A 38-year-old African American female with refractory stage IV mycosis fungoides with large cell transformation was admitted to the hospital for initiation of ICE chemotherapy. Patient had extensive cutaneous and muscle involvement of the lymphoma and had failed multiple lines of chemotherapy regimens including romidepsin and rituximab, brentuximab, and gemcitabine. Laboratory testing prior to initiation of ICE therapy was normal except for low serum albumin level of 1.7 g/dL. Patient received ICE therapy with etoposide 100 mg/m2 on days 1 to 3, ifosfamide 5000 mg/m2 on day 2 infused over 24 hours, and carboplatin with an AUC of 5 on day 3. She was premedicated with aprepitant for prevention of nausea. She was alert and oriented prior to and during the infusion but became lethargic, somnolent, and confused within 6 to 8 hours of completion of ifosfamide infusion. Physical examination was significant for random jerky movements of both upper and lower extremities, twitching of the right eye, and somnolence. The patient’s evaluation for sudden neurological changes included complete blood count, comprehensive metabolic panel, computed tomography scan of the head, and infectious workup (blood cultures, urine culture, and chest X-ray), all of which were negative. She received naloxone with no reversal of mental status changes. Based on the timing of the infusion and change in mental status, patient was diagnosed with IME and MB was immediately initiated at a dose of 50 mg every 4 hours. An improvement in the patient’s mental status was noticed within 12 hours of initiation of MB, and the patient was back to her baseline in 72 hours (received 18 total doses). Given the neurotoxicity, patient was not rechallenged with ifosfamide and was switched to a different chemotherapeutic regimen.
This is a 13-year-old boy with no pathological history, hospitalized in the\nhematology-oncology department for abdominal rhabdomyosarcoma. The history of the disease\ngoes back to 3 months of his hospitalization by the installation of abdominal pains with\nprogressive deterioration of the general condition. On admission, the patient was conscious\nwith a GCS score 15/15, apyretic with impaired general condition, weight = 30 kg. Physical\nexamination revealed a large papable abdominal mass extending from the epigastric to the\nright hypochondrium. Ultrasound then abdomino-pelvic Computed tomography (CT) scan confirmed\nthe diagnosis by objectifying a median retro-peritoneum mass. The biological assessment was\nnormal. An ultrasound-guided biopsy was performed. The histological diagnosis was in favor\nof an undifferentiated sarcoma. Extension workup revealed lung micronodules and peritoneal\nnodules under the liver. The child was put on anti-cancer treatment combining\nifosfamide-vincristine-actinomycin (IVA) and MesnaR to prevent urological\ntoxicity. The dosages of these molecules were: Ifosfamide (3 g/m2/day) 3 g/day as\nan infusion administered over 3 hours, vincristine (1.5 mg/m2/day) 1.5 mg by slow\ndirect intravenous injection, actinomycine (1.5 mg/m2/day) 1.5 mg as a slow\ndirect intravenous injection and MesnaR at a dose of 900 mg/day. Ten days after\ntreatment, the child developed seizures. An emergency computed tomography was performed\nshowing hypo-dense right frontal brain lesions (). There was no sensory or motor deficit. To\nbetter characterize, we performed a cerebral magnetic resonance imaging (MRI) which\nobjectified the subcortical lesions in T2 and FLAIR hyper signal, in T1 hypo signal, without\nrestriction of the diffusion sequence and without enhancement after injection of gadolinium\n(). Knowing the side\neffect of ifosfamide, the IVA-based protocol was stopped and modified by the\nVincristine-Actinomycin-Cyclophosphamide (VAC) protocol. The evolution was marked by the\ndefinitive cessation of seizures without other signs. No biological abnormality was detected\nand no specific treatment was added outside of the new protocol. Two weeks after stopping\nifosfamide, we performed a control brain MRI which revealed that the previously described\nbrain lesions had disappeared (). Faced with the favorable clinical course and the disappearance of the brain\nlesions, the diagnosis of IIE was retained.