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Pseudoprogression (PsP) in glioblastoma presents a significant obstacle in distinguishing genuine tumour recurrence from treatment-induced contrast enhancement on MRI. Only retrospectively identifiable, PsP is believed to be at least partly a result of radiochemotherapy-based alterations in the blood–brain barrier (BBB). Radiation-induced hypoxia has been suggested to upregulate vascular endothelial growth factor, which then mediates blood vessel permeability and fosters BBB dysregulation.
Typically understood to occur within the first 12 weeks following radiotherapy, PsP has recently been demonstrated to also appear significantly later (‘late pseudoprogression’).1
Given its ability to mimic true tumour development, late PsP can lead to interference with treatment course or unwarranted surgical intervention. Thus, its prompt and definitive detection serves a critical role in glioblastoma management.
Positron emission tomography (PET) using radiolabelled amino acids such as O-(2-(18F)fluoroethyl)-L-tyrosine ((18F)FET) has proven a useful tool in the differentiation of true tumour progression from treatment-induced changes, as tracer uptake reflects amino acid transport rather than inflammatory processes. The purpose of this study was to further substantiate the available data on the suitability of (18F)FET-PET in suspected late PsP.
Materials and methods
This retrospective study included 36 consecutive patients (22 males and 14 females, ages ranging from 24 to 75 years, with a mean of 54±14) with histopathologically confirmed glioblastoma. Between April 2010 and August 2016, patients were referred to (18F)FET-PET/CT due to suspicion of recurrence/disease progression as determined by the Response Assessment in Neuro-Oncology (RANO) working group criteria.2 The interval between cessation of radiotherapy and …
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