SummaryWe assessed the safety and efficacy of melphalan, arsenic trioxide (ATO) and ascorbic acid (AA) (MAC) combination therapy for patients with multiple myeloma (MM) who failed more than two different prior regimens. Patients received melphalan (0AE1 mg/kg p.o.), ATO (0AE25 mg/kg i.v.) and AA (1 g i.v) on days 1-4 of week 1, ATO and AA twice weekly during weeks 2-5 and no treatment during week 6 of cycle 1; during cycles 2-6, the schedule remained the same except ATO and AA were given twice weekly in week 1. Objective responses occurred in 31 of 65 (48%) patients, including two complete, 15 partial and 14 minor responses. Median progression-free survival and overall survival were 7 and 19 months respectively. Twenty-two patients had elevated serum creatinine levels (SCr) at baseline, and 18 of 22 (82%) showed decreased SCr levels during treatment. Specific grade 3/4 haematological (3%) or cardiac adverse events occurred infrequently. Frequent grade 3/4 non-haematological adverse events included fever/chills (15%), pain (8%) and fatigue (6%). This steroid-free regimen was effective and well tolerated in this heavily pretreated group. These results indicate that the MAC regimen is a new therapeutic option for patients with relapsed or refractory MM.

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Dihydropyrimidine dehydrogenase deficiency is diagnosed more frequently and is now generally accepted as a potentially life-threatening condition. It predisposes patients receiving treatment with fluoropyrimidines such as 5-fluorouracil (5-FU) to severe and, in case of complete dihydropyrimidine dehydrogenase deficiency, often fatal toxicity. A patient who had severe side effects following standard dose adjuvant 5-FU exposure was diagnosed of having hereditary partial dihydropyrimidine dehydrogenase deficiency. When the patient relapsed with liver metastases, we treated him with the non-fluoropyrimidine cytotoxic agents irinotecan, oxaliplatin and raltitrexed in sequential manner, and were able to show that these drugs can be safely applied in patients with this metabolic defect.

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