DEXAMETHASONE tablet

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

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Active ingredient:
DEXAMETHASONE (UNII: 7S5I7G3JQL) (DEXAMETHASONE - UNII:7S5I7G3JQL)
Available from:
Bryant Ranch Prepack
Administration route:
ORAL
Prescription type:
PRESCRIPTION DRUG
Therapeutic indications:
Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity reactions, perennial or seasonal allergic rhinitis, and serum sickness. Bullous dermatitis herpetiformis, exfoliative erythroderma, mycosis fungoides, pemphigus, and severe erythema multiforme (Stevens-Johnson syndrome). 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 hyperplasia, hypercalcemia associated with cancer, and nonsuppurative thyroiditis. To tide the patient over a critical period of the disease in regional enteritis and ulcerative colitis. Acquired (autoimmune) hemolytic anemia, congenital (erythroid) hypoplastic anemia (Diamond-Blackfan anemia), idiopathic thrombocytopenic purpura in a
Product summary:
Product: 63629-4127 NDC: 63629-4127-1 35 TABLET in a BOTTLE NDC: 63629-4127-2 21 TABLET in a BOTTLE NDC: 63629-4127-3 51 TABLET in a BOTTLE NDC: 63629-4127-4 90 TABLET in a BOTTLE NDC: 63629-4127-5 120 TABLET in a BOTTLE NDC: 63629-4127-6 100 TABLET in a BOTTLE NDC: 63629-4127-7 55 TABLET in a BOTTLE NDC: 63629-4127-8 10 TABLET in a BOTTLE
Authorization status:
Abbreviated New Drug Application
Authorization number:
63629-4127-1, 63629-4127-2, 63629-4127-3, 63629-4127-4, 63629-4127-5, 63629-4127-6, 63629-4127-7, 63629-4127-8

DEXAMETHASONE- dexamethasone tablet

Bryant Ranch Prepack

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Dexamethasone Tablets USP, Dexamethasone Oral Solution USP and Dexamethasone Oral

Solution USP Intensol™ (Concentrate)

Des cription

Dexamethasone Tablets USP are available for oral administration containing either 0.5 mg, 0.75 mg, 1

mg, 1.5 mg, 2 mg, 4 mg or 6 mg of dexamethasone USP. Each tablet contains the following inactive

ingredients: lactose monohydrate, magnesium stearate, starch, sugar, D&C Yellow #10 (0.5 mg and 4

mg), FD&C Blue #1 (0.75 mg and 1.5 mg), FD&C Green #3 (4 mg and 6 mg), FD&C Red #3 (1.5 mg),

FD&C Red #40 (1.5 mg), FD&C Yellow #6 (0.5 mg and 4 mg) and Yellow Iron Oxide (1 mg).

Dexamethasone Oral Solution USP is formulated for oral administration containing 0.5 mg per 5 mL of

dexamethasone USP. The cherry brandy flavored oral solution contains the following inactive

ingredients: anhydrous citric acid, cherry brandy flavor, disodium edetate, glycerin, methylparaben,

propylene glycol, propylparaben, sorbitol solution and water.

Dexamethasone Oral Solution USP Intensol™ (Concentrate) is formulated for oral administration

containing 1 mg per mL of dexamethasone USP. In addition, the oral solution contains the following

inactive ingredients: alcohol 30% v/v, anhydrous citric acid, benzoic acid, disodium edetate, propylene

glycol and water.

Dexamethasone, a synthetic adrenocortical steroid, is a white to practically white, odorless, crystalline

powder. It is stable in air. It is practically insoluble in water. The empirical formula is C

H FO . The

molecular weight is 392.47. It is designated chemically as 9-fluoro-11β,17,21-trihydroxy-16α-

methylpregna-1,4-diene,3,20-dione and the structural formula is:

CLINICAL PHARMACOLOGY

Glucocorticoids, naturally occurring and synthetic, are adrenocortical steroids that are readily absorbed

from the gastrointestinal tract. Glucocorticoids cause varied metabolic effects. In addition, they modify

the body's immune responses to diverse stimuli. Naturally occurring glucocorticoids (hydrocortisone

and cortisone), which also have sodium-retaining properties, are 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 doses, dexamethasone almost completely lacks the sodium-retaining

property of hydrocortisone and closely related derivatives of hydrocortisone.

INDICATIONS AND USAGE

Allergic States

Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional

treatment in asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity reactions, perennial or

seasonal allergic rhinitis, and serum sickness.

Dermatologic Diseases

Bullous dermatitis herpetiformis, exfoliative erythroderma, mycosis fungoides, pemphigus, and 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 hyperplasia,

hypercalcemia associated with cancer, and 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 anemia, congenital (erythroid) hypoplastic anemia (Diamond-Blackfan

anemia), idiopathic thrombocytopenic purpura in adults, pure red cell aplasia, and selected cases of

secondary thrombocytopenia.

Mis cellaneous

Diagnostic testing of adrenocortical hyperfunction, trichinosis with neurologic or myocardial

involvement, tuberculous 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 sclerosis, cerebral edema associated with primary or metastatic brain

tumor, craniotomy, or head injury.

Ophthalmic Diseases

Sympathetic ophthalmia, temporal arteritis, uveitis, and 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

Berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with

appropriate antituberculous chemotherapy, idiopathic eosinophilic pneumonias, symptomatic

sarcoidosis.

Rheumatic Disorders

As adjunctive therapy for short-term administration (to tide the patient over an acute episode or

exacerbation) in acute gouty arthritis, acute rheumatic carditis, ankylosing spondylitis, psoriatic

arthritis, rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-

dose maintenance therapy). For the treatment of dermatomyositis, polymyositis, and systemic lupus

erythematosus.

CONTRAINDICATIONS

Systemic fungal infections (see WARNINGS: Fungal Infections) and in patients who are hypersensitive to

any components of these products.

WARNINGS

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 before, during, and after the stressful situation.

Cardio-Renal

Average and large doses of corticosteroids can cause elevation of blood pressure, sodium 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.

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; 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.

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 (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. These infections may be mild to severe. With increasing doses of

corticosteroids, the 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 PRECAUTIONS: Drug Interactions:

Amphotericin B injection and potassium-depleting agents).

Special Pathogens

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.

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 reactivity, close

observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid

therapy, these patients should receive chemoprophylaxis.

Vaccination

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 cannot be predicted. Immunization procedures may be

undertaken in patients who are receiving corticosteroids as replacement therapy, e.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 diseases, particular 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 chickenpox, prophylaxis with varicella zoster

immune globulin (VZIG) may be indicated. If exposed to measles, prophylaxis with immune globulin

(IG) may be indicated. (See the respective package inserts for VZIG and IG for complete prescribing

information.) If chickenpox develops, treatment with antiviral agents should be considered.

Ophthalmic

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. Consider referral to an ophthalmologist for patients who develop ocular symptoms or

use corticosteroid-containing products for more than 6 weeks. 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

General

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.

Since complications of treatment with corticosteroids are dependent on the size of the dose and the

duration of treatment, a risk/benefit decision must be made in each individual case as to dose and

duration of treatment and as to whether daily or intermittent therapy should be used.

Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy, most 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

corticosteroids, these agents should be used with caution in patients with congestive heart failure,

hypertension, or 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;

therefore, in any situation of stress occurring during that period, hormone therapy should be

reinstituted. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should

be administered concurrently.

Gas trointes tinal

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.

Mus culos keletal

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. 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. Special consideration should be

given to patients at increased risk of osteoporosis (e.g., postmenopausal women) before initiating

corticosteroid therapy.

Neuro-Ps ychiatric

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 (see DOSAGE AND

ADMINISTRATION).

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.g., myasthenia gravis), or in

patients receiving concomitant therapy with neuromuscular blocking drugs (e.g., pancuronium). 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.

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.

Ophthalmic

lntraocular pressure may become elevated in some individuals. If steroid therapy is continued for more

than 6 weeks, intraocular pressure should be monitored.

Information for Patients

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.

Drug Interactions

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 B, diuretics), patients should be

observed closely for development of hypokalemia. 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.

Antibiotics: Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid

clearance (see Drug Interactions, CYP 3A4 Inducers,CYP 3A4 Inhibitors, and CYP 3A4 Substrates).

Anticholinesterases: Concomitant use of anticholinesterase agents and corticosteroids may produce

severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be

withdrawn at least 24 hours before initiating corticosteroid therapy.

Anticoagulants, oral: 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.

Antidiabetics: Because corticosteroids may increase blood glucose concentrations, dosage 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. Thus, results 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 corticosteroids, resulting in decreased

blood levels and lessened physiologic activity, thus requiring an increase in corticosteroid dosage.

Estrogens, including oral contraceptives: Estrogens may decrease the hepatic metabolism of certain

corticosteroids, thereby increasing their effect.

CYP 3A4 Inducers: Dexamethasone is metabolized by CYP 3A4. Drugs which induce cytochrome P450

3A4 (CYP 3A4) enzyme activity (e.g., barbiturates, phenytoin, carbamazepine, rifampin) may enhance the

metabolism of corticosteroids and require that the dosage of the corticosteroid be increased.

CYP 3A4 Inhibitors: Concomitant administration of dexamethasone with erythromycin, a moderate CYP

3A4 inhibitor, has the potential to result in increased plasma concentrations of dexamethasone.

Ketoconazole, a strong CYP3A4 inhibitor, has been reported to decrease the metabolism of certain

corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. In addition,

ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency

during corticosteroid withdrawal. Co-administration with other drugs which strongly inhibit CYP 3A4

(e.g., itraconazole, clarithromycin, ritonavir, cobicistat-containing products) may lead to increased plasma

concentrations of corticosteroids and potentially increase the risk for systemic corticosteroid side

effects. Consider the benefit of co-administration versus the potential risk of systemic corticosteroid

effects, in which case patients should be monitored for systemic corticosteroid side effects.

CYP 3A4 Substrates: Dexamethasone is a moderate inducer of CYP 3A4. Co-administration with other

drugs that are metabolized by CYP 3A4 (e.g., indinavir, erythromycin) may increase their clearance,

resulting in decreased plasma concentration.

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 experience, there have been reports of both increases and decreases in

phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control.

Skin Tests: Corticosteroids may suppress reactions to skin tests.

Thalidomide: Co-administration with thalidomide should be employed cautiously, as 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:

Infections: Vaccination).

Carcinogenesis, Mutagenesis, Impairment 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 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.

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 growth, interfere

with endogenous corticosteroid production, or cause other untoward effects. Because of the potential

for serious adverse reactions in nursing infants from corticosteroids, a decision should be made

whether to discontinue nursing or to discontinue the drug, taking 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 corticosteroids, which 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 corticosteroids, e.g., severe asthma and wheezing, are based

on adequate and well-controlled trials conducted in adults, on 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 adults, pediatric patients should be carefully observed with frequent measurements

of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the presence of

infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.

Pediatric patients who are treated with corticosteroids by any route, including systemically administered

corticosteroids, may 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 monitored, and 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

corticosteroids, pediatric 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 general, dose selection for an

elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the

greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other

drug therapy. In particular, the increased risk of diabetes mellitus, fluid retention and hypertension in

elderly patients treated with corticosteroids should be considered.

ADVERSE REACTIONS

(Listed alphabetically, under each subsection)

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

Allergic Reactions

Anaphylactoid reaction, anaphylaxis, angioedema.

Cardiovas cular

Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive

heart failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants, myocardial

rupture following recent myocardial infarction (see WARNINGS: Cardio-Renal), edema, pulmonary

edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis.

Dermatologic

Acne, allergic dermatitis, dry scaly skin, ecchymoses and petechiae, erythema, impaired wound healing,

increased sweating, rash, striae, suppression of reactions to skin tests, thin fragile skin, thinning scalp

hair, urticaria.

Endocrine

Decreased carbohydrate and glucose tolerance, development of cushingoid state, hyperglycemia,

glycosuria, hirsutism, hypertrichosis, increased requirements for insulin or oral hypoglycemic agents

in diabetes, manifestations of latent diabetes mellitus, menstrual irregularities, secondary adrenocortical

and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or illness),

suppression of growth in pediatric patients.

Fluid and Electrolyte Disturbances

Congestive heart failure in susceptible patients, fluid retention, hypokalemic alkalosis, potassium loss,

sodium retention, tumor lysis syndrome.

Gas trointes tinal

Abdominal distention, elevation in serum liver enzyme levels (usually reversible upon discontinuation),

hepatomegaly, increased appetite, nausea, pancreatitis, peptic ulcer with possible perforation and

hemorrhage, perforation of the small and large intestine (particularly in patients with inflammatory

bowel disease), ulcerative esophagitis.

Metabolic

Negative nitrogen balance due to protein catabolism.

Mus culos keletal

Aseptic necrosis of femoral and humeral heads, loss of muscle mass, muscle weakness, osteoporosis,

pathologic fracture of long bones, steroid myopathy, tendon rupture, vertebral compression fractures.

Neurological/Ps ychiatric

Convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with

papilledema (pseudotumor cerebri) usually following discontinuation of treatment, insomnia, mood

swings, neuritis, neuropathy, paresthesia, personality changes, psychic disorders, vertigo.

Ophthalmic

Exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts, vision

blurred.

Other

Abnormal fat deposits, decreased resistance to infection, hiccups, increased or decreased motility and

number of spermatozoa, malaise, moon face, weight gain.

OVERDOSAGE

Treatment of overdosage is by supportive and symptomatic therapy. In the case of acute overdosage,

according to the patient's condition, supportive therapy may include gastric lavage or emesis.

DOSAGE AND ADMINISTRATION

For Oral Administration

The initial dosage varies from 0.75 mg 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 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 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 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 the corticosteroid 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 30 mg of dexamethasone

for a week followed by 4 mg to 12 mg every other day for one month have been shown to be effective

(see PRECAUTIONS: Neuro-Psychiatric).

In pediatric patients, the initial dose of dexamethasone may vary depending on the specific disease entity

being treated. The range of initial doses is 0.02 mg to 0.3 mg/kg/day in three or four divided doses (0.6

mg to 9 mg/m bsa/day).

For the purpose of comparison, the following is the equivalent milligram dosage of the various

corticos teroids :

Cortisone, 25 mg

Triamcinolone, 4 mg

Hydrocortisone, 20 mg

Paramethasone, 2 mg

Prednisolone, 5 mg

Betamethasone, 0.75 mg

Prednisone, 5 mg

Dexamethasone, 0.75 mg

Methylprednisolone, 4 mg

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 spaces, their relative properties may

be greatly altered.

In acute, self-limited allergic disorders or acute exacerbations of chronic allergic disorders, the following

dosage schedule combining parenteral and oral therapy is suggested:

Dexamethasone sodium phosphate injection, 4 mg per mL

First Day

1 or 2 mL, intramuscularly

Dexamethasone tablets, 0.75 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 episodes, while minimizing the risk

of overdosage in chronic cases.

In cerebral edema, dexamethasone sodium phosphate injection 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 tumors, maintenance therapy with either

dexamethasone sodium phosphate injection or dexamethasone tablets in a dosage of 2 mg two or three

times daily may be effective.

Dexamethasone Suppression Tests

Proper Use of an Intensol

An Intensol is a concentrated oral solution as compared to standard oral liquid medications. It is

recommended that an Intensol be mixed with liquid or semi-solid food such as water, juices, soda or

soda-like beverages, applesauce and puddings.

Use only the calibrated dropper provided with this product. Draw into the dropper the amount

prescribed for a single dose. Then squeeze the dropper contents into a liquid or semi-solid food. Stir

the liquid or food gently for a few seconds. The Intensol formulation blends quickly and completely.

The entire amount of the mixture, of drug and liquid or drug and food, should be consumed immediately.

Do not store for future use.

HOW SUPPLIED

Product: 63629-4127

NDC: 63629-4127-1 35 TABLET in a BOTTLE

NDC: 63629-4127-2 21 TABLET in a BOTTLE

NDC: 63629-4127-3 51 TABLET in a BOTTLE

NDC: 63629-4127-4 90 TABLET in a BOTTLE

NDC: 63629-4127-5 120 TABLET in a BOTTLE

NDC: 63629-4127-6 100 TABLET in a BOTTLE

NDC: 63629-4127-7 55 TABLET in a BOTTLE

NDC: 63629-4127-8 10 TABLET in a BOTTLE

Tests for Cushing’s syndrome

Give 1 mg of dexamethasone orally at 11:00 p.m. Blood is drawn for plasma cortisol

determination at 8:00 a.m. the following morning.

For greater accuracy, give 0.5 mg of dexamethasone orally every 6 hours for 48 hours. Twenty-

four hour urine collections are made for determination of 17-hydroxycorticosteroid excretion.

Test to distinguish Cushing’s syndrome due to pituitary ACTH excess from Cushing’s syndrome

due to other causes.

Give 2 mg of dexamethasone orally every 6 hours for 48 hours. Twenty-four hour urine

collections are made for determination of 17-hydroxycorticosteroid excretion.

Dexamethasone 1.5mg Tablet

DEXAMETHASONE

dexamethasone tablet

Product Information

Product T ype

HUMAN PRESCRIPTION DRUG

Ite m Code (Source )

NDC:6 36 29 -4127(NDC:0 0 54-418 2)

Route of Administration

ORAL

Active Ingredient/Active Moiety

Ingredient Name

Basis of Strength

Stre ng th

DEXAMETHASO NE (UNII: 7S5I7G3JQL) (DEXAMETHASONE - UNII:7S5I7G3JQL)

DEXAMETHASONE

1.5 mg

Inactive Ingredients

Ingredient Name

Stre ng th

FD&C BLUE NO . 1 (UNII: H3R47K3TBD)

FD&C RED NO . 3 (UNII: PN2ZH5LOQY)

FD&C RED NO . 4 0 (UNII: WZB9 127XOA)

LACTO SE MO NO HYDRATE (UNII: EWQ57Q8 I5X)

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

STARCH, CO RN (UNII: O8 232NY3SJ)

SUCRO SE (UNII: C151H8 M554)

Product Characteristics

Color

PINK

S core

2 pieces

S hap e

ROUND

S iz e

6 mm

Bryant Ranch Prepack

Flavor

Imprint Code

54;9 43

Contains

Packag ing

#

Item Code

Package Description

Marketing Start Date

Marketing End Date

1

NDC:6 36 29 -4127-1

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

0 2/0 8 /20 10

2

NDC:6 36 29 -4127-2

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

0 2/0 8 /20 10

3

NDC:6 36 29 -4127-3

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

0 2/0 8 /20 10

4

NDC:6 36 29 -4127-4

9 0 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 2/0 8 /20 10

5

NDC:6 36 29 -4127-5

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

0 2/0 8 /20 10

6

NDC:6 36 29 -4127-6

10 0 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 2/0 8 /20 10

7

NDC:6 36 29 -4127-7

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

0 2/0 8 /20 10

8

NDC:6 36 29 -4127-8

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

0 2/0 8 /20 10

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

ANDA

ANDA0 8 46 10

0 5/19 /19 75

Labeler -

Bryant Ranch Prepack (171714327)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Bryant Ranch Prepack

171714327

REPACK(6 36 29 -4127) , RELABEL(6 36 29 -4127)

Revised: 1/2020

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