so one can [35:<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. b 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 n o 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. n o 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 therefore, 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 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 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. Cancer Chemotherapy-induced Nausea and Vomiting Prevention of nausea and vomiting associated with emetogenic cancer chemotherapy . 100 101 102 103 104 129 130 131 Addition of dexamethasone to monotherapy with a selective 5-HT 3 antagonist (e.g., granisetron, ondansetron) or a substituted benzamide (e.g., metoclopramide) increases antiemetic efficacy; combined therapy may be useful for nausea and vomiting refractory to monotherapy. Cerebral Edema To decrease cerebral edema associated with brain tumors and neurosurgery (e.g., craniotomy). a b c d f Cerebral edema associated with pseudotumor cerebri may also benefit, but efficacy of glucocorticoids is controversial and remains to be established. b Edema resulting from brain abscesses is less responsive than that resulting from brain tumors. b Pharmacologic management of cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy. a c d f Head Injury Efficacy of glucocorticoid therapy is not established; such therapy can be detrimental and is associated with a substantial increase in risk of death. Use in improving outcomes or reducing intracranial pressure in patients with head injury not recommended. 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 Bacterial Meningitis Short-term adjunctive therapy (i.e., IV dexamethasone for the first 2 4 days of anti-infective therapy) of bacterial meningitis . To benefit CSF abnormalities involving prostaglandin, lactate, glucose, and protein concentrations and to decrease neurologic manifestations and sequelae (e.g., development of hearing loss). b AAP currently recommends that adjunctive therapy with IV dexamethasone for bacterial meningitis be considered on an individualized basis in infants and children 6 weeks of age after weighing the relative risks and benefits. 127 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 syndrome a 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 Diagnostic Uses Diagnosis (dexamethasone suppression test; DST) of adrenocortical hyperfunction (e.g., Cushing s syndrome, adrenal hyperplasia, adrenal adenoma). a b d f Inhibits pituitary corticotropin (ACTH) release and decreases output of endogenous corticosteroids when given in an amount that does not itself appreciably affect levels of urinary 17-hydroxycorticosteroids. b Diagnosis (DST) of mental depression; however, considerable controversy currently exists regarding the clinical utility of the test. Sensitivity of DST in depression is relatively modest (about 40 50%), and a positive test result (nonsuppression) does not appear to reliably predict response to antidepressant therapy and a negative test result (suppression) is not an indication for withholding antidepressant therapy. Dexpak Dosage and Administration General Route of administration and dosage depend on the condition being treated and the patient response. a b d Alternate-day Therapy Alternate-day therapy in which a single dose is administered every other morning is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions. b This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects. b Because dexamethasone s HPA-axis suppression persists for 2.75 days, alternate-day regimens are not appropriate. b If alternate-day therapy is preferred, only use a short-acting glucocorticoid that suppresses the HPA axis> <1.5 days after a single oral dose (e.g., prednisone, prednisolone, methylprednisolone). b Some conditions (e.g., rheumatoid arthritis, ulcerative colitis) require daily glucocorticoid therapy because symptoms of the underlying disease cannot be controlled by alternate-day therapy. b Discontinuance of Therapy A steroid withdrawal syndrome consisting of lethargy, fever, myalgia can develop following abrupt discontinuance. b d Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly). b d If used for only brief periods (a few days) in emergency situations, may reduce and discontinue dosage quite rapidly. a b Very gradually withdraw systemic glucocorticoids until recovery of HPA-axis function occurs following long-term therapy with pharmacologic dosages. a (See Adrenocortical Insufficiency under Warnings.) Exercise caution when transferring from systemic glucocorticoid to oral or nasal inhalation corticosteroid therapy. b Many methods of slow withdrawal or tapering have been described. b In one suggested regimen, decrease by 0.375 0.75 mg every 3 7 days of until the physiologic dose (0.75 mg) is reached. b f Other recommendations state that decrements usually should not exceed 0.375 mg every 1 2 weeks. b When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient has been receiving. b After 2 4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily is reached. b For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days). a b Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days. a b Administration Administer dexamethasone orally; administer dexamethasone sodium phosphate by IV injection or infusion, or IM injection. a c d f Administer dexamethasone sodium phosphate for local effect by intra-articular, intralesional, intrasynovial, or soft-tissue injection. g Generally reserve IM or IV therapy for patients who are not able to take the drug orally or for use in an emergency situation. b d If an adequate clinical response does not occur after a reasonable period, discontinue the injection and transfer the patient to other therapy. d Oral Administration Administer dexamethasone orally as tablets, a solution, a or concentrate solution. a Dilution May dilute the oral concentrate in juice or other flavored liquid diluent or in semisolid food (e.g., applesauce) prior to administration. a Use only the calibrated dropper provided by the manufacturer. a Draw into the dropper the amount of concentrate solution prescribed. a Squeeze the dropper contents into a liquid or semi-solid food. a Stir the liquid or food gently for a few seconds. a Consume the liquid or food containing dexamethasone immediately. a IV Administration Administer dexamethasone sodium phosphate by IV injection or infusion. d For solution and drug compatibility information, see Compatibility under Stability. Dilution When dexamethasone sodium phosphate is administered by IV infusion, the drug can be added to dextrose or sodium chloride injections. d Solutions used for IV administration for further dilution of the injection should be preservative free when used in neonates, especially premature neonates. d Use within 24 hours. d IM Administration Administer dexamethasone sodium phosphate by IM injection. d Although rapidly absorbed from IM injection sites, consider the slower rate of absorption compared to IV administration. d Do not administer IM for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]). d Dosage Available as dexamethasone and dexamethasone sodium phosphate. Dosage of dexamethasone sodium phosphate is expressed in terms of dexamethasone phosphate. d 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 as soon as possible. b d Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma). b d 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. b High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides. b Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris. b Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible. b Massive dosages may be required for the treatment of shock. b Pediatric Patients Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area. c Usual Dosage Oral 0.024 0.34 mg/kg daily or 0.66 10 mg/m 2 daily, administered in 4 divided doses. g IV or IM 6 40 mcg/kg or 0.235 1.25 mg/m 2 IM or IV 1 or 2 times daily. g Intra-articular, Intrasynovial, Intralesional, or Soft-tissue Injection Dosage varies depending on location, size, and degree of inflammation. g Adolescents: 0.2 6 mg, repeated at 3-day to 3-week intervals if necessary. g Large joints (e.g., knee), Adolescents: 2 4 mg every 2 3 weeks as needed. g Smaller joints, Adolescents: 0.8 1 mg repeated every 2 3 weeks as needed. g Bursae, Adolescents: 2 3 mg every 3 5 days as needed. g Ganglia, Adolescents: 1 2 mg repeated as needed. g Soft tissues, Adolescents: 0.4 6 mg repeated as needed; 0.4 1 mg for tendon sheath inflammation and 2 6 mg for soft-tissue infiltration. g Bacterial Meningitis IV Infants and children: 0.15 mg/kg 4 times daily for the first 2 4 days of anti-infective therapy. 110 112 113 114 115 116 119 127 128 136 Alternatively, 0.4 mg/kg every 12 hours for the first 2 4 days of anti-infective therapy. 127 Croup IM Single dose of 0.6 mg/kg. j Adults Usual Dosage Oral Usually, 0.75 6 mg daily, depending on disease being treated, and usually divided into 2 4 doses. g IV or IM Usually, 0.5 24 mg daily, depending on the condition being treated and patient response. g Intra-articular, Intrasynovial, Intralesional, or Soft-tissue Injection Dosage varies depending on location, size, and degree of inflammation. g 0.2 6 mg, repeated at 3-day to 3-week intervals if necessary. g Large joints (e.g., knee): 2 4 mg every 2 3 weeks as needed. g Smaller joints: 0.8 1 mg repeated every 2 3 weeks as needed. g Bursae: 2 3 mg every 3 5 days as needed. g Ganglia: 1 2 mg repeated as needed. g Soft tissues: 0.4 6 mg repeated as needed; 0.4 1 mg for tendon sheath inflammation and 2 6 mg for soft-tissue infiltration. g Allergic Conditions IM then Oral For acute self-limited allergic conditions or acute exacerbations of chronic allergic disorders, initially 4 8 mg IM on the first day; 3 mg orally in 2 divided doses on the second and third days; 1.5 mg orally in 2 divided doses on the fourth day; and a single oral daily dose of 0.75 mg on the fifth and sixth days; then discontinue the drug. a f g Tuberculosis Meningitis IM Initially, an IM dosage of 8 12 mg daily tapered over 6 8 weeks. 137 139 No additional benefit from higher dosages but may be associated with more frequent adverse effects. 137 139 Antenatal Use in Preterm Labor IM 6 mg every 12 hours or 4 mg every 8 hours, for 2 days in preterm labor that begins at 24 34 weeks gestation. b g Beneficial effects on fetal maturation are greatest> 24 hours after initiating therapy and extend up to at least 7 days. A single course for all pregnant women between 24 34 weeks gestation who are at risk of preterm delivery within 7 days; do not routinely repeat antenatal courses of antenatal glucocorticoids since risks and benefits remain to be fully elucidated. Attempt antenatal administration of even a partial course unless immediate delivery is anticipated since some benefit is likely. Shock IV Life-threatening shock: Massive doses such as 1 6 mg/kg as a single IV injection or a 40-mg IV injection repeated every 2 6 hours if needed. d g Alternatively, 20 mg by IV injection initially followed by continuous IV infusion of 3 mg/kg per 24 hours. d g Continue high-dose therapy only until the patient s condition has stabilized and usually not beyond 48 72 hours. d g Cancer Chemotherapy-induced Nausea and Vomiting Prevention IV Usually, 10 20 mg IV before administration of the chemotherapy. 100 101 102 103 104 Additional IV or oral doses (usually lower than the initial dose) may be needed for 24 72 hours. 101 102 103 104 Cerebral Edema IV then IM or Oral Initially, 10 mg IV, then 4 mg IM every 6 hours for 2 4 days, then taper over 5 7 days. a d IM or IV or Oral In patients with recurrent or inoperable brain tumors, maintenance dosage of 2 mg IM, IV, or orally 2 or 3 times daily. a d g When possible, replace IM with oral therapy 1 3 mg 3 times daily. g Bacterial Meningitis IV 0.15 mg/kg 4 times daily for the first 2 4 days of anti-infective therapy. 110 112 113 114 115 116 119 127 128 136 Alternatively, 0.4 mg/kg every 12 hours for the first 2 4 days of anti-infective therapy. 127 Diagnostic Uses Cushing s Syndrome Oral Initially, 0.5 mg every 6 hours for 48 hours after baseline 24-hour urinary 17-hydroxycorticosteroid (17-OHCS) concentrations are determined. f g During the second 24 hours of administration, collect the urine and analyze for 17-OHCS. g Alternatively, after a baseline plasma cortisol determination, administer 1-mg orally at 11 p.m., and determine plasma cortisol concentrations at 8 a.m. the following morning. f Plasma cortisol and urinary output of 17-OHCS are depressed following administration in healthy individuals but remain at basal levels in patients with Cushing s syndrome. g To distinguish adrenal tumor from adrenal hyperplasia, 2 mg orally every 6 hours for 48 hours. f g During the second 24 hours of administration, collect the urine and analyze for 17-OHCS. g In adrenal hyperplasia, urinary 17-OHCS levels are decreased and remain at basal levels in patients with adrenocortical tumors. g Depression Oral If used for dexamethasone suppression test (DST) for depression, 1 mg at 11 p.m. Following day, obtain venous blood samples at 8 a.m., 4 p.m. and 11 p.m.; usually, only at 11 p.m. for outpatients. Depending on assay used, a serum cortisol concentration >4.5 5 mcg/dL for any blood sample is abnormal and represents a positive test. Cautions for Dexpak Contraindications Known hypersensitivity to dexamethasone, any ingredient in the respective formulation, or any other corticosteroid. a b Systemic fungal infections a unless needed to control drug reactions due to amphotericin B. d Concurrent administration of live virus vaccines in patients receiving immunosuppressive doses of corticosteroids. d IM administration for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]). d Warnings/Precautions Warnings Nervous System Effects May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses. d Use may aggravate emotional instability or psychotic tendencies. d Use with caution in patients with myasthenia gravis receiving anticholinesterase therapy. d 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.) 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. 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 dexamethasone very gradually following long-term therapy with pharmacologic dosages. b (See Discontinuance of Therapy under Dosage and Administration: General.) Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods. b 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 f If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal. b Immunosuppression Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. d Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients. d (See Increased Susceptibility to Infection under Warnings.) Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. d If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained. d May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison s disease). d Increased Susceptibility to Infection Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection. f 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. 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. b 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, IG, acyclovir). 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. 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. f Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. b d Observe closely for evidence of reactivation. d Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis. d Can reactivate latent amebiasis. d Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy. b d 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. 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. 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). Tendon rupture, particularly of the Achilles tendon. 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. Fluid and Electrolyte Disturbances Sodium retention with resultant edema, potassium loss, and elevation of BP may occur but is less common with dexamethasone than with average or large doses of cortisone or hydrocortisone. d Risk is increased with high-dose dexamethasone for prolonged periods. b Edema and CHF (in susceptible patients) may occur. b d Dietary salt restriction is advisable and potassium supplementation may be necessary. b Increased calcium excretion and possible hypocalcemia. b Ocular Effects 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. d 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 d Endocrine and Metabolic Effects 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. 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 d 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. b d Sensitivity Reactions Anaphylactic and hypersensitivity reactions reported. b d General Precautions Monitoring 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 on all patients. b Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease. During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations. GU Effects Increased or decreased motility and number of sperm in some men. b d 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. d Use with caution in patients with active or latent peptic ulcer. d Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids. d Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids. b d Antenatal Risks in Preterm Labor Short-term adverse effects of antenatal administration include transient neonatal and maternal adrenal suppression and increased risk of infection. No long-term sequelae were noted in children up to 12 years of age who had been exposed to short-term antenatal glucocorticoids. Specific Populations Pregnancy Category C. d Lactation Glucocorticoids are dis leading
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