Reciprocal Relationship Between a Ph-Negative Clone With Trisomy 8 Associated With Severe Myelodysplasia and a Ph-Positive Clone Following Imatinib Treatment in a Patient With Accelerated-Phase Chronic Myelogenous Leukemia (CML)

✍ Scribed by Paulina Patchenko; Abraham Klepfish; Luba Trakhtenbrot; Rachel Rothman; Eliezer A Rachmilewitz

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 224 KB
• Volume: 77
• Category: Article
• ISSN: 0361-8609
• DOI: 10.1002/ajh.20226

✦ Synopsis

Cytarabine-Induced Neurotoxicity Responding to Methyl Prednisolone

To the Editor: Neurotoxicity is a well-recognized complication following high-dose cytosine arabinoside (HIDAC). The pathophysiology of this toxicity is unknown, although an immune-mediated mechanism is hypothesized. We describe a patient with AML who suffered both cerebellar toxicity and peripheral neuropathy following high-dose cytarabine and showed excellent response to methylprednisolone.

A 40-year-old married woman was diagnosed with acute myeloid leukemia, FAB-M2, in August 2002. She received standard induction chemotherapy with cytarabine and daunorubicin in 7-day and 3-day regimens, respectively. Her bone marrow on day 21 showed marrow to be in remission. She was given consolidation chemotherapy in the form of HIDAC in the dose of 3 g/m 2 twice daily. She developed high-grade fever on day 3, and the last dose of HIDAC was withheld. She received a total of 22.5 g of cytarabine. On day 7, she developed slurring of speech followed by gait ataxia, diplopia, dysmetria, and dysdiadochokinesia. Brain MRI on day 10 showed early cerebellar atrophy. On day 35, she noted increased weakness and paresthesias of upper and lower limbs but without an increase in uncoordination. She had proximal muscle weakness of both upper and lower limbs, absent deep tendon reflexes along with impaired joint position, and light touch sensation in a glove-and-stocking pattern. Her nerve conduction study was suggestive of distal symmetrical sensorimotor largefiber polyneuropathy. A sural nerve biopsy was nondiagnostic. Cerebrospinal fluid analysis showed no cells, proteins 45 mg (40-75 mg), sugar 54 mg (corresponding blood sugar 78 mg). She was administered methyl prednisolone 1 g IV each day for 3 days followed by oral steroids (1 mg/kg). After about 6 days, she started showing improvement in her power. She continued to improve gradually. Her power in the lower and upper limbs along with cerebellar functions improved by more than 90% over next 3-4 weeks. She was able to walk independently with no uncoordination. She refused any further chemotherapy, relapsed 3 months later, and died.

The present case describes a patient with AML who had both cerebellar toxicity and peripheral neuropathy, thus implicating HIDAC as the causative agent [1][2][3]. The cause of peripheral neuropathy has been attributed to