# The role of dexamethasone during treatment phases in glioblastoma: Insights from a retrospective observational study

**Authors:** Juliane Göbel, Maximilian Scheer, Clemens Kirchner, Sandra Leisz, Julian Prell, Christian Strauss, Sebastian Simmermacher, Stefan Rampp

PMC · DOI: 10.1016/j.bas.2026.105968 · 2026-02-09

## TL;DR

This study finds that dexamethasone affects survival in glioblastoma patients differently depending on the treatment phase, with benefits post-surgery but risks during adjuvant therapy.

## Contribution

The study identifies phase-specific effects of dexamethasone on survival outcomes in glioblastoma patients and suggests optimal dose thresholds for each treatment phase.

## Key findings

- Dexamethasone use postoperatively was linked to improved overall and progression-free survival.
- Higher dexamethasone doses during adjuvant therapy were associated with worse survival outcomes.
- Patients not receiving dexamethasone during adjuvant therapy had significantly longer survival times.

## Abstract

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults. Dexamethasone (DEX) is commonly used to manage peritumoral edema, but its impact on overall survival (OS) and progression-free survival (PFS) remains unclear across treatment phases.

In this retrospective single-center study, we analyzed data from 106 GBM patients treated between 2016 and 2020 at the University Hospital Halle. We examined the effects of DEX on OS and PFS during the preoperative, postoperative, and adjuvant therapy phases using Kaplan-Meier and Cox regression analyses. Cutoff analyses identified phase-specific DEX dose thresholds.

Preoperatively, DEX had no significant effect on OS (HR: 0.998, p = 0.379) or PFS (HR: 0.998, p = 0.373), though a positive trend is possible. Postoperatively, DEX was associated with improved OS (HR: 0.995, p = 0.017) and PFS (HR: 0.995, p = 0.029). Conversely, during adjuvant therapy, higher DEX doses trended toward worse OS (HR: 1.001, p = 0.069) and PFS (p = 0.258). Patients not receiving DEX during adjuvant therapy had significantly longer OS (17.9 vs. 6.4 months, p < 0.001) and PFS (9 vs. 4.6 months, p = 0.007).

DEX influences survival outcomes differently across treatment phases. Higher doses may be beneficial pre- and postoperatively but detrimental during adjuvant therapy. These findings underscore the importance of phase-specific DEX dosing and support further research into optimal corticosteroid strategies in GBM care.

•Dexamethasone shows phase-dependent effects on survival in GBM patients, with potential benefits in the postoperative phase but negative trends during adjuvant therapy.•Postoperative DEX use was associated with improved overall (HR: 0.995, p = 0.017) and progression-free survival (HR: 0.995, p = 0.029), while adjuvant phase use was linked to worse outcomes.•Cutoff analyses identified critical DEX dose thresholds: >60 mg preoperatively, up to 140 mg postoperatively, and <40 mg during adjuvant therapy for favorable survival outcomes.•Patients not receiving DEX during adjuvant therapy had significantly longer survival (OS: 17.9 vs. 6.4 months, p < 0.001; PFS: 9 vs. 4.6 months, p = 0.007), underscoring the need for cautious corticosteroid use.

Dexamethasone shows phase-dependent effects on survival in GBM patients, with potential benefits in the postoperative phase but negative trends during adjuvant therapy.

Postoperative DEX use was associated with improved overall (HR: 0.995, p = 0.017) and progression-free survival (HR: 0.995, p = 0.029), while adjuvant phase use was linked to worse outcomes.

Cutoff analyses identified critical DEX dose thresholds: >60 mg preoperatively, up to 140 mg postoperatively, and <40 mg during adjuvant therapy for favorable survival outcomes.

Patients not receiving DEX during adjuvant therapy had significantly longer survival (OS: 17.9 vs. 6.4 months, p < 0.001; PFS: 9 vs. 4.6 months, p = 0.007), underscoring the need for cautious corticosteroid use.

## Linked entities

- **Chemicals:** dexamethasone (PubChem CID 5743)
- **Diseases:** glioblastoma (MONDO:0018177)

## Full-text entities

- **Genes:** OCLN (occludin) [NCBI Gene 100506658] {aka BLCPMG, PPP1R115, PTORCH1}, AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177] {aka RAGE, SCARJ1, sRAGE}, PDCD1 (programmed cell death 1) [NCBI Gene 5133] {aka ADMIO4, AIMTBS, CD279, PD-1, PD1, SLEB2}, MGMT (O-6-methylguanine-DNA methyltransferase) [NCBI Gene 4255], CLDN5 (claudin 5) [NCBI Gene 7122] {aka AWAL, BEC1, CPETRL1, TMDVCF, TMVCF}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, IDH1 (isocitrate dehydrogenase (NADP(+)) 1) [NCBI Gene 3417] {aka HEL-216, HEL-S-26, IDCD, IDH, IDP, IDPC}, TJP1 (tight junction protein 1) [NCBI Gene 7082] {aka ZO-1}
- **Diseases:** hyperglycemia (MESH:D006943), glioma (MESH:D005910), edema (MESH:D004487), Tumor (MESH:D009369), delirium (MESH:D003693), brain swelling (MESH:D001929), bleeding (MESH:D006470), neurological deficits (MESH:D009461), death (MESH:D003643), thrombosis (MESH:D013927), symptoms (MESH:D012816), toxicity (MESH:D064420), CNS tumors (MESH:D016543), infections (MESH:D007239), GBM (MESH:D005909), infectious complications (MESH:D003141), brain tumor (MESH:D001932)
- **Chemicals:** bevacizumab (MESH:D000068258), GTR (-), DEX (MESH:D003907), TMZ (MESH:D000077204)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12925272/full.md

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Source: https://tomesphere.com/paper/PMC12925272