METICORTELONE
Clinical safety rating: caution
Comprehensive clinical and safety monograph for METICORTELONE (METICORTELONE).
Corticosteroid with glucocorticoid and mineralocorticoid activity; binds to glucocorticoid receptors, modulating gene expression to suppress inflammation and immune response.
| Metabolism | Hepatic via CYP3A4; primarily metabolized to inactive metabolites. |
| Excretion | Renal: <5% unchanged; hepatic metabolism to inactive metabolites, primarily conjugated and excreted in urine; <2% fecal |
| Half-life | Terminal elimination half-life: 3.0-3.5 hours; clinical context: requires multiple daily doses for sustained effect; biological half-life (duration of HPA suppression) longer (~24-36 hours) due to intracellular activity |
| Protein binding | 75-80% bound, primarily to corticosteroid-binding globulin (CBG, transcortin) and albumin |
| Volume of Distribution | 0.5-1.0 L/kg; clinical meaning: moderate tissue distribution, indicating extensive extravascular distribution and high tissue penetration |
| Bioavailability | Oral: approximately 80-90% (well absorbed); IM: 100% |
| Onset of Action | Oral: 1-2 hours (peak effect at 2-4 hours); IM: 2-3 hours; IV: immediate (within minutes) after bolus |
| Duration of Action | Oral: 12-36 hours (dosing interval 4-6 hours for anti-inflammatory effect, but once daily possible for replacement); IM: 4-6 days; duration of adrenal suppression longer than anti-inflammatory effect |
Prednisolone: 5-60 mg orally once daily or divided twice daily; methylprednisolone: 4-48 mg orally once daily or divided twice daily. Dose and duration vary by indication.
| Dosage form | INJECTABLE |
| Renal impairment | No specific GFR-based adjustment required; caution in severe renal impairment due to fluid retention. |
| Liver impairment | Child-Pugh A: No adjustment. Child-Pugh B: Reduce dose by 50%. Child-Pugh C: Reduce dose by 75% or consider alternative. |
| Pediatric use | 0.14-2 mg/kg/day orally divided every 6-12 hours; maximum 60 mg/day. Use lowest effective dose. |
| Geriatric use | Start at lowest effective dose; monitor for osteoporosis, hypertension, hyperglycemia, and immunosuppression. Use minimum duration. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for METICORTELONE (METICORTELONE).
| Breastfeeding | Prednisolone is excreted into breast milk in low concentrations (M/P ratio approximately 0.2-0.4). Maternal doses up to 40 mg/day produce negligible infant exposure (<10% of maternal dose). Avoid high-dose or prolonged therapy; consider timing doses after breastfeeding to minimize exposure. |
| Teratogenic Risk | Prednisolone (active metabolite of Meticortelone) crosses placenta but is largely inactivated by 11β-hydroxysteroid dehydrogenase type 2. First trimester: increased risk of cleft palate (odds ratio ~3.4) with high doses (>10-20 mg/day). Second/third trimesters: associated with fetal growth restriction, adrenal suppression, and preterm birth. Risk is dose- and duration-dependent. |
■ FDA Black Box Warning
None.
| Serious Effects |
Systemic fungal infections; hypersensitivity to corticosteroids; administration of live or live-attenuated vaccines in patients receiving immunosuppressive doses.
| Precautions | Adrenal suppression with prolonged use; increased susceptibility to infections; masking of infection signs; osteoporosis; glaucoma; cataracts; Cushing's syndrome; growth suppression in children; psychiatric disturbances; cardiovascular effects (hypertension, fluid retention); gastrointestinal perforation risk. |
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| Fetal Monitoring | Maternal: blood pressure, blood glucose (especially in gestational diabetes), signs of infection, adrenal function if prolonged therapy. Fetal: serial ultrasound for growth (every 4-6 weeks) if chronic use; monitor for adrenal insufficiency in neonates after late-term exposure. |
| Fertility Effects | No direct impairment of fertility in humans. High doses may disrupt menstrual cycles via HPA axis suppression, but effects are reversible upon dose reduction or discontinuation. No evidence of permanent ovarian toxicity. |