The relationship of erythropoietin receptor expression and prognosis in glioblastoma multiforme patients.

BACKGROUND:: Glioblastoma multiforme (GBM) is the most common primary brain tumor characterized with poor prognosis and short survival. In addition to the standard treatment protocols, targeted molecular treatment options are under trial. In the recent trials, erythropoietin and erythropoietin receptor were found to be linked with the progression of GBM cells. AIM:: In this study, we compared the expression of EPOR with survival in GBM patients with mortality. MATERIALS AND METHODS:: Twenty-six patients operated for GBM in 2012-2014 were enrolled in this study. Tumor tissues were stained with EPOR, epidermal growth factor receptor, vascular endothelial growth factor, and assigned as (1+), (2+), and (3+) according to their immunohistochemical staining levels. The average postoperative follow-up time was 9.3 months. Kaplan-Meier's survival test and Spearman's correlation test were used in statistical analysis. RESULTS:: EPOR 1(+) stained group showed a median survival of 8 months (95% confidence interval [CI]: 0.954-15.046). EPOR 2(+) stained group showed a median survival of 6 months (95% CI: 2.901-9.090) EPOR 3(+) stained group showed a median survival of 2 months (95% CI: 0.400-3.600). (Kaplan-Meier P = 0.002). CONCLUSION:: These results portrayed that EPOR staining levels were inversely proportional with average survival time. In the future, specific inhibitors of this molecule could be used to form a novel treatment option for GBM.

Serum hyaluronidase levels in patients with aneurysmal subarachnoid haemorrhage.

INTRODUCTION: The purpose of this study was to investigate the time course(s) of the serum hyaluronidase levels in patients with aneurysmal subarachnoid haemorrhage and to show whether there is a correlation between symptomatic vasospasm and serum levels of hyaluronidase. METHODS: This prospective, open, non-randomised clinical study consisted of 20 patients with aneurysmal subarachnoid haemorrhage, and eight patients with normotensive hydrocephalus who served as the control group. Serum hyaluronidase levels were detected within the first three days, days five and seven after aneurysmal subarachnoid haemorrhage, and the results were compared with those from the control group. The results were also compared with those of the clinical parameters, including the patient's outcome at six months and symptomatic vasospasm. RESULTS: Mean serum hyaluronidase levels were higher on days five and seven, and comparisons with either day five (p-value is 0.001) and/or day seven (p-value is 0.00001) showed a statistical difference between subarachnoid haemorrhage and controls. However, no relationship was found between elevated serum hyaluronidase levels and the clinical parameters including symptomatic vasospasm (p-value is greater than 0.05) and outcome at sixth months (p-value is greater than 0.05). CONCLUSION: Our results indicate that serum hyaluronidase is elevated in the acute stage(s) of subarachnoid haemorrhage; however, no difference was found between serum hyaluronidase levels and subarachnoid haemorrhage severity. Clinical studies with larger population of patients with aneurysmal subarachnoid haemorrhage are required.

Relationship between DNA damage and total antioxidant capacity in patients with glioblastoma multiforme.

AIMS: To assess oxidative DNA damage and total antioxidant capacity (TAC) in glioblastoma multiforme (GBM) and to compare the results with normal brain tissues. MATERIALS AND METHODS: Oxidative DNA damage and TAC were evaluated in GBM tissues extracted from 26 patients and in normal brain tissues of 15 subjects who underwent autopsy within the first 4h of death. Oxidative DNA damage was assessed by measuring 8-hydroxy-2-deoxyguanosine (8-OH-dG) using the 8-OH-dG enzyme immunoassay kit, a quantitative assay for 8-OH-dG, and TAC was analysed using the ImAnOx colorimetric test system for the determination of antioxidative capacity. The results were compared between two groups and any correlation between 8-OH-dG and TAC was sought. RESULTS: The median level of TAC in GBM (121.5 nmol/g wet tissue) was remarkably lower than that in normal brain tissue (298 nmol/g wet tissue). The difference was statistically significant (P=0.00001). In contrast, oxidative DNA damage was significantly higher in patients with GBM (74.9 ng/g wet tissue) than in controls (34.71 ng/g wet tissue). Again, the difference was statistically significant (P=0.00001). We also found a negative correlation between oxidative DNA damage and TAC (P<0.001). CONCLUSIONS: These findings indicate that the degree of oxidative DNA damage is increased and TAC is decreased in GBM. Oxidative DNA damage is correlated with the levels of TAC.

Phenytoin-induced parkinsonism.

This report presents a 30-year-old man who developed subacute phenytoin-induced cerebellar ataxia and parkinsonism that resolved after discontinuation of the phenytoin treatment. Phenytoin was started for seizure prophylaxis in another health institution where he was referred for bilateral intracerebral orbitofrontal haemorrhage due to a head trauma. To our knowledge, there has been only one other case report describing phenytoin-induced parkinsonism, which was also reversible. The issue of the development of parkinsonism due to the phenytoin toxicity in the case of bilateral orbitofrontal lesion is addressed.