Can You Take Bepridil with Kenalog-40?

Using triamcinolone together with alcohol or grapefruit may increase the risk of side effects of triamcinolone. You may want to limit your consumption of grapefruit, grapefruit juice, and/or alcohol during treatment with triamcinolone. Talk to your doctor if you have any questions or concerns. You should seek immediate medical attention if you experience any unusual bleeding or bruising, or have other signs and symptoms of bleeding such as dizziness; lightheadedness; red or black, tarry stools; coughing up or vomiting fresh or dried blood that looks like coffee grounds; severe headache; and weakness. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Grapefruit juice may increase the blood levels of certain medications such as bepridil. You may want to limit your consumption of grapefruit and grapefruit juice during treatment with bepridil. However, if you have been regularly consuming grapefruit or grapefruit juice with the medication, then it is advisable for you to talk with your doctor before changing the amounts of these products in your diet, as this may alter the effects of your medication. Contact your doctor if your condition changes or you experience increased side effects. Orange juice is not expected to interact.

Bepridil and ethanol (alcohol) may have additive effects in lowering your blood pressure. You may experience headache, dizziness, lightheadedness, fainting, and/or changes in pulse or heart rate. These side effects are most likely to be seen at the beginning of treatment, following a dose increase, or when treatment is restarted after an interruption. Let your doctor know if you develop these symptoms and they do not go away after a few days or they become troublesome. Avoid driving or operating hazardous machinery until you know how the medications affect you, and use caution when getting up from a sitting or lying position. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Using bepridil together with multivitamin with minerals can decrease the effects of bepridil. Talk with your doctor before using bepridil and multivitamin with minerals together. You may need a dose adjustment or need your blood pressure checked more often if you take both medications. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

The use of bepridil is contraindicated in patients with a history of serious ventricular arrhythmias; patients with congenital or acquired QT interval prolongation syndromes; and patients treated concomitantly with class IA or III antiarrhythmic drugs or other medications that are known to produce increases in the QT interval or cause torsade de pointes. Bepridil has class I antiarrhythmic properties and can induce new arrhythmias, including ventricular tachycardia and ventricular fibrillation. Patients with other severe arrhythmias may have increased susceptibility to the proarrhythmic effects of bepridil, but use in such patients has been limited. Bepridil can also cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Although the absolute safe upper limit of QT is not known, the manufacturer recommends that the dosage be reduced in patients whose QT interval exceeds 0.52 seconds during treatment. If prolongation remains excessive, the drug should be discontinued.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

Bepridil may have a negative inotropic effect, particularly at high dosages. Congestive heart failure has been observed infrequently (approximately 1%) in U.S. controlled clinical trials. However, experience with the use of bepridil in the presence of significantly impaired ventricular function is limited, and there is little information on the effect of concomitant administration with digoxin. Therapy with bepridil should be administered cautiously in patients with congestive heart failure, especially if they have severe left ventricular dysfunction (e.g., ejection fraction < 30%) or if they are receiving a beta-adrenergic blocker. Likewise, bepridil should not be given to patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating bepridil therapy.

Bepridil can cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of bepridil on the QT interval and should be corrected prior to institution of bepridil therapy. In addition, patients who experience frequent, severe, and/or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with bepridil.

Bepridil can cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of bepridil on the QT interval and should be corrected prior to institution of bepridil therapy. In addition, patients who experience frequent, severe, and/or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with bepridil.

The use of some calcium channel blockers (CCBs) is contraindicated in patients with severe bradyarrhythmia, sick sinus syndrome (unless a functioning pacemaker is present), or heart block greater than the first degree (unless a functioning pacemaker is present). CCBs like bepridil, diltiazem and verapamil have a negative effect on AV conduction and the SA node and may exacerbate these conditions.

Bepridil has class I antiarrhythmic properties and can induce new arrhythmias, including ventricular tachycardia and ventricular fibrillation. In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia Suppression Trial involving patients with asymptomatic, non-life-threatening ventricular arrhythmias who have had myocardial infarctions for less than two years previously, an excess rate of mortality/nonfatal cardiac arrest was seen in patients treated with the class I antiarrhythmic agents, encainide and flecainide, compared with that seen in patients assigned to matched placebo-treated groups. Although the applicability of these results to other antiarrhythmic agents is uncertain, the manufacturer recommends generally avoiding the use of bepridil in the post-infarction period. There is also limited experience in the use of bepridil within three months following a myocardial infarction, since it was one of the exclusion criteria in U.S. clinical trials.

Bepridil can cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of bepridil on the QT interval and should be corrected prior to institution of bepridil therapy. In addition, patients who experience frequent, severe, and/or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with bepridil.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The immunosuppressant and anti-inflammatory effects of corticosteroids, particularly at higher dosages, may reduce resistance to infectious agents, increase the risk of disseminated infections, mask symptoms of infection, and reactivate or exacerbate latent/resolved infections; fatal cases have been reported. Avoid use of corticosteroids in patients with cerebral malaria. Screen patients for active (or history of) infection with tuberculosis, hepatitis, varicella, measles, and amebiasis, especially prior to prolonged treatment. Closely monitor for reactivation of latent infections; chemoprophylaxis may be required. In general, corticosteroids should not be used in patients with active infections, especially systemic fungal infections, unless medically necessary to control drug reactions. However, for corticosteroid-dependent patients who develop a severe or life-threatening infection, continuation of corticosteroid therapy with at least physiologic replacement dosages should be considered, since these patients may have secondary adrenocortical insufficiency. Removal of external steroid during periods of stress may be detrimental to these patients.

Calcium channel blockers (CCBs) are extensively metabolized by the liver. The half-lives of CCBs may be prolonged substantially in patients with severe hepatic impairment, with the potential for significant drug accumulation. In addition, the use of some CCBs has been associated with elevations in serum transaminases, both with and without concomitant elevations in alkaline phosphatase and bilirubin. While these effects may be transient and reversible, some patients have developed cholestasis or hepatocellular injury. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function is advised.

Bepridil can cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of bepridil on the QT interval and should be corrected prior to institution of bepridil therapy. In addition, patients who experience frequent, severe, and/or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with bepridil.

Bepridil may have a negative inotropic effect, particularly at high dosages. Congestive heart failure has been observed infrequently (approximately 1%) in U.S. controlled clinical trials. However, experience with the use of bepridil in the presence of significantly impaired ventricular function is limited, and there is little information on the effect of concomitant administration with digoxin. Therapy with bepridil should be administered cautiously in patients with congestive heart failure, especially if they have severe left ventricular dysfunction (e.g., ejection fraction < 30%) or if they are receiving a beta-adrenergic blocker. Likewise, bepridil should not be given to patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating bepridil therapy.

Bepridil has class I antiarrhythmic properties and can induce new arrhythmias, including ventricular tachycardia and ventricular fibrillation. In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia Suppression Trial involving patients with asymptomatic, non-life-threatening ventricular arrhythmias who have had myocardial infarctions for less than two years previously, an excess rate of mortality/nonfatal cardiac arrest was seen in patients treated with the class I antiarrhythmic agents, encainide and flecainide, compared with that seen in patients assigned to matched placebo-treated groups. Although the applicability of these results to other antiarrhythmic agents is uncertain, the manufacturer recommends generally avoiding the use of bepridil in the post-infarction period. There is also limited experience in the use of bepridil within three months following a myocardial infarction, since it was one of the exclusion criteria in U.S. clinical trials.

According to the manufacturer, there have been two cases of marked leukopenia and neutropenia reported in U.S. clinical trials of over 800 patients treated with bepridil for up to five years. Both involved diabetic and elderly patients, with one case resulting in death and the other recovering after discontinuation of the drug. In a postmarketing report, a 72-year-old man with severe angina pectoris developed fever and chills associated with an absolute neutrophil count of 35/mm3 six weeks after switching from diltiazem and nitrates to bepridil and nitrates. A bone marrow biopsy revealed profound myeloid hypoplasia. The patient recovered after discontinuation of bepridil and institution of granulocyte colony-stimulating factor and broad-spectrum antibiotics. Therapy with bepridil should be administered cautiously in patients with preexisting neutropenia or agranulocytosis. The drug should be withdrawn promptly if these conditions develop during therapy.

Bepridil has class I antiarrhythmic properties and can induce new arrhythmias, including ventricular tachycardia and ventricular fibrillation. In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia Suppression Trial involving patients with asymptomatic, non-life-threatening ventricular arrhythmias who have had myocardial infarctions for less than two years previously, an excess rate of mortality/nonfatal cardiac arrest was seen in patients treated with the class I antiarrhythmic agents, encainide and flecainide, compared with that seen in patients assigned to matched placebo-treated groups. Although the applicability of these results to other antiarrhythmic agents is uncertain, the manufacturer recommends generally avoiding the use of bepridil in the post-infarction period. There is also limited experience in the use of bepridil within three months following a myocardial infarction, since it was one of the exclusion criteria in U.S. clinical trials.

The use of certain parenteral formulations of dexamethasone, hydrocortisone, methylprednisolone, prednisolone and triamcinolone is considered by the drug manufacturers to be contraindicated in neonates, particularly premature infants and infants of low birth weight. Some formulations of these drugs contain benzyl alcohol which, when used in bacteriostatic saline intravascular flush and endotracheal tube lavage solutions, has been associated with fatalities and severe respiratory and metabolic complications in low-birth-weight premature infants. However, many experts feel that, in the absence of benzyl alcohol-free equivalents, the amount of the preservative present in these formulations should not necessarily preclude their use if they are clearly indicated. The American Academy of Pediatrics considers benzyl alcohol in low doses (such as when used as a preservative in some medications) to be safe for newborns. Continuous infusions of high dosages of medications containing benzyl alcohol may, however, cause toxicity and should be avoided if possible.

The use of some calcium channel blockers (CCBs) is contraindicated in patients with severe bradyarrhythmia, sick sinus syndrome (unless a functioning pacemaker is present), or heart block greater than the first degree (unless a functioning pacemaker is present). CCBs like bepridil, diltiazem and verapamil have a negative effect on AV conduction and the SA node and may exacerbate these conditions.

The use of bepridil is contraindicated in patients with a history of serious ventricular arrhythmias; patients with congenital or acquired QT interval prolongation syndromes; and patients treated concomitantly with class IA or III antiarrhythmic drugs or other medications that are known to produce increases in the QT interval or cause torsade de pointes. Bepridil has class I antiarrhythmic properties and can induce new arrhythmias, including ventricular tachycardia and ventricular fibrillation. Patients with other severe arrhythmias may have increased susceptibility to the proarrhythmic effects of bepridil, but use in such patients has been limited. Bepridil can also cause torsade de pointes type ventricular tachycardia secondary to its ability to prolong the QT interval. In U.S. clinical trials, the mean prolongations of QTc and QT were 8% and 10%, respectively, but increases of 25% or more occurred in 5% of the studied population for QTc and 8.7% for QT. Although the absolute safe upper limit of QT is not known, the manufacturer recommends that the dosage be reduced in patients whose QT interval exceeds 0.52 seconds during treatment. If prolongation remains excessive, the drug should be discontinued.

Corticosteroids can raise blood glucose level by antagonizing the action and suppressing the secretion of insulin, which results in inhibition of peripheral glucose uptake and increased gluconeogenesis. Therapy with corticosteroids should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during corticosteroid therapy, and their antidiabetic regimen adjusted accordingly.

Corticosteroids mimic the effects of endogenous cortisol and aldosterone. Use of these agents may aggravate conditions of hyperadrenocorticalism in a dose-dependent manner.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Long-term therapy with corticosteroids should be administered cautiously in patients with a history of cataracts, glaucoma, or increased intraocular pressure.

Corticosteroids may have enhanced effects on patients with cirrhosis due to decreased metabolism of these agents. Patients with cirrhosis should be monitored more closely for excessive cortisol effects. Dosage adjustments may be required in these patients.

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer periods. Therapy with corticosteroids should be administered cautiously in patients with preexisting fluid retention, hypertension, congestive heart failure, and/or renal dysfunction. Dietary sodium restriction and potassium supplementation may be advisable.

Corticosteroids may aggravate the symptoms of psychosis and emotional instability. Patients with these conditions should be monitored for increased or worsened symptoms during corticosteroid therapy.

Corticosteroids can raise blood glucose level by antagonizing the action and suppressing the secretion of insulin, which results in inhibition of peripheral glucose uptake and increased gluconeogenesis. Therapy with corticosteroids should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during corticosteroid therapy, and their antidiabetic regimen adjusted accordingly.

Corticosteroids may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with corticosteroids should be avoided or administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer periods. Therapy with corticosteroids should be administered cautiously in patients with preexisting fluid retention, hypertension, congestive heart failure, and/or renal dysfunction. Dietary sodium restriction and potassium supplementation may be advisable.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Long-term therapy with corticosteroids should be administered cautiously in patients with a history of cataracts, glaucoma, or increased intraocular pressure.

Corticosteroids may cause peptic ulcer disease and gastrointestinal (GI) hemorrhage, usually when given in high dosages or for prolonged periods. However, even conventional dosages may aggravate symptoms in patients with a history of peptic ulcers. Delayed healing of ulcers has also been reported. Therapy with corticosteroids should be avoided or administered cautiously in patients with active or latent peptic ulcers or other risk factors for GI bleeding. Some clinicians recommend the use of prophylactic antacids or H2-antagonists between meals when large doses of corticosteroids are necessary.

Corticosteroids may increase blood coagulability and have rarely been associated with the development of intravascular thrombosis, thromboembolism, and thrombophlebitis. Therapy with corticosteroids should be administered cautiously in patients who have or may be predisposed to thrombotic or thromboembolic disorders.

In patients with latent tuberculosis or tuberculin reactivity, the use of pharmacologic dosages of corticosteroids may cause a reactivation of the disease. Close monitoring for signs and symptoms of tuberculosis is recommended if corticosteroid therapy is administered to patients with a history of tuberculosis or tuberculin reactivity. During prolonged corticosteroid therapy, tuberculosis chemoprophylaxis may be considered.

Corticosteroids mimic the effects of endogenous cortisol and aldosterone. Use of these agents may aggravate conditions of hyperadrenocorticalism in a dose-dependent manner.

Corticosteroids mimic the effects of endogenous cortisol and aldosterone. Use of these agents may aggravate conditions of hyperadrenocorticalism in a dose-dependent manner.

Corticosteroids may elevate serum triglyceride and LDL cholesterol levels if used for longer than brief periods. Patients with preexisting hyperlipidemia may require closer monitoring during prolonged corticosteroid therapy, and adjustments made accordingly in their lipid-lowering regimen.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer periods. Therapy with corticosteroids should be administered cautiously in patients with preexisting fluid retention, hypertension, congestive heart failure, and/or renal dysfunction. Dietary sodium restriction and potassium supplementation may be advisable.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Corticosteroids may have enhanced effects in hypothyroidism due to decreased metabolism of these agents. Patients with hypothyroidism should be monitored more closely for excessive cortisol effects. Dosage adjustments may be required secondary to changes in their thyroid condition.

Corticosteroids may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with corticosteroids should be avoided or administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

Corticosteroids are primarily metabolized by the liver and may have enhanced effects in patients with liver disease. Dosage adjustments may be necessary in these patients.

Although corticosteroids are commonly used in the treatment of myasthenia gravis to increase muscle strength, these agents should nevertheless be administered with caution in such setting. Patients should be treated in an intensive care unit and receive respiratory support, since muscle strength may markedly decrease initially, particularly with high dosages. Preferably, therapy should begin with relatively low dosages (15 to 25 mg/day of prednisone or equivalent) and be increased stepwise as tolerated (approximately 5 mg/day of prednisone or equivalent at 2- to 3-day intervals until marked clinical improvement or a dosage of 50 mg/day is reached). Improvement may be delayed and gradual. Thus, it is important not to discontinue therapy prematurely.

The use of corticosteroids may be associated with left ventricular free-wall rupture in patients who have had a recent myocardial infarction. Pharmacologic dosages of corticosteroids should be administered with great caution in such patients.

Toxic myopathy has been observed with the chronic use or the administration of large doses of corticosteroids, often in patients with disorders of neuromuscular transmission such as myasthenia gravis or in patients receiving neuromuscular blocking agents. Fluorinated corticosteroids such as betamethasone, dexamethasone, and triamcinolone appear to cause more severe muscle atrophy and weakness than the nonfluorinated agents. Moreover, multiple-daily doses are more toxic than once-daily or, preferably, alternate-day morning doses. Steroid myopathy is generalized and sometimes accompanied by respiratory weakness and dyspnea. In some cases, it has resulted in quadriparesis. Elevations of creatine kinase (CK) may also occur, albeit infrequently. After withdrawal of corticosteroid therapy, recovery may be slow and incomplete. Therapy with corticosteroids should be administered cautiously in patients with preexisting myopathy or myoneural disorders since these conditions may confound the diagnosis of steroid-induced myopathy. The presence of a normal serum CK level, minimal/no changes of myopathy on electromyography, and type 2 muscle fiber atrophy on biopsy are helpful in suggesting steroid-induced weakness. If steroid myopathy is suspected, a dosage reduction or discontinuation of the steroid should be considered.

Toxic myopathy has been observed with the chronic use or the administration of large doses of corticosteroids, often in patients with disorders of neuromuscular transmission such as myasthenia gravis or in patients receiving neuromuscular blocking agents. Fluorinated corticosteroids such as betamethasone, dexamethasone, and triamcinolone appear to cause more severe muscle atrophy and weakness than the nonfluorinated agents. Moreover, multiple-daily doses are more toxic than once-daily or, preferably, alternate-day morning doses. Steroid myopathy is generalized and sometimes accompanied by respiratory weakness and dyspnea. In some cases, it has resulted in quadriparesis. Elevations of creatine kinase (CK) may also occur, albeit infrequently. After withdrawal of corticosteroid therapy, recovery may be slow and incomplete. Therapy with corticosteroids should be administered cautiously in patients with preexisting myopathy or myoneural disorders since these conditions may confound the diagnosis of steroid-induced myopathy. The presence of a normal serum CK level, minimal/no changes of myopathy on electromyography, and type 2 muscle fiber atrophy on biopsy are helpful in suggesting steroid-induced weakness. If steroid myopathy is suspected, a dosage reduction or discontinuation of the steroid should be considered.

Pharmacologic dosages of corticosteroids should be used cautiously in patients with ocular herpes simplex because of the risk of corneal perforation. Corticosteroids are not recommended for patients with active ocular herpes simplex.

Corticosteroids reduce osteoblastic function and inhibit the absorption of intestinal calcium, which can result in bone resorption and bone loss during prolonged therapy. In addition, bone matrix may be affected by the protein-catabolic effects of corticosteroids, especially when given in high dosages or for prolonged periods, leading to aseptic necrosis and fractures. Long-term or high-dose corticosteroid therapy should be administered cautiously and only if necessary in patients with or at risk for osteoporosis. Adverse skeletal effects may be minimized by alternate-day or intermittent administration. Any patient receiving prolonged therapy with the equivalent of 7.5 mg prednisone/day or more are at risk for glucocorticoid-induced osteoporosis and should be managed according to The American College of Rheumatology (ACR) guidelines.

Corticosteroids may cause peptic ulcer disease and gastrointestinal (GI) hemorrhage, usually when given in high dosages or for prolonged periods. However, even conventional dosages may aggravate symptoms in patients with a history of peptic ulcers. Delayed healing of ulcers has also been reported. Therapy with corticosteroids should be avoided or administered cautiously in patients with active or latent peptic ulcers or other risk factors for GI bleeding. Some clinicians recommend the use of prophylactic antacids or H2-antagonists between meals when large doses of corticosteroids are necessary.

The use of corticosteroids may be associated with left ventricular free-wall rupture in patients who have had a recent myocardial infarction. Pharmacologic dosages of corticosteroids should be administered with great caution in such patients.

Corticosteroids may aggravate the symptoms of psychosis and emotional instability. Patients with these conditions should be monitored for increased or worsened symptoms during corticosteroid therapy.

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer periods. Therapy with corticosteroids should be administered cautiously in patients with preexisting fluid retention, hypertension, congestive heart failure, and/or renal dysfunction. Dietary sodium restriction and potassium supplementation may be advisable.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Unlike most helminths, Strongyloides stercoralis has the ability to replicate in the human host. In patients with strongyloidiasis, the use of pharmacologic or immunosuppressive dosages of corticosteroids may result in Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. Therapy with corticosteroids should be administered with extreme caution, if at all, in these patients. For patients on corticosteroids who develop known or suspected Strongyloides infestation, withdrawal of corticosteroids or reduction of the dose of corticosteroids is recommended.

In patients with scleroderma, corticosteroids may precipitate renal crisis with malignant hypertension, possibly via steroid-induced increases in renin substrate and angiotensin II levels and decreases in vasodilator prostaglandin production. Renal failure may ensue. Therapy with corticosteroids should be administered cautiously in patients with scleroderma. In addition, they should be limited to short-term use.

Corticosteroids may increase blood coagulability and have rarely been associated with the development of intravascular thrombosis, thromboembolism, and thrombophlebitis. Therapy with corticosteroids should be administered cautiously in patients who have or may be predisposed to thrombotic or thromboembolic disorders.

In patients with latent tuberculosis or tuberculin reactivity, the use of pharmacologic dosages of corticosteroids may cause a reactivation of the disease. Close monitoring for signs and symptoms of tuberculosis is recommended if corticosteroid therapy is administered to patients with a history of tuberculosis or tuberculin reactivity. During prolonged corticosteroid therapy, tuberculosis chemoprophylaxis may be considered.

Corticosteroids may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with corticosteroids should be avoided or administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.