Levothyroxine Sodium

Levothyroxine sodium may potentiate the effects of epinephrine.

May decrease or increase thyroid hormone secretion, resulting in hypothyroidism or hyperthyroidism; slowly excreted producing prolonged effects.

Concurrent use may increase therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines. Toxic effects include increased cardiac arrhythmia risk and CNS stimulation.

Levothyroxine sodium may reduce the therapeutic effects of digitalis glycosides. Serum digitalis levels may decrease when patient becomes euthyroid, necessitating an increase in digitalis glycoside dose.

Potentiates the effects of epinephrine.

Effects of epinephrine may be potentiated by levothyroxine sodium.

Effects of epinephrine may be potentiated by levothyroxine sodium.

May decrease or increase thyroid hormone secretion resulting in hypothyroidism or hyperthyroidism depending on patient thyroid status.

May potentiate clinical response of isoproterenol; hemodynamic parameters may be significantly affected.

Concurrent use may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients.

May decrease thyroid hormone secretion; long-term therapy can result in goiter and subclinical or overt hypothyroidism in up to 20% of patients.

Concurrent use may increase therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines. Toxic effects include increased cardiac arrhythmia risk and CNS stimulation.

May decrease thyroid hormone secretion, which may result in hypothyroidism when used with levothyroxine.

Levothyroxine increases response to oral anticoagulant therapy. Decrease in anticoagulant dose may be warranted with correction of hypothyroidism or dose increases. Closely monitor coagulation tests.

Iodine-containing agents may decrease or increase thyroid hormone secretion. Parenterally administered agents cause shorter duration effects than oral cholecystographic agents.

Increases L-thyroxine metabolism by inducing UGT, leading to lower T4 serum levels and increased levothyroxine requirements. Changes in thyroid status may occur if added or withdrawn.

May decrease thyroid hormone secretion, which may result in hypothyroidism when used with levothyroxine.

May decrease thyroid hormone secretion or cause hyperthyroidism; parenteral agents produce more prolonged hypothyroidism than oral agents.

Stimulates hepatic microsomal enzyme activity causing increased hepatic degradation of levothyroxine, resulting in increased levothyroxine requirements.

May decrease thyroid hormone secretion, which may result in hypothyroidism when used with levothyroxine.

Addition of levothyroxine may worsen glycemic control and increase antidiabetic agent requirements. Carefully monitor glycemic control when thyroid therapy is started, changed, or discontinued.

Effects of epinephrine may be potentiated by levothyroxine sodium.

Antacids may reduce levothyroxine absorption by affecting intragastric pH. Monitor patients appropriately.

Antacid that may affect intragastric pH and reduce levothyroxine absorption. Monitor patients appropriately.

May decrease thyroid hormone secretion and result in hypothyroidism; long-term therapy may minimally decrease T4 and T3 levels.

May decrease serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May form an insoluble chelate with levothyroxine, binding and delaying or preventing absorption, potentially resulting in hypothyroidism.

May decrease serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May potentiate the effects of epinephrine.

May alter T4 and T3 serum transport or metabolism, affecting levothyroxine efficacy.

Bile acid sequestrant known to decrease levothyroxine absorption, potentially resulting in hypothyroidism.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

Bile acid sequestrant known to decrease levothyroxine absorption, potentially resulting in hypothyroidism.

Bile acid sequestrant known to decrease levothyroxine absorption, potentially resulting in hypothyroidism.

May reduce TSH secretion transiently at doses ≥1 mcg/kg/min when levothyroxine is used.

Potentiates the pressor effects of epinephrine.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

Likely forms a ferric-thyroxine complex that reduces levothyroxine absorption, potentially resulting in hypothyroidism.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May alter T4 and T3 serum transport or metabolism, affecting levothyroxine efficacy.

May alter thyroid hormone pharmacokinetics and metabolism, potentially affecting levothyroxine efficacy.

May alter serum T4 and T3 transport affecting levothyroxine efficacy.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May alter serum T4 and T3 transport or metabolism affecting levothyroxine efficacy.

Concurrent use may cause hypothyroidism. Closely monitor TSH levels in patients receiving this tyrosine-kinase inhibitor.

Levothyroxine therapy may result in increased insulin requirements. Monitor glycemic control, especially when thyroid therapy is started, changed, or discontinued.

Phosphate binder may bind to levothyroxine and delay or prevent absorption. Administer levothyroxine at least 4 hours apart from this agent.

Antacid that may affect intragastric pH and reduce levothyroxine absorption. Monitor patients appropriately.

May cause hypochlorhydria and affect intragastric pH, reducing levothyroxine absorption. Monitor patients appropriately.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May alter T4 and T3 serum transport.

May reduce TSH secretion transiently at doses >100 mcg/day when used with levothyroxine.

May reduce levothyroxine efficacy by affecting absorption; monitor patients for changes in thyroid function.

Reduces serum protein binding of levothyroxine; total and free T4 may be reduced 20-40%, though most patients remain euthyroid. Closely monitor thyroid parameters.

At doses >2 g/day, inhibit binding of T4 and T3 to TBG and transthyretin, initially increasing FT4 followed by return to normal with possible 30% decrease in total T4.

Inhibit binding of T4 and T3 to thyroxine-binding globulin and transthyretin. Initial increase in FT4 followed by return to normal with sustained use, though total T4 may decrease up to 30%.

Inhibit binding of T4 and T3 to thyroxine-binding globulin, causing initial increase in FT4 followed by return to normal levels with total T4 potentially decreased by 30%.

Administration in patients stabilized on levothyroxine may result in increased levothyroxine levels. Monitor thyroid function.

Ion exchange resin known to decrease levothyroxine absorption, potentially resulting in hypothyroidism.

May affect intragastric pH and reduce levothyroxine absorption. Monitor patients appropriately.

May decrease serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May cause hypochlorhydria and affect intragastric pH, reducing levothyroxine absorption. Monitor patients appropriately.

May increase serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

May decrease thyroid hormone secretion, which may result in hypothyroidism when used with levothyroxine.

May decrease serum thyroxine-binding globulin concentration, resulting in initial transient increase in FT4 followed by decreased serum T4.

Chloral Hydrate Diazepam Ethionamide Lovastatin Metoclopramide 6-Mercaptopurine Nitroprusside Para-aminosalicylate sodium Perphenazine Resorcinol (excessive topical use) Thiazide Diuretics These agents have been associated with thyroid hormone and/or TSH level alterations by various mechanisms.

Chloral Hydrate Diazepam Ethionamide Lovastatin Metoclopramide 6-Mercaptopurine Nitroprusside Para-aminosalicylate sodium Perphenazine Resorcinol (excessive topical use) Thiazide Diuretics These agents have been associated with thyroid hormone and/or TSH level alterations by various mechanisms.

Chloral Hydrate Diazepam Ethionamide Lovastatin Metoclopramide 6-Mercaptopurine Nitroprusside Para-aminosalicylate sodium Perphenazine Resorcinol (excessive topical use) Thiazide Diuretics These agents have been associated with thyroid hormone and/or TSH level alterations by various mechanisms.

Chloral Hydrate Diazepam Ethionamide Lovastatin Metoclopramide 6-Mercaptopurine Nitroprusside Para-aminosalicylate sodium Perphenazine Resorcinol (excessive topical use) Thiazide Diuretics These agents have been associated with thyroid hormone and/or TSH level alterations by various mechanisms.

Slow-release formulation may decrease serum thyroxine-binding globulin concentration.

Drug or Drug Class Effect Beta-adrenergic antagonists (e.g., Propranolol > 160 mg/day) In patients treated with large doses of propranolol (> 160 mg/day), T3 and T4 levels change, TSH levels remain normal, and patients are clinically euthyroid. Drug or Drug Class Effect Beta-adrenergic antagonists (e.g., Propranolol > 160 mg/day) In patients treated with large doses of propranolol (> 160 mg/day), T3 and T4 levels change, TSH levels remain normal, and patients are clinically euthyroid.

Drugs that alter thyroid hormone secretion Drugs that may decrease thyroid hormone secretion, which may result in hypothyroidism Aminoglutethimide Amiodarone Iodide (including iodine-containing Radiographic contrast agents) Lithium Methimazole Propylthioracil (PTU) Sulfonamides Tolbutamide Long-term lithium therapy can result in goiter in up to 50% of patients, and either subclinical or overt hypothyroidism, each in up to 20% of patients. Long-term amino-glu-tethimide therapy may minimally decrease T 4 and T 3 levels and increase TSH, although all values remain within normal limits in most patients.