Dexamethasone acts because of its structural similarity to endogenous glucocorticoids. Unbound, it can penetrate the membrane of the cell and then bind with high affinity to intracellular glucocorticoid receptors.
The anti-inflammatory (anti-inflammatory) effect is achieved by interfering with the so-called arachidonic acid metabolism. The active substance causes fewer prostaglandins and leukotrienes to be produced at the end of this metabolism. These are significantly involved in the inflammatory process of the human body.
Dexamethasone has an anti-allergic effect by preventing the release of histamine while reducing the number and activity of certain B and T lymphocytes.
It also has minimal mineralocorticoid activity.
All effects of dexamethasone occur with a time delay of 1-3 days, due to its complex mechanism of action.
Dexamethasone is approximately 77% protein-bound in plasma. The majority is bound to serum albumin. Dexamethasone is metabolized in the liver by the enzyme CYP3A4, so drug interactions may occur. Corticosteroids are generally excreted predominantly in the urine. However, <10% of dexamethasone is excreted in the urine. The mean half-life of a tablet is 4 hours. After intramuscular injection, the half-life is approximately 3-6 hours.
Known drug interactions are:
- Inducers of hepatic microsomal enzymes (CYP450) such as barbiturates, phenytoin, and rifampicin may decrease the half-life of dexamethasone.
- Concomitant treatment with oral contraceptives may increase its volume of distribution.