Liothyronine Sodium Tablets. These Highlights Do Not Include All The Information Needed To Use Liothyronine Sodium Tablets Safely And Effectively. See Full Prescribing Information For Liothyronine Sodium Tablets.

Limitations of Use

• Liothyronine sodium tablets are not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients as there are no clinical benefits and overtreatment with liothyronine sodium tablets may induce hyperthyroidism [see Warnings and Precautions (5.4)] .
• Liothyronine sodium tablets are not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis.

Store at 20°C to 25°C (68°F to 77°F) [see USP Controlled Room Temperature]

Concurrent use of ketamine and liothyronine sodium tablets may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients.

The signs and symptoms of overdosage are those of hyperthyroidism [see Warnings and Precautions (5.4)and Adverse Reactions (6)] . In addition, confusion and disorientation may occur. Cerebral embolism, seizure, shock, coma, and death have been reported. Symptoms may not necessarily be evident or may not appear until several days after ingestion.

Reduce the liothyronine sodium tablets dose or temporarily discontinued if signs or symptoms of overdosage occur. Initiate appropriate supportive treatment as dictated by the patient's medical status.

For current information on the management of poisoning or overdosage, contact the National Poison Control Center at 1-800-222-1222 or www.poison.org.

Liothyronine sodium tablets contain the active ingredient, liothyronine (L-triiodothyronine or LT ₃), a synthetic form of a thyroid hormone liothyronine in sodium salt form. It is chemically designated as L-Tyrosine, O-(4-hydroxy-3-iodophenyl)-3,5-diiodo-, monosodium salt. The molecular formula, molecular weight and structural formula of liothyronine sodium are given below.

Liothyronine sodium tablets contain liothyronine sodium equivalent to liothyronine in 5 mcg, 25 mcg, and 50 mcg. Inactive ingredients consist of calcium sulfate, microcrystalline cellulose, hypromellose, talc, and colloidal silicon dioxide.

Myxedema coma is a life-threatening emergency characterized by poor circulation and hypometabolism, and may result in unpredictable absorption of thyroid hormone from the gastrointestinal tract. Use of oral thyroid hormone drug products is not recommended to treat myxedema coma. Administer thyroid hormone products formulated for intravenous administration to treat myxedema coma.

The initial dose of liothyronine sodium tablets varies with age and body weight. Dosing adjustments are based on an assessment of the individual patient's clinical and laboratory parameters [see Dosage and Administration (2.3, 2.4)] .

In pediatric patients in whom a diagnosis of permanent hypothyroidism has not been established, discontinue thyroid hormone for a trial period, but only after the child is at least 3 years of age. Obtain serum TSH, T4, and T3 levels at the end of the trial period, and use laboratory test results and clinical assessments to guide diagnosis and treatment, if warranted [see Dosage and Administration (2.6)].

Because of the increased prevalence of cardiovascular disease among the elderly, initiate liothyronine sodium tablets at less than the full replacement dose [see Dosage and Administration (2.3)and Warnings and Precautions (5.1)] . Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with thyroid hormone overtreatment in the elderly.

Liothyronine sodium tablets are indicated as a replacement therapy in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism.

Liothyronine sodium tablets are contraindicated in patients with uncorrected adrenal insufficiency [see Warnings and Precautions (5.3)] .

Adverse reactions associated with liothyronine sodium tablets therapy are primarily those of hyperthyroidism due to therapeutic overdosage [see Warnings and Precautions (5.4)and Overdosage (10)] . 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 and cramps

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

Respiratory: dyspnea

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

Dermatologic: hair loss, flushing

Endocrine: decreased bone mineral density

Reproductive: menstrual irregularities, impaired fertility

See full prescribing information for drugs that 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 liothyronine sodium tablets ( 7)

Concurrent use of sympathomimetics and liothyronine sodium tablets 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.

The onset of activity of liothyronine sodium occurs within a few hours. Maximum pharmacologic response occurs within 2 or 3 days.

Liothyronine sodium tablets are an L-triiodothyronine (T3) indicated for:

• Hypothyroidism: As replacement in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism ( 1.1)
• Pituitary Thyrotropin (Thyroid-Stimulating Hormone, TSH) Suppression: As an adjunct to surgery and radioiodine therapy in the management of well-differentiated thyroid cancer ( 1.2)
• Thyroid Suppression Test: As a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy ( 1.3)

Limitations of Use:

- Not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients. ( 1)

- Not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis. ( 1)

Liothyronine sodium tablets 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 liothyronine sodium tablets dose is increased. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments.

Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine (T3) and L-thyroxine (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.

The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues.

Addition of liothyronine sodium tablets therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control, especially when liothyronine sodium tablets are started, changed, or discontinued [see Warnings and Precautions (5.5)] .

Liothyronine sodium tablets may reduce the therapeutic effects of digitalis glycosides. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides.

• Cardiac adverse reactions in the elderly and in patients with underlying cardiovascular disease: Initiate liothyronine sodium tablets at less than the full replacement dose because of the increased risk of cardiac adverse reactions, including atrial fibrillation ( 2.3, 5.1, 8.5)
• Myxedema coma: Do not use oral thyroid hormone drug products to treat myxedema coma. ( 5.2)
• Acute adrenal crisis in patients with concomitant adrenal insufficiency: Treat with replacement glucocorticoids prior to initiation of liothyronine sodium tablets treatment ( 5.3)
• Prevention of hyperthyroidism or incomplete treatment of hypothyroidism: Proper dose titration and careful monitoring is critical to prevent the persistence of hypothyroidism or the development of hyperthyroidism. ( 5.4)
• Worsening of diabetic control: Therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control after starting, changing, or discontinuing thyroid hormone therapy ( 5.5)
• Decreased bone mineral density associated with thyroid hormone over-replacement: Over-replacement can increase bone resorption and decrease bone mineral density. Give the lowest effective dose ( 5.6)

Concurrent use of tricyclic (e.g., amitriptyline) or tetracyclic (e.g., maprotiline) antidepressants and liothyronine sodium tablets 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 central nervous system stimulation. Liothyronine sodium tablets may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on liothyronine sodium tablets may result in increased liothyronine sodium tablets requirements.

• Administer liothyronine sodium tablets orally once daily and individual dosage according to patient response and laboratory findings ( 2.1)
• See full prescribing information for recommended dosage for hypothyroidism ( 2.2) TSH suppression in well-differentiated thyroid cancer ( 2.3) and for thyroid suppression test ( 2.4)
• When switching a patient to liothyronine sodium tablets, discontinue levothyroxine therapy and initiate liothyronine sodium tablets at a low dosage. Gradually increase the dose according to the patient's response ( 2.5)
• Adequacy of therapy determined with periodic monitoring of TSH and T3 levels as well as clinical status ( 2.6)

Liothyronine sodium tablets are indicated as a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.

Tablets (round, flat, white to off-white) available as follows:

• 5 mcg: debossed "5" over "220" on one side and plain on the other
• 25 mcg: debossed "25" above the score and "222" below the score on one side and plain on the other
• 50 mcg: debossed "50" above the score and "223" below the score on one side and plain on the other

Pregnancy may require the use of higher doses of thyroid hormone ( 2.2, 8.1)

Concurrent use of tyrosine-kinase inhibitors such as imatinib may cause hypothyroidism. Closely monitor TSH levels in such patients.

The dose of liothyronine sodium tablets for hypothyroidism or pituitary Thyroid-Stimulating Hormone (TSH) suppression depends on a variety of factors including: the patient's age, body weight, cardiovascular status, concomitant medical conditions (including pregnancy), concomitant medications, co-administered food and the specific nature of the condition being treated [see Dosage and Administration (2.2, 2.3, 2.4), Warnings and Precautions (5), and Drug Interactions (7)] . Dosing must be individualized to account for these factors and dose adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters [see Dosage and Administration (2.4)] .

Administer liothyronine sodium tablets orally once daily.

Addition of thyroid hormone therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control after starting, changing, or discontinuing liothyronine sodium tablets [see Drug Interactions (7.2)].

Liothyronine sodium tablets, USP (round, flat, white to off-white) are supplied as follows:

Consider changes in TBG concentration when interpreting T4 and T3 values. Measure and evaluate unbound (free) hormone in this circumstance. Pregnancy, infectious hepatitis, estrogens, estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations. Nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, androgens and corticosteroids decrease TBG concentration. Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9000.

The recommended dose is 75 mcg to 100 mcg daily for 7 days, with radioactive iodine uptake being determined before and after the 7 day administration of liothyronine sodium tablets. If thyroid function is normal, the radioiodine uptake will drop significantly after treatment. A 50% or greater suppression of uptake indicates a normal thyroid-pituitary axis.

Assess the adequacy of therapy by periodic assessment of laboratory tests and clinical evaluation. Persistent clinical and laboratory evidence of hypothyroidism despite an apparent adequate replacement dose of liothyronine sodium tablets may be evidence of inadequate absorption, poor compliance, drug interactions, or a combination of these factors.

NDC 51407-384-01

Liothyronine

Sodium Tablets, USP

5 mcg

Rx Only

100 Tablets

NDC 51407-385-01

Liothyronine

Sodium Tablets, USP

25 mcg

Rx Only

100 Tablets

NDC 51407-386-01

Liothyronine

Sodium Tablets, USP

50 mcg

Rx Only

100 Tablets

• Thyroid hormones, including liothyronine sodium tablets, 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 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 [see Adverse Reactions (6), Drug Interactions (7.7), and Overdosage (10)] .

Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of liothyronine sodium.

Many drugs can exert effects on thyroid hormone pharmacokinetics (e.g. absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to liothyronine sodium tablets (see Tables 1 – 4).

Liothyronine sodium tablets has a rapid onset of action and residual effects of the other thyroid preparation may persist for the first several weeks after initiating liothyronine sodium tablets therapy. When switching a patient to liothyronine sodium tablets, discontinue levothyroxine therapy and initiate liothyronine sodium tablets at a low dosage. Gradually increase the liothyronine sodium tablets dose according to the patient's response.

Liothyronine sodium tablets are indicated as an adjunct to surgery and radioiodine therapy in the management of well-differentiated thyroid cancer .

Thyroid hormone increases metabolic clearance of glucocorticoids. Initiation of thyroid hormone therapy prior to initiating glucocorticoid therapy may precipitate an acute adrenal crisis in patients with adrenal insufficiency. Treat patients with adrenal insufficiency with replacement glucocorticoids prior to initiating treatment with liothyronine sodium tablets [see Contraindications (4)].

Liothyronine sodium tablets has a narrow therapeutic index. Over- or undertreatment with liothyronine sodium tablets may have negative effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function, and on glucose and lipid metabolism. Titrate the dose of liothyronine sodium tablets carefully and monitor response to titration to avoid these effects [see Dosage and Administration (2.4)]. Monitor for the presence of drug or food interactions when using liothyronine sodium tablets and adjust the dose as necessary [see Drug Interactions (7)and Clinical Pharmacology (12.3)].

The dose of liothyronine sodium tablets should target TSH levels within the desired therapeutic range. This may require higher doses, depending on the target level for TSH suppression.

Increased bone resorption and decreased bone mineral density may occur as a result of thyroid hormone over-replacement, particularly in post-menopausal women. 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. Administer the minimum dose of liothyronine sodium tablets that achieves the desired clinical and biochemical response to mitigate against this risk.

Overtreatment with thyroid hormone may cause an increase in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias, particularly in patients with cardiovascular disease and in elderly patients. Initiate liothyronine sodium tablets therapy in this population at lower doses than those recommended in younger individuals or in patients without cardiac disease [see Dosage and Administration (2.3)and Use in Specific Populations (8.5)].

Monitor for cardiac arrhythmias during surgical procedures in patients with coronary artery disease receiving suppressive liothyronine sodium tablets therapy. Monitor patients receiving concomitant liothyronine sodium tablets and sympathomimetic agents for signs and symptoms of coronary insufficiency. If cardiovascular symptoms develop or worsen, reduce or withhold the liothyronine sodium tablets dose for one week and restart at a lower dose.

Limitations of Use

• Liothyronine sodium tablets are not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients as there are no clinical benefits and overtreatment with liothyronine sodium tablets may induce hyperthyroidism [see Warnings and Precautions (5.4)] .
• Liothyronine sodium tablets are not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis.

Store at 20°C to 25°C (68°F to 77°F) [see USP Controlled Room Temperature]

Concurrent use of ketamine and liothyronine sodium tablets may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients.

The signs and symptoms of overdosage are those of hyperthyroidism [see Warnings and Precautions (5.4)and Adverse Reactions (6)] . In addition, confusion and disorientation may occur. Cerebral embolism, seizure, shock, coma, and death have been reported. Symptoms may not necessarily be evident or may not appear until several days after ingestion.

Reduce the liothyronine sodium tablets dose or temporarily discontinued if signs or symptoms of overdosage occur. Initiate appropriate supportive treatment as dictated by the patient's medical status.

For current information on the management of poisoning or overdosage, contact the National Poison Control Center at 1-800-222-1222 or www.poison.org.

Liothyronine sodium tablets contain the active ingredient, liothyronine (L-triiodothyronine or LT ₃), a synthetic form of a thyroid hormone liothyronine in sodium salt form. It is chemically designated as L-Tyrosine, O-(4-hydroxy-3-iodophenyl)-3,5-diiodo-, monosodium salt. The molecular formula, molecular weight and structural formula of liothyronine sodium are given below.

Liothyronine sodium tablets contain liothyronine sodium equivalent to liothyronine in 5 mcg, 25 mcg, and 50 mcg. Inactive ingredients consist of calcium sulfate, microcrystalline cellulose, hypromellose, talc, and colloidal silicon dioxide.

Myxedema coma is a life-threatening emergency characterized by poor circulation and hypometabolism, and may result in unpredictable absorption of thyroid hormone from the gastrointestinal tract. Use of oral thyroid hormone drug products is not recommended to treat myxedema coma. Administer thyroid hormone products formulated for intravenous administration to treat myxedema coma.

The initial dose of liothyronine sodium tablets varies with age and body weight. Dosing adjustments are based on an assessment of the individual patient's clinical and laboratory parameters [see Dosage and Administration (2.3, 2.4)] .

In pediatric patients in whom a diagnosis of permanent hypothyroidism has not been established, discontinue thyroid hormone for a trial period, but only after the child is at least 3 years of age. Obtain serum TSH, T4, and T3 levels at the end of the trial period, and use laboratory test results and clinical assessments to guide diagnosis and treatment, if warranted [see Dosage and Administration (2.6)].

Because of the increased prevalence of cardiovascular disease among the elderly, initiate liothyronine sodium tablets at less than the full replacement dose [see Dosage and Administration (2.3)and Warnings and Precautions (5.1)] . Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with thyroid hormone overtreatment in the elderly.

Liothyronine sodium tablets are indicated as a replacement therapy in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism.

Liothyronine sodium tablets are contraindicated in patients with uncorrected adrenal insufficiency [see Warnings and Precautions (5.3)] .

Adverse reactions associated with liothyronine sodium tablets therapy are primarily those of hyperthyroidism due to therapeutic overdosage [see Warnings and Precautions (5.4)and Overdosage (10)] . 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 and cramps

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

Respiratory: dyspnea

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

Dermatologic: hair loss, flushing

Endocrine: decreased bone mineral density

Reproductive: menstrual irregularities, impaired fertility

See full prescribing information for drugs that 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 liothyronine sodium tablets ( 7)

Concurrent use of sympathomimetics and liothyronine sodium tablets 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.

The onset of activity of liothyronine sodium occurs within a few hours. Maximum pharmacologic response occurs within 2 or 3 days.

Liothyronine sodium tablets are an L-triiodothyronine (T3) indicated for:

• Hypothyroidism: As replacement in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism ( 1.1)
• Pituitary Thyrotropin (Thyroid-Stimulating Hormone, TSH) Suppression: As an adjunct to surgery and radioiodine therapy in the management of well-differentiated thyroid cancer ( 1.2)
• Thyroid Suppression Test: As a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy ( 1.3)

Limitations of Use:

- Not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients. ( 1)

- Not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis. ( 1)

Liothyronine sodium tablets 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 liothyronine sodium tablets dose is increased. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments.

Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine (T3) and L-thyroxine (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.

The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues.

Addition of liothyronine sodium tablets therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control, especially when liothyronine sodium tablets are started, changed, or discontinued [see Warnings and Precautions (5.5)] .

Liothyronine sodium tablets may reduce the therapeutic effects of digitalis glycosides. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides.

• Cardiac adverse reactions in the elderly and in patients with underlying cardiovascular disease: Initiate liothyronine sodium tablets at less than the full replacement dose because of the increased risk of cardiac adverse reactions, including atrial fibrillation ( 2.3, 5.1, 8.5)
• Myxedema coma: Do not use oral thyroid hormone drug products to treat myxedema coma. ( 5.2)
• Acute adrenal crisis in patients with concomitant adrenal insufficiency: Treat with replacement glucocorticoids prior to initiation of liothyronine sodium tablets treatment ( 5.3)
• Prevention of hyperthyroidism or incomplete treatment of hypothyroidism: Proper dose titration and careful monitoring is critical to prevent the persistence of hypothyroidism or the development of hyperthyroidism. ( 5.4)
• Worsening of diabetic control: Therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control after starting, changing, or discontinuing thyroid hormone therapy ( 5.5)
• Decreased bone mineral density associated with thyroid hormone over-replacement: Over-replacement can increase bone resorption and decrease bone mineral density. Give the lowest effective dose ( 5.6)

Concurrent use of tricyclic (e.g., amitriptyline) or tetracyclic (e.g., maprotiline) antidepressants and liothyronine sodium tablets 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 central nervous system stimulation. Liothyronine sodium tablets may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on liothyronine sodium tablets may result in increased liothyronine sodium tablets requirements.

• Administer liothyronine sodium tablets orally once daily and individual dosage according to patient response and laboratory findings ( 2.1)
• See full prescribing information for recommended dosage for hypothyroidism ( 2.2) TSH suppression in well-differentiated thyroid cancer ( 2.3) and for thyroid suppression test ( 2.4)
• When switching a patient to liothyronine sodium tablets, discontinue levothyroxine therapy and initiate liothyronine sodium tablets at a low dosage. Gradually increase the dose according to the patient's response ( 2.5)
• Adequacy of therapy determined with periodic monitoring of TSH and T3 levels as well as clinical status ( 2.6)

Liothyronine sodium tablets are indicated as a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.

Tablets (round, flat, white to off-white) available as follows:

• 5 mcg: debossed "5" over "220" on one side and plain on the other
• 25 mcg: debossed "25" above the score and "222" below the score on one side and plain on the other
• 50 mcg: debossed "50" above the score and "223" below the score on one side and plain on the other

Pregnancy may require the use of higher doses of thyroid hormone ( 2.2, 8.1)

Concurrent use of tyrosine-kinase inhibitors such as imatinib may cause hypothyroidism. Closely monitor TSH levels in such patients.

The dose of liothyronine sodium tablets for hypothyroidism or pituitary Thyroid-Stimulating Hormone (TSH) suppression depends on a variety of factors including: the patient's age, body weight, cardiovascular status, concomitant medical conditions (including pregnancy), concomitant medications, co-administered food and the specific nature of the condition being treated [see Dosage and Administration (2.2, 2.3, 2.4), Warnings and Precautions (5), and Drug Interactions (7)] . Dosing must be individualized to account for these factors and dose adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters [see Dosage and Administration (2.4)] .

Administer liothyronine sodium tablets orally once daily.

Addition of thyroid hormone therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control after starting, changing, or discontinuing liothyronine sodium tablets [see Drug Interactions (7.2)].

Liothyronine sodium tablets, USP (round, flat, white to off-white) are supplied as follows:

Consider changes in TBG concentration when interpreting T4 and T3 values. Measure and evaluate unbound (free) hormone in this circumstance. Pregnancy, infectious hepatitis, estrogens, estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations. Nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, androgens and corticosteroids decrease TBG concentration. Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9000.

The recommended dose is 75 mcg to 100 mcg daily for 7 days, with radioactive iodine uptake being determined before and after the 7 day administration of liothyronine sodium tablets. If thyroid function is normal, the radioiodine uptake will drop significantly after treatment. A 50% or greater suppression of uptake indicates a normal thyroid-pituitary axis.

Assess the adequacy of therapy by periodic assessment of laboratory tests and clinical evaluation. Persistent clinical and laboratory evidence of hypothyroidism despite an apparent adequate replacement dose of liothyronine sodium tablets may be evidence of inadequate absorption, poor compliance, drug interactions, or a combination of these factors.

NDC 51407-384-01

Liothyronine

Sodium Tablets, USP

5 mcg

Rx Only

100 Tablets

NDC 51407-385-01

Liothyronine

Sodium Tablets, USP

25 mcg

Rx Only

100 Tablets

NDC 51407-386-01

Liothyronine

Sodium Tablets, USP

50 mcg

Rx Only

100 Tablets

• Thyroid hormones, including liothyronine sodium tablets, 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 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 [see Adverse Reactions (6), Drug Interactions (7.7), and Overdosage (10)] .

Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of liothyronine sodium.

Many drugs can exert effects on thyroid hormone pharmacokinetics (e.g. absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to liothyronine sodium tablets (see Tables 1 – 4).

Liothyronine sodium tablets has a rapid onset of action and residual effects of the other thyroid preparation may persist for the first several weeks after initiating liothyronine sodium tablets therapy. When switching a patient to liothyronine sodium tablets, discontinue levothyroxine therapy and initiate liothyronine sodium tablets at a low dosage. Gradually increase the liothyronine sodium tablets dose according to the patient's response.

Liothyronine sodium tablets are indicated as an adjunct to surgery and radioiodine therapy in the management of well-differentiated thyroid cancer .

Thyroid hormone increases metabolic clearance of glucocorticoids. Initiation of thyroid hormone therapy prior to initiating glucocorticoid therapy may precipitate an acute adrenal crisis in patients with adrenal insufficiency. Treat patients with adrenal insufficiency with replacement glucocorticoids prior to initiating treatment with liothyronine sodium tablets [see Contraindications (4)].

Liothyronine sodium tablets has a narrow therapeutic index. Over- or undertreatment with liothyronine sodium tablets may have negative effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function, and on glucose and lipid metabolism. Titrate the dose of liothyronine sodium tablets carefully and monitor response to titration to avoid these effects [see Dosage and Administration (2.4)]. Monitor for the presence of drug or food interactions when using liothyronine sodium tablets and adjust the dose as necessary [see Drug Interactions (7)and Clinical Pharmacology (12.3)].

The dose of liothyronine sodium tablets should target TSH levels within the desired therapeutic range. This may require higher doses, depending on the target level for TSH suppression.

Increased bone resorption and decreased bone mineral density may occur as a result of thyroid hormone over-replacement, particularly in post-menopausal women. 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. Administer the minimum dose of liothyronine sodium tablets that achieves the desired clinical and biochemical response to mitigate against this risk.

Overtreatment with thyroid hormone may cause an increase in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias, particularly in patients with cardiovascular disease and in elderly patients. Initiate liothyronine sodium tablets therapy in this population at lower doses than those recommended in younger individuals or in patients without cardiac disease [see Dosage and Administration (2.3)and Use in Specific Populations (8.5)].

Monitor for cardiac arrhythmias during surgical procedures in patients with coronary artery disease receiving suppressive liothyronine sodium tablets therapy. Monitor patients receiving concomitant liothyronine sodium tablets and sympathomimetic agents for signs and symptoms of coronary insufficiency. If cardiovascular symptoms develop or worsen, reduce or withhold the liothyronine sodium tablets dose for one week and restart at a lower dose.