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Prednisone 1mg tablet: White, or almost white, round tablet with one face embossed "1" and the other embossed "P". Diameter 6.25mm.
Prednisone 2.5mg tablet: White, or almost white, round tablet with one face embossed "2.5" and the other embossed "P". Diameter 6.25mm.
Prednisone 5mg tablet: White, or almost white, round tablet with one face embossed "5" and the other embossed "P". Diameter 6.25mm.
Prednisone 20mg tablet: Pink, round tablet with a bisecting score on one face and a "P" on the other. Diameter 6.25mm. Prednisone 20mg tablets contain FD & C Red No.3 colouring.
Prednisone tablets are gluten-free.
Prednisone is a synthetic glucocorticoid obtained by dehydrogenation of cortisone at positions 1 and 2. It is biologically inert.
Anti-inflammatory, immunosuppressant and mineralcorticoid properties are only exhibited when prednisone is converted to prednisolone in the liver.
Prednisolone is extensively bound to plasma proteins although less so than hydrocortisone (cortisol). Prednisolone is a potent therapeutic agent influencing the biochemical behaviour of most tissues of the body. Unlike hydrocortisone, prednisolone has little sodium retaining activity.
Prednisolone has a biological half-life lasting several hours, intermediate between those of cortisone (cortisol) and the longer acting glucocorticoids, such as dexamethasone. It is this intermediate duration of action which makes it suitable for the alternate-day administration regimens which have been found to reduce the risk of adrenocortical insufficiency, yet provide adequate corticosteroid coverage in some disorders.
Prednisone is readily absorbed from the gastrointestinal tract and is then converted to its active metabolite prednisolone, by hydrogenation of the ketone group at position 11, in the liver. The preconversion biological half-life of prednisone is about 60 minutes.
Prednisolone is excreted in the urine as free and conjugated metabolites together with an appreciable proportion of unchanged prednisolone. Prednisolone has a usual plasma half-life of 2 to 4 hours.
A recent review of the pharmacokinetics of prednisone and prednisolone concluded that the conversion of prednisone is probably not diminished by liver disease.
Prednisone is indicated wherever corticosteroid therapy is considered necessary eg.
Skin: Pemphigus vulgaris, allergic dermatitis, eczema, exfolliative dermatitis, dermatitis herpetiformas, dermatitis medicamentosa, erythema multiforme, disseminated lupus erythematosus, dermatomyositis, polyarteritis nodosa.
Respiratory: Severe bronchial asthma and status asthmaticus, emphysema, pulmonary fibrosis.
Adrenal: Adrenal hyperplasia (adrenogenital syndrome).
Haematological: Idiopathic thrombocytopenic purpura, acquired haemolytic anaemia, acute leukaemia.
Other: Nephrotic syndrome, iridochoroiditis ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, rheumatic fever, gout, periarthritis of the shoulder.
Prednisone is intended for oral administration only.
Adults: The initial dose is 5mg to 80mg daily depending on the condition being treated, as a single dose after breakfast, as divided doses, or as a double dose on alternate days. The maintenance dose is usually 5mg to 20mg daily. The dose should be individualised according to the severity of the disease and the patients reponse rather than by age or body weight.
For adrenogenital syndrome: 5 to 10mg a day as a single dose.
The usual adult prescribing limit is up to 250mg day.
Children: For children up to 18 months of age, dosage has not been established. For children over 18 months, initial dosage is 0.5mg/kg daily, this dosage can be doubled or trebled if necessary, continued until definitive remission occurs. Maintenance dose 0.125 to 0.25mg/kg daily.
A single daily dose is preferable over divided doses, to reduce the likelihood of adrenal suppression. The dose should be taken prior to 9am, to closely mimic the body's own maximum corticosteriod secretion. Giving the dose, usually double pre-determined daily dose, on alternate mornings may also reduce the suppression of the HPA axis. This regimen is not recommended for treatment of haematologic disorders, malignancies, ulcerative colitis, or severe conditions.
Patients with known or suspected renal insufficiency, including those already receiving replacement therapy require an increase in dosage or reinstitution of therapy prior to, during and for a time following exposure to stress.
Prednisone is contraindicated in patients with: peptic ulcer, osteoporosis, psychoses or severe psychoneuroses. Prednisone is usually contraindicated in the presence of acute infection, unless the patient is on long term prednisone whereupon the dose should be increased to counteract the increased stress of the infection.
Administration of live virus vaccines including smallpox is contraindicated in patients receiving immunosuppressive doses of prednisone 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.
Extreme caution should be exercised in the presence of congestive heart failure, diabetes mellitus, infectious disease, chronic renal failure and uraemia, quiescent tuberculosis, glaucoma, hypertension, myasthenia gravis and thromboembolic disorders.
Abrupt withdrawal of prednisone 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, dyspneoa, 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 prednisone 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 prednisone. Like all corticosteroids, prednisone increases calcium excretion.
The administration of prednisone 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 gastro-intestinal 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 prednisone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis. The prednisone must be used in conjunction with an appropriate antituberculosis regimen.
Metabolic clearance of adrenocorticoids is decreased in hypothyroid patients.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
Geriatric patients especially post menopausal women may be more likely to develop glucocorticoid induced osteoporosis.
Prednisone should be used with caution for long term therapy in children. Children and adolescents should be closely monitored for growth retardation, osteoporosis, avascular necrosis of the femoral heads, glaucoma or cataracts during prolonged therapy.
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.
Patients who have received high or prolonged doses of prednisone should be given supplementary corticosteroids to overcome periods of stress caused by anaesthesia, surgery or trauma.
Use in Pregnancy and Lactation: Since adequate information on the effects of prednisone on the developing child is not known, use in pregnancy or in women of child-bearing potential requires that the possible benefit of cortisone 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.
Embryotoxicity, teratogenicity, carcinogenicity, mutagenicity: Teratogenic effects of glucocorticoids which have been demonstrated in animal studies since 1950 have not been confirmed in man. Use of glucocorticoids in man has not shown an increase in malignant disease.
The use of prednisone 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 prednisone may result in suppression of corticotrophin secretion and atrophy of the adrenal cortex. Large doses of prednisone may produce symptoms typical of Cushing's disease.
Prednisone can decrease plasma anticholinesterase activity. This might affect the progress or treatment of myasthenia gravis.
Except for allergy the adverse effects listed have been associated with prolonged therapy and/or high doses:
Concurrent administration of inducers of hepatic enzymes such as 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.
Concurrent chronic use of antacids with prednisone may decrease absorption of these glucocorticoids; efficacy may be decreased sufficiently to require dosage adjustments in patients receiving small doses of prednisone.
Adverse effects related to prednisone normally develop only after prolonged use of doses in excess of the normal physiological requirement. Treatment is symptomatic and where possible the prednisone dose should be reduced gradually.
Store at room temperature. Protect from light and moisture and keep out of reach of children.
Prescription Medicine.
Prednisone 1mg and 2.5mg tablets are in packs of 100. Prednisone 5mg tablets in packs of 30, 100 and 500. Prednisone 20mg tablets are in packs of 30 and 100.
Prednisone is 17,21-dihydroxypregna-1,4-diene 3,11,20 trione. It has a molecular weight of 358.4 and its molecular formula is C21H26O5.
Other ingredients of the tablets are: Lactose, Maize cornflour, Polyvinylpyrrolidinone, Magnesium stearate, Talc and Sodium starch glycolate. Prednisone 20mg tablets contain FD & C Red No.3 colouring.
Douglas Pharmaceuticals Ltd
PO Box 45-027
AUCKLAND 8
Ph: (09) 835-0660
Fax: (09) 835-0665
11 June 1999