United States - English - NLM (National Library of Medicine)
PREDNISONE- prednisone tablet
NCS HealthCare of KY, LLC dba Vangard Labs
PredniSONE Tablets USP
PredniSONE Oral Solution USP
PredniSONE Intensol™ Oral Solution (Concentrate)
Prednisone Tablets USP are available for oral administration containing either 1 mg, 2.5
mg, 5 mg, 10 mg, 20 mg or 50 mg of prednisone USP. Each tablet contains the
following inactive ingredients: lactose monohydrate, magnesium stearate,
microcrystalline cellulose, pregelatinized starch, sodium starch glycolate and stearic acid
(1 mg, 2.5 mg, and 5 mg only).
Prednisone Oral Solution USP is formulated for oral administration containing 5 mg per 5
mL of prednisone USP and alcohol 5%. The oral solution contains the following inactive
ingredients: anhydrous citric acid, edetate disodium, fructose, hydrochloric acid, maltol,
peppermint oil, polysorbate 80, propylene glycol, saccharin sodium, sodium benzoate,
vanilla flavor and purified water.
Prednisone Intensol™ Oral Solution (Concentrate) is formulated for oral administration
containing 5 mg per mL of prednisone USP and alcohol 30%. In addition, the oral
solution contains the following inactive ingredients: anhydrous citric acid, poloxamer
188, propylene glycol and purified water.
Prednisone tablets contain prednisone which is a glucocorticoid. Glucocorticoids are
adrenocortical steroids, both naturally occurring and synthetic, which are readily
absorbed from the gastrointestinal tract. The chemical name for prednisone is 17,21-
dihydroxypregna-1,4-dienne-3,11,20-trione. The structural formula is represented
O M.W. 358.44
Prednisone USP is a white to partially white, crystalline powder. It is very slightly soluble
in water; slightly soluble in alcohol, chloroform, dioxane, and methanol.
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.
Glucocorticoids cause profound and varied metabolic effects. In addition, they modify
the body’s immune responses to diverse stimuli.
INDICATIONS AND USAGE
Prednisone tablets and solutions are indicated in the following conditions:
Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the
first choice: synthetic analogs may be used in conjunction with mineralocorticoids where
applicable; in infancy mineralocorticoid supplementation is of particular importance);
congenital adrenal hyperplasia; hypercalcemia associated with cancer; nonsuppurative
As adjunctive therapy for short-term administration (to tide the patient over an acute
episode or exacerbation) in: psoriatic arthritis, rheumatoid arthritis, including juvenile
rheumatoid arthritis (selected cases may require low-dose maintenance therapy),
ankylosing spondylitis, acute and subacute bursitis, acute nonspecific tenosynovitis,
acute gouty arthritis, post-traumatic osteoarthritis, synovitis of osteoarthritis,
During an exacerbation or as maintenance therapy in selected cases of: systemic lupus
erythematosus, systemic dermatomyositis (polymyositis), acute rheumatic carditis.
Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme (Stevens-
Johnson syndrome); exfoliative dermatitis; mycosis fungoides; severe psoriasis; severe
Control of severe or incapacitating allergic conditions intractable to adequate trials of
conventional treatment: seasonal or perennial allergic rhinitis; bronchial asthma; contact
dermatitis; atopic dermatitis; serum sickness; drug hypersensitivity reactions.
Severe acute and chronic allergic and inflammatory processes involving the eye and its
adnexa such as: allergic corneal marginal ulcers, herpes zoster ophthalmicus, anterior
segment inflammation, diffuse posterior uveitis and choroiditis, sympathetic ophthalmia,
allergic conjunctivitis, keratitis, chorioretinitis, optic neuritis, iritis and iridocyclitis.
Symptomatic sarcoidosis; Loeffler’s syndrome not manageable by other means;
berylliosis; fulminating or disseminated pulmonary tuberculosis when used concurrently
with appropriate antituberculous chemotherapy; aspiration pneumonitis.
Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults;
acquired (autoimmune) hemolytic anemia; erythroblastopenia (RBC anemia); congenital
(erythroid) hypoplastic anemia.
For palliative management of: leukemias and lymphomas in adults, acute leukemia of
To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without
uremia, of the idiopathic type or that due to lupus erythematosus.
To tide the patient over a critical period of the disease in: ulcerative colitis, regional
Tuberculous meningitis with subarachnoid block or impending block when used
concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic
or myocardial involvement.
Prednisone tablets and oral solutions are contraindicated in systemic fungal infections
and known hypersensitivity to components.
Rare instances of anaphylactoid reactions have occurred in patients receiving
corticosteroid therapy (see ADVERSE REACTIONS: Allergic Reactions).
Increased dosage of rapidly acting corticosteroids is indicated in patients on
corticosteroid therapy subjected to any unusual stress before, during and after the
Average and large doses of hydrocortisone or cortisone can cause elevation of blood
pressure, salt and water retention, and increased excretion of potassium. These effects
are less likely to occur with the synthetic derivatives except when used in large doses.
Dietary salt restriction and potassium supplementation may be necessary. All
corticosteroids increase calcium excretion.
Literature reports suggest an apparent association between use of corticosteroids and
left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy
with corticosteroids should be used with great caution in these patients.
Corticosteroids can produce reversible hypothalamic-pituitary adrenal (HPA) axis
suppression with the potential for corticosteroid insufficiency after withdrawal of
treatment. Adrenocortical insufficiency may result from too rapid withdrawal of
corticosteroids and may be minimized by gradual reduction of dosage. This type of
relative insufficiency may persist for up to 12 months after discontinuation of therapy;
therefore, in any situation of stress occurring during that period, hormone therapy
should be reinstituted. If the patient is receiving steroids already, dosage may have to be
Metabolic clearance of corticosteroids is decreased in hypothyroid patients and
increased in hyperthyroid patients. Changes in thyroid status of the patient may
necessitate adjustment in dosage.
Patients who are on corticosteroids are more susceptible to infections than are healthy
individuals. There may be decreased resistance and inability to localize infection when
corticosteroids are used. Infection with any pathogen (viral, bacterial, fungal, protozoan
or helminthic) in any location of the body may be associated with the use of
corticosteroids alone or in combination with other immunosuppressive agents that
affect cellular immunity, humoral immunity, or neutrophil function.
These infections may
be mild, but may be severe and at times fatal. With increasing doses of corticosteroids,
the rate of occurrence of infectious complications increases.
Corticosteroids may also
mask some signs of current infection.
Corticosteroids may exacerbate systemic fungal infections and therefore should not be
used in the presence of such infections unless they are needed to control life-
threatening drug reactions. There have been cases reported in which concomitant use
of amphotericin B and hydrocortisone was followed by cardiac enlargement and
congestive heart failure (see PRECAUTIONS: Drug Interactions: Amphotericin B Injection
and Potassium-Depleting Agents).
Latent disease may be activated or there may be an exacerbation of intercurrent
infections due to pathogens, including those caused by Amoeba, Candida,
Cryptococcus, Mycobacterium, Nocardia, Pneumocystis, Toxoplasma.
It is recommended that latent amebiasis or active amebiasis be ruled out before initiating
corticosteroid therapy in any patient who has spent time in the tropics or any patient
with unexplained diarrhea.
Similarly, corticosteroids should be used with great care in patients with known or
suspected Strongyloides (threadworm) infestation. In such patients, corticosteroid-
induced immunosuppression may lead to Strongyloides hyperinfection and
dissemination with widespread larval migration, often accompanied by severe
enterocolitis and potentially fatal gram-negative septicemia.
Corticosteroids should not be used in cerebral malaria.
The use of prednisone in active tuberculosis should be restricted to those cases of
fulminating or disseminated tuberculosis in which the corticosteroid is used for
management of the disease in conjunction with an appropriate antituberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity,
close observation is necessary as reactivation of the disease may occur. During
prolonged corticosteroid therapy, these patients should receive chemoprophylaxis.
Administration of live or live, attenuated vaccines is contraindicated in
patients receiving immunosuppressive doses of corticosteroids. Killed or
inactivated vaccines may be administered. However, the response to such
vaccines may be diminished and cannot be predicted. Indicated immunization
procedures may be undertaken in patients receiving nonimmunosuppressive doses of
corticosteroids as replacement therapy (e.g., for Addison’s disease).
Chickenpox and measles can have a more serious or even fatal course in pediatric and
adult patients on corticosteroids. In pediatric and adult patients who have not had these
diseases, particular care should be taken to avoid exposure. How the dose, route and
duration of corticosteroid administration affect the risk of developing a disseminated
infection is not known. The contribution of the underlying disease and/or prior
corticosteroid treatment to the risk is also not known. If exposed to chickenpox,
prophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If exposed to
measles, prophylaxis with pooled intramuscular immunoglobulin (IG) may be indicated.
(See the respective package inserts for complete VZIG and IG prescribing information.)
If chickenpox develops, treatment with antiviral agents may be considered.
Use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with
possible damage to the optic nerves, and may enhance the establishment of secondary
ocular infections due to bacteria, fungi or viruses. The use of oral corticosteroids is not
recommended in the treatment of optic neuritis and may lead to an increase in the risk
of new episodes. Corticosteroids should not be used in active ocular herpes simplex
because of possible corneal perforation.
The lowest possible dose of corticosteroids should be used to control the condition
under treatment. When reduction in dosage is possible, the reduction should be gradual.
Since complications of treatment with glucocorticoids are dependent on the size of the
dose and the duration of treatment, a risk/benefit decision must be made in each
individual case as to dose and duration of treatment and as to whether daily or
intermittent therapy should be used.
Kaposi’s sarcoma has been reported to occur in patients receiving corticosteroid
therapy, most often for chronic conditions. Discontinuation of corticosteroids may
result in clinical improvement.
As sodium retention with resultant edema and potassium loss may occur in patients
receiving corticosteroids, these agents should be used with caution in patients with
congestive heart failure, hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual
reduction of dosage. This type of relative insufficiency may persist for up to 12 months
after discontinuation of therapy following large doses for prolonged periods; therefore,
in any situation of stress occurring during that period, hormone therapy should be
reinstituted. Since mineralocorticoid secretion may be impaired, salt and/or a
mineralocorticoid should be administered concurrently.
There is an enhanced effect of corticosteroids on patients with hypothyroidism.
Steroids should be used with caution in active or latent peptic ulcers, diverticulitis, fresh
intestinal anastomoses, and nonspecific ulcerative colitis, since they may increase the
risk of a perforation.
Signs of peritoneal irritation following gastrointestinal perforation in patients receiving
corticosteroids may be minimal or absent.
There is an enhanced effect due to decreased metabolism of corticosteroids in patients
Corticosteroids decrease bone formation and increase bone resorption both through
their effect on calcium regulation (i.e., decreasing absorption and increasing excretion)
and inhibition of osteoblast function. This, together with a decrease in the protein matrix
of the bone secondary to an increase in protein catabolism, and reduced sex hormone
production, may lead to inhibition of bone growth in pediatric patients and the
development of osteoporosis at any age. Growth and development of infants and
children on prolonged corticosteroid therapy should be carefully observed. Special
consideration should be given to patients at increased risk of osteoporosis (e.g.,
postmenopausal women) before initiating corticosteroid therapy.
Inclusion of therapy for osteoporosis prevention or treatment should be considered. To
minimize the risk of glucocortoicoid-induced bone loss, the smallest possible effective
dosage and duration should be used. Lifestyle modification to reduce the risk of
osteoporosis (e.g., cigarette smoking cessation, limitation of alcohol consumption,
participation in weight-bearing exercise for 30-60 minutes daily) should be encouraged.
Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate,
risedronate), and a weight-bearing exercise program that maintains muscle mass are
suitable first-line therapies aimed at reducing the risk of adverse bone effects. Current
recommendations suggest that all interventions be initiated in any patient in whom
glucocorticoid therapy with at least the equivalent of 5 mg of prednisone for at least 3
months is anticipated; in addition, sex hormone replacement therapy (combined
estrogen and progestin in women; testosterone in men) should be offered to such
patients who are hypogonadal or in whom replacement is otherwise clinically indicated
and biphosphonate therapy should be initiated (if not already) if bone mineral density
(BMD) of the lumbar spine and/or hip is below normal.
Although controlled clinical trials have shown corticosteroids to be effective in speeding
the resolution of acute exacerbations of multiple sclerosis, they do not show that they
affect the ultimate outcome or natural history of the disease. The studies do show that
relatively high doses of corticosteroids are necessary to demonstrate a significant
effect. (See DOSAGE AND ADMINISTRATION: Multiple Sclerosis.)
An acute myopathy has been observed with the use of high doses of corticosteroids,
most often occurring in patients with disorders of neuromuscular transmission (e.g.,
myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular
blocking drugs (e.g., pancuronium). This acute myopathy is generalized, may involve
ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine
kinase may occur. Clinical improvement or recovery after stopping corticosteroids may
require weeks to years.
Psychiatric derangements may appear when corticosteroids are used, ranging from
euphoria, insomnia, mood swings, personality changes, and severe depression, to frank
psychotic manifestations. Also, existing emotional instability or psychotic tendencies
may be aggravated by corticosteroids.
Intraocular pressure may become elevated in some individuals. If steroid therapy is
continued for more than 6 weeks, intraocular pressure should be monitored.
Information for Patients
Patients should be warned not to discontinue the use of corticosteroids abruptly or
without medical supervision. As prolonged use may cause adrenal insufficiency and
make patients dependent on corticosteroids, they should advise any medical attendants
that they are taking corticosteroids and they should seek medical advice at once should
they develop an acute illness including fever or other signs of infection. Following
prolonged therapy, withdrawal of corticosteroids may result in symptoms of the
corticosteroid withdrawal syndrome including, myalgia, arthralgia, and malaise.
Persons who are on corticosteroids should be warned to avoid exposure to chickenpox
or measles. Patients should also be advised that if they are exposed, medical advice
should be sought without delay.
Amphotericin B Injection and Potassium-Depleting Agents:
When corticosteroids are administered concomitantly with potassium-depleting agents
(e.g., amphotericin B, diuretics), patients should be observed closely for
development of hypokalemia. In addition, there have been cases reported in which
concomitant use of amphotericin B and hydrocortisone was followed by cardiac
enlargement and congestive heart failure.
Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid
clearance (see PRECAUTIONS: Drug Interactions: Hepatic Enzyme Inducers, Inhibitors
Concomitant use of anticholinesterase agents (e.g., neostigmine, pyridostigmine)
and corticosteroids may produce severe weakness in patients with myasthenia gravis. If
possible, anticholinesterase agents should be withdrawn at least 24 hours before
initiating corticosteroid therapy. If concomitant therapy must occur, it should take place
under close supervision and the need for respiratory support should be anticipated.
Co-administration of corticosteroids and warfarin usually results in inhibition of
response to warfarin, although there have been some conflicting reports. Therefore,
coagulation indices should be monitored frequently to maintain the desired anticoagulant
Because corticosteroids may increase blood glucose concentrations, dosage
adjustments of antidiabetic agents may be required.
Serum concentrations of isoniazid may be decreased.
Since systemic steroids, as well as bupropion, can lower the seizure threshold,
concurrent administration should be undertaken only with extreme caution; low initial
dosing and small gradual increases should be employed.
Cholestyramine may increase the clearance of corticosteroids.
Increased activity of both cyclosporine and corticosteroids may occur when the two are
used concurrently. Convulsions have been reported with this concurrent use.
Patients on digitalis glycosides may be at increased risk of arrhythmias due to
Estrogens, Including Oral Contraceptives:
Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby
increasing their effect.
Post-marketing surveillance reports indicate that the risk of tendon rupture may be
increased in patients receiving concomitant fluoroquinolones (e.g., ciprofloxacin,
levofloxacin) and corticosteroids, especially in the elderly. Tendon rupture can occur
during or after treatment with quinolones.
Hepatic Enzyme Inducers, Inhibitors and Substrates:
Drugs which induce cytochrome P450 3A4 (CYP 3A4) enzyme activity (e.g.,
barbiturates, phenytoin, carbamazepine, rifampin) may enhance the metabolism
of corticosteroids and require that the dosage of the corticosteroid be increased. Drugs
which inhibit CYP 3A4 (e.g., ketoconazole, itraconazole, ritonavir, indinavir,
macrolide antibiotics such as erythromycin) have the potential to result in
increased plasma concentrations of corticosteroids. Glucocorticoids are moderate
inducers of CYP 3A4. Co-administration with other drugs that are metabolized by CYP
3A4 (e.g., indinavir, erythromycin) may increase their clearance, resulting in
decreased plasma concentration.
Ketoconazole has been reported to decrease the metabolism of certain corticosteroids
by up to 60%, leading to increased risk of corticosteroid side effects. In addition,
ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal
insufficiency during corticosteroid withdrawal.
Nonsteroidal Anti-Inflammatory Agents (NSAIDS):
Concomitant use of aspirin (or other nonsteroidal anti-inflammatory agents) and
corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used
cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of
salicylates may be increased with concurrent use of corticosteroids; this could lead to
decreased salicylate serum levels or increase the risk of salicylate toxicity when
corticosteroid is withdrawn.
In post-marketing experience, there have been reports of both increases and decreases
in phenytoin levels with dexamethasone co-administration, leading to alterations in
seizure control. Phenytoin has been demonstrated to increase the hepatic metabolism of
corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid.
Increased doses of quetiapine may be required to maintain control of symptoms of
schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer.
Corticosteroids may suppress reactions to skin tests.
Co-administration with thalidomide should be employed cautiously, as toxic epidermal
necrolysis has been reported with concomitant use.
Patients on corticosteroid therapy may exhibit a diminished response to toxoids and live
or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also
potentiate the replication of some organisms contained in live attenuated vaccines.
Routine administration of vaccines or toxoids should be deferred until corticosteroid
therapy is discontinued if possible (see WARNINGS: Infection: Vaccination).
Carcinogenesis, Mutagenesis, Impairment of Fertility
No adequate studies have been conducted in animals to determine whether
corticosteroids have a potential for carcinogenesis or mutagenesis. Steroids may
increase or decrease motility and number of spermatozoa in some patients.
Pregnancy Category C: Corticosteroids have been shown to be teratogenic in many
species when given in doses equivalent to the human dose. Animal studies in which
corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an