic leukemia, the differential diagnosis includes a leukemic infiltration of the nervous system, drug toxicity, infection, and other neurological disorders. We describe a 16-year-old girl with acute lymphoblastic leukemia that appeared to be complicated by vincristine-induced peripheral and cranial polyneuropathy after induction chemotherapy. She presented with right ptosis six weeks after the first dose of vincristine, and her neurological symptoms progressed to peripheral polyneuropathy. She recovered from these neurological symptoms over the next three months. Leukemic involvement of the nervous system and other neurological disorders could be excluded as potential causes of the neurological symptoms. This report shows that vincristine-induced neurotoxicity should be considered as a cause of cranial neuropathy that develops during the treatment of acute lymphoblastic leukemia.
Adolescent ; Cranial Nerve Diseases ; Diagnosis, Differential ; Drug Toxicity ; Humans ; Induction Chemotherapy ; Leukemia ; Leukemic Infiltration ; Nervous System ; Nervous System Diseases ; Polyneuropathies ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Vincristine

Dexmedetomidine, which is a selective alpha2-adrenoceptor agonist, was recently introduced into clinical practice for its analgesic properties. The purpose of this study was to evaluate the effects of dexmedetomidine in a vincristine-evoked neuropathic rat models. Sprague-Dawley rats were injected intraperitoneally with vincristine or saline (0.1 mg/kg/day) using a 5-day-on, 2-day-off schedule for 2 weeks. Saline and dexmedetomidine (12.5, 25, 50, and 100 microg/kg) were injected to rats developed allodynia 14 days after vincristine injection, respectively. We evaluated allodynia at before, 15, 30, 60, 90, 120, 180, and 240 min, and 24 hr after intraperitoneal drug (normal saline or dexmedetomidine) injection. Saline treatment did not show any differences for all the allodynia. Maximal paw withdrawal thresholds to mechanical stimuli were 3.0 +/- 0.4, 9.1 +/- 1.9, 13.0 +/- 3.6, 16.6 +/- 2.4, and 24.4 +/- 1.6 g at saline, 12.5, 25, 50, and 100 microg/kg dexmedetomidine injection, respectively. Minimal withdrawal frequency to cold stimuli were 73.3 +/- 4.2, 57.1 +/- 6.8, 34.3 +/- 5.7, 20.0 +/- 6.2, and 14.3 +/- 9.5 g at saline, 12.5, 25, 50, and 100 microg/kg dexmedetomidine injection, respectively. Dexmedetomidine shows a dose-dependent antiallodynic effect on mechanical and cold stimuli in vincristine-evoked neuropathic rat models (P < 0.05).
Analgesics/*therapeutic use ; Animals ; Behavior, Animal/drug effects ; Dexmedetomidine/*therapeutic use ; Disease Models, Animal ; Hyperalgesia/chemically induced/*drug therapy ; Injections, Intraperitoneal ; Male ; Pain Threshold ; Rats ; Rats, Sprague-Dawley ; Vincristine/toxicity

Dexmedetomidine, which is a selective alpha2-adrenoceptor agonist, was recently introduced into clinical practice for its analgesic properties. The purpose of this study was to evaluate the effects of dexmedetomidine in a vincristine-evoked neuropathic rat models. Sprague-Dawley rats were injected intraperitoneally with vincristine or saline (0.1 mg/kg/day) using a 5-day-on, 2-day-off schedule for 2 weeks. Saline and dexmedetomidine (12.5, 25, 50, and 100 microg/kg) were injected to rats developed allodynia 14 days after vincristine injection, respectively. We evaluated allodynia at before, 15, 30, 60, 90, 120, 180, and 240 min, and 24 hr after intraperitoneal drug (normal saline or dexmedetomidine) injection. Saline treatment did not show any differences for all the allodynia. Maximal paw withdrawal thresholds to mechanical stimuli were 3.0 +/- 0.4, 9.1 +/- 1.9, 13.0 +/- 3.6, 16.6 +/- 2.4, and 24.4 +/- 1.6 g at saline, 12.5, 25, 50, and 100 microg/kg dexmedetomidine injection, respectively. Minimal withdrawal frequency to cold stimuli were 73.3 +/- 4.2, 57.1 +/- 6.8, 34.3 +/- 5.7, 20.0 +/- 6.2, and 14.3 +/- 9.5 g at saline, 12.5, 25, 50, and 100 microg/kg dexmedetomidine injection, respectively. Dexmedetomidine shows a dose-dependent antiallodynic effect on mechanical and cold stimuli in vincristine-evoked neuropathic rat models (P < 0.05).
Analgesics/*therapeutic use ; Animals ; Behavior, Animal/drug effects ; Dexmedetomidine/*therapeutic use ; Disease Models, Animal ; Hyperalgesia/chemically induced/*drug therapy ; Injections, Intraperitoneal ; Male ; Pain Threshold ; Rats ; Rats, Sprague-Dawley ; Vincristine/toxicity