Name of Active Substance(s): Hydrocortisone BP/Ph. Eur.
Strength of Active Substance(s): 10 mg Hydrocortisone BP/Ph. Eur.
Pharmacology: Pharmacodynamics: Hydrocortisone or cortisol is a natural glucocorticoid (corticosteroid hormone). It acts by binding to steroid receptors in the cytoplasm. It acts mainly by reducing the local inflammation reaction. It alleviates inflammation symptoms and eliminates allergic symptoms.
Pharmacokinetics: Hydrocortisone is absorbed rapidly and completely from the alimentary tract. Because of first-pass metabolism, its bioavailability varies between 25% and 90%. In plasma, the peak concentration of hydrocortisone is reached in 1-2 hours after dosing. It is bound to plasma transcortin and albumin. At low concentrations, 10% of hydrocortisone is free; at higher concentrations, the binding capacity of transcortin is saturated and the proportion of free drug can increase to 40-50%. Its volume of distribution is 0.4-0.7 l/kg. The pharmacological half-life of hydrocortisone averages 1.5 hours, but the half-life of biological effect is considerably longer, approx. 10 hours. Hydrocortisone penetrates the placenta and is excreted in small amounts in breast milk. The elimination of hydrocortisone may be prolonged in liver diseases and shortened in thyrotoxicosis.
Adrenocortical insufficiency (Addison's disease), diminution of anterior pituitary function (hypopituitarism), congenital adrenal hyperplasia. Conditions where systemic glucocorticoid therapy is indicated.
Recommended dose: Posology: As replacement therapy, 20 to 30 mg daily, usually approximately 2/3 of this amount in the morning and 1/3 in the early evening. If necessary, the morning dose may be taken in 2 parts. In the other indications, 40 to 200 mg daily; in short-term use in special indications, even higher doses.
Paediatric population: In children, the dosage is individual. In adrenocortical insufficiency, 7.5 to 15 mg/m2/day divided in 3 equal doses (first thing in the morning, in the afternoon, and late in the evening); the morning dose may also be larger than the other doses. In congenital adrenal hyperplasia, usually 10 mg/m2/day divided in 3 doses. In hypopituitarism, 2.5 mg 3 times daily.
Dosing in special situations: Hydrocortisone replacement therapy: In patients receiving hydrocortisone replacement therapy, the dosage of Hydrocortisone should be increased 2-4-fold in stressful situations, such as in connection with injuries, infections or surgery. If necessary, the patient should be switched to parenteral treatment.
Pharmacological glucocorticoid therapy: Long-term systemic glucocorticoid therapy causes adrenocortical insufficiency that may persist for months after treatment cessation. Therefore, the dosage of Hydrocortisone should be increased in stressful situations such as in connection with infections.
In order to avoid glucocorticoid withdrawal syndrome, long-term treatment with corticosteroids should be discontinued gradually over several weeks. Dosing on alternate days reduces the risk of adrenocortical insufficiency and of the withdrawal syndrome associated with treatment cessation.
Instructions for Use: The patient should take this medicine by mouth. The amount to take each day will depend on the illness. The number of tablets to be taken will be on the label of the medicine. If unsure about the dose to take, talk to a doctor or pharmacist. Hydrocortisone can be taken with or without food.
Mode of Administration: Oral.
Symptoms and Treatment of Overdose: Acute massive overdose of hydrocortisone is not likely. Remarkably high doses are tolerated without serious adverse reactions. Treatment of oral overdose is supportive; if necessary, medicinal carbon may be given and gastric lavage performed.
Tuberculosis and other acute or chronic bacteria and viral infections without antibiotic or chemotherapeutic protection, hypersensitivity to any ingredient of the preparation.
In patients receiving hydrocortisone substitution therapy, the dosage of hydrocortisone in stress situations, e.g. trauma, infections, or surgery, must be increased 2-4 fold and, if necessary, the patient must be transferred to parenteral therapy.
Long-term systemic glucocorticoid therapy causes adrenocortical insufficiency which may last for months after the treatment has been stopped. Therefore, in stress situations, e.g. infections, the dosage of Hydrocortisone must be increased.
To avoid the withdrawal syndrome of glucocorticoid therapy, long-term corticosteroid therapy must be withdrawn gradually over a period of several weeks. Dosing on alternate days reduces the risk of adrenocortical insufficiency and the withdrawal syndrome associated with stopping the treatment. Caution should be exercised when administrating pharmaceutical dose of hydrocortisone to patients with acute psychosis, peptic ulcer, diabetes, osteoporosis, glaucoma or hypertension.
Glucocorticoids may reduce the potency of vaccines and increase the risk of neurological complications of vaccination. Live virus vaccines can cause an infection in patients receiving corticosteroids.
Pheochromocytoma crisis, which may be fatal, has been reported after administration of systemic corticosteroids. Corticosteroids should only be administered to patients with suspected or identified pheochromocytoma after an appropriate risk/benefit evaluation.
Effects on Ability to Drive and Use Machine: Hydrocortisone may cause vertigo, visual field loss and muscle wasting and weakness. If affected, patients should not drive or operate machinery.
Hydrocortisone penetrates the placenta. There is however no reason to abstain from clearly indicated therapy. A newborn of a mother who has received pharmacologic doses of hydrocortisone during pregnancy should be monitored for potential hypoadrenalism. Hydrocortisone is excreted in breast milk. Breast feeding is possible during pharmacological low dose therapy. When doses exceed 100 mg/day, nursing should be avoided for a few hours after drug administration.
No adverse reactions are anticipated from substitution therapy with physiologic doses. Short-term hydrocortisone therapy even at high dose is generally harmless.
In long-term high dose therapy, adverse reactions occur frequently. Hydrocortisone has the same adverse reactions as other glucocorticoids. It also has a mineralocorticoid effect. Hydrocortisone causes adrenocortical insufficiency in long-term high dose therapy. Therefore, stress, e.g. surgery or infection, can cause hypotension, hypoglycemia, or even death, unless the steroid dose is increased to adjust to the stress. Glucocorticoid withdrawal syndrome will follow abrupt withdrawal of long-term steroid therapy.
Phenytoin, phenobarbital, carbamazepine, rifampicin, and antithyroid drugs increase the clearance of hydrocortisone and reduce its half-life.
Hydrocortisone may weaken the effect of anticoagulants and antidiabetics.
In combination with anticholinesterase, corticosteroids can cause muscle weakness in patients with myasthenia gravis.
Systemic glucocorticoid therapy increases the risk of hypokalemia in patients receiving diuretics or amphotericin B. Glucocorticoids may increase the risk of anti-inflammatory analgesic-induced peptic ulcer.
Co-treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic side effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side effects, in which case patients should be monitored for systemic corticosteroid side effects.
Store below 30°C. Store in the original packaging and protect from light.
H02AB09 - hydrocortisone ; Belongs to the class of glucocorticoids. Used in systemic corticosteroid preparations.
Renson tab 10 mg
3 × 10's
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