6-ketoprostaglandin-f1-alpha and Meningeal-Neoplasms

The pathophysiological mechanisms to explain peritumoral edema have not been clarified. Multiple aspects of brain edema secondary to supratentorial meningiomas were prospectively investigated in a group of 29 patients who underwent surgery consecutively. Sixty-nine tumor samples were analyzed for prostanoid levels. Levels of 6-keto-PGF1 alpha, the stable metabolite of prostacycline, were found to correlate well with the extent of edema (r = 0.51, P < 0.01). The ratio, 6-keto-PGF1 alpha x PGE2/TXB2, was found to have the best correlation with edema index (extension/tumor volume) (r = 0.69, P < 0.005). A case of a hemangiopericytic meningioma with the largest edema extent within the study group also exhibited the highest level of 6-keto-PGF1 alpha (2420 pg/mg protein). Steroid treatment (dosage, duration of therapy, and their product) did not correlate with prostaglandin levels. These findings may explain the inconsistent clinical effects of steroids on meningioma-induced edema. Possible explanations for this phenomenon are discussed. Otherwise, histology, pathological features of tumor aggressiveness, or mechanical parameters, such as its volume, location, and insertion site, did not correlate well with edema parameters or with prostaglandin levels. Similarly, tumor water content, imaging parameters in computed tomography and magnetic resonance, and operative findings (including dissection plane, vascularity, and tumor firmness) did not correlate well with edema parameters. Although a direct cause-effect relationship between prostaglandins and peritumoral edema is not conclusively established, the circumstantial evidence of the ability of prostaglandins to induce vasogenic brain edema and the robust association with peritumoral edema is persuasive.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Aged, 80 and over; Blood-Brain Barrier; Brain; Brain Edema; Brain Neoplasms; Dexamethasone; Female; Humans; Magnetic Resonance Imaging; Male; Meningeal Neoplasms; Meningioma; Middle Aged; Premedication; Prostaglandins; Supratentorial Neoplasms; Tomography, X-Ray Computed

The specific mechanism underlying the genesis of vasogenic brain edema is still debated: the role of arachidonic acid is considered extremely important, as it is a possible activator of self-maintaining reactions enhancing the release of vasoactive and cytotoxic compounds. The relationship between arachidonic acid metabolism and brain edema has been studied primarily in brain tissue samples or in the extracellular fluid, whereas the residual capacity of perilesional tissue to synthesize and release eicosanoids has not been investigated. In the present study, perilesional samples of brain tissue were available from 4 patients operated on for brain metastasis, from 8 patients who had malignant neuroepithelial tumors, from 4 with meningiomas, and from 5 with subarachnoid hemorrhage. A brain edema index was calculated from the preoperative computed tomographic scan. The "ex vivo" method allowed determination of the residual capacity of endogenous arachidonic acid metabolism. The edema index is significantly higher in patients with brain metastasis (6.5 +/- 0.8) and neuroepithelial tumors (3.6 +/- 0.2) than in those with meningiomas (1.5 +/- 0.06), subarachnoid hemorrhage (1.7 +/- 0.18), and in controls. In patients with metastatic and neuroepithelial tumors there is a significant correlation between peritumoral brain edema and the capacity to synthesize leukotriene C4 (P less than 0.05); the capacity to synthesize leukotriene C4 is also significantly elevated after subarachnoid hemorrhage (13.91 +/- 2.6 ng/ml of incubation medium) when compared with control cases (5.56 +/- 0.91). The capacity to synthesize prostacyclin is significantly higher in patients with brain metastasis than in those with neuroepithelial tumors and meningiomas (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Brain Edema; Brain Neoplasms; Dinoprostone; Humans; Meningeal Neoplasms; Meningioma; SRS-A; Subarachnoid Hemorrhage

Tumour cell-rich platelet-free preparations were isolated from 21 fresh samples of human intracranial tumours using enzymic digestion, followed by discontinuous density gradient centrifugation on Percoll and (14 preparations) adherence on plastic. Of the disaggregated cells 79.8 to 97.7% (mean 86.2%) were tumour cells, and mean cell viability was 82.6%. All the tumours produced prostaglandin (PG), E2, F2 alpha, 6 oxo F1 alpha and Thromboxane B2 during 16 hours of incubation but the amount varied widely. Highest production of PGE2 and TXB2 per 10(5) cells was by the eight meningiomas in which the prostanoid profile closely resembled that of circulating monocytes.

Topics: 6-Ketoprostaglandin F1 alpha; Astrocytoma; Brain Neoplasms; Dinoprost; Dinoprostone; Glioblastoma; Glioma; Humans; Meningeal Neoplasms; Meningioma; Monocytes; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane B2; Thromboxanes