The magnitude and relative importance of the effects noted below are likely to be patient specific and may vary by
such factors as age, gender, race, intercurrent illnesses, dose of either agent, additional concomitant medications,
and timing of drug administration. Any agent that alters thyroid hormone synthesis, secretion, distribution, effect
on target tissues, metabolism, or elimination may alter the optimal therapeutic dose of levothyroxine sodium.
Levoxine Sodium Absorption: The following agents may bind and decrease absorption of
levothyroxine sodium from the gastrointestinal tract: aluminum hydoxide, cholestyramine resin, colestipol
hydrochloride, ferrous sulfate, sodium polystyrene sulfonate, soybean flour (e.g., infant formula),
Binding to Serum Proteins: The following agents may either inhibit levothyroxine sodium binding to
serum proteins or alter the concentrations of serum binding proteins: androgens and related anabolic hormones,
asparaginase, clofibrate, estrogens and estrogen-containing compounds, 5-fluorouracil, furosemide, glucocorticoids,
meclofenamic acid, mefenamic acid, methadone, perphenazine, phenylbutazone, phenytoin, salicylates, tamoxifen.
Thyroid Physiology: The following agents may alter thyroid hormone or TSH levels, generally by
effects on thyroid hormone synthesis, secretion, distribution, metabolism, hormone action, or elimination, or altered
TSH secretion: aminoglutethimide, p-aminosalicylic acid, amiodarone, androgens and related anabolic hormones, complex
anions (thiocyanate, perchlorate, pertechnetate), antithyroid drugs, b-adrenergic blocking
agents, carbamazepine, chloral hydrate, diazepam, dopamine and dopamine agonists, ethionamide, glucocorticoids,
heparin, hepatic enzyme inducers, insulin, iodinated cholestographic agents, iodine- containing compounds, levodopa,
lovastatin, lithium, 6-mercaptopurine, metoclopramide, mitotane, nitroprusside, phenobarbital, phenytoin, resorcinol,
rifampin, somatostatin analogs, sulfonamides, sulfonylureas, thiazide diuretics.
Adrenocorticoids: Metabolic clearance of adrenocorticoids is decreased in hypothyroid patients and
increased in hyperthyroid patients, and may therefore change with changing thyroid status.
Amiodarone: Amiodarone therapy alone can cause hypothyroidism or hyperthyroidism.
Anticoagulants (Oral): The hypoprothrombinemic effect of anticoagulants may be potentiated,
apparently by increased catabloism of vitamin K-dependent clotting factors.
Antidiabetic Agents (Insulin, Sulfonylureas): Requirements for insulin or oral antidiabetic agents
may be reduced in hypothyroid patients with diabetes mellitus and may subsequently increase with the initiation of
thyroid hormone replacement therapy.
b-Adrenergic Blocking Agents: Actions of some of beta-blocking agents may
be impaired when hypothyroid patients become euthyroid.
Cytokines (interferon, interleukin): Cytokines have been reported to induce both hyperthyroidism and
Digitalis Glycosides: Therapeutic effects of digitalis glycosides may be reduced. Serum digitalis
levels may be decreased in hyperthyroidism or when a hypothyroid patient becomes euthyroid.
Ketamine: Marked hypertension and tachycardia have been reported in association with concomitant
administration of levothyroxine sodium and ketamine.
Maprotiline: Risk of cardiac arrhythmias may increase.
Sodium Iodide (123I and 131I), Sodium Pertechnetate Tc99m: Uptake of
radiolabeled ions may be decreased.
Somatrem/Somatropin: Excessive concurrent use of thyroid hormone may accelerate epiphyseal closure.
Untreated hypothyroidism may interfere with the growth response to somatrem or somatropin.
Theophylline: Theophylline clearance may decrease in hypothyroid patients and return toward normal
when a euthyroid state is achieved.
Tricyclic Antidepressants: Concurrent use may increase the therapeutic and toxic effects of both
drugs, possibly due to increased catecholamine sensitivity. Onset of action of tricyclics may be accelerated.
Sympathomimetic Agents: Possible increased risk of coronary insufficiency in patients with coronary