LAUSR

A 52-year-old female underwent surgery in March 2009 or a localized non-secretory adrenocortical carcinoma (ACC) f 17 cm. A Weiss score of 9 with a mitotic rate of more han 5/50HPF and a Ki67 of 10% were reported at pathology. aseline imaging work-up showed pulmonary micronodules, epatic and bones metastases and peritoneal carcinomatosis Fig. 1A). Mitotane therapy was started in April 2009, with arboplatin-etoposide (MPE) because of pejorative prognostic actors. Response to treatment was evaluated every 2 months ith CT based on RECIST 1.0 criteria and mitotane plasma evel was monitored monthly (Fig. 1). The therapeutic winow of mitotane plasma level was reached with a daily dose of g/day 4 months after treatment initiation. Furthermore, a peak f 20 mg/L was reached twice on month 4 (19.2 mg/L) and on onth 5 (20.6 mg/L). Along with that mitotane levels, a progresive disease was found until month 6 evaluation (Fig. 1B–D). maging work-up performed at month 8 after 6 cycles of EP nd 2 cycles of carboplatin-etoposide found a stable disease nd only mitotane was continued and decreased due to side ffects at maximum tolerated dose. Locoregional approaches o treat the symptomatic bones metastasis were performed at onth 10 (cimentoplasty, osteosynthesis and cryotherapy). A umor response (hepatic partial response and pulmonary comlete response) was observed for the first time 10 months after EP initiation, 2 months after the end of carboplatin-etoposide nd 6 months after mitotane peak was reached (Fig. 1F). Under itotane alone, tumor response lasted 21 months after treatment nitiation (Fig. 1G and H). At this time, because of progression in epatic targets concomitant with a plasma mitotane level above 4 mg/L, radiofrequency was performed, making RECIST criteia not usable anymore on the liver while bone metastases were ll treated with loco-regional approaches. Since 2010, the dis-