Letter to the Editor: Vincristine-related (VCR) peripheral neuropathy during treatment of pediatric acute lymphoblastic leukemia (ALL) is relatively common, whereas severe neurologic complications are rarely described [1,2].
Our experience with such an event is instructive. Our patient was a 5-year old girl who developed an acute VCR-related flaccid paralysis while on treatment for ALL. She was enrolled in the ALL95 medium risk protocol of the Associazione Italiana Emato-Oncologia Pediatrica (AIEOP) whose induction phase consists of four weekly doses of vincristine 1.5 mg/m 2 , daunomycin 30 mg/m 2 , asparaginase 5000 U/m 2 plus prednisone 60 mg/m 2 /day for 5 weeks associated with five triple intrathecal (TIT) injections of methotrexate, prednisone, and cytarabine. The patient achieved marrow remission on Day ΓΎ 14 and tolerated this part of the protocol well. She then entered the consolidation phase: four high-dose methotrexate courses (2 g/m 2 ) in association with TIT every 2 weeks. Subsequently she began the reinduction phase which in turn comprised of four weekly doses of doxorubicin 30 mg/m 2 , vincristine 1.5 mg/m 2 , asparaginase 10000 U/m 2 plus dexamethasone 10 mg/m 2 /day for 4 weeks. No other cytotoxic drugs were administered; ranitidine was given to prevent steroid-related gastritis. The chemotherapy schedule was uneventful up to the second vincristine dose of the reinduction.
Then during dexamethasone therapy at 10 mg/m 2 /day (cumulative dose 150 mg/m 2 ) the patient showed a quickly progressive lower limb hypotonia and hyperesthesia. The cumulative dose of vincristine was 9 mg/m 2 at that point. The neuropathy evolved to flaccid paralysis of the legs and high grade paresthesia. Upper extremities involvement was represented by weakness and paresthesia. The neuropathy was evaluated as grade 4 according to WHO scoring system.
Electrophysiologic studies (peroneal nerve), showed normal motor conduction velocity, decreased action potential amplitudes, and not evocable sensory nerve action potentials thus indicating an axonal rather than a demyelinating neuropathy.
Also electromyography of the anterior tibial muscle showed signs of denervation.