Corticosteroids in brain cancer patients: benefits and pitfalls

Abstract

Glucocorticoids have been used for decades in the treatment of brain tumor patients and belong to the most powerful class of agents in reducing tumor-associated edema and minimizing side effects and the risk of encephalopathy in patients undergoing radiation therapy. Unfortunately, corticosteroids are associated with numerous and well-characterized adverse effects, constituting a major challenge in patients requiring long-term application of corticosteroids. Novel anti-angiogenic agents, such as bevacizumab (Avastin®), which have been increasingly used in cancer patients, are associated with significant steroid-sparing effects, allowing neuro-oncologists to reduce the overall use of corticosteroids in patients with progressive malignant brain tumors. Recent experimental studies have revealed novel insights into the mechanisms and effects of corticosteroids in cancer patients, including modulation of tumor biology, angiogenesis and steroid-associated neurotoxicity. This article summarizes current concepts of using corticosteroids in brain cancer patients and highlights potential pitfalls in their effects on both tumor and neural progenitor cells.

NLRC5/MHC class I transactivator is a target for immune evasion in cancer

“…Because brain mass is limited by the skull, unlike other cancers, one major life-threatening complications of brain tumors is the development of brain edema, which is associated with inflammatory events including impaired blood-brain barrier and destruction of normal brain tissues (31,32). In fact, patients with brain tumors are commonly treated with anti-inflammatory drugs such as corticosteroids (32,33). Taken together, these findings show that NLRC5 expression is correlated with higher survival in multiple cancer types, with the exception of brain cancer, in which it appears to be a negative prognostic factor.…”

Use of Dexamethasone in Patients with High-Grade Glioma: A Clinical Practice Guideline

“…In a recent review of the role of steroids in the management of brain metastases, Ryken and colleagues concluded that symptomatic patients should be treated with a starting dose of 4-8 mg daily; if the patient exhibits severe symptoms associated with increased intracranial pressure, a dose of 16 mg daily or higher could be considered 9 . Two recent comprehensive reviews recommend an initial intravenous loading dose of 10-20 mg dexamethasone when a patient presents with acute neurologic symptoms caused by a brain tumour or spinal cord lesion; the loading dose should be followed by maintenance dosing with oral or intravenous dexamethasone in divided doses totalling to 4-24 mg daily 13,14 .…”

“…Most patients begin to improve symptomatically within hours of dexamethasone administration, achieving maximum benefit within 24-72 hours 13 . A high rate of side effects is associated with prolonged dexamethasone use, as is a risk of suppression of the hypothalamic-pituitary-adrenocortical axis.…”

“…A high rate of side effects is associated with prolonged dexamethasone use, as is a risk of suppression of the hypothalamic-pituitary-adrenocortical axis. Dexamethasone should therefore be tapered once symptoms begin to improve 13,14,18 .…”

“…Lowering the dose or switching medications might reduce the extent of the myopathy. Switching from a fluorinated to a non-fluorinated corticosteroid might reduce myopathy 13,24,28 .…”