Methyl prednisolone is an analogue of prednisolone, found to be five times more potent in its anti-inflammatory properties than hydrocortisone. It is a systemic synthetic corticosteroid. It is more potent than prednisolone as it is more lipophilic. Methylprednisolone action like other corticosteroids bind to glucocorticoid receptors, inhibit pro-inflammatory signals and promote anti-inflammatory signals, hence its clinical use as an anti-inflammatory and immunosuppressive agent. Derivatives of methylprednisolone include methylprednisolone acetate succinate and methylprednisolone sodium. Methyl prednisolone formulations for various routes of administrations are indicated in various condition. Parenteral - intra-articular injections are given in the short term management of rheumatoid arthritis, synovitis of osteoarthritis, epicondylitis, acute gout and intra-lesional injections are indicated for discoid lupus erythematosus, lichen simplex and complex, psoriatic plaques, localized hypertrophic infiltrated inflammatory lesions of granuloma annulare and necrobiosis. it is mostly used parenterally however oral, rectal and topical generic preparations are also available. The pharmacokinetics of methyl prednisolone is linear. It diffuses passively across the cellular membrane and binds to the intracellular glucocorticoid receptor to form a complex. The methylprednisolone-glucocorticoid complex translocates into the nucleus, interacts with specific DNA sequences, enhances or surpresses the transcription of specific genes. It binds and blocks promoter sites of proinflammatory genes, promotes expression of anti-inflammatory gene products, inhibits the synthesis of inflammatory cytokines by blocking the function of transcription factors such as nuclear factor-kappa-B (NF-kB), suppresses the synthesis of cyclooxygenase (COX)- 2 which is responsible for the production of prostaglandins in damaged tissue leading to the inflammation cascade, inhibits cell mediated immunologic functions e.g. those dependent on lymphocytes. the use of methylprednisolone results in a reduced ability of leukocytes to adhere to vascular endothelium and leave circulation. It controls inflammation by reversing capillary permeability, suppressing fibroblast migration, controlling the rate of protein synthesis and stabilize lysosomes at the cellular level.

Methyl Prednisolone Pathway References