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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 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.
DailyMed will deliver notification of updates and additions to Drug Label information currently shown on this site through its RSS feed. DailyMed will deliver this notification to your desktop, Web browser, or e-mail depending on the RSS Reader you select to use. Due to inconsistencies between the drug labels on DailyMed and the pill images provided by RxImage , we no longer display the RxImage pill images associated with drug labels.
We anticipate reposting the images once we are able identify and filter out images that do not match the information provided in the drug labels. Drug Label Info. NDC National Drug Code - Each drug product is assigned this unique number which can be found on the drug's outer packaging.
Drug Label Information Updated August 5, If you are a consumer or patient please visit this version. Prednisone tablets 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 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.
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 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.
Systemic fungal infections and known hypersensitivity to components. 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. The benefits of ADT should not encourage the indiscriminate use of steroids. 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. 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. Exogenous corticosteroids suppress adrenocortical activity the least, when given at the time of maximal activity am. 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. Once control is again established alternate day therapy may be re-instituted. Prednisone Tablets, USP are available in the following strengths and package sizes:. Dispense in tight, light-resistant container. Keep patient under close observation of a physician. Manufactured by: Jubilant Cadista Pharmaceuticals Inc. See package insert for complete product information.
DailyMed will deliver notification of updates and additions to Drug Label information currently shown on this site through its RSS feed. DailyMed will deliver this notification to your desktop, Web browser, or e-mail depending on the RSS Reader you select to use. Due to inconsistencies between the drug labels on DailyMed and the pill images provided by RxImage , we no longer display the RxImage pill images associated with drug labels.
We anticipate reposting the images once we are able identify and filter out images that do not match the information provided in the drug labels. Drug Label Info. NDC National Drug Code - Each drug product is assigned this unique number which can be found on the drug's outer packaging. Drug Label Information Updated January 31, If you are a consumer or patient please visit this version. The chemical name for prednisone is pregna-1, 4-diene-3, 11, trione, 17, dihydroxy- The structural formula is represented below:.
ACTIONS Naturally occurring glucocorticoids hydrocortisone and cortisone , which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states.
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.
The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. Corticosteroids should not be used in active ocular herpes simplex because of possible corneal perforation.
The lowest possible dose of corticosteroids should be used to control the condition under treatment. When reduction in dosage is possible, the reduction should be gradual. Discontinuation of corticosteroids may result in clinical improvement. As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy following large doses for prolonged periods; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. 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. Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation i. 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. Inclusion of therapy for osteoporosis prevention or treatment should be considered. To minimize the risk of glucocortoicoid-induced bone loss, the smallest possible effective dosage and duration should be used.
Lifestyle modification to reduce the risk of osteoporosis e. Calcium and vitamin D supplementation, bisphosphonate e. 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. 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. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis.
Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored. 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. When corticosteroids are administered concomitantly with potassium-depleting agents e. 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.
Concomitant use of anticholinesterase agents e. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated.
Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required.
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.
Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use. Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. Post-marketing surveillance reports indicate that the risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones e.
Tendon rupture can occur during or after treatment with quinolones. Drugs which inhibit CYP 3A4 e. Glucocorticoids are moderate inducers of CYP 3A4. Co-administration with other drugs that are metabolized by CYP 3A4 e. In addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal.
Concomitant use of aspirin or other nonsteroidal anti-inflammatory agents and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids; this could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. In post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control.
Phenytoin has been demonstrated to increase the hepatic metabolism of corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid. Increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer. Co-administration with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use. Patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response.
Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. No adequate studies have been conducted in animals to determine whether corticosteroids have a potential for carcinogenesis or mutagenesis. Steroids may increase or decrease motility and number of spermatozoa in some patients. Pregnancy Category C : Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose.
Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an 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. It is also used to treat high blood calcium due to cancer and adrenal insufficiency along with other steroids.
Prednisone is derived from cortisone. Prednisone was patented in and, in , it was approved for medical use in the United States. Prednisone is a globally found drug. Prednisone suppliers market it in the final dosage form of 1 mg, 2. To treat most of the diseases with Prednisone, an adult patient should take the Initial dose of 5 mg to 60 mg orally per day. At the maintenance dose, the patient, under medical advice, can adjust or maintain the initial dose until a satisfactory response is obtained.
During a Prednisone treatment, it is advised to avoid alcohol and take Prednisone medicine with food; it reduces irritation. Taking Prednisone can cause some side effects that may include aggression, agitation, blurred vision, decrease in the amount of urine, dizziness, fast, slow, pounding, or irregular heartbeat or pulse, headache, irritability, mood changes. An online search for the wholesale price for sale of Prednisone for distributors will reveal a wide range of costs.
It will vary from store to store depending on your visit and the country of the wholesale market. Prednisone prices can fluctuate from the countries that sell the medications. In the US, Prednisone costs depend on the final dosage form. As Prednisone is a globally found drug, on the internet, you can encounter fraudulent websites that will want to sell Prednisone with some risks for you and your clients.
By using Pipelinepharma B2B marketplace, you avoid the time-consuming sourcing, and you directly find qualified sellers of Prednisone that have been through quality control procedures to assure they were qualified partners. Thanks to the intuitive online marketplace, you will find Prednisone and many other drugs quickly and efficiently.
If you are a consumer or patient please visit this version. Prednisone is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract.
Prednisone, USP is a white to partially white, crystalline powder. It is very slightly soluble in water; slightly soluble in alcohol, chloroform, dioxane, and methanol. The chemical name for prednisone is 17,dihydroxypregna-1,4-dienne-3,11,trione. The structural formula is represented below:. PredniSONE Tablets, USP contain the following inactive ingredients: lactose monohydrate, magnesium stearate, microcrystalline cellulose, pregelatinized starch, sodium starch glycolate and stearic acid 5 mg only.
Naturally occurring glucocorticoids hydrocortisone and cortisonewhich 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. 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.
As adjunctive therapy for short-term administration to tide the patient over an acute episode or exacerbation in:. Rheumatoid arthritis, including juvenile rheumatoid arthritis selected cases may require low-dose maintenance therapy. Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment:. Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: Allergic corneal marginal ulcers.
Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy. To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus.
Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy. 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. Since adequate human reproduction studies have not been done with corticosteroids, the use of these drugs in pregnancy, nursing mothers or women of child-bearing 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 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. Children who are on immunosuppressant drugs are more susceptible to infections than healthy children. Chickenpox and measles, for example, can have a more serious or even fatal course in children on immunosuppressant corticosteroids.
In such children, or in adults who have not had these diseases, particular care should be taken to avoid exposure. If chickenpox develops treatment with antiviral agents may be considered. 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. 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. 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.
Convulsions have been reported with concurrent use of methylprednisolone and cyclosporin. 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.
Increased intracranial pressure with papilledema pseudotumor cerebri usually after treatment Convulsions. Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or illness. The initial dosage of prednisone may vary from 5 mg to 60 mg of 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. 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. If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. In the treatment of acute exacerbations of multiple sclerosis daily doses of 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 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 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. DailyMed will deliver notification of updates and additions to Drug Label information currently shown on this site through its RSS feed.
DailyMed will deliver this notification to your desktop, Web browser, or e-mail depending on the RSS Reader you select to use. Due to inconsistencies between the drug labels on DailyMed and the pill images provided by RxImagewe no longer display the RxImage pill images associated with drug labels. We anticipate reposting the images once we are able identify and filter out images that do not match the information provided in the drug labels. Drug Label Info. NDC National Drug Code - Each drug product is assigned this unique number which can be found on the drug's outer packaging.
Drug Label Information Updated August 5, If you are a consumer or patient please visit this version. Prednisone tablets 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 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.
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 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.
Prednisone is a globally found drug. Roxane Laboratories Inc, Ferndale Laboratories Inc, Sandoz Inc, Teva Pharmaceuticals USA Inc, Phoenix. Township Line Road, Suite Yardley, PA , USA; Tel.: Manufacturing Facilites; Kiley Drive Salisbury, MD Prednisone was patented in and approved for medical use in the United States in It is on the World Health Organization's List of Essential. Packager: Hikma Pharmaceuticals USA Inc. Category: HUMAN PRESCRIPTION DRUG LABEL; DEA Schedule: None; Marketing Status: Abbreviated New Drug Application. Manufactured By. Dosage range is the same for prednisone and prednisolone. If you are a consumer or patient please visit this version. Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial involvement. In addition, they modify the body's immune responses to diverse stimuli. Pemphigus Bullous dermatitis herpetiformis Severe erythema multiforme Stevens-Johnson syndrome Exfoliative dermatitis Mycosis fungoides Severe psoriasis Severe seborrheic dermatitis.Drug facts, warnings, and ingredients follow. Each tablet contains the following inactive ingredients: lactose monohydrate, magnesium stearate, microcrystalline cellulose, pregelatinized starch, sodium starch glycolate and stearic acid 5 mg only. Prednisone tablets contain prednisone which is a glucocorticoid.
Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. The chemical name for prednisone is 17,dihydroxypregna-1,4-dienne-3,11,trione. The structural formula is represented below:. Prednisone USP is a white to partially white, crystalline powder. It is very slightly soluble in water; slightly soluble in alcohol, chloroform, dioxane, and methanol.
Naturally occurring glucocorticoids hydrocortisone and cortisone , which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states.
Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. Primary or secondary adrenocortical insufficiency hydrocortisone or cortisone is the first choice: synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy mineralocorticoid supplementation is of particular importance ; congenital adrenal hyperplasia; hypercalcemia associated with cancer; nonsuppurative thyroiditis.
As adjunctive therapy for short-term administration to tide the patient over an acute episode or exacerbation in: psoriatic arthritis, rheumatoid arthritis, including juvenile rheumatoid arthritis selected cases may require low-dose maintenance therapy , ankylosing spondylitis, acute and subacute bursitis, acute nonspecific tenosynovitis, acute gouty arthritis, post-traumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis.
During an exacerbation or as maintenance therapy in selected cases of: systemic lupus erythematosus, systemic dermatomyositis polymyositis , acute rheumatic carditis. Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme Stevens-Johnson syndrome ; exfoliative dermatitis; mycosis fungoides; severe psoriasis; severe seborrheic dermatitis. Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment: seasonal or perennial allergic rhinitis; bronchial asthma; contact dermatitis; atopic dermatitis; serum sickness; drug hypersensitivity reactions.
Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: allergic corneal marginal ulcers, herpes zoster ophthalmicus, anterior segment inflammation, diffuse posterior uveitis and choroiditis, sympathetic ophthalmia, allergic conjunctivitis, keratitis, chorioretinitis, optic neuritis, iritis and iridocyclitis.
Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; acquired autoimmune hemolytic anemia; erythroblastopenia RBC anemia ; congenital erythroid hypoplastic anemia. For palliative management of: leukemias and lymphomas in adults, acute leukemia of childhood. To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus.
To tide the patient over a critical period of the disease in: ulcerative colitis, regional enteritis. Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial involvement. Prednisone tablets are contraindicated in systemic fungal infections and known hypersensitivity to components. 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.
Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary.
All corticosteroids increase calcium excretion. Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy with corticosteroids should be used with great caution in these patients.
Corticosteroids can produce reversible hypothalamic-pituitary adrenal HPA axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. Adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted.
If the patient is receiving steroids already, dosage may have to be 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. 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.
With increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. 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.
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. The use of prednisone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for management of the disease in conjunction with an appropriate antituberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Killed or inactivated vaccines may be administered. However, the response to such vaccines may be diminished and cannot be predicted. Indicated immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids as replacement therapy e. 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. 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. If chickenpox develops, treatment with antiviral agents may be considered.
Use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to bacteria, fungi or viruses. The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. Corticosteroids should not be used in active ocular herpes simplex because of possible corneal perforation. The lowest possible dose of corticosteroids should be used to control the condition under treatment.
When reduction in dosage is possible, the reduction should be gradual. Discontinuation of corticosteroids may result in clinical improvement. As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy following large doses for prolonged periods; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted.
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. Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation i.
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.
Inclusion of therapy for osteoporosis prevention or treatment should be considered. To minimize the risk of glucocortoicoid-induced bone loss, the smallest possible effective dosage and duration should be used. Lifestyle modification to reduce the risk of osteoporosis e.
Calcium and vitamin D supplementation, bisphosphonate e. 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.
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. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations.
Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored. 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.
When corticosteroids are administered concomitantly with potassium-depleting agents e. 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. Concomitant use of anticholinesterase agents e. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated.
Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect.
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