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Type of organic compound that contains a characteristic arrangement of four cycloalkane rings joined to one another.

The steroid core is composed of seventeen carbon atoms bonded together in the form of four fused rings: three cyclohexane rings (designated as rings A, B and C in the figure to the right) and one cyclopentane ring (the D ring). Individual steroids vary, first and primarily, by the oxidation state of the carbon atoms in the rings and by the chains and functional groups attached to this four-ring system; second, steroids can vary more markedly via changes to the ring structure (e.g., via ring scissions that produce secosteroids like vitamin D3, see below). Sterols are a particularly important form of steroids, with sterols having a cholestane-derived framework and an hydroxyl group at the C-3 ring position being the most prominent (e.g., as in cholesterol, shown at right).

Hundreds of distinct steroids are found in animals, fungi, plants, and elsewhere. All natural steroids are made in living cells, either from the sterol lanosterol (animals and fungi, see examples) or from cycloartenol (plants). Both lanosterol and cycloartenol are derived via cyclization of the triterpenoid squalene.


A steroid hormone (abbreviated as sterone) is a steroid that acts as a hormone. Steroid hormones can be grouped into five groups by the receptors to which they bind:



Mineralocorticoids, androgens, estrogens, and progestogens. Vitamin D derivatives are a sixth closely related hormone system with homologous receptors. They have some of the characteristics of true steroids as receptor ligands, but lack the planar fused four ring system of true steroids.

see 21 aminosteroid.


Steroid hormones help control metabolism, inflammation, immune functions, salt and water balance, development of sexual characteristics, and the ability to withstand illness and injury. The term steroid describes both hormones produced by the body and artificially produced medications that duplicate the action for the naturally occurring steroids.

Patients with pituitary adenomas usually receive “stress dose” steroids in the peri-operative periods.

Though randomized controlled trials(RCT) have not been performed to assess the necessity of steroid coverage, there are several studies that explained the changes of adrenal function during peri-operative peroids.

Steroids are very commonly administered concurrently with temozolomide and radiotherapy after the initial surgical resection of glioblastoma (GBM) to control neurological morbidity. Although the potent anti-inflammatory effect of steroids is well documented to ameliorate vasogenic edema in these tumors, the deleterious effects of steroids on the efficacy of alkylating agents or radiotherapy have been a matter of debate 1) 2) 3) 4).

Pitter et al., performed a retrospective analysis of glioblastoma patient cohorts to determine the prognostic role of steroid administration. A disease-relevant mouse model of glioblastoma was used to characterize the effects of dexamethasone on tumour cell proliferation and death, and to identify gene signatures associated with these effects. A murine anti-VEGFA antibody was used in parallel as an alternative for oedema control.

They applied the dexamethasone-induced gene signature to The Cancer Genome Atlas glioblastoma dataset to explore the association of dexamethasone exposure with outcome. Mouse experiments were used to validate the effects of dexamethasone on survival in vivo Retrospective clinical analyses identified corticosteroid use during radiotherapy as an independent indicator of shorter survival in three independent patient cohorts. A dexamethasone-associated gene expression signature correlated with shorter survival in The Cancer Genome Atlas patient dataset. In glioma-bearing mice, dexamethasone pretreatment decreased tumour cell proliferation without affecting tumour cell viability, but reduced survival when combined with radiotherapy. Conversely, anti-VEGFA antibody decreased proliferation and increased tumour cell death, but did not affect survival when combined with radiotherapy. Clinical and mouse experimental data suggest that corticosteroids may decrease the effectiveness of treatment and shorten survival in glioblastoma. Dexamethasone-induced anti-proliferative effects may confer protection from radiotherapy- and chemotherapy-induced genotoxic stress. This study highlights the importance of identifying alternative agents such as vascular endothelial growth factor antagonists for managing oedema in glioblastoma patients. Beyond the established adverse effect profile of protracted corticosteroid use, this analysis substantiates the request for prudent and restricted use of corticosteroids in glioblastoma 5).

Side effects

Steroids may have central nervous system side effects affecting whole body, including steroid-induced mental agitation and psychosis.

In the absence of a meta-analysis, most weight should be placed on the result of the largest trial. The increase in mortality with steroids in this trial suggest that steroids should no longer be routinely used in people with traumatic head injury 6)

Piette C, Munaut C, Foidart JM, Deprez M. Treating gliomas with glucocorticoids: from bedside to bench. Acta Neuropathol. 2006;112(6):651–664.
Wang H, Li M, Rinehart JJ, Zhang R. Pretreatment with dexamethasone increases antitumor activity of carboplatin and gemcitabine in mice bearing human cancer xenografts: in vivo activity, pharmacokinetics, and clinical implications for cancer chemotherapy. Clin Cancer Res. 2004;10(5):1633–1644.
Weller M, Schmidt C, Roth W, Dichgans J. Chemotherapy of human malignant glioma: prevention of efficacy by dexamethasone? Neurology. 1997;48(6):1704–1709.
Shields LB, Shelton BJ, Shearer AJ, et al. Dexamethasone administration during definitive radiation and temozolomide renders a poor prognosis in a retrospective analysis of newly diagnosed glioblastoma patients. Radiat Oncol. 2015;10:222.
Pitter KL, Tamagno I, Alikhanyan K, Hosni-Ahmed A, Pattwell SS, Donnola S, Dai C, Ozawa T, Chang M, Chan TA, Beal K, Bishop AJ, Barker CA, Jones TS, Hentschel B, Gorlia T, Schlegel U, Stupp R, Weller M, Holland EC, Hambardzumyan D. Corticosteroids compromise survival in glioblastoma. Brain. 2016 May;139(Pt 5):1458-71. doi: 10.1093/brain/aww046. Epub 2016 Mar 28. PubMed PMID: 27020328; PubMed Central PMCID: PMC5006251.
Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD000196. Review. PubMed PMID: 15674869.
steroid.txt · Last modified: 2017/02/07 12:06 (external edit)