Interactions between Hydrocortisone and Trileptal

Hydrocortisone has a moderate potential interaction with Abnormal Glucose Tolerance.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Adrenal Insufficiency.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Adrenal Tumor.

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

The OXcarbazepine in Trileptal has a moderate potential interaction with Arrhythmia.

Aromatic antiepileptic drugs such as phenytoin, carbamazepine, and oxcarbazepine, inhibit voltage- gated sodium channels and reduce membrane excitability in neurons and muscle and can be associated with cardiovascular effects. Individual agents have demonstrated AV heart block, including second and third-degree block following treatment. This occurred generally, but not solely in patients with underlying EKG abnormalities or risk factors for conduction abnormalities. Therapy with these agents should be considered and administered cautiously in patients with a history of cardiovascular disease and conduction abnormalities.

The OXcarbazepine in Trileptal has a moderate potential interaction with Bone Marrow Depression/Low Blood Counts.

Rare events of pancytopenia, leukopenia, and agranulocytosis have been reported in patients treated with oxcarbazepine during postmarketing observations. Discontinuation of the drug should be considered if any evidence of these hematologic events develop. Therapy with oxcarbazepine should be administered with caution in patients with preexisting blood dyscrasias and/or bone marrow depression. Complete blood counts, including platelets and possibly reticulocytes and serum iron, should be performed prior to initiating therapy and regularly during therapy.

The OXcarbazepine in Trileptal has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Aromatic antiepileptic drugs such as phenytoin, carbamazepine, and oxcarbazepine, inhibit voltage- gated sodium channels and reduce membrane excitability in neurons and muscle and can be associated with cardiovascular effects. Individual agents have demonstrated AV heart block, including second and third-degree block following treatment. This occurred generally, but not solely in patients with underlying EKG abnormalities or risk factors for conduction abnormalities. Therapy with these agents should be considered and administered cautiously in patients with a history of cardiovascular disease and conduction abnormalities.

Hydrocortisone has a moderate potential interaction with Cataract.

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.

Hydrocortisone has a moderate potential interaction with Cirrhosis.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Cirrhosis.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

The OXcarbazepine in Trileptal has a major potential interaction with Depression.

Antiepileptic drugs can increase depression and suicidal thoughts or behaviors in patients receiving these drugs for any indication. Patients should be monitored for the emergence or worsening of depression, suicidal thoughts and unusual changes in mood or behavior. Caregivers and family should be alert for the emergence or worsening of symptoms. Behaviors of concern should be reported immediately to the healthcare providers.

Hydrocortisone has a moderate potential interaction with Depression.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Depression.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

Hydrocortisone has a moderate potential interaction with Diabetes Mellitus.

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.

Hydrocortisone has a moderate potential interaction with Diverticulitis.

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.

Hydrocortisone has a moderate potential interaction with Electrolyte Abnormalities.

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.

Hydrocortisone has a moderate potential interaction with Fluid Retention.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Fluid Retention.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

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.

Hydrocortisone has a moderate potential interaction with Heart Attack.

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.

Hydrocortisone has a moderate potential interaction with Heart Failure.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Heart Failure.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Herpetic Keratitis.

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.

Hydrocortisone has a moderate potential interaction with High Blood Pressure.

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.

Hydrocortisone has a moderate potential interaction with High Cholesterol.

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.

Hydrocortisone has a moderate potential interaction with History, Peptic Ulcer.

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.

Hydrocortisone has a moderate potential interaction with History, Thrombotic/Thromboembolic Disorder.

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.

Hydrocortisone has a moderate potential interaction with History, Tuberculosis.

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.

Hydrocortisone has a moderate potential interaction with Hyperadrenocorticism.

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

Hydrocortisone has a moderate potential interaction with Hyperaldosteronism.

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

Hydrocortisone has a moderate potential interaction with Hypernatremia.

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.

Hydrocortisone has a moderate potential interaction with Hypocalcemia.

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.

Hydrocortisone has a moderate potential interaction with Hypokalemia.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Hyponatremia.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a major potential interaction with Infection.

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.

Hydrocortisone has a moderate potential interaction with Intestinal Anastomoses.

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.

The OXcarbazepine in Trileptal has a major potential interaction with Liver Disease.

Most anticonvulsants are primarily metabolized by the liver. Metabolic activity may be decreased in patients with liver disease, resulting in elevated drug levels and increased risk of toxicity. Therapy with anticonvulsants should be administered cautiously in patients with mild and moderate liver impairment. Therapy with these drugs is mostly not recommended in patients with severe liver impairment. Caution is also advised when treating patients with a history of liver disease, since the use of some anticonvulsants has been associated with hepatotoxicity. Baseline and periodic evaluation of liver function is recommended. Therapy should be discontinued and not readministered if evidence of liver damage is observed and felt to be drug-related.

Hydrocortisone has a moderate potential interaction with Liver Disease.

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.

Hydrocortisone has a moderate potential interaction with Myasthenia Gravis.

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.

Hydrocortisone has a moderate potential interaction with Myoneural Disorder.

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.

Hydrocortisone has a moderate potential interaction with Myopathy.

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.

Hydrocortisone has a moderate potential interaction with Osteoporosis.

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.

Hydrocortisone has a moderate potential interaction with Peptic Ulcer.

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 OXcarbazepine in Trileptal has a moderate potential interaction with Polydipsia.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Post MI Syndrome.

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.

Hydrocortisone has a major potential interaction with Prematurity/Underweight in Infancy.

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.

Hydrocortisone has a moderate potential interaction with Psychosis.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Psychosis.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

The OXcarbazepine in Trileptal has a major potential interaction with Renal Dysfunction.

Most anticonvulsants are primarily excreted by the kidney. The plasma clearance may be decreased and the half-life prolonged in patients with impaired renal function. Therapy with anticonvulsants should be administered cautiously in patients with significant renal dysfunction. In most cases it is recommended to adjust the dosage in patients with CrCl <50 mL/min to half the usual starting dose and then increase slowly to achieve the desired clinical response. The renal function should be monitored regularly in patients receiving therapy.

Hydrocortisone has a moderate potential interaction with Renal Dysfunction.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Renal Dysfunction.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Seizures.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with SIADH.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Hydrocortisone has a moderate potential interaction with Strongyloidiasis.

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.

Hydrocortisone has a moderate potential interaction with Systemic Sclerosis.

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.

Hydrocortisone has a moderate potential interaction with Thrombotic/Thromboembolic Disorder.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Thyroid Disease.

Decreased values for thyroid function tests, especially T4 have been observed with the administration of oxcarbazepine. This should be taken into account in patients with thyroid disorders.

Hydrocortisone has a moderate potential interaction with Tuberculosis, Latent.

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.

Hydrocortisone has a moderate potential interaction with Ulcerative Colitis.

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.

Hydrocortisone has a moderate potential interaction with Underactive Thyroid.

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.

The OXcarbazepine in Trileptal has a moderate potential interaction with Underactive Thyroid.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.