Short-term high dose steroid therapy does not affect the hypothalamic-pituitary-adrenal axis in relapsing multiple sclerosis patients. Clinical assessment by the insulin tolerance test

Lević, Z; Micić, D.; Nikolić, Jasmina B.; Stojisavljević, N.; Sokić, Dragoslav; Jankovic, Snezana; Kendereški, Aleksandra; Mavra, Milica

doi:10.1007/bf03347855

Cited by 31 publications

(20 citation statements)

References 10 publications

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“…In line with our findings, it was shown that high-dose i.v. methylprednisolone (1 g per patient) can immediately reduce the peak cortisol levels (Trotter & Garvey 1980, Levic et al 1996. But in contrast to our data, presumably because of the large dose applied, full recovery needed here about 9 days after the last dose, but a symptom of prolonged HPA axis suppression was not seen.…”

Section: Resultscontrasting

confidence: 97%

Comparison of the hypothalamic–pituitary–adrenal axis susceptibility upon single-dose i.m. depot versus long-acting i.v. triamcinolone acetonide therapy: a direct pharmacokinetic correlation

Abraham

Demiraj

Ungemach

2006

Journal of Endocrinology

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The effects of single injections of glucocorticoid (GC) depot suspension and of long-acting GC were studied in conscious dogs. Both the depot suspension GC triamcinolone-16,17-aacetonide (TAA) and the long-acting triamcinolone acetonide-21-dihydrogen phosphate (TAA-DHP) decreased basal and ACTH-stimulated cortisol levels and in a specific timedependent way. Before treatment, all dogs had normal basal and peak cortisol responses to ACTH challenge (13-15 and O120 nmol/l at 1 h respectively). Intravenous TAA-DHP reduced cortisol levels for 12 h, i.m. TAA reduced cortisol levels as of 1 . 5 h and the effect lasted for at least 4 weeks. Both treatments blunted the peak response to ACTH. ACTH elevated cortisol levels to or above baseline values within 10 days following TAA-DHP treatment, but the TAA treatment suppressed an ACTH response for at least 4 weeks. Kinetic analysis of both the preparations demonstrated rapid absorption (t max , 0 . 6-1 . 5 h) and low maximum plasma concentrations (peak C max , 2 . . 51 nmol/l) of the steroids; indeed, the terminal half-life of TAA-DHP (13 . 9G1 . 3 h) was very much shorter than that of TAA (125 . 9G15 . 8 h). In addition, the mean residence time differed very much (11 vs 160 h for TAA-DHP and TAA respectively), in line with a delayed elimination of the depot compared with the long-acting formulation. Application of these TAA formulations needs careful evaluation for their surprisingly different effects on endocrine stress axis activity.

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Section: Resultscontrasting

confidence: 97%

Comparison of the hypothalamic–pituitary–adrenal axis susceptibility upon single-dose i.m. depot versus long-acting i.v. triamcinolone acetonide therapy: a direct pharmacokinetic correlation

Abraham

Demiraj

Ungemach

2006

Journal of Endocrinology

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“…[1][2][3] Inflammatory attack results from the interaction of T lymphocytes with other components of the immune system. Intravenous (IV) treatment with high-dose glucocorticoids (GCs) has now become the standard therapy in patients with an acute relapse of disease or a rapidly progressive deterioration of chronic progressive MS. 4 Short-term highdose corticosteroid therapy does not affect the hypothalamic-pituitary-adrenal axis in these patients 5 and does not reduce bone density. 6,7 Several studies 4,[8][9][10][11][12] on GC treatment yielded controversial results as to the most effective dose and form of application.…”

Section: Discussionmentioning

confidence: 99%

High-Dose Methylprednisolone Therapy in Multiple Sclerosis Induces Apoptosis in Peripheral Blood Leukocytes

Leussink¹,

Jung²,

Merschdorf³

et al. 2001

Arch Neurol

119

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“…Even inhaled glucocorticoid treatment can lead to adrenocortical insufficiency [14,15,16]. Only few results of adrenocortical function in relation to intermittent glucocorticoid pulse therapy have been reported [17,18,19]. …”

Section: Discussionmentioning

confidence: 99%

Methylprednisolone Pulse Treatment of Graves' Ophthalmopathy Is Not Associated with Secondary Adrenocortical Insufficiency

2015

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Objective: Graves' ophthalmopathy (GO) is an inflammatory disease in the orbital region. The first-line medical treatment is glucocorticoids. An important potential side effect of glucocorticoid treatment is suppression of the hypothalamic-pituitary-adrenal (HPA) axis with impairment of endogenous cortisol production, implicating symptoms of adrenocortical insufficiency, especially in the period after cessation of therapy with possible risks in cases of intercurrent illness. The aim of this study was to evaluate HPA axis function before and after methylprednisolone pulse treatment of GO. Study Design: HPA axis function was evaluated by measurements of plasma ACTH and an ACTH stimulation test with plasma cortisol measurements at 0 and 30 min after an intravenous bolus of synthetic ACTH (Synacthen® 250 µg). This was done in 12 patients with GO before and at cessation of methylprednisolone pulse treatment (500 mg i.v. per week for 6 weeks followed by 250 mg i.v. per week for an additional 6 weeks). Results: All patients included fulfilled the criteria of intact HPA axis function before and at cessation of methylprednisolone pulse treatment. Data are given as medians (with ranges). Before glucocorticoid treatment basal plasma cortisol was 290 nM (196-579) and 786 nM (612-1,050) after ACTH stimulation. At cessation of therapy the corresponding values were 309 nM (88-718) and 852 nM (524-1,011), respectively. Thus, all patients passed a 30-min stimulated plasma cortisol of 500 nM. Before treatment plasma ACTH was 4.2 pmol/l (4-16) and at cessation of therapy the corresponding value was 4.8 pmol/l (2-9; p = 0.27). Conclusion: Transient suppression of the HPA axis with secondary adrenocortical insufficiency does not seem to be a common phenomenon after intravenous methylprednisolone pulse therapy for GO. Therefore, routine precautions are not necessary. However, our results do not exclude that transient secondary adrenocortical insufficiency might occur occasionally.

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Short-term high dose steroid therapy does not affect the hypothalamic-pituitary-adrenal axis in relapsing multiple sclerosis patients. Clinical assessment by the insulin tolerance test

Cited by 31 publications

References 10 publications

Comparison of the hypothalamic–pituitary–adrenal axis susceptibility upon single-dose i.m. depot versus long-acting i.v. triamcinolone acetonide therapy: a direct pharmacokinetic correlation

Comparison of the hypothalamic–pituitary–adrenal axis susceptibility upon single-dose i.m. depot versus long-acting i.v. triamcinolone acetonide therapy: a direct pharmacokinetic correlation

High-Dose Methylprednisolone Therapy in Multiple Sclerosis Induces Apoptosis in Peripheral Blood Leukocytes

Methylprednisolone Pulse Treatment of Graves' Ophthalmopathy Is Not Associated with Secondary Adrenocortical Insufficiency

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