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Hydrocortisone 5mg tablet: White, round, biconvex tablet having a diameter of 6.5mm.
Hydrocortisone 20mg tablet: White, round, biconvex tablet having a diameter of 7.94mm, breakline on one face and dp logo on the other.
Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. It exhibits anti-inflammatory and immunosuppressant properties inhibiting the clinical manifestations of disease in a wide range of disorders.
Hydrocortisone is well absorbed after oral administration achieving peak blood concentrations after one hour. Plasma protein binding is greater than 90%. Hydrocortisone is primarily bound to plasma globulin. Globulins have a high affinity for hydrocortisone but low binding capacity. Plasma albumin may also bind hydrocortisone. Although albumin has a low affinity for hydrocortisone it does have a high binding capacity.
Only unbound form of hydrocortisone is pharmacologically active. Hydrocortisone is metabolised in the liver by hydrogenation to tetrahydrocortisone and other degraded forms. These are then excreted in the urine as glucuronide conjugates, with a small proportion of unchanged hydrocortisone. The biological half-life of hydrocortisone is about 100 minutes.
Replacement therapy in Addisons disease or chronic adrenocortical insufficiency secondary to hypopituitarism.
Inhibition of the secondary increase in ACTH secretion when aminoglutethimide is administered for breast or prostatic cancer.
As replacement therapy: The normal requirement is 10-30mg daily (usually 20mg in the morning and 10mg at night to mimic the circadian rhythm of the body).
As combination therapy with aminoglutethimide: 40mg daily given as 10mg with breakfast, 10mg with dinner and 20mg at bedtime.
Hydrocortisone is contraindicated in patients with peptic ulcer, osteoporosis, psychoses or severe psychoneuroses.
Hydrocortisone is usually contraindicated in the presence of acute infection, unless the patient is on long term hydrocortisone whereupon the dose should be increased to counteract the increased stress of the infection.
Extreme caution should be exercised in the presence of congestive heart failure, diabetes mellitus, infectious disease, chronic renal failure and uraemia, and quiescent tuberculosis.
Abrupt withdrawal of hydrocortisone after chronic use may precipitate acute adrenal insufficiency as a result of the suppression of corticotrophin at the anterior pituitary. Symptoms of adrenal insufficiency include malaise, muscle weakness, mental changes, muscle and joint pain, desquamation of the skin, dyspnoea, anorexia, nausea and vomiting, fever, hypoglycaemia, hypotension and dehydration.
The withdrawal symptoms may simulate a clinical relapse of the disease for which the patient is undergoing treatment. Withdrawal of hydrocortisone should always be gradual, the rate depending upon the individual patients response, the dose and duration of therapy.
Corticosteroid induced elevation of blood pressure, salt and water retention and increased potassium excretion are possible with high doses of hydrocortisone. Like all corticosteroids, hydrocortisone increases calcium excretion.
Administration of live virus vaccines including smallpox is contraindicated in patients receiving immunosuppressive doses of hydrocortisone since the expected serum antibody response may not be obtained. Immunisation procedures may, however, be undertaken in patients who are receiving corticosteroids as replacement therapy.
The administration of hydrocortisone may mask some signs of infection or allow new infections to develop. Decreased resistance and inability to localise infection may be noted.
It has been observed that in cerebral malaria, the use of corticosteroids was associated with prolongation of coma and a higher incidence of pneumonia and gastrointestinal bleeding.
Corticosteroids may activate latent amoebiasis, therefore, it is recommended that latent or active amoebiasis be ruled out before initiating corticosteroid treatment in any patient who has spent time in the tropics or has unexplained diarrhoea.
Prolonged corticosteroid use may produce posterior, sub-capsular cataracts, glaucoma with possible damage to the optic nerves and may enhance the establishment of secondary ocular infections due to fungi or viruses.
The use of hydrocortisone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis. The hydrocortisone must be used in conjunction with an appropriate antituberculosis regimen.
Patients with hypothyroidism and cirrhosis manifest an enhanced effect if given corticosteroids.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
The use of corticosteroids may cause psychic derangements ranging from euphoria, insomnia, mood swings, personality changes and severe depression to frank psychotic manifestations.
Corticosteroids should be used with caution in non-specific ulcerative colitis if there is a probability of impending perforation, abscess or other pyogenic infection.
Steroids may increase or decrease motility and number of spermatozoa in some patients.
Use in Pregnancy and Lactation: Since adequate information on the effects of hydrocortisone on the developing child is not known, use in pregnancy or in women of child-bearing potential requires that the possible benefit of hydrocortisone to the mother be weighed against the potential hazards to the mother and/or foetus.
Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production or cause other unwanted effects. Mothers should, therefore, be advised not to nurse if corticosteroids are required.
Patients who have received high or prolonged doses of hydrocortisone should be given supplementary corticosteroids to overcome periods of stress caused by anaesthesia, surgery or trauma.
The use of hydrocortisone may cause disturbance of electrolyte balance with retention of sodium and water and increased excretion of potassium. There may be disturbances of some aspects of metabolism including gluconeogenesis, calcium balance that may lead to osteoporosis and hyperglycaemia. Tissue repair and healing may be delayed, with an associated increase in the liability for infection.
Prolonged administration of hydrocortisone may result in suppression of corticotrophin secretion and atrophy of the adrenal cortex. Large doses of hydrocortisone may produce symptoms typical of Cushing's disease.
Except for allergy the adverse effects listed have been associated with prolonged therapy and/or high doses:
Adrenal suppression
Allergy
Blood/vascular disorders:
Development of diabetes mellitus
Effects on bones and joints:
Effects on eyes:
Effects on growth:
Effects on heart:
Effects on muscle:
Effects on skin:
Effects on gastrointestinal tract:
Mental effects:
Metabolic effects:
Other effects:
Concurrent administration of barbiturates, phenylbutazone, phenytoin or rifampicin may reduce the effects of corticosteroids. The action of anti-coagulants may be reduced by corticosteroids.
Excessive potassium loss may occur if corticosteroids are administered concurrently with a potassium-depleting diuretic such as the thiazides or frusemide.
Adverse effects related to hydrocortisone normally develop only after prolonged use of doses in excess of the normal physiological requirement. Treatment is symptomatic and where possible the hydrocortisone dose should be reduced gradually.
Store at room temperature. Protect from light and moisture and keep out of reach of children.
Prescription Medicine.
Hydrocortisone 5mg and 20mg tablets are available in quantities of 100.
Hydrocortisone is 11β,17,21,-trihydroxy pregn-4-ene-3,20-dione. It has a molecular formula and weight of C21H30O5 and 362.47 respectively.
Other ingredients of the tablets are: Lactose, Maize cornflour, Talc, Magnesium stearate and Polyvinylpyrrolidinone
Douglas Pharmaceuticals Ltd
P O Box 45-027
Te Atatu Peninsula
AUCKLAND 0651
New Zealand
Ph: (09) 835-0660
Fax: (09) 835-0665
19 October 2007