RESUMEN
Lipoleiomyoma is a type of tumor usually found in the uterine corpus. The pathophysiology is unclear; however, it is commonly seen in obese perimenopausal and postmenopausal women. While intrauterine lipoleiomyoma may be surveilled, there is less information about the management of extrauterine lipoleiomyoma, especially significantly large tumors. This is a case involving a 51-year-old female who was incidentally found to have a 23-cm extrauterine lipoleiomyoma emanating from the peritoneum between uterosacral ligaments. She underwent hand-assisted laparoscopic removal of an intra-abdominal tumor, which was found to be an extrauterine lipoleiomyoma. Six months later, she was found to have a recurrent mass on a follow-up computed tomography (CT) of the abdomen and pelvis. She underwent a robotic-assisted total abdominal hysterectomy, bilateral salpingo-oophorectomy, and removal of the recurrent tumor. While the mass is benign in nature, the mass effect that it may cause prompts a discussion about the best course of management and an investigation into recurrence rates, specifically in similar extrauterine presentations.
RESUMEN
Cyclophilins have diverse functions that may affect the course of central nervous system (CNS) inflammatory disorders. Anti-inflammatory and neuroprotective mechanisms may be targeted by inhibition of cyclophilin A-dependent and cyclophilin D-dependent functions, respectively. We tested the effect of cyclophilin inhibition on CNS inflammation by administering N-methyl-4-isoleucine-cyclosporin (NIM811) to mice undergoing experimental allergic encephalomyelitis (EAE). Treatment with NIM811 resulted in significant reduction of EAE clinical severity. Analysis of mitochondrial calcium retention capacity and the course of EAE in cyclophilin D knockout mice indicated that the effect of NIM811 on EAE was not entirely cyclophilin D-dependent. NIM811-treated EAE animals showed reduction in interleukin-2 expression and reduction in CNS inflammatory infiltrates. These results indicate that anti-inflammatory rather than neuroprotective mechanisms associated with cyclophilins are likely involved in the mechanism of NIM811 in EAE.