P14.02 Acute ataxia secondary to capecitabine

Abstract

INTRODUCTION: Capecitabine is an oral prodrug of 5-Fluorouracil (5-FU). It is metabolized to its cytotoxic form, 5-FU, by the enzyme thymidine phosphorylase and is used to treat breast and gastrointestinal adenocarcinomas. The cerebellar toxicity of 5-FU is well known, and the median time from treatment initiation to development symptoms is 9 weeks. Neurotoxicity secondary to capecitabine is rare, but it has been described neuropathy and encephalopathy with confussion and ataxia. Neurological side effects are more frequent in patients with dihydropyrimidine dehydrogenase deficiency. We report a case of acute ataxia in a patient treated with capecitabine with complete resolution of the symptomatology with medication withdrawal PATIENTS AND METHODS: A 57-years-old woman with metastasic invasive ductal breast carcinoma, hormone receptor positive, with hepatic dissemination at diagnosis, treated with radiotherapy and phenolisation of the liver metastases. Two days after the beginning of capecitabine, the patient complained about instability and headache, what was worsening during the next few days, adding dysarthria, left lateropulsion and inability to walk. The patient didn't improve with prednisone 30 mg/day, and was admitted in hospital. Neurological evaluation showed nystagmus in all directions of gaze and normal saccadic movements, scanning dysarthria and dysmetria and postural tremor in left upper limb. Truncal and gait ataxia was moderated. RESULTS: Laboratory blood test, included serum ammonia and thiamine were normal. MRI showed restricted diffusion in diffusion-weighted imaging in splenium of corpus callosum and in the posterior centrum semiovale. The changes in FLAIR and T2 secuences were subtle. Capecitabine was retired and added dexametasone 4mg/tid. The patient symptomatology improved in the next 24-48 h until full recovery. A new MRI one month later showed complete resolution of the diffusion and FLAIR changes. CONCLUSIONS: Acute ataxia and diffuse white matter encephalopathy can be a side effect of capecitabine. Onset of neurological symptoms is notably sooner than 5-FU. Despite the low frequency of neurological complications, clinicians must be aware. Resolution of symptomatology can be complete with the interruption of medication.