Page 298 - Personalised medicine of fluoropyrimidines using DPYD pharmacogenetics Carin Lunenburg

Chapter 11
after toxicity was resolved. A reduced enzyme activity of 3.8 nmol/(mg*h) and two variants (DPYD*2A and c.1236G>A/c.1129-5923C>G) were found. Approximately a year later, the patient was again treated with the unknown reduced capecitabine dose and oxaliplatin, which was stopped after six cycles due to toxicity. No additional analyses for this study were performed for this patient.
Patient 7
A 61 year old patient was diagnosed with disseminated colorectal cancer (pT4N1M1) who underwent surgical hemicolectomy. Palliative chemotherapy consisting of capecitabine (1,000 mg/m2 twice daily, day 1─14), oxaliplatin (130 mg/m2, day 1) and bevacizumab (7.5 mg/kg, day 1) was started. After eleven days of chemotherapy, the patient was admitted to the hospital with CTC-AE grade 3 diarrhea and nausea with vomiting, and CTC-AE grade 2 fever. Capecitabine was stopped immediately. Loperamide therapy was started but the diarrhea persisted. The patient was discharged from the hospital after 13 days. The measured DPD enzyme activity was low (1.6 nmol/(mg*h)), and DPYD genotype was DPYD*2A and c.1236G>A/c.1129-5923C>G, both measured after therapy. No additional analyses for this study were performed for this patient.
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