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Transverse myelopathy: case report A 13-year-old girl developed transverse myelopathy during treatment with methotrexate and cytarabine for B-cell acute lymphoblastic leukaemia (ALL). The girl was diagnosed with B-cell ALL. Later, she also developed lymphoblastic meningitis. She received treatment with prednisolone 1620 mg/m2, dexamethasone 252 mg/m2, pegaspargase [PEG-asparaginase] 9898 U/m2, high dose IV methotrexate 5 g/m2/course and cytarabine [cytosine arabinoside] 2 g/m2 along with various concomitant medications. Later she started intrathecal (IT) chemotherapy with methotrexate 12mg, cytarabine 15mg [aracytine] and methylprednisolone 30mg [solumedrol]. During the treatment she developed toxicities in the form of corticosteroid induced insulin-dependent diabetes, cholestatic jaundice, and major hypertriglyceridemia associated with pegaspargase therapy. She also developed severe corticosteroid-induced osteonecrosis in both knees. She suffered from pulmonary aspergillosis. Following 7 months of intensive chemotherapy, she began to experience symmetric distal hypoesthesia in lower limbs and numbness in feet with slight ataxia. Electromyographic examination revealed a reduction in sensory and motor nerve conduction velocity, and reduced motor response amplitude. Distal motor latencies were also prolonged, which was compatible with demyelinating and axonal polyneuropathy. The girl started receiving vitamin-B-complex [vitamin-B] supplementation. However, no clinical benefit was noted. The numbness gradually became more significant and hypoesthesia of lower limbs ascended to lower abdomen and perineum. She experienced loss of sensitivity during defecation and miction with intermittent urinary and fecal incontinence. Clinical examination showed a sensory level around T10, paraparesis with areflexia, static and kinetic ataxia impairing walk. The MRI in short TI inversion recovery ponderation revealed homogenous hyperintensity in posterior segment from T9 to T11, without gadolinium enhancement, suggested a dorsal myelitis. Differential diagnosis of postinfectious acute myelopathy or toxic transverse myelitis was established. She was admitted and a lumbar puncture showed a slightly elevated cerebrospinal fluid (CSF) protein without lymphoblastic invasion. CSF was negative for JC/BK virus, Mycoplasma, and Herpes simplex virus infections. CSF analysis revealed low level of methionine, highlighted blood-brain barrier integrity. Based on these findings and clinical presentation, she was diagnosed with transverse myelopathy related to the methotrexate and cytarabine. IT injections of methotrexate and cytarabine were stopped. She achieved CNS prophylaxis through methylprednisolone IT injections alone. Prior to the first clinical myelitis symptoms she received 4 courses of IV methotrexate and 16 IT chemotherapy injections. Scheduled doses of IV methotrexate were also cancelled. She achieved transient clinical improvement following 3 courses of methylprednisone. Due to persistent symptoms dextromethorphan was initiated alo