Levothroid

Last updated on RxList: 6/14/2021

Drug Summary

What Is Levothroid?

Levothroid (levothyroxine sodium) is a replacement for a hormone that is normally produced by your thyroid gland to regulate the body's energy and metabolism used to treat hypothyroidism (low thyroid hormone). Levothroid is also used to treat or prevent goiter (enlarged thyroid gland), which can be caused by hormone imbalances, radiation treatment, surgery, or cancer.

What Are Side Effects of Levothroid?

Common side effects of Levothroid include:

  • hair loss during the first few months of treatment. This side effect is usually temporary as your body adjusts to Levothroid.

Contact your doctor if you experience serious side effects of Levothroid including:

  • headache,
  • sleep problems (insomnia),
  • feeling nervous or irritable,
  • fever,
  • hot flashes,
  • sweating,
  • pounding heartbeats or fluttering in your chest,
  • changes in your menstrual periods,
  • appetite changes, or
  • weight changes.

Dosage for Levothroid

For adult hypothyroidism, Levothroid is started at 12.5-125 mcg/day taken orally. Dose may differ with individuals based on age, the presence of cardiovascular disease, tolerance, side effects, and blood levels of thyroid hormone. It may take one to three weeks before effects are seen.

What Drugs, Substances, or Supplements Interact with Levothroid?

Levothroid may interact with calcium carbonate, ferrous sulfate iron supplement, sucralfate, sodium polystyrene sulfonate, antacids that contain aluminum, and cholesterol-lowering drugs. Tell your doctor all medications or supplements you are taking.

Levothroid During Pregnancy or Breastfeeding

Current information shows that Levothroid may be used during pregnancy. Tell your doctor if you are pregnant as your dose may need to be adjusted. This medication passes into breast milk but is unlikely to harm a nursing infant. Consult your doctor before breastfeeding.

Additional Information

Our Levothroid (levothyroxine sodium) Side Effects Drug Center provides a comprehensive view of available drug information on the potential side effects when taking this medication.

Description for Levothroid

LEVOTHROID® (levothyroxine sodium) Tablets, USP contains synthetic crystalline L-3, 3', 5, 5'-tetraiodothyronine sodium salt [levothyroxine (T4) sodium]. Synthetic T4 is identical to that produced in the human thyroid gland. Levothyroxine (T4) sodium has an empirical formula of C15H10I4N NaO4 x H2O, molecular weight of 798. 86 g/mol (anhydrous), and structural formula as shown:

LEVOTHROID® (levothyroxine sodium) Structural Formula Illustration

Inactive Ingredients: Microcrystalline cellulose, calcium phosphate dibasic, povidone and magnesium stearate. The following are the coloring additives per tablet strength.

Strength (mcg) Color additive(s)
25 FD&C Yellow No.6 Aluminum Lake
50 None
75 FD&C Blue No.2 Aluminum Lake, FD&C Red No.40 Aluminum Lake
88 FD&C Yellow No.6 Aluminum Lake, FD&C Blue No.1 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
100 FD&C Yellow No.6 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
112 D&C Red No.27 Aluminum Lake, D&C Red No.30 Aluminum Lake
125 FD&C Blue No.1 Aluminum Lake, FD&C Red No.40 Aluminum Lake, FD&C Yellow No.6 Aluminum Lake
137 FD&C Blue No.1 Aluminum Lake
150 FD&C Blue No.2 Aluminum Lake
175 FD&C Blue No.1 Aluminum Lake, D&C Red No.30 Aluminum Lake, D&C Red No.27 Aluminum Lake
200 FD&C Red No.40 Aluminum Lake
300 FD&C Yellow No.6 Aluminum Lake, FD&C Blue No.1 Aluminum Lake, D&C Yellow No.10 Aluminum Lake

Uses for Levothroid

Levothyroxine sodium is used for the following indications

Hypothyroidism

As replacement or supplemental therapy in congenital or acquired hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. Specific indications include: primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) hypothyroidism and subclinical hypothyroidism. Primary hypothyroidism may result from functional deficiency, primary atrophy, partial or total congenital absence of the thyroid gland, or from the effects of surgery, radiation, or drugs, with or without the presence of goiter.

Pituitary TSH Suppression

In the treatment or prevention of various types of euthyroid goiters (see WARNINGS and PRECAUTIONS), including thyroid nodules (see WARNINGS and PRECAUTIONS), subacute or chronic lymphocytic thyroiditis (Hashimoto's thyroiditis), multinodular goiter (see WARNINGS and PRECAUTIONS) and, as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer.

Dosage for Levothroid

General Principles

The goal of replacement therapy is to achieve and maintain a clinical and biochemical euthyroid state. The goal of suppressive therapy is to inhibit growth and/or function of abnormal thyroid tissue. The dose of LEVOTHROID® (levothyroxine sodium) that is adequate to achieve these goals depends on a variety of factors including the patient's age, body weight, cardiovascular status, concomitant medical conditions, including pregnancy, concomitant medications, and the specific nature of the condition being treated (see WARNINGS and PRECAUTIONS). Hence, the following recommendations serve only as dosing guide-lines. Dosing must be individualized and adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters (see PRECAUTIONS, Laboratory Tests).

LEVOTHROID® (levothyroxine sodium) is administered as a single daily dose, preferably one-half to one hour before breakfast. LEVOTHROID® (levothyroxine sodium) should be taken at least 4 hours apart from drugs that are known to interfere with its absorption (see PRECAUTIONS, DRUG INTERACTIONS).

Due to the long half-life of levothyroxine, the peak therapeutic effect at a given dose of levothyroxine sodium may not be attained for 4-6 weeks. Caution should be exercised when administering LEVOTHROID® (levothyroxine sodium) to patients with underlying cardiovascular disease, to the elderly, and to those with concomitant adrenal insufficiency (see PRECAUTIONS).

Specific Patient Populations

Hypothyroidism in Adults and in Children in Whom Growth and Puberty are Complete

(see WARNINGS and PRECAUTIONS, Laboratory Tests )

Therapy may begin at full replacement doses in otherwise healthy individuals less than 50 years old and in those older than 50 years who have been recently treated for hyperthyroidism or who have been hypothyroid for only a short time (such as a few months). The average full replacement dose of levothyroxine sodium is approximately 1. 7 mcg/kg/day (e. g. , 100-125 mcg/day for a 70 kg adult). Older patients may require less than 1 mcg/kg/day. Levothyroxine sodium doses greater than 200 mcg/day are seldom required. An inadequate response to daily doses ≥ 300 mcg/day is rare and may indicate poor compliance, malabsorption, and/or drug interactions.

For most patients older than 50 years or for patients under 50 years of age with underlying cardiac disease, an initial starting dose of 25-50 mcg/day of levothyroxine sodium is recommended, with gradual increments in dose at 6-8 week intervals, as needed. The recommended starting dose of levothyrox-ine sodium in elderly patients with cardiac disease is 12. 5-25 mcg/day, with gradual dose increments at 4-6 week intervals. The levothyroxine sodium dose is generally adjusted in 12. 5-25 mcg increments until the patient with primary hypothyroidism is clinically euthyroid and the serum TSH has normalized. In patients with severe hypothyroidism, the recommended initial levothyroxine sodium dose is 12. 5-25 mcg/day with increases of 25 mcg/day every 2-4 weeks, accompanied by clinical and laboratory assessment, until the TSH level is normalized.

In patients with secondary (pituitary) or tertiary (hypothalamic) hypothyroidism, the levothyroxine sodium dose should be titrated until the patient is clinically euthyroid and the serum free-T4 level is restored to the upper half of the normal range.

Pediatric Dosage

Congenital or Acquired Hypothyroidism

(see PRECAUTIONS, Laboratory Tests)

General Principles

In general, levothyroxine therapy should be instituted at full replacement doses as soon as possible. Delays in diagnosis and institution of therapy may have deleterious effects on the child's intellectual and physical growth and development.

Undertreatment and overtreatment should be avoided (see PRECAUTIONS, Pediatric Use).

LEVOTHROID® (levothyroxine sodium) may be administered to infants and children who cannot swallow intact tablets by crushing the tablet and suspending the freshly crushed tablet in a small amount (5-10 mL or 1-2 teaspoons) of water. This suspension can be administered by spoon or dropper. DO NOT STORE THE SUSPENSION. Foods that decrease absorption of levothyroxine, such as soybean infant formula, should not be used for administering levothyroxine sodium tablets (see PRECAUTIONS, Drug-Food Interactions).

Newborns

The recommended starting dose of levothyroxine sodium in newborn infants is 10-15 mcg/kg/day. A lower starting dose (e. g. , 25 mcg/day) should be considered in infants at risk for cardiac failure, and the dose should be increased in 4-6 weeks as needed based on clinical and laboratory response to treatment. In infants with very low (< 5 mcg/dL) or undetectable serum T4 concentrations, the recommended initial starting dose is 50 mcg/day of levothy-roxine sodium.

Infants and Children

Levothyroxine therapy is usually initiated at full replacement doses, with the recommended dose per body weight decreasing with age (see Table 3). However, in children with chronic or severe hypothyroidism, an initial dose of 25 mcg/day of levothyroxine sodium is recommended with increments of 25 mcg every 2-4 weeks until the desired effect is achieved.

Hyperactivity in an older child can be minimized if the starting dose is one-fourth of the recommended full replacement dose, and the dose is then increased on a weekly basis by an amount equal to one-fourth the full-recommended replacement dose until the full recommended replacement dose is reached.

Table 3: Levothyroxine Sodium Dosing Guidelines for Pediatric Hypothyroidism

AGE Daily Dose Per Kg Body Weighta
0-3 months 10-15 mcg/kg/day
3-6 months 8-10 mcg/kg/day
6-12 months 6-8 mcg/kg/day
1-5 years 5-6 mcg/kg/day
6-12 years 4-5 mcg/kg/day
> 12 years but growth and puberty incomplete 2-3 mcg/kg/day
Growth and puberty complete 1.7 mcg/kg/day
aThe dose should be adjusted based on clinical response and laboratory parameters (see PRECAUTIONS, Laboratory Tests and Pediatric Use).

Pregnancy

Pregnancy may increase levothyroxine requirements (see Pregnancy).

Subclinical Hypothyroidism

If this condition is treated, a lower levothyroxine sodium dose (e. g. , 1 mcg/kg/day) than that used for full replacement may be adequate to normalize the serum TSH level. Patients who are not treated should be monitored yearly for changes in clinical status and thyroid laboratory parameters.

TSH Suppression in Well-differentiated Thyroid Cancer and Thyroid Nodules

The target level for TSH suppression in these conditions has not been established with controlled studies. In addition, the efficacy of TSH suppression for benign nodular disease is controversial. Therefore, the dose of LEVOTHROID® (levothyroxine sodium) used for TSH suppression should be individualized based on the specific disease and the patient being treated.

In the treatment of well-differentiated (papillary and follicular) thyroid cancer, levothyroxine is used as an adjunct to surgery and radioiodine therapy. Generally, TSH is suppressed to < 0.1 mU/L, and this usually requires a levothyroxine sodium dose of greater than 2 mcg/kg/day. However, in patients with high-risk tumors, the target level for TSH suppression may be < 0.01 mU/L.

In the treatment of benign nodules and nontoxic multinodular goiter, TSH is generally suppressed to a higher target (e. g. , 0.1 to either 0.5 or 1.0 mU/L) than that used for the treatment of thyroid cancer. Levothyroxine sodium is contraindicated if the serum TSH is already suppressed due to the risk of precipitating overt thyrotoxicosis (see CONTRAINDICATIONS, WARNINGS and PRECAUTIONS).

Myxedema Coma

Myxedema coma is a life-threatening emergency characterized by poor circulation and hypometabolism, and may result in unpredictable absorption of levothyroxine sodium from the gastrointestinal tract. Therefore, oral thyroid hormone drug products are not recommended to treat this condition. Thyroid hormone drug products formulated for intravenous administration should be administered.

HOW SUPPLIED

LEVOTHROID® (levothyroxine sodium tablets, USP) are caplet-shaped, color-coded, potency marked tablets and are supplied as follows:

Strength (mcg) Color NDC # for bottles of 100 NDC # for bottles of 1000
25 Orange NDC 0456-1320-01 NDC 0456-1320-00
50 White NDC 0456-1321-01 NDC 0456-1321-00
75 Violet NDC 0456-1322-01 NDC 0456-1322-00
88 Mint Green NDC 0456-1329-01 NDC 0456-1329-00
100 Yellow NDC 0456-1323-01 NDC 0456-1323-00
112 Rose NDC 0456-1330-01 NDC 0456-1330-00
125 Brown NDC 0456-1324-01 NDC 0456-1324-00
137 Deep Blue NDC 0456-1331-01 NDC 0456-1331-00
150 Blue NDC 0456-1325-01 NDC 0456-1325-00
175 Lilac NDC 0456-1326-01 NDC 0456-1326-00
200 Pink NDC 0456-1327-01 NDC 0456-1327-00
300 Green NDC 0456-1328-01 NDC 0456-1328-00

Storage Conditions

Store at 25°C (77°F) with excursions permitted to 15-30°C (59-86°F). Protect from moisture and light.

Manufactured for: Forest Pharmaceuticals, Inc., Subsidiary of Forest Laboratories, Inc.,St. Louis, Missouri, 63045
by: Lloyd Pharmaceutical Division of Lloyd, Inc., Shenandoah, IA 51601
Rev. 09/05 FDA rev date: 03/10/2006

Side Effects for Levothroid

Adverse reactions associated with levothyroxine therapy are primarily those of hyperthyroidism due to therapeutic overdosage (see PRECAUTIONS and OVERDOSAGE). They include the following:

General: fatigue, increased appetite, weight loss, heat intolerance, fever, excessive sweating;

Central nervous system: headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia;

Musculoskeletal: tremors, muscle weakness;

Cardiovascular: palpitations, tachycardia, arrhythmias, increased pulse and blood pressure, heart failure, angina, myocardial infarction, cardiac arrest;

Respiratory: dyspnea;

Gastrointestinal: diarrhea, vomiting, abdominal cramps and elevations in liver function tests;

Dermatologic: hair loss, flushing;

Endocrine: decreased bone mineral density; Reproductive: menstrual irregularities, impaired fertility.

Pseudotumor cerebri and slipped capital femoral epiphysis have been reported in children receiving levothyroxine therapy. Overtreatment may result in craniosynostosis in infants and premature closure of the epiphyses in children with resultant compromised adult height.

Seizures have been reported rarely with the institution of levothyroxine therapy.

Inadequate levothyroxine dosage will produce or fail to ameliorate the signs and symptoms of hypothyroidism.

Hypersensitivity reactions to inactive ingredients have occurred in patients treated with thyroid hormone products. These include urticaria, pruritus, skin rash, flushing, angioedema, various GI symptoms (abdominal pain, nausea, vomiting and diarrhea), fever, arthralgia, serum sickness and wheezing. Hypersensitivity to levothyroxine itself is not known to occur.

Drug Interactions for Levothroid

Many drugs affect thyroid hormone pharmacokinetics and metabolism (e. g. , absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to LEVOTHROID® (levothyroxine sodium) . In addition, thyroid hormones and thyroid status have varied effects on the pharmacokinetics and actions of other drugs. A listing of drug-thyroidal axis interactions is contained in Table 2.

The list of drug-thyroidal axis interactions in Table 2 may not be comprehensive due to the introduction of new drugs that interact with the thyroidal axis or the discovery of previously unknown interactions. The prescriber should be aware of this fact and should consult appropriate reference sources (e. g. , package inserts of newly approved drugs, medical literature) for additional information if a drug-drug interaction with levothyroxine is suspected.

Table 2:Drug-Thyroidal Axis Interactions

Drugs that may reduce TSH secretion - the reduction is not sustained;therefore,hypothyroidism does not occur
Drug or Drug Class
Dopamine / Dopamine Agonists Glucocorticoids Octreotide
Effect - Use of these agents may result in a transient reduction in TSH secretion when administered at the following doses:Dopamine ( ≥ 1µ g/kg/min); Glucocorticoids (hydrocortisone ≥ 100 mg/day or equivalent);Octreotide ( > 100 µg/day).
Drugs that alter thyroid hormone secretion
Drugs that may decrease thyroid hormone secretion,which may result in hypothyroidism
Drug or Drug Class
Aminoglutethimide Iodide Methimazole
Amiodarone (including iodine-containing Radiographic contrast agents) Lithium Propylthiouracil (PTU) Sulfonamides Tolbutamide
Effect - 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. The fetus, neonate, elderly and euthyroid patients with underlying thyroid disease (e.g., Hashimoto's thyroiditis or with Grave's disease previously treated with radioiodine or surgery) are among those individuals who are particularly susceptible to iodine-induced hypothyroidism. Oral chole-cystographic agents and amiodarone are slowly excreted, producing more prolonged hypothyroidism than parenterally administered iodinated contrast agents. Long-term aminoglutethimide therapy may minimally decrease T4 and T3 levels and increase TSH, although all values remain within normal limits in most patients.
Drugs that may increase thyroid hormone secretion,which may result in hyperthyroidism
Drug or Drug Class
Amiodarone
Iodide (including iodine-containing Radiographic contrast agents)
Effect - Iodide and drugs that contain pharmacological amounts of iodide may cause hyperthyroidism in euthyroid patients with Grave's disease previously treated with antithyroid drugs or in euthyroid patients with thyroid autonomy (e.g., multinodular goiter or hyperfunctioning thyroid adenoma). Hyperthyroidism may develop over several weeks and may persist for several months after therapy discontinuation.Amiodarone may induce hyper-thyroidism by causing thyroiditis.
Drugs that may decrease T4 absorption,which may result in hypothyroidism
Drug or Drug Class
Antacids Bile Acid Sequestrants Cation Exchange Resins
- Aluminum & Magnesium - Cholestyramine - Kayexalate
Hydroxides - Colestipol Ferrous Sulfate
- Simethicone Calcium Carbonate Sucralfate
Effect - Concurrent use may reduce the efficacy of levothyroxine by binding and delaying or preventing absorption, potentially resulting in hypothy-roidism.Calcium carbonate may form an insoluble chelate with levothyroxine, and ferrous sulfate likely forms a ferric-thyroxine complex.Administer levothyroxine at least 4 hours apart from these agents.
Drugs that may alter T4 and T3 serum transport - but FT 4 concentration remains normal;and,therefore,the patient remains euthyroid
Drugs that may increase serum TBG concentration
Clofibrate Estrogens (oral) Mitotane
Estrogen-containing Heroin /Methadone Tamoxifen
Oral contraceptives 5-Fluorouracil  
Drugs that may decrease serum TBG concentration
Androgens / Anabolic Steroids Glucocorticoids  
Asparaginase Slow-Release Nicotinic Acid  
Drugs that may cause protein-binding site displacement
Drug or Drug Class
Furosemide ( > 80 mg IV) Non Steroidal Anti-Inflammatory Drugs  
Heparin - Fenamates  
Hydantoins - Phenylbutazone  
  Salicylates ( > 2 g/day)  
Effect - Administration of these agents with levothyroxine results in an initial transient increase in FT4.Continued administration results in a decrease in serum T4 and normal FT4 and TSH concentrations and, therefore, patients are clinically euthyroid. Salicylates inhibit binding of T4 and T3 to TBG and transthyretin.An initial increase in serum FT4 is followed by return of FT4 to normal levels with sustained therapeutic serum salicylate concentrations, although total-T4 levels may decrease by as much as 30%.
Drugs that may alter T4 and T3 metabolism
Drugs that may increase hepatic metabolism,which may result in hypothyroidism
Drug or Drug Class
Carbamazepine Hydantoins Phenobarbital Rifampin
Effect - Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased levothyroxine requirements. Phenytoin and carbamazepine reduce serum protein binding of levothyroxine, and total- and free-T4 may bereduced by 20% to 40%, but most patients have normal serum TSH levels and are clinically euthyroid.
Drugs that may decrease T4 5'-deiodinase activity
Drug or Drug Class    
Amiodarone    
Beta-adrenergic antagonists Glucocorticoids  
- (e.g., Propranolol > 160 mg/day) - (e.g., Dexamethasone ≥ 4 mg/day) Propylthiouracil (PTU)  
Effect - Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels.However, serum T4 levels are usually normal but may occasionally be slightly increased. In patients treated with large doses of propranolol ( > 160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and patients are clinically euthyroid.It should be noted that actions ofparticular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state.Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels.However, long-term glucocor-ticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (see above).
Miscellaneous
Drug or Drug Class
Anticoagulants (oral)    
- Coumarin Derivatives - Indandione Derivatives  
Effect - Thyroid hormones appear to increase the catabolism of vitamin K-dependent clotting factors, thereby increasing the anticoagulant activity of oral anticoagulants. Concomitant use of these agents impairs the compensatory increases in clotting factor synthesis. Prothrombin time should be carefully monitored in patients taking levothyroxine and oral anticoagulants and the dose of anticoagulant therapy adjusted accordingly.
Drug or Drug Class
Antidepressants    
- Tricyclics (e.g., Amitriptyline) - Selective Serotonin Reuptake Inhibitors  
- Tetracyclics (e.g., Maprotiline) (SSRIs;e.g., Sertraline)  
Effect - Concurrent use of tri/tetracyclic antidepressants and levothyroxine may increase the therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines.Toxic effects may include increased risk of cardiac arrhythmias and CNS stimulation;onset of action of tricyclics may be accelerated.Administration of sertraline in patients stabilized on levothyroxine may result in increased levothyroxine requirements.
Drug or Drug Class
Antidiabetic Agents - Meglitinides - Sulfonylureas
- Biguanides - Thiazolidinediones - Insulin
Effect - Addition of levothyroxine to antidiabetic or insulin therapy may result in increased antidiabetic agent or insulin requirements.Careful monitoring of diabetic control is recommended, especially when thyroid therapy is started, changed, or discontinued.
Drug or Drug Class
Cardiac Glycosides    
Effect - Serum digitalis glycoside levels may be reduced in hyperthyroidism or when the hypothyroid patient is converted to the euthyroid state. Therapeutic effect of digitalis glycosides may be reduced.
Drug or Drug Class
Cytokines - Interferon-α - Interleukin-2
Effect - Therapy with interferon-α has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both.Patients who have antithyroid antibodies before treatment are at higher risk for thyroid dysfunction during treatment.Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients.Interferon-β and -γ have not been reported to cause thyroid dysfunction.
Drug or Drug Class
Growth Hormones - Somatrem - Somatropin
Effect - Excessive use of thyroid hormones with growth hormones may accelerate epiphyseal closure. However, untreated hypothyroidism may interfere with growth response to growth hormone.
Drug or Drug Class
Ketamine    
Effect - Concurrent use may produce marked hypertension and tachycardia;cautious administration to patients receiving thyroid hormone therapy is recommended.
Drug or Drug Class
Methylxanthine Bronchodilators - (e.g., Theophylline)  
Effect - Decreased theophylline clearance may occur in hypothyroid patients; clearance returns to normal when the euthyroid state is achieved.
Drug or Drug Class
Radiographic Agents    
Radiographic Agents
Effect - Thyroid hormones may reduce the uptake of 123I, 131I, and 99mTc.
Drug or Drug Class
Sympathomimetics    
Effect - Concurrent use may increase the effects of sympathomimetics or thyroid hormone.Thyroid hormones may increase the risk of coronary insufficiency when sympathomimetic agents are administered to patients with coronary artery disease.
Drug or Drug Class
Chloral Hydrate Metoclopramide Perphenazine
Diazepam 6-Mercaptopurine Resorcinol
Ethionamide Nitroprusside (excessive topical use)
Lovastatin Para-aminosalicylate sodium Thiazide Diuretics
Effect - These agents have been associated with thyroid hormone and / or TSH level alterations by various mechanisms.

Oral anticoagulants

Levothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the LEVOTHROID® (levothyroxine sodium) dose is increased. Prothrombin time should be closely monitored to permit appropriate and timely dosage adjustments (see Table 2).

Digitalis glycosides

The therapeutic effects of digitalis glycosides may be reduced by levothyroxine. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides (see Table 2).

Drug-Food Interactions

Consumption of certain foods may affect levothyroxine absorption thereby necessitating adjustments in dosing. Soybean flour (infant formula), cotton seed meal, walnuts, and dietary fiber may bind and decrease the absorption of levothyroxine sodium from the GI tract.

Drug-Laboratory Test Interactions

Changes in TBG concentration must be considered when interpreting T4 and T3 values, which necessitates measurement and evaluation of unbound (free) hormone and/or determination of the free-T4 index (FT4I). Pregnancy, infectious hepatitis, estrogens, estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations. Decreases in TBG concentrations are observed in nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, and after androgen or corticosteroid therapy (see also Table 2). Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9000.

Warnings for Levothroid

WARNING : Thyroid hormones, including LEVOTHROID® (levothyroxine sodium) , either alone or with other therapeutic agents, should not be used for the treatment of obesity or for weight loss. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduc-tion. Larger doses may produce serious or even life threatening manifestations of toxicity, particularly when given in association with sym-pathomimetic amines such as those used for their anorectic effects.

Levothyroxine sodium should not be used in the treatment of male or female infertility unless this condition is associated with hypothyroidism. In patients with nontoxic diffuse goiter or nodular thyroid disease, particularly the elderly or those with underlying cardiovascular disease, levothyroxine sodium therapy is contraindicated if the serum TSH level is already suppressed due to the risk of precipitating overt thyrotoxicosis (see CONTRAINDICATIONS). If the serum TSH level is not suppressed, LEVOTHROID® (levothyroxine sodium) should be used with caution in conjunction with careful monitoring of thyroid function for evidence of hyperthyroidism and clinical monitoring for potential associated adverse cardiovascular signs and symptoms of hyperthyroidism.

Precautions for Levothroid

General

Levothyroxine has a narrow therapeutic index. Regardless of the indication for use, careful dosage titration is necessary to avoid the consequences of over-or under-treatment. These consequences include, among others, effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function, and on glucose and lipid metabolism. Many drugs interact with levothyroxine sodium, necessitating adjustments in dosing to maintain therapeutic response (see DRUG INTERACTIONS).

Effects on bone mineral density

In women, long-term levothyroxine sodium therapy has been associated with increased bone resorption, thereby decreasing bone mineral density, especially in post-menopausal women on greater than replacement doses or in women who are receiving suppressive doses of levothyroxine sodium. The increased bone resorption may be associated with increased serum levels and urinary excretion of calcium and phosphorous, elevations in bone alkaline phosphatase and suppressed serum parathyroid hormone levels. Therefore, it is recommended that patients receiving levothyroxine sodium be given the minimum dose necessary to achieve the desired clinical and biochemical response.

Patients with underlying cardiovascular disease

Exercise caution when administering levothyroxine to patients with cardiovascular disorders and to the elderly in whom there is an increased risk of occult cardiac disease. In these patients, levothyroxine therapy should be initiated at lower doses than those recommended in younger individuals or in patients without cardiac disease (see WARNINGS; PRECAUTIONS, Geriatric Use;and DOSAGE AND ADMINISTRATION). If cardiac symptoms develop or worsen, the levothyroxine dose should be reduced or withheld for one week and then cautiously restarted at a lower dose. Overtreatment with levothyroxine sodium may have adverse cardiovascular effects such as an increase in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias. Patients with coronary artery disease who are receiving levothyrox-ine therapy should be monitored closely during surgical procedures, since the possibility of precipitating cardiac arrhythmias may be greater in those treated with levothyroxine. Concomitant administration of levothyroxine and sympathomimetic agents to patients with coronary artery disease may precipitate coronary insufficiency.

Patients with nontoxic diffuse goiter or nodular thyroid disease

Exercise caution when administering levothyroxine to patients with nontoxic diffuse goiter or nodular thyroid disease in order to prevent precipitation of thyrotoxicosis (see WARNINGS). If the serum TSH is already suppressed, levothyrox-ine sodium should not be administered (see CONTRAINDICATIONS).

Associated endocrine disorders

Hypothalamic/pituitary hormone deficiencies

In patients with secondary or tertiary hypothyroidism, additional hypothalamic/pituitary hormone deficiencies should be considered, and, if diagnosed, treated (see PRECAUTIONS, Autoimmune polyglandular syndrome for adrenal insufficiency).

Autoimmune polyglandular syndrome

Occasionally, chronic autoimmune thyroiditis may occur in association with other autoimmune disorders such as adrenal insufficiency, pernicious anemia, and insulin-dependent diabetes mellitus. Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with levothyroxine sodium. Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated, due to increased metabolic clearance of glucocorticoids by thyroid hormone. Patients with diabetes mellitus may require upward adjustments of their antidiabetic therapeutic regimens when treated with levothyroxine (see PRECAUTIONS, DRUG INTERACTIONS).

Other associated medical conditions

Infants with congenital hypothyroidism appear to be at increased risk for other congenital anomalies, with cardiovascular anomalies (pulmonary stenosis, atrial septal defect, and ventricular septal defect) being the most common association.

Laboratory Tests

General

The diagnosis of hypothyroidism is confirmed by measuring TSH levels using a sensitive assay (second generation assay sensitivity ≤ 0. 1 mIU/L or third generation assay sensitivity ≤ 0. 01 mIU/L) and measurement of free-T4.

The adequacy of therapy is determined by periodic assessment of appropriate laboratory tests and clinical evaluation. The choice of laboratory tests depends on various factors including the etiology of the underlying thyroid disease, the presence of concomitant medical conditions, including pregnancy, and the use of concomitant medications (see PRECAUTIONS, DRUG INTERACTIONS and Drug-Laboratory Test Interactions). Persistent clinical and laboratory evidence of hypothyroidism despite an apparent adequate replacement dose of LEVOTHROID® (levothyroxine sodium) may be evidence of inadequate absorption, poor compliance, drug interactions, or decreased T4 potency of the drug product.

Adults

In adult patients with primary (thyroidal) hypothyroidism, serum TSH levels (using a sensitive assay) alone may be used to monitor therapy. The frequency of TSH monitoring during levothyroxine dose titration depends on the clinical situation but it is generally recommended at 6-8 week intervals until nor-malization. For patients who have recently initiated levothyroxine therapy and whose serum TSH has normalized or in patients who have had their dosage of levothyroxine changed, the serum TSH concentration should be measured after 8-12 weeks. When the optimum replacement dose has been attained, clinical (physical examination) and biochemical monitoring may be performed every 6-12 months, depending on the clinical situation, and whenever there is a change in the patient's status. It is recommended that a physical examination and a serum TSH measurement be performed at least annually in patients receiving LEVOTHROID® (levothyroxine sodium) (see WARNINGS, PRECAUTIONS, and DOSAGE AND ADMINISTRATION).

Pediatrics

In patients with congenital hypothyroidism, the adequacy of replacement therapy should be assessed by measuring both serum TSH (using a sensitive assay) and total- or free-T4. During the first three years of life, the serum total- or free-T4 should be maintained at all times in the upper half of the normal range. While the aim of therapy is to also normalize the serum TSH level, this is not always possible in a small percentage of patients, particularly in the first few months of therapy. TSH may not normalize due to a resetting of the pituitary-thyroid feedback threshold as a result of in utero hypothy-roidism. Failure of the serum T4 to increase into the upper half of the normal range within 2 weeks of initiation of LEVOTHROID® (levothyroxine sodium) therapy and/or of the serum TSH to decrease below 20mU/L within 4 weeks should alert the physician to the possibility that the child is not receiving adequate therapy. Careful inquiry should then be made regarding compliance, dose of medication administered, and method of administration prior to raising the dose of LEVOTHROID® (levothyroxine sodium) .

The recommended frequency of monitoring of TSH and total- or free-T4 in children is as follows: at 2 and 4 weeks after the initiation of treatment;every 1-2 months during the first year of life;every 2-3 months between 1 and 3 years of age;and every 3 to 12 months thereafter until growth is completed. More frequent intervals of monitoring may be necessary if poor compliance is suspected or abnormal values are obtained. It is recommended that TSH and T4 levels, and a physical examination, if indicated, be performed 2 weeks after any change in LEVOTHROID® (levothyroxine sodium) dosage. Routine clinical examination, including assessment of mental and physical growth and development, and bone maturation, should be performed at regular intervals (see PRECAUTIONS, Pediatric Use and DOSAGE AND ADMINISTRATION).

Secondary (pituitary) and tertiary (hypothalamic) hypothyroidism

Adequacy of therapy should be assessed by measuring serum free-T4 levels, which should be maintained in the upper half of the normal range in these patients.

Carcinogenesis, Mutagenesis, and Impairment of Fertility

Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of levothyroxine. The synthetic T4 in LEVOTHROID® (levothyroxine sodium) is identical to that produced naturally by the human thyroid gland. Although there has been a reported association between prolonged thyroid hormone therapy and breast cancer, this has not been confirmed. Patients receiving LEVOTHROID® (levothyroxine sodium) for appropriate clinical indications should be titrated to the lowest effective replacement dose.

Pregnancy

Category A

Studies in women taking levothyroxine sodium during pregnancy have not shown an increased risk of congenital abnormal-ities. Therefore, the possibility of fetal harm appears remote. LEVOTHROID® (levothyroxine sodium) should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated.

Hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, pre-eclampsia, stillbirth and premature delivery. Maternal hypothyroidism may have an adverse effect on fetal and childhood growth and development. During pregnancy, serum T4 levels may decrease and serum TSH levels increase to values outside the normal range. Since elevations in serum TSH may occur as early as 4 weeks gestation, pregnant women taking LEVOTHROID® (levothyroxine sodium) should have their TSH measured during each trimester. An elevated serum TSH level should be corrected by an increase in the dose of LEVOTHROID® (levothyroxine sodium) . Since postpartum TSH levels are similar to preconception values, the LEVOTHROID® (levothyroxine sodium) dosage should return to the pre-pregnancy dose immediately after delivery. A serum TSH level should be obtained 6-8 weeks postpartum.

Thyroid hormones cross the placental barrier to some extent as evidenced by levels in cord blood of athyreotic fetuses being approximately one-third maternal levels. Transfer of thyroid hormone from the mother to the fetus, however, may not be adequate to prevent in utero hypothyroidism.

Nursing Mothers

Although thyroid hormones are excreted only minimally in human milk, caution should be exercised when LEVOTHROID® (levothyroxine sodium) is administered to a nursing woman. However, adequate replacement doses of levothyroxine are generally needed to maintain normal lactation.

Pediatric Use

General

The goal of treatment in pediatric patients with hypothyroidism is to achieve and maintain normal intellectual and physical growth and development. The initial dose of levothyroxine varies with age and body weight (see DOSAGE AND ADMINISTRATION, Table 3). Dosing adjustments are based on an assessment of the individual patient's clinical and laboratory parameters (see PRECAUTIONS, Laboratory Tests).

In children in whom a diagnosis of permanent hypothyroidism has not been established, it is recommended that levothyroxine administration be discontinued for a 30-day trial period, but only after the child is at least 3 years of age. Serum T4 and TSH levels should then be obtained. If the T4 is low and the TSH high, the diagnosis of permanent hypothyroidism is established, and levothyroxine therapy should be reinstituted. If the T4 and TSH levels are normal, euthyroidism may be assumed and, therefore, the hypothyroidism can be considered to have been transient. In this instance, however, the physician should carefully monitor the child and repeat the thyroid function tests if any signs or symptoms of hypothyroidism develop. In this setting, the clinician should have a high index of suspicion of relapse. If the results of the levothyroxine withdrawal test are inconclusive, careful follow-up and subsequent testing will be necessary.

Since some more severely affected children may become clinically hypothyroid when treatment is discontinued for 30 days, an alternate approach is to reduce the replacement dose of levothyroxine by half during the 30-day trial period. If, after 30 days, the serum TSH is elevated above 20 mU/L, the diagnosis of permanent hypothyroidism is confirmed, and full replacement therapy should be resumed. However, if the serum TSH has not risen to greater than 20 mU/L, levothyroxine treatment should be discontinued for another 30-day trial period followed by repeat serum T4 and TSH testing.

The presence of concomitant medical conditions should be considered in certain clinical circumstances and, if present, appropriately treated (see PRECAUTIONS).

Congenital Hypothyroidism

(see PRECAUTIONS, Laboratory Tests and DOSAGE AND ADMINISTRATION)

Rapid restoration of normal serum T4 concentrations is essential for preventing the adverse effects of congenital hypothyroidism on intellectual development as well as on overall physical growth and maturation. Therefore, LEVOTHROID® (levothyroxine sodium) therapy should be initiated immediately upon diagnosis and is generally continued for life.

During the first 2 weeks of LEVOTHROID® (levothyroxine sodium) therapy, infants should be closely monitored for cardiac overload, arrhythmias, and aspiration from avid suckling.

The patient should be monitored closely to avoid undertreatment or overtreatment. Undertreatment may have deleterious effects on intellectual development and linear growth. Overtreatment has been associated with craniosynostosis in infants, and may adversely affect the tempo of brain maturation and accelerate the bone age with resultant premature closure of the epiphyses and compromised adult stature.

Acquired Hypothyroidism in Pediatric Patients

The patient should be monitored closely to avoid undertreatment and overtreatment. Undertreatment may result in poor school performance due to impaired concentration and slowed mentation and in reduced adult height. Overtreatment may accelerate the bone age and result in premature epiphy-seal closure and compromised adult stature.

Treated children may manifest a period of catch-up growth, which may be adequate in some cases to normalize adult height. In children with severe or prolonged hypothyroidism, catch-up growth may not be adequate to normalize adult height.

Geriatric Use

Because of the increased prevalence of cardiovascular disease among the elderly, levothyroxine therapy should not be initiated at the full replacement dose (see WARNINGS, PRECAUTIONS, and DOSAGE AND ADMINISTRATION).

Overdose Information for Levothroid

The signs and symptoms of overdosage are those of hyperthyroidism (see PRECAUTIONS and ADVERSE REACTIONS). In addition, confusion and disorientation may occur. Cerebral embolism, shock, coma, and death have been reported. Seizures have occurred in a child ingesting 18 mg of levothy-roxine. Symptoms may not necessarily be evident or may not appear until several days after ingestion of levothyroxine sodium.

Treatment of Overdosage

Levothyroxine sodium should be reduced in dose or temporarily discontinued if signs or symptoms of overdosage occur.

Acute Massive Overdosage

This may be a life-threatening emergency, therefore, symptomatic and supportive therapy should be instituted immediately. If not contraindicated (e. g. , by seizures, coma, or loss of the gag reflex), the stomach should be emptied by emesis or gastric lavage to decrease gastrointestinal absorption. Activated charcoal or cholestyramine may also be used to decrease absorption. Central and peripheral increased sympathetic activity may be treated by administering β-receptor antagonists, e. g. , propranolol, provided there are no medical contraindications to their use. Provide respiratory support as needed;control congestive heart failure and arrhythmia;control fever, hypoglycemia, and fluid loss as necessary. Large doses of antithyroid drugs (e. g. , methimazole or propylthiouracil) followed in one to two hours by large doses of iodine may be given to inhibit synthesis and release of thyroid hormones. Glucocorticoids may be given to inhibit the conversion of T4 to T3. Plasmapheresis, charcoal hemoperfusion and exchange transfusion have been reserved for cases in which continued clinical deterioration occurs despite conventional therapy. Because T4 is highly protein bound, very little drug will be removed by dialysis.

Contraindications for Levothroid

Levothyroxine is contraindicated in patients with untreated subclinical (suppressed serum TSH level with normal T3 and T4 levels) or overt thyrotoxico-sis of any etiology and in patients with acute myocardial infarction. Levothyroxine is contraindicated in patients with uncorrected adrenal insufficiency since thyroid hormones may precipitate an acute adrenal crisis by increasing the metabolic clearance of glucocorticoids (see PRECAUTIONS). LEVOTHROID® (levothyroxine sodium) is contraindicated in patients with hypersensitivity to any of the inactive ingredients in LEVOTHROID® tablets (see DESCRIPTION, Inactive Ingredients).

Clinical Pharmacology for Levothroid

Thyroid hormone synthesis and secretion is regulated by the hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone (TRH) released from the hypothalamus stimulates secretion of thyrotropin-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is the physiologic stimulus for the synthesis and secretion of thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), by the thyroid gland. Circulating serum T3 and T4 levels exert a feedback effect on both TRH and TSH secretion. When serum T3 and T4 levels increase, TRH and TSH secretion decrease. When thyroid hormone levels decrease, TRH and TSH secretion increase.

The mechanisms by which thyroid hormones exert their physiologic actions are not completely understood, but it is thought that their principal effects are exerted through control of DNA transcription and protein synthesis. T3 and T4 diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins. Thyroid hormones regulate multiple metabolic processes and play an essential role in normal growth and development, and normal maturation of the central nervous system and bone. The metabolic actions of thyroid hormones include augmentation of cellular respiration and thermogenesis, as well as metabolism of proteins, carbohydrates and lipids. The protein anabolic effects of thyroid hormones are essential to normal growth and development. The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deio-dination in peripheral tissues.

Levothyroxine, at doses individualized according to patient response, is effective as replacement or supplemental therapy in hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.

Levothyroxine is also effective in the suppression of pituitary TSH secretion in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, Hashimoto's thyroiditis, multinodular goiter and, as adjunctive therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer (see INDICATIONS AND USAGE, PRECAUTIONS, DOSAGE AND ADMINISTRATION).

Pharmacokinetics

Absorption

Absorption of orally administered T4 from the gastrointestinal (GI) tract ranges from 40% to 80%. The majority of the levothyroxine dose is absorbed from the jejunum and upper ileum. The relative bioavailability of LEVOTHROID® (levothyroxine sodium) tablets, compared to an equal nominal dose of oral levothy-roxine sodium solution, is approximately 94%. T4 absorption is increased by fasting, and decreased in malabsorption syndromes and by certain foods such as soybean infant formula. Dietary fiber decreases bioavailability of T4. Absorption may also decrease with age. In addition, many drugs and foods affect T4 absorption (see PRECAUTIONS, DRUG INTERACTIONS and Drug-Food Interactions).

Distribution

Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and albumin (TBA), whose capacities and affinities vary for each hormone. The higher affinity of both TBG and TBPA for T4 partially explains the higher serum levels, slower metabolic clearance, and longer half-life of T4 compared to T3. Protein-bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins (see PRECAUTIONS, DRUG INTERACTIONS and Drug-Laboratory Test Interactions). Thyroid hormones do not readily cross the placental barrier (see PRECAUTIONS, Pregnancy).

Metabolism

T4 is slowly eliminated (see Table 1). The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty-percent of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80% of the daily dose of T4 is deiodi-nated to yield equal amounts of T3 and reverse T3 (rT3). T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation.

Elimination

Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. Approximately 20% of T4 is eliminated in the stool. Urinary excretion of T4 decreases with age.

Table 1:Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients

Hormone Ratio in Thyroglobulin Biologic
Potency

(days)
Protein
Binding (%)2
Levothyroxine (T4) 10 - 20 1 6-71 99.96
Liothyronine (T3) 1 4 ≤ 2 99.5
13 to 4 days in hyperthyroidism, 9 to 10 days in hypothyroidism;
2 Includes TBG, TBPA, and TBA

Patient Information for Levothroid

Patients should be informed of the following information to aid in the safe and effective use of LEVOTHROID® (levothyroxine sodium) :

  1. Notify your physician if you are allergic to any foods or medicines, are pregnant or intend to become pregnant, are breast-feeding or are taking any other medications, including prescription and over-the-counter preparations.
  2. Notify your physician of any other medical conditions you may have, particularly heart disease, diabetes, clotting disorders, and adrenal or pituitary gland problems. Your dose of medications used to control these other conditions may need to be adjusted while you are taking LEVOTHROID® (levothyroxine sodium) . If you have diabetes, monitor your blood and/or urinary glucose levels as directed by your physician and immediately report any changes to your physi-cian. If you are taking anticoagulants (blood thinners), your clotting status should be checked frequently.
  3. Use LEVOTHROID® (levothyroxine sodium) only as prescribed by your physician. Do not discontinue or change the amount you take or how often you take it, unless directed to do so by your physician.
  4. The levothyroxine in LEVOTHROID® (levothyroxine sodium) is intended to replace a hormone that is normally produced by your thyroid gland. Generally, replacement therapy is to be taken for life, except in cases of transient hypothyroidism, which is usually associated with an inflammation of the thyroid gland (thyroiditis).
  5. Take LEVOTHROID® (levothyroxine sodium) as a single dose, preferably on an empty stomach, one-half to one hour before breakfast. Levothyroxine absorption is increased on an empty stomach.
  6. It may take several weeks before you notice an improvement in your symptoms.
  7. Notify your physician if you experience any of the following symptoms: rapid or irregular heartbeat, chest pain, shortness of breath, leg cramps, headache, nervousness, irritability, sleeplessness, tremors, change in appetite, weight gain or loss, vomiting, diarrhea, excessive sweating, heat intolerance, fever, changes in menstrual periods, hives or skin rash, or any other unusual medical event.
  8. Notify your physician if you become pregnant while taking LEVOTHROID® (levothyroxine sodium) . It is likely that your dose of LEVOTHROID® (levothyroxine sodium) will need to be increased while you are pregnant.
  9. Notify your physician or dentist that you are taking LEVOTHROID® (levothyroxine sodium) prior to any surgery.
  10. Partial hair loss may occur rarely during the first few months of LEVOTHROID® (levothyroxine sodium) therapy, but this is usually temporary.
  11. LEVOTHROID® (levothyroxine sodium) should not be used as a primary or adjunctive therapy in a weight control program.
  12. Keep LEVOTHROID® (levothyroxine sodium) out of the reach of children. Store LEVOTHROID® (levothyroxine sodium) away from heat, moisture, and light.
  13. Agents such as iron and calcium supplements and antacids can decrease the absorption of levothyroxine sodium tablets. Therefore, levothyroxine sodium tablets should not be administered within 4 hrs of these agents.
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