PREDNISONE tablet PREDNISONE tablet

United States - English - NLM (National Library of Medicine)

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Active ingredient:
PREDNISONE (UNII: VB0R961HZT) (PREDNISONE - UNII:VB0R961HZT)
Available from:
NCS HealthCare of KY, LLC dba Vangard Labs
Administration route:
ORAL
Prescription type:
PRESCRIPTION DRUG
Therapeutic indications:
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 thyroiditis. 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, epicondylitis. During an exacerbation or as maintenance therapy in selected cases of: systemic lupus erythematosus, systemic dermatomyositis (polymyositis), acut
Product summary:
PredniSONE Tablets USP 1 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 092” debossed on the other side. NDC 0615-8306-39: Blistercards of 30 Tablets 2.5 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 339” debossed on the other side. 5 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 612” debossed on the other side. NDC 0615-0536-05: Blistercards of 15 Tablets NDC 0615-0536-39: Blistercards of 30 Tablets NDC 0615-0536-30: Unit-dose Boxes of 30 Tablets 10 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 899” debossed on the other side. 20 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 760” debossed on the other side. 50 mg – White to off-white, round, biconvex tablet; scored on one side and product identification “54 [above] 343” debossed on the other side. Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.] Dispense in a tight, child-resistant container as defined in the USP/NF. PROTECT FROM MOISTURE. PredniSONE Oral Solution USP, 5 mg per 5 mL Clear, colorless, slightly viscous solution. Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.] Dispense in a tight, light-resistant, child-resistant container as defined in the USP/NF. PredniSONE Intensol™ Oral Solution (Concentrate), 5 mg per mL Clear, colorless, slightly viscous solution. Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.] Dispense only in the bottle and only with the calibrated dropper provided. Discard opened bottle after 90 days.
Authorization status:
Abbreviated New Drug Application
Authorization number:
0615-0536-05, 0615-0536-30, 0615-0536-39, 0615-8306-39

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PREDNISONE- prednisone tablet

NCS HealthCare of KY, LLC dba Vangard Labs

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PredniSONE Tablets USP

PredniSONE Oral Solution USP

PredniSONE Intensol™ Oral Solution (Concentrate)

Rx only

DESCRIPTION

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

below:

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.

CLINICAL PHARMACOLOGY

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:

Endocrine Disorders

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

thyroiditis.

Rheumatic Disorders

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,

epicondylitis.

Collagen Diseases

During an exacerbation or as maintenance therapy in selected cases of: systemic lupus

erythematosus, systemic dermatomyositis (polymyositis), acute rheumatic carditis.

Dermatologic Diseases

Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme (Stevens-

Johnson syndrome); exfoliative dermatitis; mycosis fungoides; severe psoriasis; severe

seborrheic dermatitis.

Allergic States

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.

Ophthalmic Diseases

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.

Respiratory Diseases

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.

Hematologic Disorders

Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults;

acquired (autoimmune) hemolytic anemia; erythroblastopenia (RBC anemia); congenital

(erythroid) hypoplastic anemia.

Neoplastic Diseases

For palliative management of: leukemias and lymphomas in adults, acute leukemia of

childhood.

Edematous States

To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without

uremia, of the idiopathic type or that due to lupus erythematosus.

Gastrointestinal Diseases

To tide the patient over a critical period of the disease in: ulcerative colitis, regional

enteritis.

Miscellaneous

Tuberculous meningitis with subarachnoid block or impending block when used

concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic

or myocardial involvement.

CONTRAINDICATIONS

Prednisone tablets and oral solutions are contraindicated in systemic fungal infections

and known hypersensitivity to components.

WARNINGS

General

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

stressful situation.

Cardio-Renal

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.

Endocrine

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

increased.

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.

Infection

General:

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.

Fungal Infections:

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).

Special Pathogens:

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.

Tuberculosis:

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.

Vaccination:

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).

Viral Infections:

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.

Ophthalmic:

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.

PRECAUTIONS

General Precautions

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.

Cardio-Renal

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.

Endocrine

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.

Gastrointestinal

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

with cirrhosis.

Musculoskeletal

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.

Neuro-Psychiatric

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.

Ophthalmic

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.

Drug Interactions

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.

Antibiotics:

Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid

clearance (see PRECAUTIONS: Drug Interactions: Hepatic Enzyme Inducers, Inhibitors

and Substrates).

Anticholinesterases:

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.

Anticoagulants, Oral:

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

effect.

Antidiabetics:

Because corticosteroids may increase blood glucose concentrations, dosage

adjustments of antidiabetic agents may be required.

Antitubercular Drugs:

Serum concentrations of isoniazid may be decreased.

Bupropion:

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:

Cholestyramine may increase the clearance of corticosteroids.

Cyclosporine:

Increased activity of both cyclosporine and corticosteroids may occur when the two are

used concurrently. Convulsions have been reported with this concurrent use.

Digitalis Glycosides:

Patients on digitalis glycosides may be at increased risk of arrhythmias due to

hypokalemia.

Estrogens, Including Oral Contraceptives:

Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby

increasing their effect.

Fluoroquinolones:

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:

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.

Phenytoin:

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.

Quetiapine:

Increased doses of quetiapine may be required to maintain control of symptoms of

schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer.

Skin Tests:

Corticosteroids may suppress reactions to skin tests.

Thalidomide:

Co-administration with thalidomide should be employed cautiously, as toxic epidermal

necrolysis has been reported with concomitant use.

Vaccines:

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

Teratogenic Effects:

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

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