Dexamethasone-associated regression of glioblastoma

Dexamethasone-induced regression of an intracranial space-occupying lesion is commonly characteristic of primary central nervous system lymphoma (PCNSL). However, dexamethasone does not have an established chemotherapeutic role in glioblastoma multiforme (GBM). This is a report on dexamethasone-induced regression in GBM with the aim of exploring the mechanisms behind the phenomenon.

We present the case of a 63-year-old male presenting with status epilepticus. Initial imaging showed a high-grade glioma with significant vasogenic edema. Following 23 days of dexamethasone therapy, magnetic resonance imaging demonstrated notable tumor regression, raising differential diagnoses, including lymphoma or a nonneoplastic inflammatory process. After discontinuation of dexamethasone, the tumor rapidly regrew. A biopsy confirmed the diagnosis of high-grade glioma. Immunohistochemistry revealed the following: glial fibrillary acidic protein positive, isocitrate dehydrogenase-1 (IDH-1) R132H negative, ATP-dependent helicase ATRX (ATRX) positive, p53 with 30% nuclear labeling index, and Ki-67 with maximal labeling index of 25%. The patient underwent an image-guided awake craniotomy for tumor resection.

This case demonstrates substantial dexamethasone-induced GBM regression in our patient, serving as a diagnostic confounder with PCNSL. The decision to wean steroids with the aim of increasing diagnostic yield for PCNSL resulted in a missed opportunity for early surgery for GBM, with the development of neurological symptoms, higher surgical risk and possibly shorter survival. Healthcare professionals caring for patients with suspected GBM must be aware of this potential pitfall in rare cases, planning for timely surgical intervention to optimize the outcome for such patients. This case introduces the second case of a GBM behaving in such a manner, along with molecular characterization.