Correlation of tumor plasminogen activator with peritumoral cerebral edema

Quindlen, Eugene A.; Bucher, Anita P.

doi:10.3171/jns.1987.66.5.0729

Cited by 25 publications

(7 citation statements)

References 15 publications

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“…[31] Increased vascular endothelial growth factor detected by immunostaining correlated with the degree of edema in 37 tumors examined by Goldman, et al [14] The volume of peritumoral edema in 15 meningiomas correlated with tumor plasminogen activator content in a study by Quindlen and Bucher. [32] Hirashima and coworkers [15] found that platelet-activating factor immunostaining correlated with peritumoral edema in 31 patients. The quantity and location of peritumoral edema was associated with induction of pial blood supply by meningiomas in a recent paper by Bitzer and colleagues.…”

Section: Discussionmentioning

confidence: 99%

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Mantle¹,

Lach²,

Delgado³

et al. 1999

FOC

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Object The goal of this study was to determine whether the quantity of peritumoral brain edema displayed on computerized tomography (CT) scanning could be correlated with brain invasion and subsequent recurrence of meningiomas. Methods One hundred thirty-five patients who underwent resection of intracranial meningiomas at the Ottawa Civic Hospital were followed during the period 1980 to 1998. A complete resection was defined as one in which tumor, invaded bone, and involved dura were removed. Tumors were examined microscopically for evidence of brain invasion. The mean follow-up period was 9 years (± 4 years, standard deviation [SD]) and the mean time to recurrence was 5 years (± 4 years, SD). The authors used a simple grading system based on the average thickness (in centimeters) of edema seen on an axial CT slice showing the most tumor. Edema grade was linearly related to edema volume determined by digitizing the scans (r = 0.96; 29 cases). The chance of brain invasion increased by 20% for each centimeter of edema (rs = 1, p < 0.0001; 124 cases). The presence of brain invasion was predictive of recurrence after complete resection with an accuracy of 83%, a sensitivity of 89%, and a specificity of 82%. The chance of recurrence within 10 years after complete resection was given by the equation: percentage chance of recurrence = (centimeter of edema)3 X 0.7, which can be used to predict the chance of recurrence based on findings on CT scans (rs = 1.00, p < 0.0001; 86 patients). Statistical significance was confirmed using Kaplan-Meier and univariate and multivariate analyses. Completeness of resection was the most powerful predictor of recurrence (p < 0.00001, r = 0.6), followed by edema grade and brain invasion (both p = 0.02, r = 0.1). Patient age and gender and tumor location, size, and histological subtype were nonsignificant factors. Conclusions Brain invasion causes peritumoral edema. Invaded brain tissue is also the source of residual cells in cases of tumor recurrence after gross-total resection.

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Section: Discussionmentioning

confidence: 99%

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Mantle¹,

Lach²,

Delgado³

et al. 1999

FOC

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“…Moreover, other authors suggested that an activation of local fibrinolysis [1,2,13,14] is one of the bleeding mechanisms. In addi tion, Tucker et al [15] showed that meningio ma cells in culture produced plasminogen ac tivators which have been considered as a pos sible reason of haemorrhagic events.…”

Section: Introductionmentioning

confidence: 99%

Coagulation Study in Patients Who Had Undergone Surgery for Meningioma

Dragoni

Mazzucconi²,

Acqui³

et al. 1993

Pathophysiol Haemos Thromb

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Abnormal fibrinolysis and thrombotic complications have been often observed in patients who had undergone surgery for meningioma. Fourteen patients, affected by meningioma, were studied before surgery, during surgery and 24 h after surgery in order to evaluate the modifications of the fibrinolysis system and the coagulation physiological inhibitors. Before surgery, no patient showed hyperfibrinolysis and/or modifications of coagulation physiological inhibitors. During surgery, an activation of fibrinolysis with pathological levels of tissue plasminogen activator activity (x = 6.33 U/dl, SD = 7.9, p = 0.02) and increased levels of fibrin degradation products (x = 0.21, SD = 0.18, p = 0.002) was noted. Modifications of the fibrinolysis parameters occurred only in 9/14 patients (64%). These patients presented a more vascularized tumour, revealed before surgery by computerized tomography scan and cerebral arteriography and directly confirmed during the resection. Twenty-four hours after surgery no patient presented fibrinolysis activation. There was no evidence of disseminated intravascular coagulation in our patients. None of them presented pathological decrease of the physiological coagulation inhibitors or thrombotic complications. In conclusion, during surgery, fibrinolysis parameters show important modifications in patients with vascularized meningioma suggesting an ongoing tumour-host interaction. These variations must be taken in account, in order to plan timely a correct therapeutic approach.

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“…In contrast, Bruce et al [13] found that incubation of their glioma cells with dexamethasone reduced the permeability factor. Recently, some correlation of tumor plasminogen activator (TPA) with peritumoral brain edema was indicated in the relationship between TPA levels in specimens of human brain tumors and the amount of peritumoral edema shown in computerized tomography [29]. The factor in SUP-C from C6 gliomas, however, seems to be different from TPA, even if TPA is included in the SUP-C fraction.…”

Section: Discussionmentioning

confidence: 99%

Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema

et al. 1991

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To investigate whether brain tumors secrete a factor(s) responsible for peritumoral brain edema, we studied the effect of conditioned medium from cultured C6 glioma cells on rat brain capillary permeability. Three different fractions of conditioned medium were obtained. SUP-N was a culture supernatant incubated 4 hours in serum-free medium. SUP-C was the 60-100 fold concentrated fraction obtained by dialysis-concentration of SUP-N; it contained 950 micrograms/ml of protein greater than 10 k-daltons from 3 x 10(8) cells. SUP-L was a water-dispersible lipid fraction from SUP-N; the major components of SUP-L were neutral lipids and free fatty acids. The supernatant fractions and their corresponding control solutions were infused into normal rat brain, and capillary permeability was determined using quantitative autoradiography by measuring the unidirectional entry constant, K (micrograms l/g.min), of 14C-alpha-aminoisobutyric acid (14C-AIB) into brain tissue. SUP-C and SUP-L significantly increased capillary permeability of normal brain; the effect of SUP-C was more intense and extensive than that of SUP-L. The highest mean K value (Kmax) of SUP-C was 10.83 +/- 0.99 and that of the control was 2.53 +/- 0.22 (p less than 0.001). The Kmax of SUP-L was 5.61 +/- 0.23 and that of the control was 2.67 +/- 0.36 (p less than 0.01). A time-course study after infusion of SUP-C demonstrated that more than 1.5 hours is required for the supernatant fraction to open the barrier and that the effect of SUP-C was reversible. The increase of capillary permeability induced by SUP-C was significantly inhibited by pretreatment of rats with dexamethasone (10 mg/kg, ip) 1 hour before intracerebral infusion of SUP-C (Kmax (untreated): 8.30 +/- 0.82, Kmax (treated): 1.33 +/- 0.64, p less than 0.001). These results indicate that experimental brain tumors secrete at least two different diffusible factors responsible for capillary endothelial leakage in normal brain. One is a protein of molecular weight greater than 10 k-daltons, whose effect is inhibited by glucocorticoids, and the other is a waterdispersible lipid.

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Correlation of tumor plasminogen activator with peritumoral cerebral edema

Cited by 25 publications

References 15 publications

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Coagulation Study in Patients Who Had Undergone Surgery for Meningioma

Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema

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