PrednisonePrednisone is a corticosteroid. It prevents the release of substances in the body that cause inflammation. It also suppresses the immune system. Prednisone is used as dosd anti-inflammatory or an immunosuppressant medication. Prednisone treats many different conditions such as allergic disorders, skin conditions, ulcerative colitisarthritislupus, psoriasisor breathing disorders. High dose prednisone therapy treats many different conditions such as allergic disorders, skin conditions, ulcerative colitis, arthritis, lupus, psoriasis, or breathing disorders.
Systemic corticosteroid | DermNet New Zealand
Prednisone tablets, USP contain prednisone which is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. The chemical name for prednisone is pregna-1,4-diene-3,11,trione monohydrate, 17,dihydroxy-. The structural formula is represented below:. Prednisone is a white to practically white, odorless, crystalline powder.
It is very slightly soluble in water; slightly soluble in alcohol, chloroform , dioxane, and methanol. Each tablet, for oral administration, contains 5 mg, 10 mg or 20 mg of prednisone, USP anhydrous. In addition, each tablet contains the following inactive ingredients: 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: During an exacerbation or as maintenance therapy in selected cases of: 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: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: 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.
Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; acquired autoimmune hemolytic anemia ; erythroblastopenia RBC anemia ; congenital erythroid hypoplastic anemia. For palliative management of: 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: Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial involvement.
Gastric irritation may be reduced if taken before, during, or immediately after meals or with food or milk. The maximal activity of the adrenal cortex is between 2 am and 8 am, and it is minimal between 4 pm and midnight. Exogenous corticosteroids suppress adrenocorticoid activity the least when given at the time of maximal activity am for single dose administration. Therefore, it is recommended that prednisone be administered in the morning prior to 9 am and when large doses are given, administration of antacids between meals to help prevent peptic ulcers.
Multiple dose therapy should be evenly distributed in evenly spaced intervals throughout the day. Do not stop taking this medicine without first talking to your doctor. Avoid abrupt withdraw of therapy. The initial dosage of prednisone may vary from 5 mg to 60 mg per day, depending on the specific disease entity being treated. In situations of less severity lower doses will generally suffice, while in selected patients higher initial doses may be required.
The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of time there is a lack of satisfactory clinical response, prednisone should be discontinued and the patient transferred to other appropriate therapy. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small increments at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached.
It should be kept in mind that constant monitoring is needed in regard to drug dosage. Included in the situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient's individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment; in this latter situation, it may be necessary to increase the dosage of prednisone for a period of time consistent with the patient's condition.
If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. 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. Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of corticoid is administered every other morning. The purpose of this mode of therapy is to provide the patient requiring long-term pharmacologic dose treatment with the beneficial effects of corticoids while minimizing certain undesirable effects, including pituitary -adrenal suppression, the cushingoid state, corticoid withdrawal symptoms, and growth suppression in children.
The rationale for this treatment schedule is based on two major premises: A 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. Watson Pharma Private Ltd. Cardio-Renal , necrotizing angiitis , pulmonary edema , syncope , tachycardia , thromboembolism , thrombophlebitis , vasculitis. General Precautions , lupus erythematosus-like lesions, perineal irritation, purpura , rash, striae, subcutaneous fat atrophy, suppression of reactions to skin tests, striae, telangiectasis, thin fragile skin, thinning scalp hair, urticaria.
Adrenal insufficiency-greatest potential caused by high potency glucocorticoids with long duration of action associated symptoms include; arthralgias, buffalo hump , dizziness, life-threatening hypotension , nausea, severe tiredness or weakness , amenorrhea , postmenopausal bleeding or other menstrual irregularities, decreased carbohydrate and glucose tolerance, development of cushingoid state, diabetes mellitus new onset or manifestations of latent , glycosuria, hyperglycemia , hypertrichosis, hyperthyroidism see WARNINGS: Endocrine , hypothyroidism , increased requirements for insulin or oral hypoglycemic agents in diabetics, lipids abnormal, moon face, negative nitrogen balance caused by protein catabolism , secondary adrenocortical and pituitary unresponsiveness particularly in times of stress , as in trauma , surgery or illness see WARNINGS: Endocrine , suppression of growth in pediatric patients.
Musculoskeletal , pathologic fracture of long bones, steroid myopathy , tendon rupture particularly of the Achilles tendon , vertebral compression fractures. Ophthalmic , optic nerve damage, papilledema. Infection , hiccups , immunosuppresion, increased or decreased motility and number of spermatozoa, malaise , insomnia, moon face, pyrexia.
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. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance see Hepatic Enzyme Inducers , Inhibitors and Substrates. 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. Coadministration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. 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.
Postmarketing 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. Coadministration 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 as pirin 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 postmarketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone coadministration, leading to alterations in seizure control.
Phenytoin has been demonstrated to increase the hepatic metabolism of corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid.
Increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving a glucocorticoid , a hepatic enzyme inducer. Coadministration 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.
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.