Comparison with other studies
To date there are around twenty case reports and a few small case series of no more than three paediatric patients 4. Symptom onset mostly occurred during the induction phase of treatment4. Similarly in the other cases that were identified symptoms resolved after cessation of vincristine which had variable rates of recovery from weeks to months. It is known that drugs such as itraconazole, ,erythromycin, isoniazid, phenytoin and mitomycin c may increase the toxicity of vincristine thus making neurotoxicity more likely 5,7. Further to this, hepatic impairment may also contribute as vincristine is metabolised by the cytochrome p450 enzymes. L-asparaginase, often concomitantly administered with vincristine impairs the hepatic clearance of vincristine thus increasing the chances of toxicity 5. A genetic predisposition to vincristine toxicity has also been suggested via a polymorphism of a promotor region of one of the genes that encodes microtubule formation7.
It is however possible that vcp due to vincristine is likely to be under reported with only severe cases of patients with breathing difficulties, stridor of severe hoarseness being reported. Previous studies have described prevalence rates at 1.36% 8 and 1.9%5. This also generates the discussion as to whether any other chemotherapy agents are associated with vocal cord paralysis. Vinblastine, another vinca alkaloid is implicated in adult vcp9 as well as cisplatin10 .
There has been some work to see if anticholinesterase inhibitors such as pyridostigmine given prophylactically to prevent neurotoxicity in patientsgiven vincristine however these agents do not appear to be protective5.