Background Surgery is the main treatment modality for intracranial meningiomas, but data on short-term surgical outcome are limited. The aim of this Swedish nationwide registry-based study was to benchmark the 30-day complication rate in a cohort of meningioma patients using data from the Swedish brain tumor registry (SBTR). Furthermore, we investigated outcomes for asymptomatic patients. Methods Data were collected from the SBTR for all adults with histopathologically verified intracranial meningioma between 2009 and 2015. Patient symptoms, tumor characteristics, and complications within 30 days postoperatively were analyzed. Results In total, 2324 patients, with a mean age of 58.7 years (SD 13.5), underwent surgery for intracranial meningioma and 14.1% of the patients were asymptomatic before the intervention. The most common symptom prior to treatment was focal deficit, which occurred in 1450 patients (62.4%). Moreover, within 30 days after surgery, 344 patients (14.8%) developed new neurological deficits and new-onset seizures occurred in 105 patients (4.5%), while 8.3% of asymptomatic patients developed neurological deficit and 3.7% new-onset seizures. Due to complications, reoperations were performed in 120 patients (5.2%). The postoperative 30-day mortality in the whole cohort was 1.5%. Conclusion This study benchmarks the 30-day complication rate after meningioma surgery and provides outcome data in the highly relevant group of asymptomatic patients using data from the Swedish brain tumor registry. Since surgical decision-making is a careful consideration of short-term risk versus long-term benefit, this information may be useful for both caregivers and patients.
Background: The T2-FLAIR mismatch sign is an imaging finding highly suggestive of isocitrate dehydrogenase mutated (IDH-mut) 1p19q non-codeleted (non-codel) gliomas (astrocytomas). In previous studies, it has shown excellent specificity but limited sensitivity for IDH-mut astrocytomas. Whether the mismatch sign is a marker of a clinically relevant subtype of IDH-mut astrocytomas is unknown. Methods: We included histopathologically verified supratentorial lower-grade gliomas (LGG) WHO grade II-III retrospectively during the period 2010-2016. In the period 2017-2018, patients with suspected LGG radiologically were prospectively included, and in this cohort other diagnoses than glioma could occur. Clinical, radiological and molecular data were collected. For clinical evaluation we included all patients with IDH-mut astrocytomas. In the 2010-2016 cohort DNA methylation analysis with Infinium MethylationEPIC BeadChip (Illumina) was performed for patients with an IDH-mut astrocytoma with available tissue. We aimed to examine the association of the T2-FLAIR mismatch sign with clinical factors and outcomes. Additionally, we evaluated the diagnostic reliability of the mismatch sign and its relation to methylation profiles. Results: Out of 215 patients with LGG, 135 had known IDH-mutation and 1p19q codeletion status. Fifty patients had an IDH-mut astrocytoma and 12 of these (24.0%) showed a mismatch sign. The sensitivity and specificity of the mismatch sign for IDH-mut detection were 26.4 and 97.6%, respectively. There were no differences between patients with an IDH-mut astrocytoma with or without mismatch sign when grouped according to T2-FLAIR mismatch sign with respect to baseline characteristics, clinical outcomes and methylation profiles. The overall interrater agreement between neuroradiologist and clinical neurosurgeons for the T2-FLAIR mismatch sign was significant when all 215 MRI examination assessed (κ = 0.77, p < 0.001, N = 215). Conclusion: The T2-FLAIR mismatch sign in patients with an IDH-mut astrocytoma is not associated with clinical presentation or outcome. It seems unlikely that the IDH-mut astrocytomas with mismatch sign represent a specific subentity. Finally, we have validated that the T2-FLAIR mismatch sign is a reliable and specific marker of IDH-mut astrocytomas.
Background DNA methylation profiling has facilitated and improved the classification of a wide variety of tumors of the central nervous system. In this study, we investigated the potential utility of DNA methylation profiling to achieve molecular diagnosis in adult primary diffuse lower-grade glioma (dLGG) according to WHO 2016 classification system. We also evaluated whether methylation profiling could provide improved molecular characterization and identify prognostic differences beyond the classical histological WHO grade together with IDH mutation status and 1p/19q codeletion status. All patients diagnosed with dLGG in the period 2007–2016 from the Västra Götaland region in Sweden were assessed for inclusion in the study. Results A total of 166 dLGG cases were subjected for genome-wide DNA methylation analysis. Of these, 126 (76%) were assigned a defined diagnostic methylation class with a class prediction score ≥ 0.84 and subclass score ≥ 0.50. The assigned methylation classes were highly associated with their IDH mutation status and 1p/19q codeletion status. IDH-wildtype gliomas were further divided into subgroups with distinct molecular features. Conclusion The stratification of the patients by methylation profiling was as effective as the integrated WHO 2016 molecular reclassification at predicting the clinical outcome of the patients. Our study shows that DNA methylation profiling is a reliable and robust approach for the classification of dLGG into molecular defined subgroups, providing accurate detection of molecular markers according to WHO 2016 classification.
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