PREDNISONE- prednisone tablet

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

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Active ingredient:
PREDNISONE (UNII: VB0R961HZT) (PREDNISONE - UNII:VB0R961HZT)
Available from:
Bryant Ranch Prepack
Administration route:
ORAL
Prescription type:
PRESCRIPTION DRUG
Therapeutic indications:
Prednisone tablets, USP 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 erythemato
Product summary:
Product: 71335-1294 NDC: 71335-1294-1 14 TABLET in a BOTTLE NDC: 71335-1294-2 10 TABLET in a BOTTLE NDC: 71335-1294-3 18 TABLET in a BOTTLE NDC: 71335-1294-4 20 TABLET in a BOTTLE
Authorization status:
Abbreviated New Drug Application
Authorization number:
71335-1294-1, 71335-1294-2, 71335-1294-3, 71335-1294-4

PREDNISONE- prednisone tablet

Bryant Ranch Prepack

----------

PredniSONE Tablets, USP

Revised: October 2015

Rx Only

DESCRIPTION

Prednisone tablets, USP 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 pregna-1,4-diene-3,11,20-trione

monohydrate, 17,21-dihydroxy-. The structural formula is represented below:

H O M.W. 358.44

Prednisone is a white to practically white, odorless, crystalline powder. It is very slightly soluble in

water; slightly soluble in alcohol, chloroform, dioxane, and methanol.

Each tablet, for oral administration, contains 5 mg, 10 mg or 20 mg of prednisone, USP (anhydrous). In

addition, each tablet contains the following inactive ingredients: anhydrous lactose, colloidal silicon

dioxide, crospovidone, docusate sodium, magnesium stearate and sodium benzoate.

Prednisone tablets, USP 20 mg also contain FD&C Yellow No. 6.

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, USP 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.

Mis cellaneous

Tuberculous meningitis with subarachnoid block or impending block when used concurrently with

appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial involvement.

CONTRAINDICATIONS

Prednisone tablets 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.

Gas trointes tinal

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.

Mus culos keletal

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 glucocortiocoid-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 to 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-Ps ychiatric

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

Coadministration 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

Postmarketing 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. Coadministration 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 postmarketing experience, there have been reports of both increases and decreases in phenytoin

levels with dexamethasone coadministration, 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

Coadministration 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 increased incidence of cleft palate in the offspring. There are no adequate and

well-controlled studies in pregnant women. Corticosteroids should be used during pregnancy only if

the potential benefit justifies the potential risk to the fetus. Infants born to mothers who have received

substantial doses of corticosteroids during pregnancy should be carefully observed for signs of

hypoadrenalism.

Nursing Mothers

Systemically administered corticosteroids appear in human milk and could suppress growth, interfere

with endogenous corticosteroid production, or cause other untoward effects. Because of the potential

for serious adverse reactions in nursing infants from corticosteroids, a decision should be made

whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug

to the mother.

Pediatric Use

The efficacy and safety of corticosteroids in the pediatric population are based on the well-established

course of effect of corticosteroids, which is similar in pediatric and adult populations. Published

studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic

syndrome (patients greater than 2 years of age), and aggressive lymphomas and leukemias (patients

greater than 1 month of age). Other indications for pediatric use of corticosteroids, e.g., severe asthma

and wheezing, are based on adequate and well-controlled trials conducted in adults, on the premises that

the course of the diseases and their pathophysiology are considered to be substantially similar in both

populations.

The adverse effects of corticosteroids in pediatric patients are similar to those in adults (see

ADVERSE REACTIONS). Like adults, pediatric patients should be carefully observed with frequent

measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the

presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and

osteoporosis. Pediatric patients who are treated with corticosteroids by any route, including

systemically administered corticosteroids, may experience a decrease in their growth velocity. This

negative impact of corticosteroids on growth has been observed at low systemic doses and in the

absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) axis suppression (i.e.,

cosyntropin stimulation and basal cortisol plasma levels). Growth velocity may therefore be a more

sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used

tests of HPA axis function. The linear growth of pediatric patients treated with corticosteroids should

be monitored, and the potential growth effects of prolonged treatment should be weighed against

clinical benefits obtained and the availability of treatment alternatives. In order to minimize the potential

growth effects of corticosteroids, pediatric patients should be titrated to the lowest effective dose.

Geriatric Use

Clinical studies did not include sufficient numbers of subjects aged 65 and over to determine whether

they respond differently from younger subjects. Other reported clinical experience has not identified

differences in responses between the elderly and younger patients. In general, dose selection for an

elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the

greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other

drug therapy. In particular, the increased risk of diabetes mellitus, fluid retention and hypertension in

elderly patients treated with corticosteroids should be considered.

ADVERSE REACTIONS

(listed alphabetically, under each subsection)

The following adverse reactions have been reported with prednisone or other corticosteroids:

Allergic Reactions

anaphylactoid or hypersensitivity reactions, anaphylaxis, angioedema.

Cardiovascular System

bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive

heart failure, ECG changes caused by potassium deficiency, edema, fat embolism, hypertension or

aggravation of hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture

following recent myocardial infarction (see WARNINGS: Cardio-Renal), necrotizing angiitis,

pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis.

Dermatologic

acne, acneiform eruptions, allergic dermatitis, alopecia, angioedema, angioneurotic edema, atrophy and

thinning of skin, dry scaly skin, ecchymoses and petechiae (bruising), erythema, facial edema, hirsutism,

impaired wound healing, increased sweating, Karposi’s sarcoma (see PRECAUTIONS: General

Precautions), lupus erythematosus-like lesions, perineal irritation, purpura, rash, striae, subcutaneous

fat atrophy, suppression of reactions to skin tests, striae, telangiectasis, thin fragile skin, thinning scalp

hair, urticaria.

Endocrine

Adrenal insufficiency-greatest potential caused by high potency glucocorticoids with long duration of

action (associated symptoms include; arthralgias, buffalo hump, dizziness, life-threatening hypotension,

nausea, severe tiredness or weakness), amenorrhea, postmenopausal bleeding or other menstrual

irregularities, decreased carbohydrate and glucose tolerance, development of cushingoid state,

diabetes mellitus (new onset or manifestations of latent), glycosuria, hyperglycemia, hypertrichosis,

hyperthyroidism (see WARNINGS: Endocrine), hypothyroidism, increased requirements for insulin or

oral hypoglycemic agents in diabetics, lipids abnormal, moon face, negative nitrogen balance caused by

protein catabolism, secondary adrenocortical and pituitary unresponsiveness (particularly in times of

stress, as in trauma, surgery or illness) (see WARNINGS: Endocrine), suppression of growth in

pediatric patients.

Fluid and Electrolyte Disturbances

congestive heart failure in susceptible patients, fluid retention, hypokalemia, hypokalemic alkalosis,

metabolic alkalosis, hypotension or shock-like reaction, potassium loss, sodium retention with resulting

edema.

Gastrointestinal

abdominal distention, abdominal pain,anorexia which may result in weight loss, constipation, diarrhea,

elevation in serum liver enzyme levels (usually reversible upon discontinuation), gastric irritation,

hepatomegaly, increased appetite and weight gain, nausea, oropharyngeal candidiasis, pancreatitis,

peptic ulcer with possible perforation and hemorrhage, perforation of the small and large intestine

(particularly in patients with inflammatory bowel disease), ulcerative esophagitis, vomiting.

Hematologic

anemia, neutropenia (including febrile neutropenia).

Metabolic

negative nitrogen balance due to protein catabolism.

Musculoskeletal

arthralgias, aseptic necrosis of femoral and humeral heads, increase risk of fracture, loss of muscle

mass, muscle weakness, myalgias, osteopenia, osteoporosis (see PRECAUTIONS: Musculoskeletal),

pathologic fracture of long bones, steroid myopathy, tendon rupture (particularly of the Achilles

tendon), vertebral compression fractures.

Neurological/Psychiatric

amnesia, anxiety, benign intracranial hypertension, convulsions, delirium, dementia (characterized by

deficits in memory retention, attention, concentration, mental speed and efficiency, and occupational

performance), depression, dizziness, EEG abnormalities, emotional instability and irritability, euphoria,

hallucinations, headache, impaired cognition, incidence of severe psychiatric symptoms, increased

intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of

treatment, increased motor activity, insomnia, ischemic neuropathy, long-term memory loss, mania, mood

swings, neuritis, neuropathy, paresthesia, personality changes, psychiatric disorders including steroid

psychoses or aggravation of pre-existing psychiatric conditions, restlessness, schizophrenia, verbal

memory loss, vertigo, withdrawn behavior.

Ophthalmic

blurred vision, cataracts (including posterior subcapsular cataracts), central serous chorioretinopathy,

establishment of secondary bacterial, fungal and viral infections, exophthalmos, glaucoma, increased

intraocular pressure (see PRECAUTIONS: Ophthalmic), optic nerve damage, papilledema.

Other

abnormal fat deposits, aggravation/masking of infections, decreased resistance to infection (see

WARNINGS: Infection), hiccups, immunosuppresion, increased or decreased motility and number of

spermatozoa, malaise, insomnia, moon face, pyrexia.

To report SUSPECTED ADVERSE EVENTS, contact Actavis at 1-800-272-5525 or FDA at 1-

800-FDA-1088 or http://www.fda.gov/ for voluntary reporting of adverse reactions.

DOSAGE AND ADMINISTRATION

Gastric irritation may be reduced if taken before, during, or immediately after meals or with food or

milk.

The maximal activity of the adrenal cortex is between 2 am and 8 am, and it is minimal between 4 pm and

midnight. Exogenous corticosteroids suppress adrenocorticoid activity the least when given at the time

of maximal activity (am) for single dose administration. Therefore, it is recommended that prednisone be

administered in the morning prior to 9 am and when large doses are given, administration of antacids

between meals to help prevent peptic ulcers. Multiple dose therapy should be evenly distributed in

evenly spaced intervals throughout the day.

Dietary salt restriction may be advisable in patients.

Do not stop taking this medicine without first talking to your doctor. Avoid abrupt withdraw of therapy.

The initial dosage of prednisone may vary from 5 mg to 60 mg per day, depending on the specific

disease entity being treated. In situations of less severity lower doses will generally suffice, while in

selected patients higher initial doses may be required. The initial dosage should be maintained or

adjusted until a satisfactory response is noted. If after a reasonable period of time there is a lack of

satisfactory clinical response, prednisone should be discontinued and the patient transferred to other

appropriate therapy. IT SHOULD BE EMPHASIZED THAT DOSAGE REQUIREMENTS ARE

VARIABLE AND MUST BE INDIVIDUALIZED ON THE BASIS OF THE DISEASE UNDER

TREATMENT AND THE RESPONSE OF THE PATIENT. After a favorable response is noted,

the proper maintenance dosage should be determined by decreasing the initial drug dosage in small

increments at appropriate time intervals until the lowest dosage which will maintain an adequate clinical

response is reached. It should be kept in mind that constant monitoring is needed in regard to drug

dosage. Included in the situations which may make dosage adjustments necessary are changes in clinical

status secondary to remissions or exacerbations in the disease process, the patient’s individual drug

responsiveness, and the effect of patient exposure to stressful situations not directly related to the

disease entity under treatment; in this latter situation, it may be necessary to increase the dosage of

prednisone for a period of time consistent with the patient’s condition. If after long-term therapy the

drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly.

Multiple Sclerosis

In the treatment of acute exacerbations of multiple sclerosis daily doses of 200 mg of prednisolone for

a week followed by 80 mg every other day for 1 month have been shown to be effective. (Dosage range

is the same for prednisone and prednisolone.)

Alternate Day Therapy

Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of

corticoid is administered every other morning. The purpose of this mode of therapy is to provide the

patient requiring long-term pharmacologic dose treatment with the beneficial effects of corticoids

while minimizing certain undesirable effects, including pituitary-adrenal suppression, the cushingoid

state, corticoid withdrawal symptoms, and growth suppression in children.

The rationale for this treatment schedule is based on two major premises: (a) the anti-inflammatory or

therapeutic effect of corticoids persists longer than their physical presence and metabolic effects and

(b) administration of the corticosteroid every other morning allows for re-establishment of more nearly

normal hypothalamic-pituitary-adrenal (HPA) activity on the off-steroid day.

A brief review of the HPA physiology may be helpful in understanding this rationale. Acting primarily

through the hypothalamus a fall in free cortisol stimulates the pituitary gland to produce increasing

amounts of corticotropin (ACTH) while a rise in free cortisol inhibits ACTH secretion. Normally the

HPA system is characterized by diurnal (circadian) rhythm. Serum levels of ACTH rise from a low

point about 10 pm to a peak level about 6 am. Increasing levels of ACTH stimulate adrenocortical

activity resulting in a rise in plasma cortisol with maximal levels occurring between 2 am and 8 am.

This rise in cortisol dampens ACTH production and in turn adrenocortical activity. There is a gradual

fall in plasma corticoids during the day with lowest levels occurring about midnight.

The diurnal rhythm of the HPA axis is lost in Cushing’s disease, a syndrome of adrenocortical

hyperfunction characterized by obesity with centripetal fat distribution, thinning of the skin with easy

bruisability, muscle wasting with weakness, hypertension, latent diabetes, osteoporosis, electrolyte

imbalance, etc. The same clinical findings of hyperadrenocorticism may be noted during long-term

pharmacologic dose corticoid therapy administered in conventional daily divided doses. It would

appear, then, that a disturbance in the diurnal cycle with maintenance of elevated corticoid values during

the night may play a significant role in the development of undesirable corticoid effects. Escape from

these constantly elevated plasma levels for even short periods of time may be instrumental in protecting

against undesirable pharmacologic effects.

During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with

subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA

activity is variable depending upon the dose and duration of treatment. During this time the patient is

vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal

suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that

dose administered every 6 hours, there is evidence that some suppressive effect on adrenal activity may

be carried over into the following day when pharmacologic doses are used. Further, it has been shown

that a single dose of certain corticosteroids will produce adrenocortical suppression for two or more

days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone,

are considered to be short acting (producing adrenocortical suppression for 11/4 to 11/2 days

following a single dose) and thus are recommended for alternate day therapy.

The following should be kept in mind when considering alternate day therapy:

1. Basic principles and indications for corticosteroid therapy should apply. The benefits of alternate

day therapy should not encourage the indiscriminate use of steroids.

2. Alternate day therapy is a therapeutic technique primarily designed for patients in whom long-term

pharmacologic corticoid therapy is anticipated.

3. In less severe disease processes in which corticoid therapy is indicated, it may be possible to initiate

treatment with alternate day therapy. More severe disease states usually will require daily divided high

dose therapy for initial control of the disease process. The initial suppressive dose level should be

continued until satisfactory clinical response is obtained, usually four to ten days in the case of many

allergic and collagen diseases. It is important to keep the period of initial suppressive dose as brief as

possible particularly when subsequent use of alternate day therapy is intended.

Once control has been established, two courses are available: (a) change to alternate day therapy and

then gradually reduce the amount of corticoid given every other day or (b) following control of the

disease process reduce the daily dose of corticoid to the lowest effective level as rapidly as possible

and then change over to an alternate day schedule. Theoretically, course (a) may be preferable.

4. Because of the advantages of alternate day therapy, it may be desirable to try patients on this form of

therapy who have been on daily corticoids for long periods of time (e.g., patients with rheumatoid

arthritis). Since these patients may already have a suppressed HPA axis, establishing them on alternate

day therapy may be difficult and not always successful. However, it is recommended that regular

attempts be made to change them over. It may be helpful to triple or even quadruple the daily

maintenance dose and administer this every other day rather than just doubling the daily dose if difficulty

is encountered. Once the patient is again controlled, an attempt should be made to reduce this dose to a

minimum.

5. As indicated above, certain corticosteroids, because of their prolonged suppressive effect on

adrenal activity, are not recommended for alternate day therapy (e.g., dexamethasone and

betamethasone).

6. The maximal activity of the adrenal cortex is between 2 am and 8 am, and it is minimal between 4 pm

and midnight. Exogenous corticosteroids suppress adrenocortical activity the least, when given at the

time of maximal activity (am).

7. In using alternate day therapy it is important, as in all therapeutic situations to individualize and tailor

the therapy to each patient. Complete control of symptoms will not be possible in all patients. An

explanation of the benefits of alternate day therapy will help the patient to understand and tolerate the

possible flare-up in symptoms which may occur in the latter part of the off-steroid day. Other

symptomatic therapy may be added or increased at this time if needed.

8. In the event of an acute flare-up of the disease process, it may be necessary to return to a full

suppressive daily divided corticoid dose for control. Once control is again established alternate day

therapy may be reinstituted.

9. Although many of the undesirable features of corticosteroid therapy can be minimized by alternate

day therapy, as in any therapeutic situation, the physician must carefully weigh the benefit-risk ratio for

each patient in whom corticoid therapy is being considered.

HOW SUPPLIED

Product: 71335-1294

NDC: 71335-1294-1 14 TABLET in a BOTTLE

NDC: 71335-1294-2 10 TABLET in a BOTTLE

NDC: 71335-1294-3 18 TABLET in a BOTTLE

NDC: 71335-1294-4 20 TABLET in a BOTTLE

REFERENCES

1. Fekety R. Infections associated with corticosteroids and immunosuppressive therapy. In: Gorbach

SL, Bartlett JG, Blacklow NR, eds. Infectious Diseases.

Philadelphia: WBSaunders Company 1992:1050-1.

2. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticoids.

Rev Infect Dis 1989:11(6):954-63.

Manufactured by:

Watson Pharma Private Ltd.

Verna, Salcette Goa 403 722 INDIA

Distributed by:

Actavis Pharma, Inc.

Parsippany, NJ 07054 USA

Revised: October 2015

PREDNISONE 20MG TABLET

PREDNISONE

prednisone tablet

Product Information

Product T ype

HUMAN PRESCRIPTION DRUG

Ite m Code (Source )

NDC:71335-129 4(NDC:0 59 1-5443)

Route of Administration

ORAL

Active Ingredient/Active Moiety

Ingredient Name

Basis of Strength

Stre ng th

PREDNISO NE (UNII: VB0 R9 6 1HZT) (PREDNISONE - UNII:VB0 R9 6 1HZT)

PREDNISONE

20 mg

Inactive Ingredients

Ingredient Name

Stre ng th

ANHYDRO US LACTO SE (UNII: 3SY5LH9 PMK)

CRO SPO VIDO NE, UNSPECIFIED (UNII: 2S78 30 E56 1)

DO CUSATE SO DIUM (UNII: F0 5Q2T2JA0 )

MAGNESIUM STEARATE (UNII: 70 0 9 7M6 I30 )

SO DIUM BENZO ATE (UNII: OJ245FE5EU)

SILICO N DIO XIDE (UNII: ETJ7Z6 XBU4)

FD&C YELLO W NO . 6 (UNII: H77VEI9 3A8 )

Product Characteristics

Color

ORANGE (Peach)

S core

2 pieces

S hap e

ROUND

S iz e

10 mm

Flavor

Imprint Code

DAN;DAN;5443

Contains

Packag ing

#

Item Code

Package Description

Marketing Start Date

Marketing End Date

Bryant Ranch Prepack

1

NDC:71335-129 4-1

14 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 8 /29 /20 19

2

NDC:71335-129 4-2

10 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 8 /29 /20 19

3

NDC:71335-129 4-3

18 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 8 /29 /20 19

4

NDC:71335-129 4-4

20 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 8 /29 /20 19

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

ANDA

ANDA0 8 516 1

0 1/0 1/19 9 0

Labeler -

Bryant Ranch Prepack (171714327)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Bryant Ranch Prepack

171714327

REPACK(71335-129 4) , RELABEL(71335-129 4)

Revised: 9/2019

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