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.