The mechanism of action of methylprednisolone in the treatment of multiple sclerosis

doi:10.1191/1352458505ms1190oa

Paper

The mechanism of action of methylprednisolone in the treatment of multiple sclerosis

Published Aug 1, 2005 · J. Sloka, M. Stefanelli

Multiple Sclerosis

Q1 SJR score

175

Citations

5

Influential Citations

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Abstract

Methylprednisolone plays an important role in the current treatment of multiple sclerosis (MS), particularly in the acute phase of relapse. It acts in various ways to decrease the inflammatory cycle including: dampening the inflammatory cytokine cascade, inhibiting the activation of T cells, decreasing the extravasation of immune cells into the central nervous system, facilitating the apoptosis of activated immune cells, and indirectly decreasing the cytotoxic effects of nitric oxide and tumor necrosis factor alpha. This paper reviews the most recent observations on these mechanisms both to understand the disease mechanism and its treatment. As more becomes known about these mechanisms, it may become possible to design treatment regimes that are more specific towards both the individual and the disease state.

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Study Snapshot

Methylprednisolone effectively treats multiple sclerosis by decreasing inflammation through various mechanisms, potentially leading to more specific treatment regimes for individual patients.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

The mechanism of action of methylprednisolone in the treatment of multiple sclerosis

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References

Multiple Sclerosis

Dementia occurs in 22% of multiple sclerosis patients, affecting cognitive abilities and personality, and is linked to brain atrophy.

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Multiple sclerosis research is progressing, with new experimental observations and insights into immune system interactions potentially affecting immunomodulatory therapies.

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Methylprednisolone acts on peripheral blood mononuclear cells and endothelium in inhibiting migration phenomena in patients with multiple sclerosis.

Methylprednisolone may decrease peripheral blood mononuclear cell migration through the blood-brain barrier in multiple sclerosis patients, but a single infusion may not provide persistent reduction.

Pharmacodynamics and Pharmacogenomics of Diverse Receptor-Mediated Effects of Methylprednisolone in Rats Using Microarray Analysis

Methylprednisolone has diverse pharmacogenomic effects in rats, with 20 genes showing enhanced expression and 31 genes showing reduced expression, affecting acute phase/immune response, energy metabolism, microsomal metabolism, and hepatic function.

Citations

C16 peptide and angiopoietin-1 alleviate the side effects of glucocorticoids in a rat multiple sclerosis model.

C16 peptide and angiopoietin-1 show potential as a complement to glucocorticoids for treating multiple sclerosis, with fewer side effects observed in a rat model.

A review on multiple sclerosis: Unravelling the complexities of pathogenesis, progression, mechanisms and therapeutic innovations

Multiple sclerosis (MS) is a chronic, inflammatory demyelinating disorder involving genetic, environmental, and immunological factors, with therapeutic innovations significantly improving disease management and reversing CNS damage.

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Disruption of the blood-brain barrier contributes to neuroimmunological diseases, and therapies targeting the BBB may help prevent BBB damage.

Overview of Cytomegalovirus Ocular Diseases: Retinitis, Corneal Endotheliitis, and Iridocyclitis

Cytomegalovirus ocular diseases include retinitis, corneal endotheliitis, and iridocyclitis, which often require systemic treatment in addition to topical treatment.

Corticosteroid-depending effects on peripheral immune cell subsets vary according to disease modifying strategies in multiple sclerosis

Corticosteroid treatment in multiple sclerosis (MS) has significant effects on innate immune cells, with the impact varying depending on the disease-modifying therapy used.

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Acute acquired demyelinating syndromes in children can present in unique ways, with or without Myelin oligodendrocyte glycoprotein (MOG) antibody positivity, and most respond to pulse high dose methylprednisolone injections.

Lipid metabolism is dysregulated in endocrine glands upon autoimmune demyelination

Autoimmune demyelination leads to dysregulated lipid metabolism in endocrine glands, affecting hormone levels and psychiatric symptoms.