Current Corticosteroid Treatment in Brain Tumours

Czech version

Authors: O. Kalita; M. Vaverka; L. Hrabálek
Authors‘ workplace: Neurochirurgická klinika LF UP a FN Olomouc
Published in: Cesk Slov Neurol N 2016; 79/112(5): 521-527
Category: Review Article

Overview

Considering that there is no curative treatment for the majority of malignant brain tumours, supportive therapy plays a very important role and treatment with corticosteroids is its integral part. The goal of corticosteroid therapy is to maintain adequate quality of life and functional self-sufficiency. Corticosteroids have been used to effectively treat oedema around brain tumours since 1960s. In addition to their antioedematous action, their antiemetic and antilymphocytic effect has been utilised in neurooncology. However, these positive impacts are accompanied by a range of adverse cardiovascular, muscular, and psychiatric effects. Despite the widespread use of corticosteroids in neurooncology, no relevant data have been available so far concerning their optimal and safe administration in this specific case. Although there has been a development in disease-modifying treatment modalities over the recent years, the prognosis of patients with brain tumours remain poor; therefore, maintaining an acceptable quality of life continues to be a priority. Rational corticosteroid prescription to minimise toxicity is one of the major factors affecting the quality of life in patients with brain tumours.

Key words:
brain tumours – corticosteroid treatment – adverse effects – quality of life

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.

Sources

1. Talar-Williams C, Sneller MC. Complications of corticosteroid therapy. Eur Arch Otorhinolaryngol 1994; 251 (3): 131–6.

2. Johnson AB, O’Malley BW. Steroid receptor coactivators 1, 2, and 3: critical regulators of nuclear receptor activity and steroid receptor modulator (SRM) -based cancer therapy. Mol Cell Endocrinol 2012; 348 (2): 430–9. doi: 10.1016/j.mce.2011.04.021.

3. Clark AR, Belvisi MG. Maps and legends: the quest for dissociated ligands of the glucocorticoid receptor. Pharmacol Ther 2012; 134 (1): 54–67. doi: 10.1016/j.pharmthera.2011.12.004.

4. Sandercock PA, Soane T. Corticosteroids for acute ischaemic stroke. Cochrane Database Syst Rev 2011; 9: CD000064. doi: 10.1002/14651858.CD000064.pub2.

5. Andersen C, Astrup J, Gyldensted C. Quantitation of peritumoural oedema and the effect of steroids using NMR relaxation time imaging and blood-brain barrier analysis. Acta Neurochir Suppl 1994; 60: 413–5.

6. Armitage PA, Schwindack C, Bastin ME, et al. Quantitative assessment of intracranial tumor response to dexamethasone using diffusion, perfusion and permeability magnetic resonance imaging. Magn Reson Imaging 2007; 25 (3): 303–10.

7. Stamatovic SM, Keep RF, Andjelkovic AV. Brain endothelial cell-cell junctions: how to „open“ the blood brain barrier. Curr Neuropharmacol 2008; 6 (3): 179–92. doi: 10.2174/157015908785777210.

8. Papadopoulos MC, Saadoun S, Woodrow CJ, et al. Occludin expression in microvessels of neoplastic and non-neoplastic human brain. Neuropathol Appl Neurobiol 2001; 27 (5): 384–95.

9. Liebner S, Fischmann A, Rascher G, et al. Claudin-1 and claudin-5 expression and tight junction morphology are altered in blood vessels of human glioblastoma multiforme. Acta Neuropathol 2000; 100 (3): 323–31.

10. Saadoun S, Papadopoulos MC, Davies DC, et al. Aquaporin-4 expression is increased in oedematous human brain tumours. J Neurol Neurosurg Psychiatry 2002; 72 (2): 262–5.

11. Machein MR, Plate KH. VEGF in brain tumors. J Neurooncol 2000; 50 (1–2): 109–20.

12. Machein MR, Kullmer J, Fiebich BL, et al. Vascular endothelial growth factor expression, vascular volume, and, capillary permeability in human brain tumors. Neurosurgery 1999; 44 (4): 732–40.

13. Peak SJ, Levin VA. Role of bevacizumab therapy in the management of glioblastoma. Cancer Manag Res 2010; 2: 97–104.

14. Black KL, Hoff JT, McGillicuddy JE, et al. Increased leukotriene C4 and vasogenic edema surrounding brain tumors in humans. Ann Neurol 1986; 19 (6): 592–5.

15. Nathoo N, Barnett GH, Golubic M. The eicosanoid cascade: possible role in gliomas and meningiomas. J Clin Pathol 2004; 57 (1): 6–13.

16. Piette C, Munaut C, Foidart JM, et al. Treating gliomas with glucocorticoids: from bedside to bench. Acta Neuropathol 2006; 112 (6): 651–64.

17. Osawa T, Tosaka M, Nagaishi M, et al. Factors affecting peritumoral brain edema in meningioma: special histological subtypes with prominently extensive edema. J Neurooncol 2013; 111 (1): 49–57. doi: 10.1007/s11060-012-0989-y.

18. Kim H, Lee JM, Park JS, et al. Dexamethasone coordinately regulates angiopoietin-1 and VEGF: a mechanism of glucocorticoid-induced stabilization of bloodbrain barrier. Biochem Biophys Res Commun 2008; 372 (1): 243–8. doi: 10.1016/j.bbrc.2008.05.025.

19. Kreisl TN, Kim L, Moore K, et al. Phase II trial of single- agent bevacizumab followed by bevacizumab plus iri- notecan at tumor progression in recurrent glioblastoma. J Clin Oncol 2009; 27 (5): 740–5. doi: 10.1200/JCO.2008.16.3055.

20. Badie B, Schartner JM, Paul J, et al. Dexamethasone-induced abolition of the inflammatory response in an experimental glioma model: a flow cytometry study. J Neurosurg 2000; 93 (4): 634–9.

21. Salvador E, Shityakov S, Forster C. Glucocorticoids and endothelial cell barrier function. Cell Tissue Res 2014; 355 (3): 597–605. doi: 10.1007/s00441-013-1762-z.

22. Bebawy JF. Perioperative steroids for peritumoral intracranial edema: a review of mechanisms, efficacy, and side effects. J Neurosurg Anesthesiol 2012; 24 (3): 173–7. doi: 10.1097/ANA.0b013e3182578bb5.

23. Macdonald DR, Cascino TL, Schold SC jr, et al. Response criteria for phase II studies of supratentorial malignant glioma. J Clin Oncol 1990; 8 (7): 1277–80.

24. Wen PY, Macdonald DR, Reardon DA, et al. Updated response assessment criteria for high-grade gliomas: response assessment in neuro-oncology working group. J Clin Oncol 2010; 28: 1963–72. doi: 10.1200/JCO.2009.26.3541.

25. Sionov RV, Spokoini R, Kfir-Erenfeld S, et al. Mechanisms regulating the susceptibility of hematopoietic malignancies to glucocorticoidinduced apoptosis. Adv Cancer Res 2008; 101: 127–248. doi: 10.1016/S0065-230X (08) 00406-5.

26. Kullmann MK, Grubbauer C, Goetsch K, et al. The p27-Skp2 axis mediates glucocorticoid-induced cell cycle arrest in T-lymphoma cells. Cell Cycle 2013; 12 (16): 2625–35. doi: 10.4161/cc.25622.

27. Roth P, Stupp R, Eisele G, et al. Treatment of primary CNS lymphoma. Curr Treat Options Neurol 2014; 16 (1): 277. doi: 10.1007/s11940-013-0277-y.

28. Langeveld CH, van Waas MP, Stoof JC, et al. Implication of glucocorticoid receptors in the stimulation of human glioma cell proliferation by dexamethasone. J Neurosci Res 1992; 31 (3): 524–31.

29. Zibera C, Gibelli N, Butti G, et al. Proliferative effect of dexamethasone on a human glioblastoma cell line (HU 197) is mediated by glucocorticoid receptors. Anticancer Res 1992; 12 (5): 1571–4.

30. Weller M, Schmidt C, Roth W, et al. Chemotherapy of human malignant glioma: prevention of efficacy by dexamethasone? Neurology 1997; 48 (6): 1704–9.

31. Das A, Banik NL, Ray SK. Modulatory effects of acetazolomide and dexamethasone on temozolomide-mediated apoptosis in human glioblastoma T98G and U87MG cells. Cancer Invest 2008; 26 (4): 352–8. doi: 10.1080/07357900701788080.

32. Friese MA, Platten M, Lutz SZ, et al. MICA/NKG2D-mediated immunogene therapy of experimental gliomas. Cancer Res 2003; 63 (24): 8996–9006.

33. Grunberg SM. Antiemetic activity of corticosteroids in patients receiving cancer chemotherapy: dosing, efficacy, and tolerability analysis. Ann Oncol 2007; 18 (2): 233–40.

34. Mantovani G, Maccio A, Esu S, et al. Evidence that cisplatin induces serotonin release from human peripheral blood mononuclear cells and that methylprednisolone inhibits this effect. Eur J Cancer 1996; 32A (11): 1983–5.

35. Suzuki T, Sugimoto M, Koyama H, et al. Inhibitory effect of glucocorticoids on human-cloned 5-hydroxytryptamine3A receptor expressed in xenopus oocytes. Anesthesiology 2004; 101 (3): 660–5.

36. Ho CM, Ho ST, Wang JJ, et al. Dexamethasone has a central antiemetic mechanism in decerebrated cats. Anesth Analg 2004; 99 (3): 734–9.

37. Kršek M. Systémová léčba glukokortikoidy: praktický pohled. Vnitř Lék 2015; 61 (10): 905–12.

38. Clore JN, Estep H, Ross-Clunis H, et al. Adrenocorticotropin and cortisol-induced changes in urinary sodium and potassium excretion in man: effects of spironolactone and RU 486. J Clin Endocrinol Metab 1988; 67 (4): 824–31.

39. Freiberg JM, Kinsella J, Sacktor B. Glucocorticoids increase the Na+ H+ exchange and decrease the Na+ gradient-dependent phosphate-uptake systems in renal brush border membrane vesicles. Proc Natl Acad Sci USA 1982; 79 (16): 4932–6.

40. Pilkey J, Daeninck PJ. A retrospective analysis of dexamethasone use on a Canadian palliative care unit. Prog Palliat Care 2008; 16: 63–8.

41. Hardy JR, Rees E, Ling J, et al. A prospective survey of the use of dexamethasone on a palliative care unit. Palliat Med 2001; 15 (1): 3–8.

42. Weissman DE, Dufer D, Vogel V, et al. Corticosteroid toxicity in neuro-oncology patients. J Neurooncol 1987; 5 (2): 125–8.

43. Sturdza A, Millar BA, Bana N, et al. The use and toxicity of steroids in the management of patients with brain metastases. Support Care Cancer 2008; 16 (9): 1041–8. doi: 10.1007/s00520-007-0395-8.

44. Huerta C, Johansson S, Wallander MA, et al. Risk factors and short-term mortality of venous thromboembolism diagnosed in the primary care setting in the United Kingdom. Arch Intern Med 2007; 167 (9): 935–43.

45. Johannesdottir SA, Horvath-Puho E, Dekkers OM, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med 2013; 173 (9): 743–52. doi: 10.1001/jamainternmed.2013.122.

46. Grossman E, Messerli FH. Drug-induced hypertension: an unappreciated cause of secondary hypertension. Am J Med 2012; 125 (1): 14–22. doi: 10.1016/j.amjmed.2011.05.024.

47. Lansang MC, Hustak LK. Glucocorticoid-induced diabetes and adrenal suppression: how to detect and manage them. Cleve Clin J Med 2011; 78 (11): 748–56. doi: 10.3949/ccjm.78a.10180.

48. McGirt MJ, Chaichana KL, Gathinji M, et al. Persistent outpatient hyperglycemia is independently associated with decreased survival after primary resection of malignant brain astrocytomas. Neurosurgery 2008; 63 (2): 286–91. doi: 10.1227/01.NEU.0000315282.61035.48.

49. Henson JW, Jalaj JK, Walker RW, et al. Pneumocystis carinii pneumonia in patients with primary brain tumors. Arch Neurol 1991; 48 (4): 406–9.

50. Enomoto T, Azuma A, Matsumoto A, et al. Preventive effect of sulfamethoxasole-trimethoprim on Pneumocystis jiroveci pneumonia in patients with interstitial pneumonia. Intern Med 2008; 47 (1): 15–20.

51. Pereira RM, Freire de Carvalho J. Glucocorticoid-induced myopathy. Joint Bone Spine 2011; 78 (1): 41–4. doi: 10.1016/j.jbspin.2010.02.025.

52. Williams TJ, O’Hehir RE, Czarny D, et al. Acute myopathy in severe acute asthma treated with intravenously administered corticosteroids. Am Rev Respir Dis 1988; 137 (2): 460–3.

53. Amaya-Villar R, Garnacho-Montero J, Garcia-Garmendia JL, et al. Steroid-induced myopathy in patients intubated due to exacerbation of chronic obstructive pulmonary disease. Intensive Care Med 2005; 31 (1): 157–61.

54. Levin OS, Polunina AG, Demyanova MA, et al. Steroid myopathy in patients with chronic respiratory diseases. J Neurol Sci 2014; 338 (1–2): 96–101. doi: 10.1016/j.jns.2013.12.023.

55. Qian T, Guo X, Levi AD, et al. High-dose methylprednisolone may cause myopathy in acute spinal cord injury patients. Spinal Cord 2005; 43 (4): 199–203.

56. Steinberg KP, Hudson LD, Goodman RB, et al. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med 2006; 354 (16): 1671–84.

57. Dekhuijzen PN, Decramer M. Steroid-induced myopathy and its significance to respiratory disease: a known disease rediscovered. Eur Respir J 1992; 5 (8): 997–1003.

58. Frieze DA. Musculoskeletal pain associated with corticosteroid therapy in cancer. Curr Pain Headache Rep 2010; 14 (4): 256–60. doi: 10.1007/s11916-010-0120-z.

59. Lewis DA, Smith RE. Steroid-induced psychiatric syndromes. A report of 14 cases and a review of the literature. J Affect Disord 1983; 5 (4): 319–32.

60. Bolanos SH, Khan DA, Hanczyc M, et al. Assessment of mood states in patients receiving long-term corticosteroid therapy and in controls with patient-rated and clinician-rated scales. Ann Allergy Asthma Immunol 2004; 92 (5): 500–5.

61. Compston J. Management of glucocorticoid-induced osteoporosis. Nat Rev Rheumatol 2010; 6 (2): 82–8. doi: 10.1038/nrrheum.2009.259.

62. Maricic M. Update on glucocorticoid-induced osteoporosis. Rheum Dis Clin North Am 2011; 37 (3): 415–31. doi: 10.1016/j.rdc.2011.07.003.

63. Steinbuch M, Youket TE, Cohen S. Oral glucocorticoid use is associated with an increased risk of fracture. Osteoporos Int 2004; 15 (4): 323–8.

64. Kanis JA, Johansson H, Oden A, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res 2004; 19 (6): 893–9.

65. Farhat G, Yamout B, Mikati MA, et al. Effect of antiepileptic drugs on bone density in ambulatory patients. Neurology 2002; 58 (9): 1348–53.

66. Feldkamp J, Becker A, Witte OW, et al. Long-term anticonvulsant therapy leads to low bone mineral density evidence for direct drug effects of phenytoin and carbamazepine on human osteoblast-like cells. Exp Clin Endocrinol Diabetes 2000; 108 (1): 37–43.

67. Shen C, Chen F, Zhang Y, et al. Association between use of antiepileptic drugs and fracture risk: a systematic review and meta-analysis. Bone 2014; 64: 246–53. doi: 10.1016/j.bone.2014.04.018.

68. Mathew BS, Carson KA, Grossman SA. Initial response to glucocorticoids. Cancer 2006; 106 (2): 383–7.

69. Batchelor T, Loeffler JS. Primary CNS lymphoma. J Clin Oncol 2006; 24 (8): 1281–8.

70. Mancini T, Kola B, Mantero F, et al. High cardiovascular risk in patients with Cushing’s syndrome according to 1999 WHO/ISH guidelines. Clin Endocrinol 2004; 61 (6): 768–77.

71. van Raalte DH, Ouwens DM, Diamant M. Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options? Eur J Clin Invest 2009; 39 (2): 81–93. doi: 10.1111/j.1365-2362.2008.02067.x.

72. Mazziotti G, Gazzaruso C, Giustina A. Diabetes in Cushing syndrome: basic and clinical aspects. Trends Endocrinol Metab 2011; 22 (12): 499–506. doi: 10.1016/j.tem.2011.09.001.

73. Munir A, Newell-Price J. Management of diabetes mellitus in Cushing’s syndrome. Neuroendocrinology 2010; 92 (Suppl 1): S82–5.

74. Vlček J. Lékové interakce z pohledu klinického farmaceuta. Practicus 2009; 1: 10–5.

75. Stanbury RM, Graham EM. Systemic corticosteroid therapy-side effects and their management. Br J Ophthalmol 1998; 82: 704–8.

76. Manson SC, Brown RE, Cerulli A, et al. The cumulative burden of oral corticosteroid side effects and the economic implications of steroid use. Respir Med 2009; 103 (7): 975–94. doi: 10.1016/j.rmed.2009.01.003.

77. Weissman DE, Dufer D, Vogel V, et al. Corticosteroid toxicity in neuro-oncology patients. J Neurooncol 1987; 5 (2): 125–8.

78. The Boston Collaborative Drug Surveillance Program. Acute adverse reactions to prednisone in relation to dosage. Clin Pharmacol Ther 1972; 13 (5): 694–8.

79. Encio IJ, Detera-Wadleigh SD. The genomic structure of the human glucocorticoid receptor. J Biol Chem 1991; 266 (11): 7182–8.

80. Turner JD, Schote AB, Macedo JA, et al. Tissue specific glucocorticoid receptor expression, a role for alternative first exon usage? Biochem Pharmacol 2006; 72 (11): 1529–37.

81. Zhou J, Cidlowski JA. The human glucocorticoid receptor: one gene, multiple proteins and diverse responses. Steroids 2005; 70 (5–7): 407–17.

82. Schaaf MJ, Cidlowski JA. Molecular determinants of glucocorticoid receptor mobility in living cells: the importance of ligand affinity. Mol Cell Biol 2003; 23 (6): 1922–34.

83. Cadepond F, Schweizer-Groyer G, Segard-Maurel I, et al. Heat shock protein 90 as a critical factor in maintaining glucocorticosteroid receptor in a nonfunctional state. J Biol Chem 1991; 266 (9): 5834–41.

84. Johnson AB, O’Malley BW. Steroid receptor coactivators 1, 2, and 3: critical regulators of nuclear receptor activity and steroid receptor modulator (SRM) -based cancer therapy. Mol Cell Endocrinol 2012; 348 (2): 430–9. doi: 10.1016/j.mce.2011.04.021.

85. Clark AR, Belvisi MG. Maps and legends: the quest for dissociated ligands of the glucocorticoid receptor. Pharmacol Ther 2012; 134 (1): 54–67. doi: 10.1016/j.pharmthera.2011.12.004.

86. Xu J, Winkler J, Derendorf H. A pharmacokinetic/pharmacodynamic approach to predict total prednisolone concentrations in human plasma. J Pharmacokinet Pharmacodyn 2007; 34 (3): 355–72.

87. Hempen C, Weiss E, Hess CF. Dexamethasone treatment in patients with brain metastases and primary brain tumors: do the benefits outweigh the side-effects? Support Care Cancer 2002; 10 (4): 322–8.

88. Galicich JH, French LA. Use of dexamethasone in the treatment of cerebral edema resulting from brain tumors and brain surgery. Am Pract Dig Treat 1961; 12: 169–74.

89. Mitchell CD, Richards SM, Kinsey SE, et al. Research Council Childhood Leukaemia Working. Benefit of dexamethasone compared with prednisolone for childhood acute lymphoblastic leukaemia: results of the UK Medical Research Council ALL97 randomized trial. Br J Haematol 2005; 129 (6): 734–45.

90. Hanks GW, Trueman T, Twycross RG. Corticosteroids in terminal cancer – a prospective analysis of current practice. Postgrad Med J 1983; 59 (697): 702–6.

91. Aulakh R, Singh S. Strategies for minimizing corticosteroid toxicity: a review. Indian J Pediatr 2008; 75 (10): 1067–73. doi: 10.1007/s12098-008-0211-6.

92. Kirkham SR. The palliation of cerebral tumours with high dose dexamethasone: a review. Palliat Med 1988; 2: 27–33.

93. Vecht CJ, Hovestadt A, Verbiest HB, et al. Dose-effect relationship of dexamethasone on Karnofsky performance in metastatic brain tumors: a randomized study of doses of 4, 8, and 16 mg per day. Neurology 1994; 44 (4): 675–80.

94. Marantidou A, Levy C, Duquesne E, et al. Steroid requirements during radiotherapy for malignant gliomas. J Neurooncol 2010; 100 (1): 89–94. doi: 10.1007/s11060-010-0142-8.

95. Weissman DE, Janjan NA, Erickson B, et al. Twice-daily tapering dexamethasone treatment during cranial radiation for newly diagnosed brain metastases. J Neurooncol 1991; 11 (3): 235–9.

96. Ryken TC, McDermott M, Robinson PD, et al. The role of steroids in the management of brain metastases: a systematic review and evidence-based clinical practice guideline. J Neurooncol 2010; 96 (1): 103–14. doi: 10.1007/s11060-009-0057-4.

97. Kostaras X, Cusano F, Kline GA, et al. Use of dexamethasone in patients with high-grade glioma: a clinical practice guideline. Curr Oncol 2014; 21 (3): e493–503. doi: 10.3747/co.21.1769.

98. Debono M, Mallappa A, Gounden V, et al. Hormonal circadian rhythms in patients with congenital adrenal hyperplasia: identifying optimal monitoring times and novel disease biomarkers. Eur J Endocrinol 2015; 173 (6): 727–37. doi: 10.1530/EJE-15-0064.

99. Kala M. Neurologické diagnózy v diferencované hospicové péči – dvě kazuistiky. Cesk Slov Neurol N 2013; 76/109 (6): 756–8.

100. Vredenburgh J, Cloughesy TF, Samant M, et al. Corticosteroid use in patients with glioblastoma at first or second relapse treated with bevacizumab in the brain study. Oncologist 2010; 15 (12): 1329–34. doi: 10.1634/theoncologist.2010-0105.

101. Cohen MH, Shen YL, Keegan P, et al. FDA drug approval summary: bevacizumab (Avastin) as treatment of recurrent glioblastoma multiforme. Oncologist 2009; 14 (11): 1131–8. doi: 10.1634/theoncologist.2009-0121.

102. Agar M, Koh ES, Gibbs E, et al. Validating self-report and proxy reports of the Dexamethasone Symptom Questionnaire Chronic for the evaluation of longer-term corticosteroid toxicity. Support Care Cancer 2016; 24 (3): 1209–18. doi: 10.1007/s00520-015-2897-0.

103. Roth P, Happold C, Weller M. Corticosteroid use in neuro-oncology: an update. Neurooncol Pract 2015; 2 (1): 6–12.

104. Schiff D, Lee EQ, Nayak L, et al. Medical management of brain tumors and the sequelae of treatment. Neuro Oncol 2015; 17 (4): 488–504. doi: 10.1093/neuonc/nou304.

105. Gannon C, McNamara P. A retrospective observation of corticosteroid use at the end of life in a hospice. J Pain Symptom Manage 2002; 24 (3): 328–35.