Decadron

Description for Decadron

DECADRON® (dexamethasone tabletsUSP) tabletsfor oral administrationare supplied in two potencies0.5 mgand 0.75 mg. Inactive ingredients are calcium phosphatelactosemagnesium stearateand starch. Tablets DECADRON 0.5 mg also contain D&C Yellow 10 and FD&C Yellow 6. Tablets DECADRON 0.75 mg also contain FD&C Blue 1.

The molecular weight for dexamethasone is 392.47. It is designated chemically as 9-fluoro-11β,17,21trihydroxy-16α-methylpregna-1,4-diene-3,20-dione. The empirical formula is C₂₂H₂₉FO₅ and the structural formula is:

Dexamethasonea synthetic adrenocortical steroidis a white to practically whiteodorlesscrystalline powder. It is stable in the air. It is practically insoluble in water.

Uses for Decadron

Allergic States

Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in asthmaatopic dermatitiscontact dermatitisdrug hypersensitivity reactions, perennial or seasonal allergic rhinitisand serum sickness.

Dermatologic Diseases

Bullous dermatitis herpetiformisexfoliative erythrodermamycosis fungoidespemphigusand severe erythema multiforme (Stevens-Johnson syndrome).

Endocrine Disorders

Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; may be used in conjunction with synthetic mineralocorticoid analogs where applicable; in infancy mineralocorticoid supplementation is of particular importance)congenital adrenal hyperplasiahypercalcemia associated with cancerand nonsuppurative thyroiditis.

Gastrointestinal Diseases

To tide the patient over a critical period of the disease in regional enteritis and ulcerative colitis.

Hematologic Disorders

Acquired (autoimmune) hemolytic anemiacongenital (erythroid) hypoplastic anemia (Diamond-Blackfan anemia)idiopathic thrombocytopenic purpura in adultspure red cell aplasiaand selected cases of secondary thrombocytopenia.

Miscellaneous

Diagnostic testing of adrenocortical hyperfunctiontrichinosis with neurologic or myocardial involvementtuberculous meningitis with subarachnoid block or impending block when used with appropriate antituberculous chemotherapy.

Neoplastic Diseases

For the palliative management of leukemias and lymphomas.

Nervous System

Acute exacerbations of multiple sclerosiscerebral edema associated with primary or metastatic brain tumorcraniotomyor head injury.

Ophthalmic Diseases

Sympathetic ophthalmiatemporal arteritisuveitisand ocular inflammatory conditions unresponsive to topical corticosteroids.

Renal Diseases

To induce a diuresis or remission of proteinuria in idiopathic nephrotic syndrome or that due to lupus erythematosus.

Respiratory Diseases

Berylliosisfulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapyidiopathic eosinophilic pneumoniassymptomatic sarcoidosis.

Rheumatic Disorders

As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in acute gouty arthritisacute rheumatic carditisankylosing spondylitispsoriatic arthritisrheumatoid arthritisincluding juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy). For the treatment of dermatomyositispolymyositisand systemic lupus erythematosus.

Dosage for Decadron

For Oral Administration

The initial dosage varies from 0.75 to 9 mg a day depending on the disease being treated.

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 notedthe proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage that maintains an adequate clinical response is reached.

Situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease processthe patient’s individual drug responsivenessand 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 the corticosteroid for a period of time consistent with the patient’s condition. If after long-term therapy the drug is to be stoppedit is recommended that it be withdrawn gradually rather than abruptly.

In the treatment of acute exacerbations of multiple sclerosisdaily doses of 30 mg of dexamethasone for a week followed by 4 to 12 mg every other day for one month have been shown to be effective (see PRECAUTIONSNeuro-Psychiatric).

In pediatric patientsthe initial dose of dexamethasone may vary depending on the specific disease entity being treated. The range of initial doses is 0.02 to 0.3 mg/kg/day in three or four divided doses (0.6 to 9 mg/m²bsa/day).

For the purpose of comparisonthe following is the equivalent milligram dosage of the various corticosteroids:

Cortisone25	Triamcinolone4
Hydrocortisone20	Paramethasone2
Prednisolone5	Betamethasone0.75
Prednisone5	Dexamethasone0.75
Methylprednisolone4

These dose relationships apply only to oral or intravenous administration of these compounds. When these substances or their derivatives are injected intramuscularly or into joint spacestheir relative properties may be greatly altered.

In acuteself-limited allergic disorders or acute exacerbations of chronic allergic disorders, the following dosage schedule combining parenteral and oral therapy is suggested:

Dexamethasone Sodium Phosphate injectionUSP 4 mg per mL:

First Day
1 or 2 mLintramuscularly
DECADRON tablets0.75 mg:
Second Day
4 tablets in two divided doses
Third Day
4 tablets in two divided doses
Fourth Day
2 tablets in two divided doses
Fifth Day
1 tablet
Sixth Day
1 tablet
Seventh Day
No treatment
Eighth Day
Follow-up visit

This schedule is designed to ensure adequate therapy during acute episodeswhile minimizing the risk of overdosage in chronic cases.

In cerebral edemaDexamethasone Sodium Phosphate injectionUSP is generally administered initially in a dosage of 10 mg intravenously followed by 4 mg every six hours intramuscularly until the symptoms of cerebral edema subside. Response is usually noted within 12 to 24 hours and dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days. For palliative management of patients with recurrent or inoperable brain tumorsmaintenance therapy with either Dexamethasone Sodium Phosphate injectionUSP or DECADRON tablets in a dosage of 2 mg two or three times daily may be effective.

Dexamethasone Suppression Tests

1. Tests for Cushing's syndrome Give 1.0 mg of DECADRON orally at 11:00 p.m. Blood is drawn for plasma cortisol determination at 8:00 a.m. the following morning.
   For greater accuracygive 0.5 mg of DECADRON orally every 6 hours for 48 hours. Twenty-four hour urine collections are made for determination of 17-hydroxycorticosteroid excretion.
2. Test to distinguish Cushing's syndrome due to pituitary ACTH excess from Cushing's syndrome due to other causes.
   Give 2.0 mg of DECADRON orally every 6 hours for 48 hours. Twenty-four hour urine collections are made for determination of 17-hydroxycorticosteroid excretion.

HOW SUPPLIED

Tablets DECADRON are compressedpentagonal-shaped tabletscolored to distinguish potency. They are scored and coded on one side and embossed with DECADRON on the other. They are available as follows:

No. 7601 — 0.75 mgbluish-green in color and coded MSD 63.

NDC 0006-0063-12 5-12 PAK* (package of 12)
NDC 0006-0063-68 bottles of 100.

No. 7598 — 0.5 mgyellow in color and coded MSD 41.

NDC 0006-0041-68 bottles of 100.

Storage

Store at controlled room temperature 20 to 25°C (68 to 77°F).

Manufactured by: Merck Sharp & Dohme Corp.a subsidairy of Merck & Co.Inc.Whitehouse StationNJ 08889USA. Revised: July 2016

Side Effects for Decadron

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

Allergic Reactions

Anaphylactoid reactionanaphylaxisangioedema.

Cardiovascular

Bradycardiacardiac arrestcardiac arrhythmiascardiac enlargementcirculatory collapsecongestive heart failurefat embolismhypertensionhypertrophic cardiomyopathy in premature infantsmyocardial rupture following recent myocardial infarction (see WARNINGSCardio-Renal)edemapulmonary edemasyncopetachycardiathromboembolismthrombophlebitisvasculitis.

Dermatologic

Acneallergic dermatitisdry scaly skinecchymoses and petechiaeerythemaimpaired wound healingincreased sweatingrashstriaesuppression of reactions to skin teststhin fragile skinthinning scalp hairurticaria.

Endocrine

Decreased carbohydrate and glucose tolerancedevelopment of cushingoid statehyperglycemiaglycosuriahirsutismhypertrichosisincreased requirements for insulin or oral hypoglycemic agents in diabetesmanifestations of latent diabetes mellitusmenstrual irregularitiessecondary adrenocortical and pituitary unresponsiveness (particularly in times of stressas in traumasurgeryor illness)suppression of growth in pediatric patients.

Fluid And Electrolyte Disturbances

Congestive heart failure in susceptible patientsfluid retentionhypokalemic alkalosispotassium losssodium retentiontumor lysis syndrome.

Gastrointestinal

Abdominal distentionelevation in serum liver enzyme levels (usually reversible upon discontinuation)hepatomegalyincreased appetitenauseapancreatitispeptic ulcer with possible perforation and hemorrhageperforation of the small and large intestine (particularly in patients with inflammatory bowel disease)ulcerative esophagitis.

Metabolic

Negative nitrogen balance due to protein catabolism.

Musculoskeletal

Aseptic necrosis of femoral and humeral headsloss of muscle massmuscle weaknessosteoporosispathologic fracture of long bonessteroid myopathytendon rupturevertebral compression fractures.

Neurological/Psychiatric

Convulsionsdepressionemotional instabilityeuphoriaheadacheincreased intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of treatmentinsomniamood swingsneuritisneuropathyparesthesiapersonality changespsychic disordersvertigo.

Ophthalmic

Exophthalmosglaucomaincreased intraocular pressureposterior subcapsular cataracts.

Other

Abnormal fat depositsdecreased resistance to infectionhiccupsincreased or decreased motility and number of spermatozoamalaisemoon faceweight gain.

Drug Interactions for Decadron

Aminoglutethimide

Aminoglutethimide may diminish adrenal suppression by corticosteroids.

Amphotericin B Injection And Potassium-Depleting Agents

When corticosteroids are administered concomitantly with potassium-depleting agents (e.g.amphotericin Bdiuretics)patients should be observed closely for development of hypokalemia. In additionthere have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure.

Antibiotics

Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance (see DRUG INTERACTIONS, Hepatic Enzyme InducersInhibitors and Substrates).

Anticholinesterases

Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possibleanticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.

AnticoagulantsOral

Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarinalthough there have been some conflicting reports. Thereforecoagulation indices should be monitored frequently to maintain the desired anticoagulant effect.

Antidiabetics

Because corticosteroids may increase blood glucose concentrationsdosage adjustments of antidiabetic agents may be required.

Antitubercular Drugs

Serum concentrations of isoniazid may be decreased.

Cholestyramine

Cholestyramine may increase the clearance of corticosteroids.

Cyclosporine

Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use.

Dexamethasone Suppression Test (DST)

False-negative results in the dexamethasone suppression test (DST) in patients being treated with indomethacin have been reported. Thusresults of the DST should be interpreted with caution in these patients.

Digitalis Glycosides

Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia.

Ephedrine

Ephedrine may enhance the metabolic clearance of corticosteroidsresulting in decreased blood levels and lessened physiologic activitythus requiring an increase in corticosteroid dosage.

EstrogensIncluding Oral Contraceptives

Estrogens may decrease the hepatic metabolism of certain corticosteroidsthereby increasing their effect.

Hepatic Enzyme InducersInhibitors And Substrates

Drugs which induce cytochrome P450 3A4 (CYP 3A4) enzyme activity (e.g.barbituratesphenytoincarbamazepinerifampin) may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. Drugs which inhibit CYP 3A4 (e.g.ketoconazolemacrolide antibiotics such as erythromycin) have the potential to result in increased plasma concentrations of corticosteroids. Dexamethasone is a moderate inducer of CYP 3A4. Co-administration with other drugs that are metabolized by CYP 3A4 (e.g.indinavirerythromycin) may increase their clearanceresulting in decreased plasma concentration.

Ketoconazole

Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%leading to increased risk of corticosteroid side effects. In additionketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal.

Nonsteroidal Anti-Inflammatory Agents (NSAIDS)

Concomitant use of aspirin (or other nonsteroidal anti-inflammatory agents) and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids.

Phenytoin

In post-marketing experiencethere have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administrationleading to alterations in seizure control.

Skin Tests

Corticosteroids may suppress reactions to skin tests.

Thalidomide

Co-administration with thalidomide should be employed cautiouslyas toxic epidermal necrolysis has been reported with concomitant use.

Vaccines

Patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. Routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible (see WARNINGS, InfectionsVaccination).

Warnings for Decadron

General

Rare instances of anaphylactoid reactions have occurred in patients receiving corticosteroid therapy (see ADVERSE REACTIONS).

Increased dosage of rapidly acting corticosteroids is indicated in patients on corticosteroid therapy subjected to any unusual stress beforeduringand after the stressful situation.

Cardio-Renal

Average and large doses of corticosteroids can cause elevation of blood pressuresodium and water retentionand 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; thereforetherapy with corticosteroids should be used with great caution in these patients.

Endocrine

Corticosteroids can produce reversible hypothalamic-pituitary adrenal (HPA) axis suppression with the potential for glucocorticosteroid 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 months after discontinuation of therapy; thereforein any situation of stress occurring during that periodhormone therapy should be reinstituted. If the patient is receiving steroids alreadydosage 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.

Infections

General

Patients who are on corticosteroids are more susceptible to infections than are healthy individuals. There may be decreased resistance and inability to localize infection when corticosteroids are used. Infection with any pathogen (viralbacterialfungalprotozoan or helminthic) in any location of the body may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents. These infections may be mild to severe. W ith increasing doses of corticosteroidsthe rate of occurrence of infectious complications increases. Corticosteroids may also mask some signs of current infection.

Fungal Infections

Corticosteroids may exacerbate systemic fungal infections and therefore should not be used in the presence of such infections unless they are needed to control life-threatening drug reactions. There have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure (see DRUG INTERACTIONSAmphotericin B Injection And Potassium-Depleting Agents).

Special Pathogens

Latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogensincluding those caused by AmoebaCandidaCryptococcusMycobacteriumNocardiaPneumocystisToxoplasma.

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.

Similarlycorticosteroids should be used with great care in patients with known or suspected Strongyloides (threadworm) infestation. In such patientscorticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migrationoften accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

Corticosteroids should not be used in cerebral malaria.

Tuberculosis

The use of corticosteroids 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 reactivityclose observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapythese patients should receive chemoprophylaxis.

Vaccination

Administration of live or liveattenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered. Howeverthe response to such vaccines cannot be predicted. Immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapye.g.for Addison’s disease.

Viral Infections

Chickenpox and measles can have a more serious or even fatal course in pediatric and adult patients on corticosteroids. In pediatric and adult patients who have not had these diseasesparticular care should be taken to avoid exposure. The contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. If exposed to chickenpoxprophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If exposed to measlesprophylaxis with immune globulin (IG) may be indicated. (See the respective package inserts for VZIG and IG for complete prescribing information.) If chickenpox developstreatment with antiviral agents should be considered.

Ophthalmic

Use of corticosteroids may produce posterior subcapsular cataractsglaucoma with possible damage to the optic nervesand may enhance the establishment of secondary ocular infections due to bacteriafungior 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.

Precautions for Decadron

General

The lowest possible dose of corticosteroids should be used to control the condition under treatment. W hen reduction in dosage is possiblethe reduction should be gradual.

Since complications of treatment with corticosteroids are dependent on the size of the dose and the duration of treatmenta risk/benefit decision must be made in each individual case as to dose and duration of treatment and as to whether daily or intermittent therapy should be used.

Kaposi’s sarcoma has been reported to occur in patients receiving corticosteroid therapymost often for chronic conditions. Discontinuation of corticosteroids may result in clinical improvement.

Cardio-Renal

As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroidsthese agents should be used with caution in patients with congestive heart failurehypertensionor renal insufficiency.

Endocrine

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; thereforein any situation of stress occurring during that periodhormone therapy should be reinstituted. Since mineralocorticoid secretion may be impairedsalt and/or a mineralocorticoid should be administered concurrently.

Gastrointestinal

Steroids should be used with caution in active or latent peptic ulcersdiverticulitisfresh intestinal anastomosesand nonspecific ulcerative colitissince 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.

Musculoskeletal

Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation (i.e.decreasing absorption and increasing excretion) and inhibition of osteoblast function. Thistogether with a decrease in the protein matrix of the bone secondary to an increase in protein catabolismand reduced sex hormone productionmay lead to inhibition of bone growth in pediatric patients and the development of osteoporosis at any age. Special consideration should be given to patients at increased risk of osteoporosis (e.g.postmenopausal women) before initiating corticosteroid therapy.

Neuro-Psychiatric

Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosisthey do not show that they affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect. (See DOSAGE AND ADMINISTRATION.)

An acute myopathy has been observed with the use of high doses of corticosteroidsmost often occurring in patients with disorders of neuromuscular transmission (e.g.myasthenia gravis)or in patients receiving concomitant therapy with neuromuscular blocking drugs (e.g.pancuronium). This acute myopathy is generalizedmay involve ocular and respiratory musclesand may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.

Psychic derangements may appear when corticosteroids are usedranging from euphoriainsomniamood swingspersonality changesand severe depressionto frank psychotic manifestations. Alsoexisting emotional instability or psychotic tendencies may be aggravated by corticosteroids.

Ophthalmic

Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeksintraocular pressure should be monitored.

CarcinogenesisMutagenesisImpairment Of Fertility

No adequate studies have been conducted in animals to determine whether corticosteroids have a potential for carcinogenesis or mutagenesis.

Steroids may increase or decrease motility and number of spermatozoa in some patients.

Pregnancy

Teratogenic Effects

Pregnancy Category C.

Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant miceratsand rabbits have yielded an increased incidence of cleft palate in the offspring. There are no adequate and well-controlled studies in pregnant women. Corticosteroids should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Infants born to mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.

Nursing Mothers

Systemically administered corticosteroids appear in human milk and could suppress growthinterfere with endogenous corticosteroid productionor cause other untoward effects. Because of the potential for serious adverse reactions in nursing infants from corticosteroidsa decision should be made whether to discontinue nursing or to discontinue the drugtaking into account the importance of the drug to the mother.

Pediatric Use

The efficacy and safety of corticosteroids in the pediatric population are based on the well-established course of effect of corticosteroidswhich is similar in pediatric and adult populations. Published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (patients >2 years of age)and aggressive lymphomas and leukemias (patients >1 month of age). Other indications for pediatric use of corticosteroidse.g.severe asthma and wheezingare based on adequate and well-controlled trials conducted in adultson the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations.

The adverse effects of corticosteroids in pediatric patients are similar to those in adults (see ADVERSE REACTIONS). Like adultspediatric patients should be carefully observed with frequent measurements of blood pressureweightheightintraocular pressureand clinical evaluation for the presence of infectionpsychosocial disturbancesthromboembolismpeptic ulcerscataractsand osteoporosis. Pediatric patients who are treated with corticosteroids by any routeincluding systemically administered corticosteroidsmay experience a decrease in their growth velocity. This negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) axis suppression (i.e.cosyntropin stimulation and basal cortisol plasma levels). Growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The linear growth of pediatric patients treated with corticosteroids should be monitoredand the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of treatment alternatives. In order to minimize the potential growth effects of corticosteroidspediatric patients should be titrated to the lowest effective dose.

Geriatric Use

Clinical studies did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In generaldose selection for an elderly patient should be cautioususually starting at the low end of the dosing rangereflecting the greater frequency of decreased hepaticrenalor cardiac functionand of concomitant disease or other drug therapy. In particularthe increased risk of diabetes mellitusfluid retention and hypertension in elderly patients treated with corticosteroids should be considered.

Overdose Information for Decadron

Treatment of overdosage is by supportive and symptomatic therapy. In the case of acute overdosageaccording to the patient’s conditionsupportive therapy may include gastric lavage or emesis.

Contraindications for Decadron

Systemic fungal infections (see WARNINGSFungal infections).

DECADRON tablets are contraindicated in patients who are hypersensitive to any components of this product.

Clinical Pharmacology for Decadron

Glucocorticoidsnaturally occurring and syntheticare adrenocortical steroids that are readily absorbed from the gastrointestinal tract. Glucocorticoids cause varied metabolic effects. In additionthey modify the body's immune responses to diverse stimuli. Naturally occurring glucocorticoids (hydrocortisone and cortisone)which also have sodium-retaining propertiesare used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs including dexamethasone are primarily used for their anti-inflammatory effects in disorders of many organ systems.

At equipotent anti-inflammatory dosesdexamethasone almost completely lacks the sodium-retaining property of hydrocortisone and closely related derivatives of hydrocortisone.

Patient Information for Decadron

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 corticosteroidsthey 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 therapywithdrawal of corticosteroids may result in symptoms of the corticosteroid withdrawal syndrome including myalgiaarthralgiaand 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 exposedmedical advice should be sought without delay.