2024 American Academy of Neurology Abstract Website

Objective:

The purpose of this study is to test the hypothesis that the metabolic syndrome is a risk factor for developing glioblastoma and is associated with worse survival outcomes.

Background:

A growing body of evidence is beginning to implicate mutations in genes underlying cellular metabolism in the etiology of glioblastoma. The metabolic syndrome has been found to increase the risk of developing various systemic cancers, but it is not known how often the metabolic syndrome occurs in patients with glioblastoma or how it affects their clinical outcomes.

Design/Methods:

A retrospective cohort study was conducted, consisting of patients at a single institution. Clinical records from 40 patients with glioblastoma IDH wild type were reviewed as part of this interim analysis—with plans to analyze 80 patients by study completion. Records included the patient’s diagnosis, progression free survival, overall survival, treatment, tumor molecular characteristics, blood pressure, body mass index, medications, and laboratory data.

Results:

Our results demonstrate a trend that patients with the metabolic syndrome have worse overall survival compared to those who do not (16.7 months vs 8.1 months; p=0.069). Interestingly, hypertension (p=0.007), hyperglycemia (p = 0.044), and dyslipidemia (p = 0.041) were negatively associated with survival, while BMI was not. Furthermore, there was a significant negative association between overall survival and the number of metabolic risk factors that patients accumulate (i.e. BMI, HTN, etc.) (p=0.0038). However, our results demonstrate the prevalence of metabolic syndrome in GBM patients to be 30%, which is less than that of the general population, 35%.

Conclusions:

These interim results suggest that the metabolic syndrome is associated with worse survival in patients with glioblastoma IDH wild type, but that it is not a risk factor in the development of this cancer. These results support other work that has implicated metabolic dysregulation in the pathogenesis of glioblastoma.