Disease relevance of hydrocortisone

• Most patients received intrathecal hydrocortisone (HC) each treatment to minimize arachnoiditis [1].
• Stress-appropriate hypercortisolism was obtained by infusion of HC (2.0 mg/kg) over 23 h, preceded by treatment for 5 days with dexamethasone (1.5 mg/day) [2].
• An initial study was performed on 10 postmenopausal patients with advanced breast cancer who had taken 1000 mg AG per day and 20 mg hydrocortisone (HC) twice daily (b.d.) for greater than 3 months [3].
• Cells from patients with ANLL display variable inhibition by HC which is probably not mediated by specific receptors [4].
• Larger doses of ID HC did not prevent local doxorubicin toxicity and were inherently toxic to the skin [5].

High impact information on hydrocortisone

• Disruption of CD40L-CD40 interactions by soluble CD40-Ig fusion protein or anti-CD40L mAb blocked the capacity of HC to induce IgE synthesis in normal B cells [6].
• HC upregulated CD40L mRNA expression in PBMCs and surface expression of CD40L in PBMCs as well as in purified populations of T and B cells [6].
• In this study we demonstrate that HC fails to induce IgE synthesis in B cells from CD40 ligand-deficient (CD40L-deficient) patients [6].
• Hydrocortisone (HC) blocked the inhibitory effect if added either in the IL-4 preincubation phase or during the colony formation stage, implying that HC blocked both induction of the inhibitory activity and its release or its effector function [7].
• The comparative effectiveness of intrathecal (IT) combination chemotherapy using two agents, methotrexate (MTX) and hydrocortisone (HDC), and three agents, MTX, HDC, and cytosine arabinoside (CA), in treating meningeal leukemia was determined in a randomized Southwest Oncology Group study [8].

Chemical compound and disease context of hydrocortisone

• Aminoglutethimide (AG) and hydrocortisone (HC) were given to 20 patients with advanced prostatic cancer resistant to conventional hormonal therapy [9].

Biological context of hydrocortisone

• However, beta-EP at concentrations of 10(-9) M or greater significantly inhibited cell growth in serum-free medium containing DHT, HC, or bFGF, with the greatest inhibition again occurring in medium with DHT [10].
• It also inhibited HC-induced apoptosis in the T cell hybridoma line 2B4.11, which is sensitive to GC [11].
• Thus, the metabolic changes in response to HC-accelerated gluconeogenesis in the liver, which can be reversed by insulin, are likely to produce oxidative stress that leads to cataract formation [12].
• As T3 and HCT probably stimulate GH gene transcription at different sites, insulin may suppress GH gene expression at a more distal site [13].
• These results suggest that increases in the circulating levels of T4 and HC in suckling rats and mastication in the weaning period are involved in development of the postnatal development of the facial part of the skull [14].

Anatomical context of hydrocortisone

• The effect was specific to both components of the system (i.e., HC as apoptosis inducer and SP as its inhibitor), as judged from comparison to three other apoptosis-inducing means (irradiation, thymic epithelial cells, or retinoic acid), and to two other neuropeptides (somatostatin and vasoactive intestinal peptide) [11].
• Since aromatase is more sensitive than desmolase to AG in vitro, lower doses of AG alone (i.e. without HC) were assessed for endocrine effects in 13 further post-menopausal women with advanced breast cancer [3].
• HL60 cells were resistant to HC at concentrations up to 10(-4) M but blast CFC showed a wide range of response [4].
• Fifteen day old chick embryos were administered with 0.25 micromol hydrocortisone succinate sodium (HC), and then 12-30 nmol of thyroxine 4 hr after HC administration [15].
• Similar findings are observed in experiments performed in the absence of HC and 1,25(OH)2D3, indicating that HC and 1,25(OH)2D3 are not needed for OPGL-induced osteoclast differentiation [16].

Associations of hydrocortisone with other chemical compounds

• These results suggest that SC115 tumor cells in primary culture are stimulated to grow in a dose-responsive manner by DHT, HC, or bFGF in both serum-containing and serum-free media [10].
• This study evaluated whether selected hormones, 3,5,3'-triiodothyronine (T3), hydrocortisone (HC), or insulin, would influence the binding of L-tryptophan to rat hepatic nuclei or nuclear envelopes [17].
• After injection of hydrocortisone-succinate (Hydro) (200 micrograms/150 g rat) into the inferior vena cava of adrenalectomized rats, 3H-dexamethasone (3H-Dex) binding in liver cytosol rapidly decreased within 5 min, followed by a rapid replenishment [18].
• The effects of antipsoriatic agents such as hydrocortisone (HC), cyclosporin A (CsA), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and its analogue MC903 on IL-1 production by keratinocytes were also investigated [19].

Gene context of hydrocortisone

• However, peak GH-responses to PD in combination with GHRH were reduced during HC (80 mg/day for 1 day) compared to no glucocorticoid pretreatment in all patients [20].
• Conversely, following HC exposure, the GR was downregulated and AhR levels were elevated [21].
• The inhibitory effect was complete if SP was given with HC or within 1 h after it; partial inhibitory effect could be seen at 2 h and no effect at 3 h [11].
• IL-1 release by both NHK and HSC-1 cells was accelerated by stimulation with rIFN-gamma dose-dependently, although IL-1 alpha was released only transiently by rIFN-gamma-stimulated NHKs in serum-free keratinocyte growth medium containing HC [19].
• The data show that physiological doses of insulin antagonize T3-induced stimulation of GH secretion and also partially block the synergistic stimulation of GH by T3 and HCT [13].

Analytical, diagnostic and therapeutic context of hydrocortisone

• Administration of HYD for the first 8 days after ERC lesion, and then cessation of treatment for the remaining 7 days, also resulted in outgrowth lower than that of controls but higher than that of groups treated for the entire 15 days [22].
• AG + HC produced relief of bone pain in 12 patients (75%) and only 4 required narcotics after treatment [9].
• CONCLUSION: Application of our treatment protocol of a tapered course of 1200 mg HC significantly and rapidly improves recovery outcomes in patients of SSNHL [23].
• STUDY DESIGN AND SETTING: We conducted a retrospective study of 112 patients presenting to Saitama Medical Center. Patients received tapering courses of hydrocortisone (HC) with an initial dose of either 1200 mg or 600 mg [23].

References