| Generic Name: |
Methylprednisolone
|
| Therapeutic Category: |
Glucocorticoids
|
| Pharmacological Class: |
Corticosteroids
|
| Composition: |
Each uncoated tablet contains
- Methylprednisolone IP 4mg
- Methylprednisolone IP 8mg
- Methylprednisolone IP 16mg
|
| Pregnancy Category: |
C
This drug should only be used during pregnancy if the benefit outweighs the potential risk to the fetus.
|
| LACTATION: |
Benefit should outweigh risk
Excreted into human milk: Yes
Maternal oral doses up to 40 mg/day are not likely to cause systemic effects in infants, however, doses higher than that may cause a degree of adrenal suppression.
|
| Presentation: |
INCOR M 4 – 10 X 10’s
INCOR M 8 – 10 X 10’s
INCOR M 16 – 10 X 10’s
|
| INDICATIONS:: |
- Endocrine disorders.
- Allergic disorders.
- Skin disorders.
- Arteritis/ collagenosis.
- Respiratory disease.
- Ocular disease.
- Blood disorders.
- Cardiovascular disorders.
- Rheumatoid arthritis.
- Hypercalcemia.
- Gastrointestinal disorders.
|
| MECHANISM OF ACTION: |
Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt – retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.
Glucortocoids cause profound and varied metabolic effects. In addition, they modify the body’s immune responses to diverse stimuli.
|
| DOSAGE: |
• Rheumatoid Arthritis
Severe: 12-16 mg
Moderately severe: 8-12 mg
Moderate: 4-8 mg
Children: 4-8 mg
• Systemic Lupus Erythematosus (SLE)
20-40 mg/day for mild to moderate disease.
• Dermatological Conditions
16-40 mg/day until symptoms subside, followed by gradual tapering.
• Oncology (Palliative Management of Inflammatory Symptoms or as Part of Chemotherapy)
Oral: 16-32 mg/day for symptomatic control (e.g., inflammation, swelling).
|
| PHARMACOKINETICS: |
Absorption: Well absorbed orally with a bioavailability of about 89%.
Distribution: Widely distributed across tissues; crosses the placenta.
Metabolism: Metabolized primarily in the liver via the cytochrome P450.
System Excretion: Excreted in the urine; half-life ranges from 18-36 hours.
|
| ADVERSE EFFECTS: |
The adverse effects are Infection (including increased susceptibility and severity of infections with suppression of clinical symptoms and signs),Cushingoid, Sodium retention; Fluid retention,Affective disorder (including Depressed mood and Euphoric mood),Hypertension,Peptic ulcer (with possible Peptic ulcer perforation and Peptic ulcer haemorrhage),Skin atrophy; Acne,Blood potassium decreased.
|
| CONTRAINDICATIONS: |
• In patients who have systemic fungal infections.
•In patients who have hypersensitivity to the active substance.
•In patients who have systemic infections unless specific anti-infective therapy is employed.
|
| PRECAUTIONS: |
• Tuberculosis:
Those with a previous history of, or X-ray changes characteristic of, tuberculosis. The emergence of active tuberculosis can however, be prevented by the prophylactic use of anti-tuberculosis therapy.
•Hepatic disease: In patients with acute and active hepatitis, protein binding of the glucocorticoids will be reduced and peak concentrations of administered glucocorticoids increased. Elimination of prednisolone will also be impaired. There is an enhanced effect of corticosteroids in patients with cirrhosis.
•Corticosteroid requirements may be reduced in menopausal and post-menopausal women.
•Patients with a history of severe affective disorders and particularly those with a previous history of steroid-induced psychoses.
|
| DRUG INTERACTIONS: |
•Antacids
The absorption of prednisolone may be reduced by large doses of some antacids such as magnesium trisilicate or aluminium hydroxide.
•Anticoagulants
Response to anticoagulants may be reduced or, less often, enhanced by corticosteroids. Close monitoring of the INR or prothrombin time is required to avoid spontaneous bleeding.
•Antidiabetic agents
Glucocorticoids may increase blood glucose levels. Patients with diabetes mellitus receiving concurrent insulin and/or oral hypoglycemic agents may require dosage adjustments of such therapy.
•Antibacterials
Rifamycins accelerate metabolism of corticosteroids and thus may reduce their effect. Erythromycin inhibits metabolism of methylprednisolone and possibly other corticosteroids.
|
