Thyroid

Class: Thyroid Agents
ATC Class: H03AA05
VA Class: HS851
CAS Number: 8028-36-2
Brands: Armour Thyroid, Nature-Throid, Westhroid

Introduction

Natural thyroid agent; cleaned, dried, and powdered thyroid gland (obtained from domesticated animals) containing tetraiodothyronine (thyroxine, T₄) and triiodothyronine (liothyronine, T₃).^{a b c d h}

Uses for Thyroid

Hypothyroidism

Replacement or supplemental therapy in congenital or acquired hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.^{a b c} Specific indications include primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) hypothyroidism.^{a b c}

Not considered drug of choice for replacement therapy^{a c d e} because of potential problems (e.g., variability in T₄:T₃ ratio, fluctuating and often elevated T₃ concentrations).^{a c m} Levothyroxine is considered drug of choice for replacement therapy.^{a c d e i m}

For the treatment of congenital hypothyroidism (cretinism),^{a b c} levothyroxine is considered drug of choice.^{a c}

Pituitary TSH Suppression

Treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto’s thyroiditis), and multinodular goiter.^{a b c}

Adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer.^{b c}

Efficacy of TSH suppression for benign nodular disease remains controversial.^{p q r}

Diagnosis of Thyroid Disorders

Used diagnostically in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.^{b c} Use with caution in patients in whom there is a strong suspicion of thyroid gland autonomy because exogenous hormone effects will be additive to endogenous source.^b

Thyrotoxicosis

Has been used in combination with antithyroid agents for the treatment of thyrotoxicosis to prevent goitrogenesis and hypothyroidism.^{a c}

May occasionally be useful to prevent antithyroid agent-induced hypothyroidism in the management of thyrotoxicosis during pregnancy; however, combination therapy generally considered unnecessary because it may increase the requirement for antithyroid agents and, therefore, the risk of fetal hypothyroidism.^{a c}

Other Uses

See Unlabeled Uses under Cautions.

Thyroid Dosage and Administration

General

• 
  

  Initially, monitor response to therapy about every 6–8 weeks.^{e m} Once normalization of thyroid function and serum TSH concentrations has been achieved, patients may be evaluated less frequently (i.e., every 6–12 months).^{e m} However, if dosage is changed, measure serum TSH concentrations after 8–12 weeks.^m

  
  


• 
  

  Commercially available natural thyroid preparations have different T₄:T₃ ratios and fluctuating T₃ concentrations.^{a c m} Do not switch from one manufacturer's natural thyroid preparation to another manufacturer's preparation unless under the direction and supervision of a clinician.^a

  
  


• 
  

  Natural and synthetic thyroid agent preparations are not necessarily directly comparable; however, the following equivalencies have been suggested based on clinical response:^c

  
  

Equivalencies of Thyroid Preparations Based on Clinical Responsec

Thyroid Agent	Approximate Equivalent Dosage
Levothyroxine Sodium	100 mcg or less
Liothyronine Sodium	25 mcg
Liotrix (Levothyroxine Sodium/Liothyronine Sodium)	50 mcg/12.5 mcg (Thyrolar)
Thyroglobulin	65 mg
Thyroid	60–65 mg (1 grain)

Administration

Oral Administration

Administer orally, usually as a single daily dose before breakfast.^{a b c}

Dosage

Each 65 mg of thyroid contains approximately 38 and 9 mcg of measurable levothyroxine and T₃, respectively.^{a b} Each 60–65 mg of thyroid is approximately clinically equivalent to 100 mcg or less of levothyroxine sodium or to 25 mcg of liothyronine sodium.^{a c d} (See General under Dosage and Administration.)

Adjust dosage carefully according to clinical and laboratory response to treatment. ^{a b c} Avoid undertreatment or overtreatment.^{b c} (See Therapy Monitoring under Cautions.)

Initiate dosage at a lower level in geriatric patients, in patients with functional or ECG evidence of cardiovascular disease, and in patients with severe, long-standing hypothyroidism or other endocrinopathies.^{a b c}

Pediatric Patients

Hypothyroidism

Oral

Initiate therapy at full replacement dosages as soon as possible after diagnosis of hypothyroidism to prevent deleterious effects on intellectual and physical growth and development.^{a b c o} The following dosages have been recommended:

Dosage for Management of Hypothyroidism in Pediatric Patientsb

Age	Daily Dosage
0–6 months	15–30 mg or 4.8–6 mg/kg
6–12 months	30–45 mg or 3.6–4.8 mg/kg
1–5 years	45–60 mg or 3–3.6 mg/kg
6–12 years	60–90 mg or 2.4–3 mg/kg
>12 years	>90 mg or 1.2–1.8 mg/kg

When transient hypothyroidism is suspected, therapy may be temporarily discontinued when the child is >3 years of age to reassess the condition.^{b o} (See Pediatric Use under Cautions.)

Adults

Hypothyroidism

Oral

Usual initial dosage is 15–30 mg daily.^{b d} May increase dosage in increments of 15 mg at intervals of 2–3 weeks.^b

For management of long-standing myxedema, usual initial dosage is 15 mg daily.^b

Usual maintenance dosage is 60–120 mg daily.^b Failure to respond adequately to oral dosages of 180 mg daily suggests presence of malabsorption or patient noncompliance.^b

Pituitary TSH Suppression

Thyroid Cancer

Oral

Administration of dosages higher than those used for replacement therapy usually is required to suppress TSH concentrations to low or undetectable concentrations.^b

Special Populations

Patients with Cardiovascular Disease

Hypothyroidism

Initiate therapy at lower dosages than those recommended in patients without cardiovascular disease.^{b c}

Usual initial dosage is 15–30 mg daily.^b If angina appears or if cardiovascular disease is aggravated, reduce dosage or temporarily withhold therapy and then cautiously restart therapy at a lower dosage.^{b c}

Geriatric Patients

Hypothyroidism

Initiate therapy at lower dosages than those recommended in younger patients.^{b c}

Usual initial dosage is 15–30 mg daily.^b If cardiovascular disease is aggravated, reduce dosage or temporarily withhold therapy and then cautiously restart therapy at a lower dosage.^{b c}

Cautions for Thyroid

Contraindications

• 
  

  Untreated thyrotoxicosis.^{b c}

  
  


• 
  

  AMI uncomplicated by hypothyroidism.^c

  
  


• 
  

  Uncorrected adrenal insufficiency.^{b c}

  
  


• 
  

  Known hypersensitivity to any ingredient in the formulation.^{b c} (See Sensitivity Reactions under Cautions.)

  
  

Warnings/Precautions

Warnings

Unlabeled Uses

Should not be used for the treatment of obesity or for weight loss either alone or with other therapeutic agents.^{b c m} In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction.^{b c} Larger doses may produce serious or life-threatening toxicity, particularly when given in conjunction with sympathomimetic amines (e.g., anorectic agents).^{b c}

Should not be used in the treatment of male or female infertility unless this condition is associated with hypothyroidism.^{b c m}

Sensitivity Reactions

Hypersensitivity to thyroid hormone not known to occur;^b however, concern for allergic reactions to animal proteins exists.ⁱ Hypersensitivity reactions to inactive ingredients of thyroid hormone products have been reported and include urticaria, pruritus, rash, flushing, angioedema, abdominal pain, nausea, vomiting, diarrhea, fever, arthralgia, serum sickness, and wheezing.^c

May rarely cause GI intolerance in patients highly sensitive to pork or corn.^c

Major Toxicities

Effects on Bone Mineral Density

Potential for excessive doses to result in hypermetabolic state^b and decreased bone mineral density.^{c n} Use lowest dose necessary to achieve desired clinical and biochemical response.ⁿ

General Precautions

Therapy Monitoring

Thyroid agents have a narrow therapeutic index.^c Avoid undertreatment or overtreatment, that may result in adverse effects on growth and development in pediatric patients, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, GI function, and glucose and lipid metabolism.^c

Periodically perform appropriate laboratory tests (e.g., serum TSH, total or free T₄, total T₃) and clinical evaluations to monitor adequacy of therapy.^{b c i m}

Preexisting Cardiovascular Disease

Use with extreme caution.^{b c} (See Patients with Cardiovascular Disease under Dosage and Administration.) Patients with CHD should be monitored closely during surgical procedures due to increased risk of arrhythmias.^c

Associated Endocrine Disorders

Hypopituitarism, adrenal insufficiency, and other endocrine disorders such as diabetes mellitus and diabetes insipidus are characterized by signs and symptoms that may be diminished in severity or obscured by hypothyroidism.^c Thyroid agents may aggravate the intensity of previously obscured symptoms in patients with endocrine disorders, and appropriate adjustment of therapy for these concomitant disorders may be required.^{b c}

In patients with secondary or tertiary hypothyroidism, consider possibility of additional hypothalamic/pituitary hormone deficiencies and treat if diagnosed.ⁿ

Chronic autoimmune thyroiditis may occur in association with other autoimmune disorders (e.g., adrenal insufficiency, pernicious anemia, type 1 diabetes mellitus).^{e f}

Patients with concomitant adrenal insufficiency should be treated with replacement corticosteroids prior to initiation of thyroid agents.^c Failure to do so may precipitate an acute adrenal crisis due to increased metabolic clearance of corticosteroids when the thyroid agent is initiated.^c

Patients with diabetes mellitus may require increased dosages of antidiabetic agents when treated with thyroid agents.^b

Specific Populations

Pregnancy

Category A.^{b h}

During pregnancy in hypothyroid patients, serum free T₄ levels may decrease and serum TSH levels increase to values outside the normal range.^{f n} Elevations in serum TSH may occur at 4 weeks' gestation;ⁿ monitor TSH levels during each trimester (or every 6 weeks) and adjust thyroid dosage accordingly.^{d e m} Reduce dosage to pre-pregnancy level immediately after delivery, since postpartum TSH concentrations are similar to preconception levels;ⁿ measure serum TSH concentrations 6–8 weeks postpartum.^m

Lactation

Although thyroid hormones are minimally distributed into human milk, exercise caution when administering to a nursing woman.^{b c n} However, adequate replacement dosages generally are needed to maintain normal lactation.ⁿ

Pediatric Use

The goal of treatment in pediatric patients with hypothyroidism is to achieve and maintain normal intellectual and physical growth and development.^c Initiate therapy immediately upon diagnosis.^{b c} Maintain therapy for life, unless transient hypothyroidism is suspected.^{b c}

Neonates with suspected hypothyroidism should receive thyroid agent therapy pending results of confirmative tests.^c If a positive diagnosis cannot be made on the basis of laboratory findings but there is a strong clinical suspicion of congenital hypothyroidism, initiate replacement therapy to achieve euthyroidism until the child is 1–2 years of age.^c During the first 2 weeks of therapy, closely monitor infants for cardiac overload, arrhythmias, and aspiration resulting from avid suckling.^c Evaluate infant’s clinical response to therapy about 6 weeks after initiation of thyroid agent therapy and at least at 6 and 12 months of age and yearly thereafter.^c

When transient hypothyroidism is suspected, temporarily discontinue therapy for 2–8 weeks to reassess the condition when the child is >3 years of age.^{b o} If the diagnosis of permanent hypothyroidism is confirmed, reinstitute full replacement therapy.^o However, if serum concentrations of free T₄ and TSH are normal, discontinue thyroid agent therapy and monitor carefully;^{b o} repeat thyroid function tests if manifestations of hypothyroidism develop.^o

In pediatric patients with transient severe hypothyroidism, reduce replacement dosage by half for 30 days.^o If, after 30 days, serum TSH >20 mU/L, consider the hypothyroidism permanent and reinstitute full replacement therapy.^o However, if serum free TSH has not increased, temporarily discontinue thyroid agent therapy for another 30 days, then repeat serum free T₄ and TSH measurements.^o Reinstitute or discontinue replacement therapy based on laboratory findings.^o

Monitor patients closely to avoid undertreatment or overtreatment.^c Undertreatment may result in impaired intellectual development, poor school performance (due to impaired concentration and slowed mentation), and reduced adult height.^c Overtreatment may result in craniosynostosis in infants and accelerate aging of bones, resulting in premature epiphyseal closure and compromised adult stature.^{b c}

Treated children may manifest a period of catch-up growth, which may be adequate in some cases to achieve normal adult height.^c In children with severe or long-standing hypothyroidism, catch-up growth may not be adequate to achieve normal adult height.^c

Pseudotumor cerebri and slipped capital femoral epiphysis have been reported in children receiving thyroid agents.^c

Geriatric Use

Because of the increased risk of cardiovascular disease among geriatric patients, thyroid therapy should not be initiated at the full replacement dose.^{b c m} (See Geriatric Patients under Dosage and Administration.)

Common Adverse Effects

Adverse reactions result from overdosage and resemble manifestations of hyperthyroidism,^{a b c} including fatigue, weight loss, increased appetite, heat intolerance, fever, excessive sweating, headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia, tremor, muscle weakness, palpitations, tachycardia, arrhythmias, increased heart rate and BP, heart failure, angina, AMI, cardiac arrest, diarrhea, vomiting, abdominal cramps, elevations in liver function tests, hair loss, flushing, decreased bone mineral density, menstrual irregularities, and impaired fertility.^c

Interactions for Thyroid

Drugs Affecting Hepatic Microsomal Enzymes

Potential increased metabolism of thyroid hormone with drugs that induce hepatic microsomal enzymes, resulting in increased thyroid agent dosage requirements.^c

Drugs That May Decrease T₄ 5'-Deiodinase Activity

Inhibitors of T₄ 5’-deiodinase decrease peripheral conversion of T₄ to T₃, resulting in decreased T₃ concentrations.^{c s} However, serum T₄ concentrations usually remain within normal range, but may occasionally be slightly increased.^{c n}

Specific Drugs and Foods

Drug	Interaction	Comments
Amiodarone	Decreased metabolism of T4 to T3c
Anticoagulants, oral (e.g., coumarins)	Potentiation of anticoagulant activityb c	Carefully monitor PT and adjust anticoagulant dosage accordingly when thyroid agent therapy is initiatedb c
Antidepressants (tricyclics, tetracyclics, SSRIs)	Increased risk of cardiac arrhythmias and CNS stimulation when levothyroxine is used with tricyclics or tetracyclicsc Faster onset of action of tricyclics following concomitant use with levothyroxinec Sertraline may increase levothyroxine requirementsc
Antidiabetic agents (biguanides, meglitinides, sulfonylureas, thiazolidinediones, insulin)	Thyroid agents may cause increased antidiabetic agent or insulin requirementsb c	Carefully monitor diabetic control, especially when thyroid therapy is initiated, changed, or discontinuedb c
β-Adrenergic blocking agents (e.g., propranolol hydrochloride dosages >160 mg daily)	Decreased metabolism of T4 to T3c Impaired antihypertensive effects when hypothyroid patient is converted to euthyroid statec
Bile acid sequestrants (e.g., cholestyramine, colestipol)	Impaired thyroid agent absorptionb c	Administer thyroid agents ≥4 hours apart from these agentsb c
Carbamazepine	Potential increased metabolism of thyroid agentc	May require thyroid agent dosage increasec
Cardiac glycosides	Decreased serum digitalis glycoside concentrations in patients with hyperthyroidism or in patients with hypothyroidism in whom a euthyroid state has been achieved; potential for reduced therapeutic effects of digitalis glycosides with thyroid usec	May need to increase dosage of digitalis glycoside when hypothyroidism has been correctedd n
Corticosteroids (e.g., dexamethasone at dosages ≥4 mg daily)	Decreased metabolism of T4 to T3.c Short-term administration of large doses of corticosteroids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levelsc
Estrogen or estrogen-containing oral contraceptives	Possible decreased free T4 concentrationsb	Patients without a functioning thyroid gland may require thyroid dosage increaseb
Ferrous sulfate	Delayed or impaired thyroid absorptionc	Administer thyroid agents ≥4 hours apart from this agentc
Food with large amounts of fiber (e.g., cotton seed meal, infant soybean formula, soybean flour, walnuts)	Decreased levothyroxine absorptionn
Furosemide (at IV dosages >80 mg)	Concomitant use with levothyroxine produces transient increases in serum free T4 concentrations; continued administration results in a decrease in serum T4 and normal free T4 and TSH concentrations, and therefore, patients are clinically euthyroidc
GI drugs (e.g., antacids [aluminum hydroxide, magnesium hydroxide, calcium carbonate], simethicone, sucralfate)	Delayed or impaired thyroid agent absorptionc	Administer thyroid agents ≥4 hours apart from these agents
Growth hormones (e.g., somatropin)	Excessive use of thyroid agents with growth hormones may accelerate epiphyseal closure; however, untreated hypothyroidism may interfere with growth response to growth hormonec
Heparin	Concomitant use with levothyroxine produces transient increases in serum free T4 concentrations; continued administration results in a decrease in serum T4 and normal free T4 and TSH concentrations, and therefore, patients are clinically euthyroidc
Hydantoins (e.g., phenytoin)	Potential increased metabolism of thyroid agentc Reduced levothyroxine serum protein bindingc Concomitant use with levothyroxine produces transient increases in serum free T4 concentrations; continued administration results in a decrease in serum T4 and normal free T4 and TSH concentrations, and therefore, patients are clinically euthyroidc	May require thyroid dosage increasec
Ketamine	Risk of marked hypertension and tachycardiac	Use with cautionc
NSAIAs (e.g., fenamates, phenylbutazone)	Concomitant use with levothyroxine produces transient increases in serum free T4 concentrations; continued administration results in a decrease in serum T4 and normal free T4 and TSH concentrations, and therefore, patients are clinically euthyroidc
Phenobarbital	Potential increased metabolism of thyroid agentc	May require thyroid agent dosage increasec
Radiographic agents	Reduced uptake of 123I, 131I, and 99mTcc
Rifampin	Potential increased metabolism of thyroid agentc	May require thyroid agent dosage increasec
Salicylates (dosages >2 g daily)	Inhibit binding of T4 and T3 to TBG and transthyretin; initially increases serum free T4 followed by return to normal concentrations with sustained therapeutic serum salicylate concentrations, although total T4 concentrations may decrease by as much as 30%c
Sodium polystyrene sulfonate	Delayed or impaired thyroid absorptionc	Administer thyroid agents ≥4 hours apart from this agentc
Sympathomimetic agents	Potentiation of sympathomimetic effects; increased risk of coronary insufficiency in patients with CHDc	Observe patient carefully when sympathomimetic agent is administeredc
Xanthine derivatives (e.g., theophylline)	Clearance of xanthine derivatives may be decreased in hypothyroid patients but returns to normal when the euthyroid state is achievedc

Drugs Affecting Thyroid Function or Thyroid Function Tests

Various drugs or concomitant medical conditions (e.g., pregnancy, infectious hepatitis) may adversely affect thyroid function (e.g., alter endogenous thyroid hormone secretion, reduce TSH secretion) resulting in hypothyroidism or hyperthyroidism or interfere with laboratory tests used to assess thyroid function.^{b c} Consult specialized references for information.

Some drugs may affect transport of thyroid hormones (T₃, T₄, levothyroxine) by affecting serum thyroxine-binding globulin (TBG) concentrations.^{c n} However, free T₄ concentrations may remain normal and the patient may remain euthyroid.^{c n} Monitor therapy and adjust thyroid dosage as necessary.^c

Drugs Affecting Thyroxine Binding Globulin Concentrations^{b c}

• Drugs That May Increase Serum TBG Concentration


• 
  

  Estrogens, oral (including estrogen-containing oral contraceptives)^{b c}

  
  


• 
  

  Fluorouracil^c

  
  


• 
  

  Methadone^c

  
  


• 
  

  Mitotane^c

  
  


• 
  

  Tamoxifen^c

  
  

• Drugs That May Decrease Serum TBG Concentration


• 
  

  Androgens^c

  
  


• 
  

  Asparaginase^c

  
  


• 
  

  Corticosteroids^c

  
  


• 
  

  Niacin (sustained-release)^c

  
  

Thyroid Pharmacokinetics

Absorption

Bioavailability

Levothyroxine: Variably absorbed from the GI tract (range: 40–80%).^{b c} Extent of absorption is increased in the fasting state and decreased in malabsorption states.^{b c}

Liothyronine: Almost completely absorbed from the GI tract (about 95%).^{b c}

Absorption of hormones contained in natural thyroid agent preparations is similar to that of synthetic hormones.^{b c d} However, commercially available natural thyroid preparations have different T₄:T₃ ratios and fluctuating T₃ concentrations.^{a c m} (See General under Dosage and Administration.)

Onset

Peak therapeutic effects may not be attained for 1–3 weeks.^c

Duration

Therapeutic effects are maintained for 1–3 weeks following discontinuance of therapy.^c

Food

Infant soybean formula may decrease absorption.ⁿ

Distribution

Extent

T₄ is distributed throughout most body tissues and fluids; highest concentrations found in liver and kidneys.^c

Thyroid hormones do not readily cross the placenta;^{b c h} however, some transfer does occur, as evidenced by levels in cord blood of athyrotic fetuses being approximately one-third maternal levels.ⁿ

Thyroid hormones are minimally distributed into breast milk.^{b c}

Plasma Protein Binding

Circulating thyroid hormones are >99% bound to serum proteins, including TBG, thyroxine-binding prealbumin (TBPA), and albumin.^{b c} T₄ is more extensively and firmly bound to TBG and TBPA than T₃.^{b c} Only unbound hormone is metabolically active.^b

Elimination

Metabolism

T₄ and T₃ are metabolized principally in the liver through sequential deiodination.^{c n} Approximately 80% of the daily dose of T₄ is deiodinated to yield equal amounts of T₃ and reverse T₃ (rT₃).ⁿ T₃ and rT₃ are further deiodinated to diiodothyronine.^{c n} Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation.^{b c}

Elimination Route

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

Half-life

T₄: Approximately 6–7 days.^c

T₃: Approximately 1–2 days.^c

These plasma half-lives are decreased in patients with hyperthyroidism and increased in those with hypothyroidism.^c

Stability

Storage

Oral

Tablets

Tight containers at 15–30°C.^{a b} Protect from moisture and light.^a

ActionsActions

• 
  

  Thyroid hormones (T₄ and T₃) regulate multiple metabolic processes, including augmentation of cellular respiration and thermogenesis, as well as metabolism of proteins, carbohydrates, and lipids.ⁿ

  
  


• 
  

  Thyroid hormones also play an essential role in normal growth and development and normal maturation of the CNS and bone.^c The protein anabolic effects of thyroid hormones are essential for normal growth and development.^{c n}

  
  


• 
  

  The physiologic actions of thyroid hormones are produced predominantly by T₃, most of which (approximately 80%) is derived from T₄ by deiodination in peripheral tissues.^{a b c}

  
  


• 
  

  T₃ is 4 times more potent than T₄.^b

  
  

Advice to Patients

• 
  

  Importance of understanding the need to continue thyroid agent therapy for life, unless transient hypothyroidism is suspected.^b

  
  


• 
  

  Importance of taking thyroid exactly as prescribed.ⁿ Do not alter regimen or discontinue therapy unless directed by a clinician.ⁿ

  
  


• 
  

  Risk of transient hair loss.^{b c} Importance of immediately informing a clinician if 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 occurs.^{b c e m n}

  
  


• 
  

  Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and herbal supplements, as well as concomitant illnesses (e.g., cardiovascular disease, diabetes mellitus, clotting disorders, adrenal or pituitary gland problems.)^{b c}

  
  


• 
  

  In patients with diabetes mellitus, importance of monitoring blood and/or urinary glucose levels and immediately reporting any changes to a clinician.^{b c n} In patients receiving concomitant anticoagulant therapy, importance of monitoring clotting status frequently.^{b c}

  
  


• 
  

  Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.^b Dosage may need to be increased during pregnancy.^e

  
  


• 
  

  Importance of informing physician or dentist of current thyroid hormone therapy prior to any surgery.^c

  
  


• 
  

  Importance of informing patients of other important precautionary information.^b (See Cautions.)

  
  

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Thyroid

Routes	Dosage Forms	Strengths	Brand Names	Manufacturer
Oral	Tablets	15 mg*	Armour Thyroid	Forest
		16.25 mg	Nature-Throid	Western Research
		30 mg*	Armour Thyroid	Forest
		32.5 mg	Nature-Throid	Western Research
			Westhroid	Western Research
		60 mg*	Armour Thyroid	Forest
		65 mg*	Nature-Throid	Western Research
			Westhroid	Western Research
		90 mg*	Armour Thyroid	Forest
		120 mg*	Armour Thyroid	Forest
		130 mg*	Nature-Throid	Western Research
			Westhroid	Western Research
		180 mg*	Armour Thyroid	Forest
		195 mg	Nature-Throid	Western Research
		240 mg	Armour Thyroid	Forest
		300 mg*	Armour Thyroid	Forest

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 03/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Armour Thyroid 120MG Tablets (FOREST): 30/$18.99 or 90/$34.97

Armour Thyroid 15MG Tablets (FOREST): 30/$14.99 or 60/$18.97

Armour Thyroid 180MG Tablets (FOREST): 30/$23.99 or 90/$52.97

Armour Thyroid 240MG Tablets (FOREST): 30/$29.99 or 90/$69.97

Armour Thyroid 30MG Tablets (FOREST): 30/$14.99 or 90/$22.97

Armour Thyroid 300MG Tablets (FOREST): 30/$32.99 or 90/$79.97

Armour Thyroid 60MG Tablets (FOREST): 30/$14.99 or 60/$19.98

Armour Thyroid 90MG Tablets (FOREST): 30/$18.99 or 60/$25.98

Nature-Throid 130MG Tablets (RLC LABS): 100/$29.99 or 200/$45.97

Nature-Throid 32.5MG Tablets (RLC LABS): 100/$19.99 or 200/$28.98

Disclaimer

This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.

The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.

AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions June 2008. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

References

a. AHFS Drug Information 2008. McEvoy GK, ed. Thyroid. Bethesda, MD: American Society of Health-System Pharmacists; 2008:3308-9.

b. Forest Pharmaceuticals, Inc. Armour Thyroid (thyroid) tablets prescribing information. St. Louis, MO; 2002 Nov.

c. AHFS Drug Information 2008. McEvoy GK, ed. Thyroid Agents General Statement. Bethesda, MD: American Society of Health-System Pharmacists; 2008:3298-302.

d. Anon. Drugs for hypothyroidism and hyperthyroidism. Treat Guidel Med Lett. 2006; 4:17-24.

e. American Association of Clinical Endocrinologists. Medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism, 2006 amended version. Endocr Pract. 2002; 8:457-69. [PubMed 15260011]

f. American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists, number 37, August 2002: Thyroid disease in Pregnancy. Obstet Gynecol. 2002; 100:387-96. [PubMed 12166417]

g. Baxter K, ed. Stockley's Drug Interactions. 7th edition. London, UK: Pharmaceutical Press; 2006: 317-8.

h. Thyroid. In: Briggs GG, Freeman RK, Yaffe SJ. Drugs in pregnancy and lactation. 7th ed. Philadelphia, PA: Lippincott, Williams, & Wilkins, 2005:1578-9.

i. Dong BJ. Thyroid Disorders. In: Koda-Kimble MA, Young LY, eds. Applied therapeutics: The clinical use of drugs. 8th ed. Philadelphia, PA: Lippincott Williams, & Wilkins; 2005:49-1–49-19.

j. Surks MI, Ortiz E, Daniels GH et al. Subclinical thyroid disease: Scientific review and guidelines for diagnosis and management. JAMA. 2004; 291:228-38. [PubMed 14722150]

l. Col NF, Surks MI, and Daniels GH. Subclinical thyroid disease: Clinical applications. JAMA. 2004; 291:239-43. [PubMed 14722151]

m. Singer PA, Cooper DS, Levy EG et al. Treatment guidelines for patients with hyperthyroidism and hypothyroi