BACKGROUND

Meningioma is the most frequent primary benign intracranial tumor, with a higher incidence in women. Treatment with progesterone acetates, including cyproterone, nomegestrol, chlormadinone, promegestone, medrogestone, and medroxyprogesterone acetate, has been identified as a risk factor of meningioma, particularly in the anterior and middle cranial fossae. Discontinuation of these treatments often leads to volume stabilization or regression of the tumor.

CASE DESCRIPTION

A 42-year-old woman undergoing treatment with nomegestrol acetate (NA) presented with headaches and visual loss in her right eye. She was diagnosed with a large spheno-orbital meningioma invading the sphenoid and ethmoid sinuses, associated with hyperostosis of the sphenoid wing. An initial resection was performed using an extended endonasal approach. Immunohistochemistry confirmed a chondroid meningioma, Grade II, with progestin receptor in 100% of the tumor cell nuclei and a Ki-67 proliferation index of 3-5%. NA was immediately stopped on diagnosis. Despite the cessation of the NA, the intraosseous sphenoidal part of the tumor continued to grow, leading to optic nerve compression. A second surgery was performed using a right fronto-temporo-orbito-zygomatic approach. Examination of the dura of the middle fossa showed subtle tumoral infiltration, while the Ki-67% index was estimated at 1%. Examination of the sphenoid bone demonstrated reactive hyperostosis with minimal to no tumor infiltration.

CONCLUSION

This case illustrates that the proliferative activity of the progestin-associated meningioma does not account for intraosseous progression within the sphenoid bone following cessation of progestin therapy. Our observations suggest an upregulation of osteogenesis in infiltrated bone, even as the dural part of the meningioma regresses.