Hydrocortisone Acetate

The following local adverse reactions are reported infrequently with topical corticosteroids, but may occur more frequently with use of occlusive dressings. These reactions are listed in an approximate decreasing order of occurrence beginning with column 1:

Patients using topical corticosteroids should receive the following information and instructions:

1. This medication is to be used as directed by the physician. It is for external use only. Avoid contact with eyes.
2. Patients should be advised not to use this medication for any disorder other than for which it was prescribed.
3. The treated skin area should not be bandaged or otherwise covered or wrapped as to be occlusive unless directed by the physician.
4. Patients should report any signs of local adverse reactions especially under occlusive dressing.
5. Parents of pediatric patients should be advised not to use tight-fitting diapers or plastic pants on a child being treated in the diaper area, as these garments may constitute occlusive dressings.

Apply the medication as soon as you remember. If it is almost time for the next dose, skip the missed dose and use the medicine at the next regularly scheduled time. Do not use extra medicine to make up the missed dose.

• Elocon
• Hydro 35

• Ultravate

© Carmol HC Patient Information is supplied by Cerner Multum, Inc. and Carmol HC Consumer information is supplied by First Databank, Inc., used under license and subject to their respective copyrights.

Glucocorticoid secreted by the adrenal cortex; also exhibits mineralocorticoid activity.a

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

When used for anti-inflammatory and immunosuppressant properties, synthetic glucocorticoids that have minimal mineralocorticoid activity are preferred.b

Adrenocortical Insufficiency

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

Hydrocortisone or cortisone (in conjunction with liberal salt intake) is usually the corticosteroid of choice for replacement therapy in patients with adrenocortical insufficiency, because these drugs have both glucocorticoid and mineralocorticoid properties.a b Concomitant administration of a more potent mineralocorticoid (fludrocortisone) may be required in some patients.b

In suspected or known adrenal insufficiency, parenteral therapy may be used preoperatively or during serious trauma, illness, or shock unresponsive to conventional therapy.c d e

In shock, IV therapy in conjunction with other therapy for shock is essential; hydrocortisone is preferred.b

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.a c d f

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; an additional mineralocorticoid may be necessary in conjunction through at least 5–7 years of age.b

A glucocorticoid, usually alone, for long-term therapy after early childhood.b

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

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.a b c d e f

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.b

Treatment of hypercalcemia associated with sarcoidosis†.b

Treatment of hypercalcemia associated with vitamin D intoxication†.b

Not effective for hypercalcemia caused by hyperparathyroidism†.b

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.a c d e f

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

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

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

Rheumatic Disorders and Collagen Diseases

Short-term palliative treatment of acute episodes or exacerbations and systemic complications of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, Reiter syndrome†, rheumatic fever† [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, dematomyositis† [polymyositis], polyareteristis nodosa†, vasculitis†) refractory to more conservative measures.a c d f

Relieves inflammation and suppresses symptoms but not disease progression.b

Rarely indicated as maintenance therapy.b

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.a b c d f

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

Local injection can provide dramatic relief initially for articular manifestations of rheumatic disorders (e.g., rheumatoid arthritis) that involve only a few persistently inflamed joints or for inflammation of tendons or bursae;b inflammation tends to recur and sometimes is more intense after drug cessation.b

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

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.b

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

Primary treatment to control symptoms and prevent severe, often life-threatening complications of dermatomyositis† and polymyositis†, polyarteritis nodosa†, relapsing polychondritis†, polymyalgia rheumatica† and giant-cell (temporal) arteritis†, or mixed connective tissue disease syndrome†.b 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.b

Polymyositis† associated with malignancy and childhood dermatomyositis may not respond well.b

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

In osteoarthritis†, intra-articular injections may be beneficial but should be limited in number as joint damage may occur.b

Dermatologic Diseases

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

Usually reserved for acute exacerbations unresponsive to conservative therapy.b

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

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

Chronic skin disorders seldom an indication for systemic glucocorticoids.b

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

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

Rarely indicated for alopecia† (areata, totalis, or universalis); may stimulate hair growth, but hair loss returns when the drug is discontinued.b

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment and control of acute manifestations, including anaphylactic and anaphylactoid reactions, angioedema†, acute noninfectious laryngeal edema, serum sickness, allergic symptoms of trichinosis, urticarial transfusion reactions†, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.a b c d f

Systemic therapy usually reserved for acute conditions and severe exacerbations.b

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

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

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.b

To reduce scarring in ocular injuries†.b

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye and adnexa (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).a c d

Acute optic neuritis optimally treated with intial high-dose IV therapy followed by chronic oral therapy.b Can slow progression to clinically definite multiple sclerosis.b

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

Systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.b

Asthma

Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.b j

Systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.j

Because onset of effects is delayed, do not use alone for emergency treatment.b

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.j

In hospital management of an acute asthma exacerbation, may give systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.b

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthmab (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).b

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.b

Oral glucocorticoids with minimal mineralocorticoid activity and relatively short half-life (e.g., prednisone, prednisolone, methylprednisolone) are preferred.

COPD

For severe exacerbations of COPD, a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.

Effects in stable COPD are much less dramatic than in asthma, and role of glucocorticoids in the management of stable COPD is limited to very specific indications.

Sarcoidosis

Management of symptomatic sarcoidosis.a b c d f

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

Advanced Pulmonary and Extrapulmonary Tuberculosis

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.a

Adjunctive glucocorticoid therapy may enhance short-term resolution of disease manifestations (e.g., clinical and radiographic abnormalities) in advanced pulmonary tuberculosis and also may reduce mortality associated with certain forms of extrapulmonary disease (e.g., meningitis, pericarditis).

Systemic adjunctive glucocorticoids may reduce sequelae (e.g., intellectual impairment) and/or improve survival in moderate to severe tuberculous meningitis.

Systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion) in acute tuberculous pericarditis.

Hastens the resolution of pain, dyspnea, and fever associated with tuberculous pleurisy.b

Lipid Pneumonitis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids in lipid pneumonitis.b

Pneumocystis jiroveci Pneumonia

Systemic adjunctive glucocorticoids decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death in moderate to severe Pneumocystis jiroveci (Pneumocystis carinii) pneumonia in acquired immunodeficiency syndrome† (AIDS).

Prevents early deterioration in oxygenation associated with antipneumocystis therapy; initiate adjunctive glucocorticoid therapy as early as possible in moderate to severe pneumocystis pneumonia.

Not known whether patients with mild pneumocystis pneumonia (arterial oxygen pressure >70 mm Hg or arterial-alveolar gradient <35 mm Hg on room air) will have clinically important benefit with adjunctive glucocorticoid therapy.

Other glucocorticoids (e.g., oral prednisone, parenteral methylprednisolone) generally are preferred.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.a b c d e f

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.a b c d e f

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.a b c d e f

Anthrax

Adjunct to anti-infective therapy in the treatment of anthrax† in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

For cutaneous anthrax† if there are signs of systemic involvement or extensive edema involving the neck and thoracic region, anthrax meningitis†, and inhalational anthrax† that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

Antenatal Use in Preterm Labor

Short-course IM betamethasone or dexamethasone are preferred in selected women with preterm labor to hasten fetal maturation† (e.g., lungs, cerebral blood vessels), including women with preterm premature rupture of membranes, preeclampsia, or third-trimester hemorrhage. Insufficient experience to evaluate efficacy of hydrocortisone.

Postnatal Use for Bronchopulmonary Dysplasia

Has been used for prevention or treatment of bronchopulmonary dysplasia in very low-birth-weight infants (i.e., <1.5 kg) who require mechanical ventilation. However, the AAP states that routine use of systemic glucocorticoids in such patients is not recommended.

May provide short-term pulmonary benefits but does not reduce mortality and is associated with an increased risk of serious adverse effects (e.g., hyperglycemia, hypertension, GI bleeding or intestinal perforation, hypertrophic obstructive cardiomyopathy, poor weight gain, poor growth of head circumference) and long-term sequelae (e.g., neurodevelopmental delay, cerebral palsy, impaired cognitive function, and stunted growth at or before school age).

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.a b c d f

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

Glucocorticoids, immune globulin IV (IGIV), or splenectomy are first-line therapies for moderate to severe ITP, depending on the extent of bleeding involved.

May not affect or prevent renal complications in Henoch-Schoenlein purpura.b

Insufficient evidence of effectiveness in aplastic anemia in children, but widely used.b

Shock

Although IV glucocorticoids may be life-saving in shock secondary to adrenocortical insufficiency (see Adrenocortical Insufficiency under Uses), the value of the drugs in the treatment of shock resulting from other causes† is controversial.b

Management of shock should be based on specific treatment of the primary cause and secondary abnormalities, and glucocorticoids, if used, should be regarded only as adjunctive supportive treatment.

Value in adjunctive treatment of septic shock† is particularly controversial. Conflicting evidence regarding effects of high-dose regimens on morbidity and mortality in septic shock.

Pericarditis

To reduce the pain, fever, and inflammation of pericarditis†, including that associated with MI.b

Glucocorticoids can provide effective symptomatic relief, but aspirin considered the treatment of choice for postmyocardial infarction pericarditis because of greater evidence establishing benefit.

Important to distinguish between pain caused by pericarditis and that caused by ischemia since management will differ.

Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development.

Glucocorticoids may cause thinning of developing scar and myocardial rupture.

Management of tuberculous pericarditis. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.)

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, and celiac disease†.a b c d f

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.b

Rarely indicated for maintenance therapy in chronic GI diseases (e.g., ulcerative colitis, celiac disease) since does not prevent relapses and may produce severe adverse reactions with long-term administration.b

Occasionally, low dosages, in conjunction with other supportive therapy, may be useful for disease unresponsive to the usual therapy indicated for chronic conditions.b

Crohn’s Disease

Management of mildly to moderately active and moderately to severely active Crohn’s disease.f

Some experts state that conventional glucocorticoids should not be used for the management of mildly to moderately active disease, because of the high incidence of adverse effects and their use should be reserved for patients with moderately to severely active disease.

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease†. Once patients respond to parenteral therapy, they should gradually be switched to an equivalent regimen of an oral glucocorticoid.

Glucocorticoids should not be used for maintenance therapy of Crohn’s disease, because they usually do not prevent relapses and the drugs may produce severe adverse reactions with long-term administration.

Glucocorticoids have been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease† in pediatric patients.

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).a b c d e f

Treatment of breast cancer; glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.b

Glucocorticoids alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer.

Head Injury

Efficacy of glucocorticoid therapy is not established in patients with head injury; such therapy can be detrimental and is associated with a substantial increase in risk of death. Use to improve outcome or reduce intracranial pressure not recommended in patients with head injury.

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria caused by Plasmodium falciparum; no longer recommended for this condition.b

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis†.

Anti-inflammatory and immunomodulating effects accelerate neurologic recovery by restoring the blood-brain barrier, reducing edema, and possibly improving axonal conduction.

Shortens the duration of relapse and accelerates recovery; remains to be established whether the overall degree of recovery improves or the long-term course is altered.

Myasthenia Gravis

Management of myasthenia gravis†, usually when there is an inadequate response to anticholinesterase therapy.

Parenterally for the treatment of myasthenic crisis.

Organ Transplants

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

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

Trichinosis

Treatment of trichinosis with neurologic or myocardial involvement.a c d f

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.a c d f f

Can induce diuresis and remission of proteinuria in nephrotic syndromea b c d f secondary to primary renal disease, especially when there is minimal renal histologic change.b

Treatment of lupus nephritis.a b c d

Contraindications

• Known hypersensitivity to hydrocortisone, any ingredient in the respective formulation, or any other corticosteroid.b

• Systemic fungal infectionsb unless needed to control drug reactions due to amphotericin B.d

• Concurrent administration of live virus vaccines in patients receiving immunosuppressive doses of corticosteroids.g

• IM administration for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]).

• Hydrocortisone sodium succinate injection preparations containing benzyl alcohol in premature infants.c (See Pediatric Use under Cautions.)

Warnings/Precautions

Warnings

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

Use with caution in patients with myasthenia gravisc receiving anticholinesterase therapy.

Serious, potentially permanent, and sometimes fatal adverse neurologic events (e.g., spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, brain edema) reported rarely, often within minutes to 48 hours following epidural glucocorticoid injection given either with or without fluoroscopic guidance.1000 1001 1002 1003

FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use.1000 1001 (See Advice to Patients.)

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).b

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.b

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.b d

Withdraw hydrocortisone very gradually following long-term therapy with pharmacologic dosages.b c (See Discontinuance of Therapy under Dosage and Administration.)

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

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.b Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.b c

If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal.b

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

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.c f If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained.c f May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease).c f

Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection.f c f

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.c f

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

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

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.c f

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.c f

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

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba).

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.

May exacerbate fungal infections and should not be used in the presence of such infection unless needed to control drug reactions to amphotericin B; however, cases of cardiac enlargement and CHF have been reported with concomitant use of hydrocortisone and amphotericin B.d

Not effective and can have detrimental effects (prolongation of coma, higher incidence of pneumonia and GI bleeding) in the management of cerebral malaria.b d f

Can reactivate tuberculosis.c d f Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy.b d Observe closely for evidence of reactivation.c d f Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis.c d f

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

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.b These adverse effects may be especially serious in geriatric or debilitated patients.b A high-protein diet may help to prevent adverse effects associated with protein catabolism.b

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).c

Tendon rupture, particularly of the Achilles tendon.c

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.

To minimize the risk of glucocorticoid-induced bone loss, the smallest possible effective dosage and duration should be used. Topical and inhaled preparations should be used whenever possible.

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

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.

Glucocorticoid-induced bone loss can be both prevented and treated. Baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip should be obtained when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and appropriate preventive therapy should be initiated. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate, risedronate), and a weight-bearing exercise program that maintains muscle mass are suitable first-line therapies aimed at reducing the risk of adverse bone effects.

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur with average or large doses of hydrocortisone.b c Edema and CHF (in susceptible patients) may occur.b c

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

Increased calcium excretion and possible hypocalcemia.b c

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

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

Cortical blindness has occurred following epidural glucocorticoid injection.1001 1002 1003

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.b c

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.b Corticosteroids have also been reported to increase or decrease motility and number of sperm in some men.c

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

Exaggerated response to the glucocorticoids in hypothyroidism.b c

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

Sensitivity Reactions

Anaphylactic and hypersensitivity reactions.b d

Certain tablet formulations contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin.

Some commercially available formulations contain sulfites that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals.b Overall prevalence of sulfite sensitivity in the general population is unknown but probably low; appears to occur more frequently in asthmatic than in nonasthmatic individuals.b

General Precautions

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

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

During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations.

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

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.c

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 of corticosteroids.b

Various dermatologic effects (i.e., impaired wound healing, skin atrophy and thinning, acne, increased sweating, hirsutism, facial erythema, striae, petechiae, ecchymoses, easy bruising) are associated with systemic glucocorticoids.b

Kaposi’s sarcoma reported in patients receiving glucocorticoids; discontinuance may result in clinical remission.c d

Specific Populations

Category C.d

Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants.d Discontinue nursing (in mothers taking pharmacologic doses) because of potential risk to nursing infants.c d

With long-term use, may delay growth and maturation in children and adolescents.b c Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.a c d Titrate dosage to the lowest effective level.b Alternate-day therapy may minimize growth suppression and should be instituted if growth suppression occurs.b

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DXA]) in children and adolescents are similar to those in adults.

Ensure children and adolescents consistently ingest adequate calcium and vitamin D either through diet or supplementation.

Some commercially available injections contain benzyl alcohol as a preservative.b Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (when large amounts administered [100–400 mg/kg daily]), although causal relationship not established.b

Some manufacturers state that benzyl alcohol-containing injectable preparations are contraindicated in premature infants and use should be avoided whenever possible; AAP states that presence of small amounts in a commercially available injection should not proscribe its use when the medication is indicated in neonates and comparable benzyl alcohol-free preparations are not available.b

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.b May be especially serious in geriatric or debilitated patients.b

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

Use with caution in patients with osteoporosis.d

Patients with cirrhosis show an exaggerated response to glucocorticoids.b c

Use with caution.c

Common Adverse Effects

Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.h i (See Warnings/Precautions under Cautions.)

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: potential pharmacokinetic interaction (decreased hydrocortisone clearance).c e

Inducers of CYP3A4: potential pharmacokinetic interaction (increased hydrocortisone clearance).a c

Specific Drugs