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Betamethasone (Monograph)

Brand name: Celestone Soluspan
Drug class: Adrenals
ATC class: H02AB01
VA class: HS051
CAS number: 378-44-9

Medically reviewed by on Feb 27, 2023. Written by ASHP.


Synthetic glucocorticoid; minimal mineralocorticoid activity.

Uses for Betamethasone

Treatment of a wide variety of diseases and conditions principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for effects on blood and lymphatic systems in the palliative treatment of various diseases.

Usually, inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.

Adrenocortical Insufficiency

Corticosteroids are administered in physiologic dosages to replace deficient endogenous hormones in patients with adrenocortical insufficiency.

Cortisone or hydrocortisone is the corticosteroid of choice for replacement therapy in patients with adrenocortical insufficiency because these drugs have both glucocorticoid and mineralocorticoid properties.

If betamethasone is used, must also administer a mineralocorticoid, particularly in infants.

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome (also known as congenital adrenal hyperplasia).

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; addition of a mineralocorticoid may be necessary through at least 5–7 years of age. After early childhood, a glucocorticoid alone is used for long-term therapy throughout life.

In hypertensive forms, a short-acting glucocorticoid with minimal mineralocorticoid activity (e.g., methylprednisolone, prednisone) is preferred; avoid long-acting glucocorticoids (e.g., dexamethasone, betamethasone) because of tendency toward overdosage and growth retardation.


Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis [off-label].

Treatment of hypercalcemia associated with vitamin D intoxication [off-label].

Not effective for hypercalcemia caused by hyperparathyroidism [off-label].


Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.

Anti-inflammatory action relieves fever, acute thyroid pain, and swelling.

May reduce orbital edema in endocrine exophthalmos (thyroid ophthalmopathy).

Usually reserved for palliative therapy in severely ill patients unresponsive to salicylates and thyroid hormones.

Rheumatic Disorders and Collagen Diseases

Short-term adjunctive treatment of acute episodes or exacerbations of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, acute and subacute bursitis, epicondylitis, acute nonspecific tenosynovitis, peritendinitis, ankylosing spondylitis, Reiter syndrome [off-label], rheumatic fever [off-label] [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, polyarteritis nodosa, vasculitis) refractory to more conservative measures.

Relieves inflammation and suppresses symptoms but not disease progression.

Rarely indicated as maintenance therapy.

May be used as maintenance therapy (e.g., in rheumatoid arthritis, acute gouty arthritis, systemic lupus erythematosus, acute rheumatic carditis) as part of a total treatment program in selected patients when more conservative therapies have proven ineffective.

Glucocorticoid withdrawal is extremely difficult if used for maintenance; relapse and recurrence usually occur with drug discontinuance.

Local injection (intra-articular or soft tissue administration) can provide initial relief of articular manifestations of an acute episode of a rheumatic condition (e.g., acute gouty arthritis, acute and subacute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, synovitis of osteoarthritis).

Local injection can prevent invalidism by facilitating movement of joints that might otherwise become immobile.

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.

Adjunctively for severe systemic complications of Wegener’s granulomatosis, but cytotoxic therapy is the treatment of choice.

Primary treatment to control symptoms and prevent severe, often life-threatening complications in patients with dermatomyositis and polymyositis, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica and giant-cell (temporal) arteritis, or mixed connective tissue disease syndrome. High dosage may be required for acute situations; after a response has been obtained, drug must often be continued for long periods at low dosage.

Rarely indicated in psoriatic arthritis, diffuse scleroderma (progressive systemic sclerosis), acute and subacute bursitis, or osteoarthritis; risks outweigh benefits.

Dermatologic Diseases

Treatment of pemphigus and pemphigoid, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, lichen planus, uncontrollable eczema, cutaneous sarcoidosis, mycosis fungoides, severe psoriasis, and severe seborrheic dermatitis.

Usually reserved for acute exacerbations unresponsive to conservative therapy.

Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris and pemphigoid, and high or massive doses may be required.

For control of severe or incapacitating allergic conditions (e.g., contact dermatitis, atopic dermatitis) intractable to adequate trials of conventional treatment.

Chronic skin disorders seldom an indication for systemic glucocorticoids.

Intralesional injections occasionally indicated for localized chronic skin disorders (e.g., keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, granuloma annulare) unresponsive to topical therapy.

Rarely indicated for psoriasis; if used, exacerbation may occur when the drug is withdrawn or dosage is decreased.

Rarely indicated systemically for alopecia (areata, totalis, or universalis). May stimulate hair growth, but hair loss returns when the drug is discontinued.

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment and control of acute manifestations, including atopic dermatitis, contact dermatitis, serum sickness, allergic symptoms of trichinosis, transfusion reactions, drug hypersensitivity reactions, and seasonal or perennial rhinitis.

Systemic therapy usually reserved for acute conditions and severe exacerbations.

For acute conditions, usually used in high dosage and with other therapies (e.g., antihistamines, sympathomimetics).

Reserve prolonged treatment of chronic allergic conditions for disabling conditions unresponsive to more conservative therapy and when risks of long-term glucocorticoid therapy are justified.

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.

To reduce scarring in ocular injuries.

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye that are intractable to adequate trials of conventional treatment (e.g., allergic conjunctivitis, keratitis, allergic corneal marginal ulcers, herpes zoster ophthalmicus, iritis and iridocyclitis, chorioretinitis, diffuse posterior uveitis and choroiditis, anterior segment inflammation, optic neuritis, sympathetic ophthalmia).

Less severe allergic and inflammatory allergic conditions of the eye are treated with topical (to the eye) corticosteroids.

Glucocorticoids used systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.


Corticosteroids are used as adjunctive treatment of acute asthma exacerbations and for maintenance treatment of persistent asthma.

Systemic glucocorticoids (usually prednisone, prednisolone, and dexamethasone) are used for treatment of moderate to severe acute exacerbations of asthma; speeds resolution of airflow obstruction and reduces rate of relapse.


Management of symptomatic sarcoidosis.

Systemic glucocorticoids are indicated for hypercalcemia; ocular, CNS, glandular, myocardial, or severe pulmonary involvement; or severe skin lesions unresponsive to intralesional injections of glucocorticoids.


Systemically as adjunctive therapy with effective antimycobacterial agents (e.g., streptomycin, isoniazid) to suppress manifestations related to the host’s inflammatory response to the bacillus (Mycobacterium tuberculosis) and ameliorate complications in severe pulmonary or extrapulmonary tuberculosis.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.


Symptomatic relief of acute manifestations of berylliosis.

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.

Antenatal Use in Preterm Labor

Corticosteroids have been used for short-course IM therapy in selected women with preterm labor to accelerate fetal maturation (e.g., lungs, cerebral blood vessels), including women with premature rupture of membranes, preeclampsia, or third-trimester hemorrhage.

The American College of Obstetricians and Gynecologists (ACOG) guideline states that administration of betamethasone may be considered in pregnant women between 34 0/7 weeks and 36 6/7 weeks of gestation who are at risk of preterm birth within 7 days, and who have not received a course of antenatal corticosteroids.

Combined effects on multiple organ maturation reduces neonatal morbidity and mortality.

Antenatal corticosteroid administration has resulted in significantly lower severity and frequency of respiratory distress syndrome in the neonate.

Betamethasone and dexamethasone are the most widely studied corticosteroids for this use.

Hematologic Disorders

Management of hematologic disorders such as acquired (autoimmune) hemolytic anemia, pure red cell aplasia, and selected cases of secondary thrombocytopenia.

High or even massive dosages decrease bleeding tendencies and normalize blood counts; does not affect the course or duration of hematologic disorders.

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis (Crohn’s disease), or celiac disease.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).

Low Back Pain

Systemic corticosteroids have been used symptomatic relief of low back pain, however current evidence suggests that corticosteroids do not seem to be effective for improving radicular or nonradicular low back pain.

Organ Transplants

In massive dosage, used concomitantly with other immunosuppressive drugs to prevent rejection of transplanted organs.

Incidence of secondary infections is high with immunosuppressive drugs; limit to clinicians experienced in their use.


Treatment of trichinosis with neurologic or myocardial involvement.

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.

Can induce diuresis and remission of proteinuria in nephrotic syndrome.

Treatment of lupus nephritis.

Carpal Tunnel Syndrome

Local injection into the tissue near the carpal tunnel has been used in a limited number of patients to relieve symptoms (e.g., pain, edema, sensory deficit) of carpal tunnel syndrome.

Betamethasone Dosage and Administration


Discontinuance of Therapy


Administer by IM injection; do not administer IV.

May administer locally by intra-articular, intralesional, or soft tissue injection for some conditions.

Safety and efficacy of epidural administration of corticosteroids not established; corticosteroids are not approved for this use.

IM Administration

Administer betamethasone sodium phosphate and betamethasone acetate by IM injection. Generally reserve IM therapy for patients who are not able to take oral glucocorticoids.

Intra-articular, Intralesional, and Soft-tissue Administration

Administer betamethasone sodium phosphate and betamethasone acetate by intra-articular, intralesional (intradermal, not sub-Q), or soft-tissue injection.

Intra-articular injection may produce systemic as well as local effects.

For intra-articular injections, use a 20- to 24-gauge needle; verify needle placement (aspirate a few drops of synovial fluid) prior to drug administration with a second syringe.

Avoid intra-articular injection into a previously infected joint. Prior to intra-articular administration, examine the joint fluid to exclude septic arthritis. Symptoms of septic arthritis include local swelling, further restriction of joint motion, fever, or malaise. If septic arthritis is confirmed, institute appropriate antimicrobial therapy.

Do not inject drug into unstable joints.

For management of tenosynovitis and tendinitis, inject into affected tendon sheaths rather than into tendons.

For dermatologic conditions, use a tuberculin syringe with a 25-gauge, ½-inch needle for intralesional administration.

For disorders of the foot (bursitis, tenosynovitis, acute gouty arthritis), use a tuberculin syringe with a 25-gauge, 3/4-inch needle for intra-articular or soft-tissue administration.

May mix injection with a local anesthetic (e.g., 1–2% lidocaine hydrochloride) using formulations that do not contain parabens or phenol. Do not mix with diluents or local anesthetics containing preservatives (e.g., parabens, phenol) because flocculation of suspension may result.


Available as betamethasone and as a fixed combination of betamethasone sodium phosphate and betamethasone acetate. Dosage of betamethasone sodium phosphate is expressed in terms of betamethasone. Each mL of the fixed-combination injectable suspension contains 3 mg of betamethasone (as betamethasone sodium phosphate) and 3 mg of betamethasone acetate.

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug gradually as soon as possible.

If a satisfactory response is not obtained, discontinue betamethasone and substitute other appropriate therapy.

Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma).

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases; after a response has been obtained, drug often must be continued for long periods at low dosage.

High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides. Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris. Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible.


Usual Dosage

Initially, 0.5–9 mg daily (0.08–1.5 mL of the suspension), depending on disease being treated. Extremely high parenteral dosage may be justified in life-threatening situations.

Rheumatic Disorders and Collagen Diseases
Bursitis, Tenosynovitis, Peritendinitis
Intralesional, Intrasynovial, or Soft-tissue Injection

Acute bursitis of subdeltoid, subacromial, olecranon, or prepatellar bursae: 6 mg (i.e., 3 mg of betamethasone as the sodium phosphate and 3 mg of betamethasone acetate in 1 mL of suspension) into the bursa as a single dose.

Recurrent acute bursitis or acute exacerbations of chronic bursitis of subdeltoid, subacromial, olecranon, or prepatellar bursae: 6 mg into bursa; repeated doses may be required. Reduce dosage for chronic bursitis once acute condition is controlled.

Bursae under heloma durum or molle: 1.5–3 mg (0.25–0.5 mL) repeated every 3 days to 1 week.

Bursae over hallus rigidus or digiti quinti varus: 3 mg (0.5 mL) repeated every 3 days to 1 week.

Tenosynovitis, periostitis of cuboid bone: 3 mg (0.5 mL) repeated every 3 days to 1 week.

Tenosynovitis or tendinitis: 6 mg for 3 or 4 injections at intervals of 1–2 weeks.

Ganglions of joint capsules and tendon sheaths: 3 mg (0.5 mL) directly into ganglion cysts.

Acute Gouty Arthritis
Intra-articular or Soft-tissue Injection

Foot: 3–6 mg (0.5–1 mL) repeated every 3 days to 1 week.

Rheumatoid Arthritis and Osteoarthritis
Intra-articular Injection

Varies depending on location, size, and degree of inflammation.

Very large joints (e.g., hip): 6–12 mg (1–2 mL of the suspension).

Large joints (e.g. knee, ankle, shoulder): 6 mg (1 mL of the suspension).

Medium joints (e.g., elbow, wrist): 3–6 mg (0.5–1 mL of the suspension).

Smaller joints (e.g., hand, chest): 1.5–3 mg (0.25–0.5 mL of the suspension).

Dermatologic Diseases
Intralesional Injection

1.2 mg/cm2 (0.2 mL) injected intradermally; do not exceed a total dosage of 6 mg/week.

Antenatal Use in Preterm Labor†

12 mg every 24 hours for 2 doses in preterm labor that begins at 24–34 weeks’ gestation.

A single course is recommended.

Prescribing Limits


Dermatologic Diseases
Intralesional Injection

Maximum total dosage of 6 mg/week.

Cautions for Betamethasone




Nervous System Effects

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression, and personality changes to frank psychoses. Use may aggravate emotional instability or psychotic tendencies.

Use with caution in patients with myasthenia gravis.

Serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids.

Efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use.

Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.

Withdraw very gradually following long-term therapy with pharmacologic dosages.

Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods.

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.

If the disease flares up during withdrawal, increase dosage and follow with a more gradual withdrawal.


Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients.

Administration of live virus or live, attenuated vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated vaccines are administered to such patients, the expected serum antibody response may not be obtained.

Increased Susceptibility to Infection

Corticosteroids increase susceptibility to and mask symptoms of infection.

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents; reactivation of latent infections also may occur.

Infections may be mild, but they can be severe or fatal, and localized infections may disseminate.

Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives.

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children. Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.

If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG).

Use with great care in patients with known or suspected Strongyloides (threadworm) infection. Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

Not effective and can have detrimental effects in the management of cerebral malaria.

Can reactivate tuberculosis. Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate antituberculosis therapy.

Can reactivate latent amebiasis. Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high protein diet may help to prevent adverse effects associated with protein catabolism.

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium).

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis. Recommendations are made according to a patient's risk of fracture.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of BP may occur but is less common with betamethasone than with average or large doses of cortisone or hydrocortisone. Risk is increased with high-dose synthetic glucocorticoids for prolonged periods. Edema and CHF (in susceptible patients) may occur.

Dietary salt restriction is advisable and potassium supplementation may be necessary.

Increased calcium excretion and possible hypocalcemia.

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased intraocular pressure (IOP) which may result in glaucoma or may occasionally damage the optic nerve.

May enhance the establishment of secondary fungal and viral infections of the eye.

Use cautiously in patients with active ocular herpes simplex infections since corneal perforation may develop.

Transient blindness, amblyopia, acute retinal necrosis syndrome, intraocular hemorrhage, and cortical blindness have occurred following epidural glucocorticoid injection

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.

Increased or decreased motility and number of sperm in some men.

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary.

Exaggerated response to the glucocorticoids in hypothyroidism.

Cardiovascular Effects

Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested.

Use with caution in patients with hypertension.

Sensitivity Reactions

Anaphylactic or anaphylactoid reactions with or without circulatory collapse, cardiac arrest, or bronchospasm. Take appropriate precautionary measures prior to administration, especially in patients with a history of allergy to any drug.

Benzalkonium Chloride Sensitivity

Injectable suspension contains benzalkonium chloride that has been associated with neurotoxic effects in animals or humans when used epidurally or intrathecally.

General Precautions


Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, BPs, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients.

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease.

GU Effects

Increased or decreased motility and number of sperm in some men.

GI Effects

Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses.

Use with caution in patients with active or latent peptic ulcer. Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids. Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages.

Specific Populations


Corticosteroids have been shown to be teratogenic in many species when administered in clinical doses. No adequate and well-controlled studies in pregnant women. Use during pregnancy only potential benefit justifies potential risk to fetus.

Observe neonates born from mothers receiving prolonged therapy for signs of hypoadrenalism.


Distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants. Exercise caution.

Pediatric Use

Efficacy and safety of corticosteroids in pediatric patients are based on the well-established course of effect of corticosteroids. Adverse effects of corticosteroids in pediatric patients are similar to those in adults.

Carefully observe pediatric patients with frequent measurements of BP, weight, height, intraocular pressure, and clinical evaluation for 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 growth velocity.

Geriatric Use

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients.

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.

Hepatic Impairment

Glucocorticoids should be used with caution in patients with cirrhosis because such patients often show exaggerated response to the drugs.

Renal Impairment

Use with caution.

Common Adverse Effects

Intra-articular and soft-tissue injection: Soft-tissue atrophy, hypopigmentation or hyperpigmentation, thin fragile skin, facial erythema.

Drug Interactions

Inhibits and is metabolized by CYP3A4.

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: Potential pharmacokinetic interaction (decreased betamethasone clearance).

Inducers of CYP3A4: Potential pharmacokinetic interaction (increased betamethasone clearance).

Specific Drugs





Increased clearance of betamethasone

Increase dosage of betamethasone

Diuretics, potassium-depleting

Enhances the potassium-wasting effects of glucocorticoids

Monitor for development of hypokalemia


Decreased clearance of betamethasone

Reduce dosage of betamethasone to avoid potential adverse effects


Increases the risk of GI ulceration

Decreased serum salicylate concentrations; when corticosteroids are discontinued, serum salicylate concentration may increase possibly resulting in salicylate intoxication

Use concurrently with caution

Observe patients receiving both drugs closely for adverse effects of either drug

May be necessary to increase salicylate dosage when corticosteroids are administered concurrently or decrease salicylate dosage when corticosteroids are discontinued


Increased clearance of betamethasone

Increase dosage of betamethasone


Increased clearance of betamethasone

Increase dosage of betamethasone


Decreased clearance of betamethasone

Reduce dosage of betamethasone to avoid potential adverse effects

Vaccines and toxoids

May cause a diminished response to toxoids and live or inactivated vaccines

May potentiate replication of some organisms contained in live, attenuated vaccines

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages)

Defer generally routine administration of vaccines or toxoids until corticosteroid therapy is discontinued

Betamethasone Pharmacokinetics



Following intra-articular administration, systemic absorption of the soluble portion (betamethasone sodium phosphate) of the injectable suspension is rapid.

Following IM administration, peak plasma concentrations occurred at 1 hour.


IM administration: Anti-inflammatory effects may appear within 1–3 hours.


IM administration: Anti-inflammatory effects or HPA suppression may persist for 7 days.



Most glucocorticoids are removed rapidly from the blood and distributed to muscles, liver, skin, intestines, and kidneys.

Distributes into breast milk and crosses the placenta.

Plasma Protein Binding

Low affinity for transcortin binding protein.



Metabolized in most tissues, but mainly in the liver, to inactive compounds.

Elimination Route

Cleared mainly by the liver, with a small amount excreted by the kidney.


In pregnant women, 7–9 hours.




Suspension for Injection

20–25°C (may be exposed to 15–30°C). Protect from light.


Advice to Patients

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Betamethasone Sodium Phosphate and Betamethasone Acetate


Dosage Forms


Brand Names



Injectable suspension

Betamethasone Sodium Phosphate 3 mg (of betamethasone) per mL with Betamethasone Acetate 3 mg/mL*

Celestone Soluspan


AHFS DI Essentials™. © Copyright 2024, Selected Revisions February 27, 2023. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

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