Eltroxin

Drug Interactions

Drug-Food Interactions

Anticoagulants

Drug-Laboratory Test Interactions

Digitalis Glycosides

ELTROXIN

Drug-Thyroidal Axis Interactions

Overview

Information for the Patient

Eltroxin

Dosage and Administration

ELTROXIN

Levothyroxine Sodium Dosing Guidelines for Pediatric Hypothyroidism

TSH Suppression in Thyroid Cancer and Thyroid Nodules

Recommended Dose and Dosage Adjustment

Adult Dosage

Administration

Missed Dose

Myxedema Coma

Dosing Considerations

Pediatric Dosage

Pediatrics

Hypothyroidism

Congenital or Acquired Hypothyroidism

Adverse Reactions

Endocrine System

General

Gastrointestinal System

Respiratory System

Adverse Drug Reaction Overview

Central Nervous System

Musculoskeletal System

Reproductive System

Dermatologic

Cardiovascular System

Indications and Clinical Use

ELTROXIN (levothyroxine sodium) is indicated as:

• replacement or supplemental therapy in patients of any age or state (including pregnancy) with hypothyroidism of any etiology except transient hypothyroidism during the recovery phase of subacute thyroiditis;

  
  

• Specific indications are: primary hypothyroidism resulting from thyroid dysfunction, primary atrophy, or partial or total absence of thyroid gland, or from the effects of surgery, radiation or drugs, with or without the presence of goiter, including subclinical hypothyroidism; secondary (pituitary) hypothyroidism; and tertiary (hypothalamic) hypothyroidism;

  
  

• A pituitary TSH suppressant in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto's), multinodular goiter, and in conjunction with surgery and radioactive iodine therapy in the management of thyrotropin-dependent well-differentiated papillary or follicular carcinoma of the thyroid.

  Overdosage

  Treatment of Overdosage

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

  
  

  In the treatment of acute massive levothyroxine sodium overdosage, symptomatic and supportive therapy should be instituted immediately. Treatment is aimed at reducing gastrointestinal absorption and counteracting central and peripheral effects, mainly those of increased sympathetic activity. Cholestyramine and activated charcoal have also been used to decrease levothyroxine sodium absorption. Beta-receptor antagonists, particularly propranolol, are useful in counteracting many of the effects of increased central and peripheral sympathetic activity, especially when no contraindications exist for its 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, carbimazole, or propylthiouracil) followed in one to two hours by large doses of iodine may be given to inhibit synthesis and release of thyroid hormones. Cardiac glycosides may be administered if congestive heart failure develops. Glucocorticoids may be administered 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. Since T₄ is extensively protein bound, very little drug will be removed by dialysis.

  Signs and Symptoms

  Excessive doses of ELTROXIN (levothyroxine sodium) result in a hypermetabolic state indistinguishable from thyrotoxicosis of endogenous origin. Signs and symptoms of thyrotoxicosis include exophthalmic goiter, weight loss, increased appetite, palpitations, nervousness, diarrhea, abdominal cramps, sweating, tachycardia, increased pulse and blood pressure, cardiac arrhythmias, angina pectoris, tremors, insomnia, heat intolerance, fever, and menstrual irregularities. 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 levothyroxine. Symptoms are not always evident or may not appear until several days after ingestion of levothyroxine sodium.

  
  
  

  Dosage Forms, Composition and Packaging

  150 µg

  Each blue, scored, round tablet, engraved with “150”, contains: levothyroxine sodium 150 µg. Nonmedicinal ingredients: acacia powder, colorcon blue, cornstarch, lactose and magnesium stearate. Gluten- and tartrazine-free. Bottles of 500.

  50 µg

  Each white, scored, round tablet, engraved with “50”, contains: levothyroxine sodium USP 50 µg. Nonmedicinal ingredients: acacia powder, cornstarch, lactose and magnesium stearate. Gluten- and tartrazine-free. Bottles of 500.

  100 µg

  Each yellow, scored, round tablet, engraved with “100”, contains: levothyroxine sodium 100 µg. Nonmedicinal ingredients: acacia powder, colorcon yellow, cornstarch, lactose and magnesium stearate. Gluten- and tartrazine-free. Bottles of 500.

  300 µg

  Each green, scored, round tablet, engraved with “300”, contains: levothyroxine sodium 300 µg. Nonmedicinal ingredients: acacia powder, colorcon green, cornstarch, lactose and magnesium stearate. Gluten- and tartrazine-free. Bottles of 100 and 500.

  200 µg

  Each pink, scored, round tablet, engraved with “200”, contains: levothyroxine sodium 200 µg. Nonmedicinal ingredients: acacia powder, cornstarch, erythrosine, lactose and magnesium stearate. Gluten- and tartrazine-free. Bottles of 500.

  
  
  

  Warnings and Precautions

  Carcinogenesis and Mutagenesis

  Although animal studies to determine the mutagenic or carcinogenic potential of thyroid hormones have not been performed, synthetic T₄ is identical to that produced by the human thyroid gland. A reported association between prolonged thyroid hormone therapy and breast cancer has not been confirmed and patients receiving levothyroxine sodium for established indications should not discontinue therapy.

  Acquired Hypothyroidism

  The initial levothyroxine sodium dose varies with age and body weight, and should be adjusted to maintain serum total T₄ or free T₄ levels in the upper half of the normal range. In general, unless there are overriding clinical concerns, children should be started on a full replacement dose. Children with underlying heart disease should be started at lower dosages, with careful upward titration. Children with severe, longstanding hypothyroidism may also be started on a lower initial dose followed by an upward titration, attempting to avoid premature epiphyseal closure. The recommended dose per body weight decreases with age (see Dosage and Administration, Recommended Dose and Dosage Adjustment, Pediatric Dosage, Table 2).

  
  

  Treated children may resume growth at a greater than normal rate (period of transient catch-up growth). In some cases the catch-up may be adequate to normalize growth. However, severe and prolonged hypothyroidism may reduce adult height. Excessive thyroxine replacement may initiate accelerated bone maturation, producing disproportionate skeletal age advancement and shortened adult stature.

  
  

  If transient hypothyroidism is suspected hypothyroidism permanence may be assessed after the child reaches 3 years of age. Levothyroxine therapy may be interrupted for 30 days and serum T₄ and TSH measured. Low T₄ and elevated TSH confirm permanent hypothyroidism; therapy should be re-instituted. If T₄ and TSH remain in the normal range, a presumptive diagnosis of transient hypothyroidism can be made. In this instance, continued clinical monitoring and periodic thyroid function test reevaluation may be warranted.

  
  

  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 sodium 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 sodium treatment should be discontinued for another 30-day trial period followed by repeat serum T₄ and TSH testing.

  Pediatrics (All ages including neonates)

  
  
  

  Associated Endocrine Disorders

  
  
  

  Patients with Nontoxic Diffuse Goiter or Nodular Thyroid Disease

  In patients with non-toxic diffuse goiter or nodular thyroid disease, particularly the elderly or those with underlying cardiovascular disease, levothyroxine 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, 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.

  Geriatrics (>50 years of age)

  Because of the increased prevalence of cardiovascular disease among the elderly, levothyroxine therapy should not be initiated at the full replacement dose (see Warnings and Precautions and Dosage and Administration).

  Pregnant Women

  Studies in pregnant women have not shown that levothyroxine sodium increases the risk of fetal abnormalities if administered during pregnancy. If levothyroxine sodium is used during pregnancy, the possibility of fetal harm appears remote.

  
  

  Thyroid hormones cross the placental barrier to some extent. T₄ levels in the cord blood of athyroid fetuses have been shown to be about one-third of maternal levels. Nevertheless, maternal-fetal transfer of T₄ may not prevent in utero hypothyroidism.

  
  

  Hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, preeclampsia, stillbirth and premature delivery. Maternal hypothyroidism may have an adverse effect on fetal and childhood growth and development. On the basis of current knowledge, levothyroxine sodium should therefore not be discontinued during pregnancy, and hypothyroidism diagnosed during pregnancy should be treated. Studies have shown that during pregnancy T₄ concentrations may decrease and TSH concentrations may increase to values outside normal ranges. Postpartum values are similar to preconception values. Elevations in TSH may occur as early as the fourth week of gestation.

  
  

  Pregnant women who are maintained on levothyroxine sodium should have their TSH measured periodically. An elevated TSH should be corrected by an increase in levothyroxine sodium dose. After pregnancy, the dose can be decreased to the optimal preconception dose. A serum TSH level should be obtained six to eight weeks postpartum.

  Autoimmune Polyglandular Syndrome

  Use of levothyroxine sodium in patients with concomitant diabetes mellitus, diabetes insipidus or adrenal cortical insufficiency may aggravate the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases may therefore be required. Treatment of myxedema coma may require simultaneous administration of glucocorticoids (see Dosage and Administration).

  Congenital Hypothyroidism

  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.

  
  

  Rapid restoration of normal serum T₄ concentrations is essential to prevent deleterious neonatal thyroid hormone deficiency effects on intelligence, overall growth, and development. Treatment should be initiated immediately upon diagnosis and generally maintained for life. The therapeutic goal is to maintain serum total T₄ or FT₄ in the upper half of the normal range and serum TSH in the normal range.

  
  

  An initial starting dose of 10 to 15 µg/kg/day (ages 0 to 3 months) will generally increase serum T₄ concentrations to the upper half of the normal range in less than 3 weeks. Clinical assessment of growth, development, and thyroid status should be monitored frequently. In most cases, the levothyroxine sodium dose per body weight will decrease as the patient grows through infancy and childhood (see Dosage and Administration, Recommended Dose and Dosage Adjustment, Pediatric Dosage, Table 2). Prolonged use of large doses in infants may be associated with temperament problems, which appear to be transient.

  
  

  Thyroid function tests (serum total T₄ or FT₄, and TSH) should be monitored closely and used to determine the adequacy of levothyroxine sodium therapy. Serum T₄ normalization is usually followed by a rapid decline in TSH. Nevertheless, TSH normalization may lag behind T₄ normalization by 2 to 3 months or longer. The relative serum TSH elevation is more marked in the early months, but can persist to some degree throughout life. In rare patients TSH remains relatively elevated despite clinical euthyroidism and age-specific normal total T₄ or FT₄ levels. Increasing the levothyroxine sodium dosage to suppress TSH into the normal range may produce overtreatment, with an elevated serum T₄ and clinical features of hyperthyroidism including: irritability, increased appetite with diarrhea, and sleeplessness. Another risk of prolonged overtreatment in infants is premature cranial synostosis.

  Special Populations

  
  
  

  Hematologic

  T₄ enhances the response to anticoagulant therapy. Prothrombin time should be closely monitored in patients taking both levothyroxine sodium and oral anticoagulants, and the dosage of anticoagulant adjusted accordingly.

  General

  ELTROXIN (levothyroxine sodium) 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).

  
  

  The bioavailability of levothyroxine may differ to some extent among marketed brands. Once the patient is stabilized on a particular brand of levothyroxine sodium caution should be exercised when a change in drug product brand is implemented.

  
  

  It has been shown that differences in formulations of levothyroxine, despite an identical content of active ingredient, may be associated with differences in fractional gastrointestinal absorption. These differences may not be observed through measurement of total T₃ and T₄ serum levels. It is therefore, recommended that patients who are switched from one levothyroxine formulation to another be retitrated to the desired thyroid function. Accuracy in retitration can best be achieved by using sensitive thyrotropin assays.

  
  

  Seizures have been reported rarely in association with the initiation of levothyroxine sodium therapy, and may be related to the effect of thyroid hormone on seizure threshold.

  
  

  Lithium blocks the TSH-mediated release of T₄ and T₃. Thyroid function should therefore be carefully monitored during lithium initiation, stabilization, and maintenance. If hypothyroidism occurs during lithium treatment, a higher than usual levothyroxine sodium dose may be required.

  Hypothalamic/pituitary Hormone Deficiencies

  In patients with secondary or tertiary hypothyroidism, additional hypothalamic/pituitary hormone deficiencies should be considered, and, if diagnosed, treated for adrenal insufficiency.

  Monitoring and Laboratory Tests

  Treatment of patients with levothyroxine sodium requires periodic assessment of thyroid status by appropriate laboratory tests and clinical evaluation. Selection of appropriate tests for the diagnosis and management of thyroid disorders depends on patient variables such as presenting signs and symptoms, pregnancy, and concomitant medications. A measurement of free T₄ and TSH levels, using a sensitive TSH assay, are recommended to confirm a diagnosis of thyroid disease. Normal ranges for these parameters are age-specific in newborns and younger children.

  
  

  TSH alone or initially may be useful for thyroid disease screening and for monitoring therapy for primary hypothyroidism as a linear inverse correlation exists between serum TSH and free T₄. Measurement of total serum T₄ and T₃, resin T₃ uptake, and free T₃ concentrations may also be useful. Antithyroid microsomal antibodies are an indicator of autoimmune thyroid disease. Positive microsomal antibody presence in an euthyroid patient is a major risk factor for the development of hypothyroidism. An elevated serum TSH in the presence of a normal T₄ may indicate subclinical hypothyroidism. Intracellular resistance to thyroid hormone is quite rare, and is suggested by clinical signs and symptoms of hypothyroidism in the presence of high serum T₄ levels. Adequacy of levothyroxine sodium therapy for hypothyroidism of pituitary or hypothalamic origin should be assessed by measuring free T₄, which should be maintained in the upper half of the normal range. Measurement of TSH is not a reliable indicator of response to therapy for this condition. Adequacy of levothyroxine sodium therapy for congenital and acquired pediatric hypothyroidism should be assessed by measuring serum total T₄ or free T₄; these should be maintained in the upper half of the normal range. In congenital hypothyroidism, serum TSH normalization may lag behind serum T₄ normalization by 2 to 3 months or longer. In rare patients, serum TSH remains relatively elevated despite clinical euthyroidism and age-specific normal T₄ or free T₄ levels (see Warnings and Precautions, Special Populations, Pediatrics (All ages including neonates)).

  Endocrine and Metabolism

  Thyroid hormones, either alone or together 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 reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.

  Effects on Bone Mineral Density

  In women, long-term levothyroxine therapy has been associated with increased bone resorption, thereby decreasing bone mineral density, especially in postmenopausal women on greater 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.

  Sexual Function/Reproduction

  The use of levothyroxine sodium is also unjustified in the treatment of male or female infertility unless this condition is associated with hypothyroidism.

  Nursing Women

  Minimal amounts of thyroid hormones are excreted in human milk. Thyroid hormones are not associated with serious adverse reactions and do not have known tumorigenic potential. While caution should be exercised when levothyroxine sodium is administered to a nursing woman, adequate replacement doses of levothyroxine sodium are generally needed to maintain normal lactation.

  Cardiovascular

  Levothyroxine sodium should be used with caution in patients with cardiovascular disorders, including angina, coronary artery disease, and hypertension, and in the elderly who have a greater likelihood of occult cardiac disease. In these patients, levothyroxine sodium therapy should be initiated at lower doses than those recommended in younger individuals or in patients without cardiac diseases (see Warnings and Precautions, Special Populations, Geriatrics (>50 years of age) and Dosage and Administration). If cardiac symptoms develop or worsen, the levothyroxine sodium dose should be reduced or withheld for one week and then cautiously restarted at a lower dose. Over-treatment 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 levothyroxine sodium 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 thyroid hormone and sympathomimetic agents to patients with coronary artery disease may increase the risk of coronary insufficiency.

  
  
  

  Storage and Stability

  Store between 15 and 25°C. Protect from light.

  Action and Clinical Pharmacology

  Distribution

  Distribution of thyroid hormones in human body tissues and fluids has not been fully elucidated. More than 99% of circulating hormones is bound to serum proteins, including thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and albumin (TBA). T₄ is more extensively and firmly bound to serum proteins than is T₃. Only unbound thyroid hormone is metabolically active. The higher affinity of TBG and TBPA for T₄ partly explains the higher serum levels, slower metabolic clearance, and longer serum elimination half-life of this hormone.

  
  

  Certain drugs and physiologic conditions can alter the binding of thyroid hormones to serum proteins and/or the concentrations of the serum proteins available for thyroid hormone binding. These effects must be considered when interpreting the results of thyroid function tests. (See Warnings and Precautions, Monitoring and Laboratory Tests and Drug Interactions).

  Pharmacokinetics

  
  
  

  ELTROXIN
  
  Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients

  
  

  Hormone	Ratio in Thyroglobulin	Biologic Potency	t½ (days)	Protein Binding (%)b
  Levothyroxine, T4	10 to 20	14	6 to 7a	99.96
  Liothyronine T3	1		<2	99.5

  ^a. Three to four days in hyperthyroidism, nine to ten days in hypothyroidism.
  ^b. Includes TBG, TBPA, and TBA.
  
  

  ---

  
  
  

  Absorption Few clinical studies have evaluated the kinetics of orally administered thyroid hormone. In animals, the most active sites of absorption appear to be the proximal and mid-jejunum. T4 is not absorbed from the stomach and little, if any, drug is absorbed from the duodenum. There seems to be no absorption of T4 from the distal colon in animals. A number of human studies have confirmed the importance of an intact jejunum and ileum for T4 absorption and have shown some absorption from the duodenum. Studies involving radioiodinated T4 fecal tracer excretion methods, equilibration, and AUC methods have shown that absorption varies from 48 to 80 percent of the administered dose. The extent of absorption is increased in the fasting state and decreased in malabsorption syndromes, such as sprue. Absorption may also decrease with age. The degree of T4 absorption is dependent on the product formulation as well as on the character of the intestinal contents, the intestinal flora, including plasma protein and soluble dietary factors, which bind thyroid hormone, making it unavailable for diffusion. Decreased absorption may result from administration of infant soybean formula, ferrous sulfate, sodium polystyrene sulfonate, aluminum hydroxide, sucralfate, or bile acid sequestrants. T4 absorption following intramuscular administration is variable. The relative bioavailability of levothyroxine sodium tablets, compared to an equal nominal dose of oral levothyroxine sodium solution, is approximately 93%. Mechanism of Action The synthesis and secretion of the major thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), from the normally functioning thyroid gland are regulated by complex feedback mechanisms of the hypothalamic-pituitary-thyroid axis. The thyroid gland is stimulated to secrete thyroid hormones by the action of thyrotropin (thyroid stimulating hormone, TSH), which is produced in the anterior pituitary gland. TSH secretion is in turn controlled by thyrotropin-releasing hormone (TRH) produced in the hypothalamus, circulating thyroid hormones, and possibly other mechanisms. Thyroid hormones circulating in the blood act as feedback inhibitors of both TSH and TRH secretion. Thus, when serum concentrations of T3 and T4 are increased, secretion of TSH and TRH decreases. Conversely, when serum thyroid hormone concentrations are decreased, secretion of TSH and TRH is increased. Administration of exogenous thyroid hormones to euthyroid individuals results in suppression of endogenous thyroid hormone secretion. The mechanisms by which thyroid hormones exert their physiologic actions have not been completely elucidated, but it is thought that their principal effects are exerted through control of DNA transcription and protein synthesis. T4 and T3 are transported into cells by passive and active mechanisms. T3 in cell cytoplasm and T3 generated from T4 within the cell diffuse into the nucleus and bind to thyroid receptor proteins, which appear to be primarily attached to DNA. Receptor binding leads to activation or repression of DNA transcription, thereby altering the amounts of mRNA and resultant proteins. Changes in protein concentrations are responsible for the metabolic changes observed in organs and tissues. Thyroid hormones enhance oxygen consumption of most body tissues and increase the basal metabolic rate and metabolism of carbohydrates, lipids, and proteins. Thus, they exert a profound influence on every organ system and are of particular importance in the development of the central nervous system. Thyroid hormones also appear to have direct effects on tissues, such as increased myocardial contractility and decreased systemic vascular resistance. The physiologic effects of thyroid hormones are produced primarily by T3, a large portion of which (approximately 80%) is derived from the deiodination of T4 in peripheral tissues. About 70 to 90 percent of peripheral T3 is produced by monodeiodination of T4 at the 5 position (outer ring). Peripheral monodeiodination of T4 at the 5 position (inner ring) results in the formation of reverse triiodothyronine (rT3), which is calorigenically inactive. 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 Clinical Use, Warnings and Precautions and Dosage and Administration). Metabolism The liver is the major site of degradation for both hormones. T4 and T3 are conjugated with glucuronic and sulfuric acids and excreted in the bile. There is an enterohepatic circulation of thyroid hormones, as they are liberated by hydrolysis in the intestine and reabsorbed. A portion of the conjugated material reaches the colon unchanged, is hydrolyzed there, and is eliminated as free compounds in the feces. In man, approximately 20 to 40 percent of T4 is eliminated in the stool. About 70 percent of the T4 secreted daily is deiodinated to yield equal amounts of T3 and rT3. Subsequent deiodination of T3 and rT3 yields multiple forms of diiodothyronine. A number of other minor T4 metabolites have also been identified. Although some of these metabolites have biologic activity, their overall contribution to the therapeutic effect of T4 is minimal. Contraindications ELTROXIN (levothyroxine sodium) is contraindicated in: Patients with an apparent hypersensitivity to thyroid hormones or any of the inactive product constituents. Patients with untreated subclinical (suppressed serum TSH with normal T3 and T4 levels) or overt thyrotoxicosis of any etiology. Patients with acute myocardial infarction. Patients with uncorrected adrenal insufficiency, as thyroid hormones increase tissue demands for adrenocortical hormones and may thereby precipitate acute adrenal crisis (see Warnings and Precautions). Your Shopping Cart You currently have no items in your cart. 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