Can you take Amiodarone with Interferon alfa-2b?

Interferon alfa-2b has a major potential interaction with Arrhythmia.

Hypertension, arrhythmias, angina, myocardial infarction, cardiomyopathy, and congestive heart failure have been reported during interferon therapy. Therapy with interferons should be administered with caution in patients with compromised cardiac function.

Interferon alfa-2b has a major potential interaction with Autoimmune Disorders.

Antiviral interferons may exacerbate autoimmune disorders such as myositis, thyroiditis, systemic lupus erythematosus, rheumatoid arthritis, psoriasis, or autoimmune hepatitis. Therapy should be avoided or administered with extreme caution in patients with autoimmune disorders.

Interferon alfa-2b has a moderate potential interaction with Bone Marrow Depression/Low Blood Counts.

Interferons (alfa and gamma) induce a dose-dependent, generally mild, myelosuppression. Leukopenia is the primary manifestation. Thrombocytopenia and anemia occur less frequently. Therapy with interferons (alfa and gamma) should be administered cautiously to patients with bone marrow suppression. Clinical monitoring of hematopoietic function is recommended.

Amiodarone has a major potential interaction with Cardiogenic Shock.

The use of amiodarone is contraindicated for use in patients with cardiogenic shock, severe sinus node dysfunction causing marked sinus bradycardia, second- or third-degree AV block, or symptomatic bradycardia in the absence of a functioning pacemaker.

Interferon alfa-2b has a major potential interaction with Cardiovascular Conditions and Disorders.

Hypertension, arrhythmias, angina, myocardial infarction, cardiomyopathy, and congestive heart failure have been reported during interferon therapy. Therapy with interferons should be administered with caution in patients with compromised cardiac function.

Interferon alfa-2b has a major potential interaction with Depression.

Interferons (alfa or beta) can induce depression and suicidal behavior. Suicidal attempts and suicides have been reported. Therapy with interferons (alfa or beta) should be administered cautiously to patients with or predisposed to mental depression. Clinical monitoring of psychological status is recommended.

Interferon alfa-2b has a moderate potential interaction with Diabetes Mellitus.

Flu-like symptoms frequently associated with interferon-alfa therapy can precipitate ketoacidosis in diabetic patients. Therapy with interferon alfa should be administered cautiously in patients with diabetes mellitus. Clinical monitoring of blood glucose concentrations and anti-diabetic therapy is recommended.

Amiodarone has a major potential interaction with Heart Block.

The use of amiodarone is contraindicated for use in patients with cardiogenic shock, severe sinus node dysfunction causing marked sinus bradycardia, second- or third-degree AV block, or symptomatic bradycardia in the absence of a functioning pacemaker.

Amiodarone has a major potential interaction with Heart Failure.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Interferon alfa-2b has a major potential interaction with Heart Failure.

Hypertension, arrhythmias, angina, myocardial infarction, cardiomyopathy, and congestive heart failure have been reported during interferon therapy. Therapy with interferons should be administered with caution in patients with compromised cardiac function.

Amiodarone has a major potential interaction with Hemodialysis.

Amiodarone and its active metabolite are not removed by hemodialysis.

Amiodarone has a moderate potential interaction with Hyperkalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Interferon alfa-2b has a major potential interaction with Hyperthyroidism.

Thyroid abnormalities, hypothyroidism or hyperthyroidism, have been reported in patients administered interferons. Therapy with interferons should be administered cautiously to patients with thyroid dysfunction. If thyroid control cannot be maintained within normal limits with medication, interferon-alfa should be discontinued. Clinical monitoring of thyroid function is recommended.

Amiodarone has a moderate potential interaction with Hyperthyroidism.

Amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and also contributes inorganic iodine that can result in altered thyroid function tests, hypothyroidism, or hyperthyroidism. Therapy with amiodarone should be administered cautiously in patients with thyroid dysfunction. Clinical monitoring, including baseline and periodic evaluation of thyroid function is recommended. Modification of thyroid therapy may be necessary.

Amiodarone has a moderate potential interaction with Hypokalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Amiodarone has a major potential interaction with Hypotension.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Interferon alfa-2b has a major potential interaction with Ischemic Heart Disease.

Hypertension, arrhythmias, angina, myocardial infarction, cardiomyopathy, and congestive heart failure have been reported during interferon therapy. Therapy with interferons should be administered with caution in patients with compromised cardiac function.

Interferon alfa-2b has a major potential interaction with Liver Disease.

Hepatotoxicity, including fatal cases, has been reported in patients treated with interferon alpha. Additionally, the risk of hepatic decompensation and death is increased in patients with cirrhosis. Any patient developing liver function abnormalities during treatment should be monitored closely and treatment should be discontinued if appropriate. Interferon-alfa is contraindicated in patients with autoimmune hepatitis and decompensated liver disease.

Amiodarone has a moderate potential interaction with Liver Disease.

There have been rare reports of fatal hepatocellular necrosis after treatment with amiodarone. In patients with life-threatening arrhythmias, the potential risk of hepatic injury should be weighed against the potential benefit of amiodarone therapy. Patients with hepatic impairment should be monitored for evidence of progressive hepatic injury. Consideration should be given to reducing the rate of administration or withdrawing treatment if needed.

Amiodarone has a moderate potential interaction with Magnesium Imbalance.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Amiodarone has a moderate potential interaction with Neurological Disorders.

Reversible and dose-related nervous system toxicity such as dizziness, paresthesia, tremor and involuntary movements, lack of coordination, abnormal gait and ataxia is commonly noted in patients receiving amiodarone. Therapy with amiodarone should be administered cautiously and dosage modifications considered in patients with or predisposed to neurologic dysfunction.

Interferon alfa-2b has a major potential interaction with Parkinsonism.

Reversible CNS effects such as seizures, mental status changes, manic behavior or psychotic reactions, gait disturbances, and dizziness have occurred in patients receiving interferons. Therapy with interferons should be administered cautiously in patients with or predisposed to seizures, psychiatric disorders, or conditions affecting posture or gait.

Amiodarone has a moderate potential interaction with Parkinsonism.

Reversible and dose-related nervous system toxicity such as dizziness, paresthesia, tremor and involuntary movements, lack of coordination, abnormal gait and ataxia is commonly noted in patients receiving amiodarone. Therapy with amiodarone should be administered cautiously and dosage modifications considered in patients with or predisposed to neurologic dysfunction.

Interferon alfa-2b has a moderate potential interaction with Peripheral Neuropathy.

Paresthesia and numbness have been reported during interferon therapy. Therapy with interferons should be administered cautiously in patients with or predisposed to peripheral neuropathy.

Amiodarone has a major potential interaction with Psoriasis.

The use of certain antimalarial agents is contraindicated in patients with known prolongation of QT interval as these patients can develop fatal arrhythmias. These drugs should also be avoided in patients with clinical conditions known to prolong the QT interval, such as uncorrected hypokalemia or hypomagnesemia, bradycardia, and certain other cardiac conditions. Caution is advised in patients taking other medications that can prolong the QT interval.

Interferon alfa-2b has a major potential interaction with Psychosis.

Reversible CNS effects such as seizures, mental status changes, manic behavior or psychotic reactions, gait disturbances, and dizziness have occurred in patients receiving interferons. Therapy with interferons should be administered cautiously in patients with or predisposed to seizures, psychiatric disorders, or conditions affecting posture or gait.

Amiodarone has a major potential interaction with Pulmonary Impairment.

Pulmonary toxicities such as hypersensitivity pneumonitis or interstitial/alveolar pneumonitis are potentially fatal (approximately 10% of the time) and have occurred in as many as 10% to 17% of patients administered daily dosages of approximately 400 mg of amiodarone. More frequently, asymptomatic abnormal diffusion capacity has been observed. Patients with preexisting pulmonary dysfunction does not appear to have an increased risk of pulmonary toxicity; however, they have a poorer prognosis if toxicity does develop. Thus, the risks and benefits of amiodarone therapy should be weighed carefully. Clinical monitoring of pulmonary function, including chest X-ray (baseline and every 3 to 6 months) and pulmonary function tests (with diffusion capacity), is recommended in all patients receiving amiodarone therapy. Any new respiratory symptom during treatment should be evaluated promptly and thoroughly, since toxicity is more likely to be reversible if diagnosed and managed early. Patients who develop hypersensitivity pneumonitis should be withdrawn permanently from amiodarone therapy and treated with steroids. In the case of interstitial/alveolar pneumonitis, steroid therapy and dosage reduction or discontinuation of amiodarone, if possible, usually result in clinical improvement. Subsequent rechallenge with amiodarone at reduced dosages does not always lead to return of toxicity and may be considered in some patients. The use of a lower loading dose and maintenance doses may also decrease the incidence of amiodarone- induced pulmonary toxicity.

Interferon alfa-2b has a major potential interaction with Renal Dysfunction.

Proteinuria (rare), not associated with a decrease in serum protein, is the most common renal toxicity observed with interferon- alfa therapy. Increased BUN and serum creatinine levels, hematuria, acute renal failure and nephrotic syndrome have also been reported. Therapy with interferon alfa should be administered cautiously to patients with severe renal dysfunction. Renal function should be evaluated in all patients before initiation of interferon- alfa therapy. In addition, patients with any degree of renal impairment should be carefully monitored for laboratory abnormalities and decreased creatinine clearance. A reduced dose of medication is recommended in patients with low CrCl (less than 50 mL/min - 30 mL/min).

Interferon alfa-2b has a major potential interaction with Seizures.

Reversible CNS effects such as seizures, mental status changes, manic behavior or psychotic reactions, gait disturbances, and dizziness have occurred in patients receiving interferons. Therapy with interferons should be administered cautiously in patients with or predisposed to seizures, psychiatric disorders, or conditions affecting posture or gait.

Interferon alfa-2b has a moderate potential interaction with Ulcerative Colitis.

Fatal and nonfatal ulcerative or hemorrhagic/ischemic colitis have been observed within 12 weeks of the start of alpha interferon treatment. Abdominal pain, bloody diarrhea, and fever are the typical manifestations. Treatment should be discontinued immediately in patients who develop these signs and symptoms. The colitis usually resolves within 1 to 3 weeks of discontinuation of alpha interferons.

Interferon alfa-2b has a major potential interaction with Underactive Thyroid.

Thyroid abnormalities, hypothyroidism or hyperthyroidism, have been reported in patients administered interferons. Therapy with interferons should be administered cautiously to patients with thyroid dysfunction. If thyroid control cannot be maintained within normal limits with medication, interferon-alfa should be discontinued. Clinical monitoring of thyroid function is recommended.

Amiodarone has a moderate potential interaction with Underactive Thyroid.

Amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and also contributes inorganic iodine that can result in altered thyroid function tests, hypothyroidism, or hyperthyroidism. Therapy with amiodarone should be administered cautiously in patients with thyroid dysfunction. Clinical monitoring, including baseline and periodic evaluation of thyroid function is recommended. Modification of thyroid therapy may be necessary.

Amiodarone has a major potential interaction with Visual Defect/Disturbance.

Optic neuropathy and/or neuritis has occurred during administration of amiodarone and has resulted in visual impairment such as changes in visual acuity, decrease in peripheral vision, and blindness. Optic toxicity can occur at any time following initiation of amiodarone. Therapy with amiodarone should be administered cautiously in patients with visual defects. Regular ophthalmologic examinations including fundoscopy and slit- lamp examinations are recommended.