Prednisone 5 MG Oral Tablet 21 Count Pack
WARNINGS
: 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.
Infections with any pathogen including viral, bacterial, fungal, protozoan or helminthic infections, 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.
1 These infections may be mild, but can be severe and at times fatal.
With increasing doses of corticosteroids, the rate of occurrence of infectious complications increases.
2 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.
Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to such vaccines may be diminished.
Indicated immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids.
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 the 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.
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.
Similarly, corticosteroids should be used with great care in patients with known or suspected Stronglyoides (threadworm) infestation.
In such patients, corticosteroid-induced immunosuppression may lead to Stronglyoides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.
DRUG INTERACTIONS
Drug Interactions The pharmacokinetic interactions listed below are potentially clinically important.
Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response.
Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance.
Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity.
Corticosteroids may increase the clearance of chronic high dose aspirin.
This could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn.
Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia.
The effect of corticosteroids on oral anticoagulants is variable.
There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids.
Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect.
DESCRIPTION
Prednisone is a glucocorticoid.
Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract.
The molecular formula for prednisone is C 21 H 26 O 5 .
Chemically, it is 17, 21-dihydroxypregna-1, 4-diene-3,11,20-trione and has the following structural formula: Prednisone is a white to practically white, odorless, crystalline powder and has a molecular weight of 358.44.
It melts at about 230°C with some decomposition.
Prednisone is very slightly soluble in water; slightly soluble in alcohol, chloroform, dioxane, and methanol.
Each tablet, for oral administration, contains 5 mg or 10 mg of prednisone.
Inactive ingredients: 5 mg: anhydrous lactose, colloidal silicon dioxide, magnesium stearate, microcrystalline cellulose, sodium starch glycolate, and talc.
10 mg: anhydrous lactose, colloidal silicon dioxide, magnesium stearate, microcrystalline cellulose, sodium starch glycolate, and talc.
Image 1
HOW SUPPLIED
Prednisone Tablets, USP 5 mg: White, Round Tablets; Debossed “West-ward 475” on one side and Scored on the other side.
Each tablet contains 5 mg of prednisone for oral administration.
Blister Pack of 21 tablets NDC# 45802- 733 -21 Blister Pack of 48 tablets NDC# 45802- 733 -67 Prednisone Tablets, USP 10 mg: White, Round Tablets; Debossed “WEST-WARD 473” on one side and Scored on the other side.
Each tablet contains 10 mg of prednisone for oral administration.
Blister Pack of 21 tablets NDC# 45802- 303 -21 Blister Pack of 48 tablets NDC# 45802- 303 -67
INDICATIONS AND USAGE
: Prednisone tablets 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 Nonsuppurative thyroiditis Hypercalcemia associated with cancer 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 Serum sickness Bronchial asthma Contact dermatitis Atopic dermatitis Drug hypersensitivity reactions Ophthalmic diseases: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa, such as: Allergic conjunctivitis Keratitis Allergic corneal marginal ulcers Herpes zoster ophthalmicus Iritis and iridocyclitis Chorioretinitis Anterior segment inflammation Diffuse posterior uveitis and choroiditis Optic neuritis Sympathetic ophthalmia 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 Eythroblastopenia (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 Nervous system: Acute exacerbations of multiple sclerosis Miscellaneous: Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy.
Trichinosis with neurologic or myocardial involvement.
PREGNANCY
USAGE IN : 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.
Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to such vaccines may be diminished.
Indicated immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids.
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 the 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.
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.
Similarly, corticosteroids should be used with great care in patients with known or suspected Stronglyoides (threadworm) infestation.
In such patients, corticosteroid-induced immunosuppression may lead to Stronglyoides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.
INFORMATION FOR PATIENTS
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.
DOSAGE AND ADMINISTRATION
: Dosage of prednisone should be individualized according to the severity of the disease and the response of the patient.
For infants and children, the recommended dosage should be governed by the same considerations rather than strict adherence to the ratio indicated by age or body weight.
Hormone therapy is an adjunct to, and not a replacement for, conventional therapy.
Dosage should be decreased or discontinued gradually when the drug has been administered for more than a few days.
The severity, prognosis, expected duration of the disease, and the reaction of the patient to medication are primary factors in determining dosage.
If a period of spontaneous remission occurs in a chronic condition, treatment should be discontinued.
Blood pressure, body weight, routine laboratory studies, including two-hour postprandial blood glucose and serum potassium, and a chest X-ray should be obtained at regular intervals during prolonged therapy.
Upper Gl X-rays are desirable in patients with known or suspected peptic ulcer disease.
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 adjustment 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 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 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 (e.g., 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 (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 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 reinstituted.
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.