PREDNISONE tablet

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

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Active ingredient:
PREDNISONE (UNII: VB0R961HZT) (PREDNISONE - UNII:VB0R961HZT)
Available from:
Direct_Rx
Administration route:
ORAL
Prescription type:
PRESCRIPTION DRUG
Therapeutic indications:
Prednisone Tablets, USP are indicated in the following conditions: 1. 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 Nonsuppurative thyroiditis 2. 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. 3. Collagen Diseases During an exacerbation or as maintenance therapy in selected cases of: Systemic lupus erythe
Product summary:
Prednisone Tablets, USP are available in the following strengths and package sizes: 5 mg (White, round tablets debossed with "TL 172" on one side and scored on the other side) Bottles of 100 Bottles of 1000 10 mg (White, round tablets debossed with "TL 173" on one side and scored on the other side) Bottles of 100 Bottles of 500 Bottles of 1000 20mg (Peach, round tablets debossed with "TL 175" on one side and scored on the other side) Bottles of 100 Bottles of 500 Bottles of 1000 Store at 20° to 25° C (68° to 77° F) [See USP Room Temperature]. Manufactured By: Jubilant Cadista Pharmaceuticals Inc. Salisbury, MD 21801, USA. Revised 01/2018
Authorization status:
Abbreviated New Drug Application
Authorization number:
61919-235-15, 61919-235-40

PREDNISONE- prednisone tablet

Direct_Rx

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PREDNISONE

Prednisone is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring

and synthetic, which are readily absorbed from the gastrointestinal tract. Prednisone is a white to

practically white, odorless, crystalline powder. It is very slightly soluble in water; slightly soluble in

alcohol, in chloroform, in dioxane, and in methanol. The chemical name for prednisone is pregna-1, 4-

diene-3, 11, 20-trione, 17, 21-dihydroxy-

The structural formula is represented below:

[Image]

Molecular weight: 358.44

Prednisone Tablets, USP are available in three strengths: 5 mg, 10 mg, and 20 mg. In addition, each

tablet contains the following Inactive Ingredients: Lactose Monohydrate, Magnesium Stearate,

Pregelatinized Starch, Sodium Lauryl Sulfate and Sodium Starch Glycolate. Also Prednisone Tablets

USP, 20 mg contains FD & C yellow #6 aluminum lake HT 15-18%.

Prednisone Tablets, USP are indicated in the following conditions:

1. 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

Nonsuppurative thyroiditis

2. 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.

3. Collagen Diseases

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

Systemic lupus erythematosus

Systemic derznatomyositis (polymyositis)

Acute rheumatic carditis

4. Dermatologic Diseases

Pemphigus

Bullous dermatitis herpetiformis

Severe erythema multiforme (Stevens-Johnson syndrome)

Exfoliative dermatitis

Mycosis fungoides

Severe psoriasis

Severe seborrheic dermatitis

5. 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

6. 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

7. 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

8. Hematologic Disorders

Idiopathic thrombocytopenic purpura in adults

Secondary thrombocytopenia in adults

Acquired (autoimmune) hemolytic anemia

Erythroblastopenia (RBC anemia)

Congenital (erythroid) hypoplastic anemia

9. Neoplastic Diseases

For palliative management of:

Leukemias and lymphomas in adults

Acute leukemia of childhood

10. 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

11. Gastrointestinal Diseases

To tide the patient over a critical period of the disease in:

Ulcerative colitis

Regional enteritis

12. Nervous System

Acute exacerbations of multiple sclerosis

13. Miscellaneous

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

appropriate antituberculous chemotherapy

Trichinosis with neurologic or myocardial involvement

Systemic fungal infections and known hypersensitivity to components.

In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting

corticosteroids before, during, and after the stressful situation is indicated.

Corticosteroids may mask some signs of infection, and new infections may appear during their use.

There may be decreased resistance and inability to localize infection when corticosteroids are used.

Prolonged 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

fungi or viruses.

Usage in pregnancy: Since adequate human reproduction studies have not been done with

corticosteroids, the use of these drugs in pregnancy, nursing mothers or women of childbearing

potential requires that the possible benefits of the drug be weighed against the potential hazards to the

mother and embryo or fetus. Infants born of mothers who have received substantial doses of

corticosteroids during pregnancy, should be carefully observed for signs of hypoadrenalism.

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.

While on corticosteroid therapy patients should not be vaccinated against smallpox. Other immunization

procedures should not be undertaken in patients who are on corticosteroids, especially on high dose,

because of possible hazards of neurological complications and a lack of antibody response.

The use of Prednisone Tablets, USP in active tuberculosis should be restricted to those cases of

fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the

disease in conjunction with an appropriate anti-tuberculous 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.

Persons who are on drugs which suppress the immune system are more susceptible to infections than

healthy individuals. Chickenpox and measles, for example, can have a more serious or even fatal course

in non-immune children or adults on corticosteroids. In such children or adults who have not had these

diseases, particular care should be taken to avoid exposure. How the dose, route and duration of

corticosteroid administration affects 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.

General Precautions

Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of

dosage. This type of relative insufficiency may persist for months after discontinuation of therapy;

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 and in those with

cirrhosis.

Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible

corneal perforation.

The lowest possible dose of corticosteroid should be used to control the condition under treatment, and

when reduction in dosage is possible, the reduction should be gradual.

Psychic 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.

Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia.

Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of

impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses;

active or latent peptic ulcer; renal insufficiency; hypertension; osteoporosis; and myasthenia gravis.

Growth and development of infants and children on prolonged corticosteroid therapy should be

carefully observed.

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 corticosteroids 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.)

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.

Convulsions have been reported with concurrent use of methylprednisolone and cyclosporine. Since

concurrent use of these agents results in a mutual inhibition of metabolism, it is possible that adverse

events associated with the individual use of either drug may be more apt to occur.

Information for patients

Persons who are on immunosuppressant doses of 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.

Fluid and Electrolyte Disturbances

Sodium retention

Fluid retention

Congestive heart failure in susceptible patients

Potassium loss

Hypokalemic alkalosis

Hypertension

Musculoskeletal

Muscle weakness

Steroid myopathy

Loss of muscle mass

Osteoporosis

Vertebral compression fractures

Aseptic necrosis of femoral and humeral heads

Pathologic fracture of long bones

Gastrointestinal

Peptic ulcer with possible perforation and hemorrhage

Pancreatitis

Abdominal distention

Ulcerative esophagitis

Dermatologic

Impaired wound healing

Thin fragile skin

Petechiae and ecchymoses

Facial erythema

Increased sweating

May suppress reactions to skin tests

Metabolic

Negative nitrogen balance due to protein catabolism

Neurological

Increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after treatment

Convulsions

Vertigo

Headache

Endocrine

Menstrual irregularities

Development of Cushingoid state

Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma,

surgery or illness

Suppression of growth in children

Decreased carbohydrate tolerance

Manifestations of latent diabetes melliltus

Increased requirements for insulin or oral hypoglycemic agents in diabetics

Ophthalmic

Posterior subcapsular cataracts

Increased intraocular pressure

Glaucoma

Exophthalmos

Additional Reactions

Urticaria and other allergic, anaphylactic or hypersensitivity reactions.

The initial dosage of prednisone Tablets, USP may vary from 5 mg to 60 mg prednisone 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 decrements 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.)

ADT ® (Alternate Day Therapy)

ADT 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 1 ¼ to 1 ½ 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 ADT

should not encourage the indiscriminate use of steroids.

2) ADT 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 ADT. 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 ADT 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 ADT, it may be desirable to try patients on this form of therapy who

have been on daily corticoids for long periods of time (eg, patients with rheumatoid arthritis). Since

these patients may already have a suppressed HPA axis, establishing them on ADT 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 (eg; 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 ADT 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 ADT 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 re-instituted.

9) Although many of the undesirable features of corticosteroid therapy can be minimized by ADT, as in

any therapeutic situation, the physician must carefully weigh the benefit-risk ratio for each patient in

whom corticoid therapy is being considered.

Prednisone Tablets, USP are available in the following strengths and package sizes:

5 mg (White, round tablets debossed with "TL 172" on one side and scored on the other side)

Bottles of 100

Bottles of 1000

10 mg (White, round tablets debossed with "TL 173" on one side and scored on the other side)

Bottles of 100

Bottles of 500

Bottles of 1000

20mg (Peach, round tablets debossed with "TL 175" on one side and scored on the other side)

Bottles of 100

Bottles of 500

Bottles of 1000

Store at 20° to 25° C (68° to 77° F) [See USP Room Temperature].

Manufactured By:

Jubilant Cadista Pharmaceuticals Inc.

Salisbury, MD 21801, USA.

Revised 01/2018

PREDNISONE

prednisone tablet

Product Information

Product T ype

HUMAN PRESCRIPTION DRUG

Ite m Code (Source )

NDC:6 19 19 -235(NDC:59 746 -173)

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

10 mg

Inactive Ingredients

Ingredient Name

Stre ng th

LACTO SE MO NO HYDRATE (UNII: EWQ57Q8 I5X)

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

STARCH, PO TATO (UNII: 8 I0 8 9 SAH3T)

SO DIUM LAURYL SULFATE (UNII: 36 8 GB5141J)

STARCH, CO RN (UNII: O8 232NY3SJ)

Product Characteristics

Color

white

S core

2 pieces

S hap e

ROUND

S iz e

9 mm

Flavor

Imprint Code

TL173

Contains

Packag ing

#

Item Code

Package Description

Marketing Start Date

Marketing End Date

1

NDC:6 19 19 -235-40

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

0 8 /29 /20 19

2

NDC:6 19 19 -235-15

15 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 40 36 2

0 8 /29 /20 19

Labeler -

Direct_Rx (079254320)

Registrant -

Direct_Rx (079254320)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Dire ct_Rx

Dire c t_Rx

0 79 254320

re pa c k(6 19 19 -235)

Revised: 6/2020

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