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Chemical structure of methylprednisolone. Corticosteroids are used during acute multiple sclerosis relapses. Administration of high doses of intravenous corticosteroids, such as methylprednisolone, is the routine therapy for acute relapses.
Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol) is a synthetic glucocorticoid, primarily prescribed for its anti-inflammatory and immunosuppressive effects. [ 4 ] [ 5 ] [ 6 ] It is either used at low doses for chronic illnesses or used concomitantly at high doses during acute flares.
Methylprednisolone acetate, sold under the brand names Depo-Medrol among others, is a synthetic glucocorticoid corticosteroid and a corticosteroid ester—specifically the C21 acetate ester of methylprednisolone—which is used in clinical and veterinary medicine.
Methylprednisolone succinate, sold under the brand name Solu-Medrol among others, is a synthetic glucocorticoid corticosteroid and a corticosteroid ester—specifically the C21 succinate ester of methylprednisolone—which is used by intravenous administration.
Common side effects with short-term use include nausea, difficulty concentrating, insomnia, increased appetite, and fatigue. [5] More severe side effects include psychiatric problems, which may occur in about 5% of people. [9] Common side effects with long-term use include bone loss, weakness, yeast infections, and easy bruising. [6]
Methylprednisolone suleptanate, sold under the brand names Medrosol and Promedrol, is a synthetic glucocorticoid corticosteroid and a corticosteroid ester—specifically, the C21 suleptanate 21-(8-(methyl-(2-sulfoethyl)amino)-1,8-dioxooctanoate) ester of methylprednisolone. [1] [2] It acts as a prodrug of methylprednisolone. [3]
Methylprednisolone aceponate, or methylprednisolone acetate propionate, sold under the brand names Advantan and Avancort, is a glucocorticoid and a corticosteroid ...
The most predictive biomarkers 36h after CAR-T infusion of CRS are a fever ≥38.9 °C (102 °F) and elevated levels of MCP-1 in serum. [12] Many of the cytokines elevated in CRS are not produced by CAR-T cells, but by myeloid cells that are pathogenically licensed through T-cell-mediated activating mechanisms.
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