Lindsay S Rowe1, John A Butman2, Megan Mackey3, Joanna H Shih4, Theresa Cooley-Zgela3, Holly Ning3, Mark R Gilbert5, DeeDee K Smart3, Kevin Camphausen3, Andra V Krauze3. 1. Radiation Oncology Branch, National Cancer Institute, 10 Center Drive Magnuson Clinical Center, Room B2-3500, Bethesda, MD, 20892, USA. Lindsay.rowe@nih.gov. 2. Radiology and Imaging Sciences, National Institutes of Health, 10 Center Drive Magnuson Clinical Center, MSC 1182, Bethesda, MD, 20892, USA. 3. Radiation Oncology Branch, National Cancer Institute, 10 Center Drive Magnuson Clinical Center, Room B2-3500, Bethesda, MD, 20892, USA. 4. Clinical Research Center, National Institutes of Health, 10 Center Drive Magnuson Clinical Center, Bethesda, MD, 20892, USA. 5. Neuro-Oncology Branch, National Cancer Institute, Building 82, Room 235A, Bethesda, MD, 20892, USA.
Abstract
INTRODUCTION: Pseudoprogression (PsP) is a diagnostic dilemma in glioblastoma (GBM) after chemoradiotherapy (CRT). Magnetic resonance imaging (MRI) features may fail to distinguish PsP from early true progression (eTP), however clinical findings may aid in their distinction. METHODS: Sixty-seven patients received CRT for GBM between 2003 and 2016, and had pre- and post-treatment imaging suitable for retrospective evaluation using RANO criteria. Patients with signs of progression within the first 12-weeks post-radiation (P-12) were selected. Lesions that improved or stabilized were defined as PsP, and lesions that progressed were defined as eTP. RESULTS: The median follow up for all patients was 17.6 months. Signs of progression developed in 35/67 (52.2%) patients within P-12. Of these, 20/35 (57.1%) were subsequently defined as eTP and 15/35 (42.9%) as PsP. MRI demonstrated increased contrast enhancement in 84.2% of eTP and 100% of PsP, and elevated CBV in 73.7% for eTP and 93.3% for PsP. A decrease in FLAIR was not seen in eTP patients, but was seen in 26.7% PsP patients. Patients with eTP were significantly more likely to require increased steroid doses or suffer clinical decline than PsP patients (OR 4.89, 95% CI 1.003-19.27; p = 0.046). KPS declined in 25% with eTP and none of the PsP patients. CONCLUSIONS: MRI imaging did not differentiate eTP from PsP, however, KPS decline or need for increased steroids was significantly more common in eTP versus PsP. Investigation and standardization of clinical assessments in response criteria may help address the diagnostic dilemma of pseudoprogression after frontline treatment for GBM.
INTRODUCTION: Pseudoprogression (PsP) is a diagnostic dilemma in glioblastoma (GBM) after chemoradiotherapy (CRT). Magnetic resonance imaging (MRI) features may fail to distinguish PsP from early true progression (eTP), however clinical findings may aid in their distinction. METHODS: Sixty-seven patients received CRT for GBM between 2003 and 2016, and had pre- and post-treatment imaging suitable for retrospective evaluation using RANO criteria. Patients with signs of progression within the first 12-weeks post-radiation (P-12) were selected. Lesions that improved or stabilized were defined as PsP, and lesions that progressed were defined as eTP. RESULTS: The median follow up for all patients was 17.6 months. Signs of progression developed in 35/67 (52.2%) patients within P-12. Of these, 20/35 (57.1%) were subsequently defined as eTP and 15/35 (42.9%) as PsP. MRI demonstrated increased contrast enhancement in 84.2% of eTP and 100% of PsP, and elevated CBV in 73.7% for eTP and 93.3% for PsP. A decrease in FLAIR was not seen in eTPpatients, but was seen in 26.7% PsP patients. Patients with eTP were significantly more likely to require increased steroid doses or suffer clinical decline than PsP patients (OR 4.89, 95% CI 1.003-19.27; p = 0.046). KPS declined in 25% with eTP and none of the PsP patients. CONCLUSIONS: MRI imaging did not differentiate eTP from PsP, however, KPS decline or need for increased steroids was significantly more common in eTP versus PsP. Investigation and standardization of clinical assessments in response criteria may help address the diagnostic dilemma of pseudoprogression after frontline treatment for GBM.
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