Peritumoral edema after stereotactic radiosurgery for intracranial meningiomas and molecular factors that predict its development.
BACKGROUND
Stereotactic radiosurgery (SRS) is an effective treatment for small and medium-sized meningiomas. Although uncommon, peritumoral edema can develop as a delayed complication after SRS. The purpose of the study was to evaluate the clinical and molecular risk factors for peritumoral edema after SRS for intracranial meningiomas.


METHODS
We retrospectively reviewed the results from 18 patients with intracranial meningiomas who underwent SRS. Tissue was obtained from 14 of these patients who also underwent surgery (13 before SRS). Peritumoral edema, before and after SRS, was estimated using the edema index. Quantitative differences in molecular markers of angiogenesis (VEGF, VRGFr) and hypoxia (HIF-1, GLUT-1, and CA-IX) as well as proliferative indices between patients with and without an elevated edema index after SRS were evaluated.


RESULTS
Of the 18 patients studied, symptomatic peritumoral edema developed in three after SRS. They were treated with steroids and one required surgical intervention. The mean time to edema onset was 5.5 months, with an average duration of 16 months. Sagittal sinus occlusion and high-grade histology appear to be more common in the edema group. VEGF and HIF-1 were found in tumors with higher edema index and the elevation of these proteins was correlated with peritumoral edema after SRS. Proliferative index was not predictive for peritumoral edema.


CONCLUSIONS
Clinical characteristics and molecular markers may identify patients with meningiomas at risk of peritumoral edema after SRS. Judicious use of steroids or perhaps the use of stereotactic fractionated radiation should be considered in these high-risk patients.
Kan
Peter
P
Department of Neurosurgery, University of Utah Health Sciences Center, 175 N. Medical Drive East, Salt Lake City, UT 84132, USA.
Liu
James K
JK
Wendland
Merideth M
MM
Shrieve
Dennis
D
Jensen
Randy L
RL
D000368:Aged; D000369:Aged, 80 and over; D000951:Antigens, Neoplasm / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology*; D000071231:Carbonic Anhydrase IX; D002256:Carbonic Anhydrases / Q000378:metabolism; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008577:Meningeal Neoplasms / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D008579:Meningioma / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D008875:Middle Aged; D011237:Predictive Value of Tests; D016634:Radiosurgery / Q000009:adverse effects*; D012189:Retrospective Studies; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D000951:Antigens, Neoplasm; D051272:Glucose Transporter Type 1; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D019394:Ki-67 Antigen; D042461:Vascular Endothelial Growth Factor A; D005169:Factor VIII; C089226:CA9 protein, human; D000071231:Carbonic Anhydrase IX; D002256:Carbonic Anhydrases