Drugs with thyroid hormone activity, alone or with other therapeutic agents, have been used for the treatment of obesity. 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.
Hypothyroidism, primary (alternative agent):
Note: Current guidelines do not recommend desiccated thyroid for treatment of hypothyroidism (primary or secondary); levothyroxine monotherapy is preferred. Avoid use during pregnancy (ATA [Jonklaas 2014]; ATA/AACE [Garber 2012]; ES [Fleseriu 2016]). Tablet strengths may vary by manufacturer in terms of grains or milligrams; dosing recommendations are based on general clinical equivalencies that 1 grain = 60 mg or 65 mg (depending on formulation).
Oral: Initial: 30 or 32.5 mg/day; in patients with cardiovascular disease or long-standing myxedema, initiate at 15 or 16.25 mg/day. May increase dose in 7.5 to 16.25 mg/day increments every 6 weeks if needed based on TSH levels; usual dose range: 60 to 130 mg/day (Hoang 2013; Shakir 2021; manufacturer's labeling). Inadequate response to doses up to 180 or 195 mg/day may suggest missed doses or malabsorption.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
(For additional information see "Thyroid extract (desiccated thyroid): Pediatric drug information")
Note: Doses presented as mg/kg/dose or mg/dose; closely review dosing units; adjust dose based upon clinical response and laboratory parameters. Tablet strengths may vary by manufacturer in terms of grains or mg; dosing recommendations are based on general clinical equivalencies that 1 grain = 60 mg or 65 mg; 1/2 grain = 30 mg or 32.5 mg; and 1/4 grain = 15 mg or 16.25 mg.
Congenital hypothyroidism: Note: Guidelines do not recommend routine use of desiccated thyroid over levothyroxine monotherapy in the management of hypothyroidism (AAP 2006; ATA [Jonklaas 2014]). Infants should have therapy initiated at full doses; Oral:
Infants 1 to 6 months: 4.8 to 6 mg/kg/dose or 15 to 32.5 mg/dose once daily
Infants >6 to 12 months: 3.6 to 4.8 mg/kg/dose or 30 to 48.75 mg/dose once daily
Children 1 to 5 years: 3 to 3.6 mg/kg/dose or 45 to 65 mg/dose once daily
Children 6 to 12 years: 2.4 to 3 mg/kg/dose or 60 to 97.5 mg/dose once daily
Adolescents: Typical doses 1.2 to 1.8 mg/kg/dose or >90 mg/dose once daily
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
Avoid use (Beers Criteria [AGS 2019]).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Armour Thyroid: 15 mg, 30 mg, 60 mg, 90 mg, 120 mg
Armour Thyroid: 180 mg [scored]
Armour Thyroid: 240 mg
Armour Thyroid: 300 mg [scored]
Nature-Throid: 16.25 mg [DSC], 32.5 mg [DSC]
Nature-Throid: 48.75 mg [DSC], 65 mg [DSC], 81.25 mg [DSC], 97.5 mg [DSC], 113.75 mg [DSC], 130 mg [DSC], 146.25 mg [DSC], 162.5 mg [DSC], 195 mg [DSC], 260 mg [DSC], 325 mg [DSC] [scored]
NP Thyroid: 15 mg, 30 mg, 60 mg, 90 mg, 120 mg
Westhroid: 32.5 mg [DSC]
Westhroid: 65 mg [DSC], 97.5 mg [DSC], 130 mg [DSC], 195 mg [DSC] [scored]
WP Thyroid: 16.25 mg [DSC], 32.5 mg [DSC]
WP Thyroid: 48.75 mg [DSC], 65 mg [DSC], 81.25 mg [DSC], 97.5 mg [DSC], 113.75 mg [DSC], 130 mg [DSC] [scored]
Generic: 15 mg [DSC], 30 mg [DSC], 60 mg [DSC], 90 mg [DSC], 120 mg [DSC]
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Generic: 30 mg, 60 mg, 125 mg
Oral: Administer on an empty stomach (eg, 30 to 60 minutes prior to breakfast) to increase absorption.
Oral: Administer on an empty stomach (eg, 30 to 60 minutes before breakfast) to increase absorption.
Hypothyroidism: Replacement or supplemental therapy in hypothyroidism
Beers Criteria: Desiccated thyroid is identified in the Beers Criteria as a potentially inappropriate medication to be avoided in patients 65 years and older (independent of diagnosis or condition) due to concerns for cardiac effects; safer alternatives available (Beers Criteria [AGS 2019]).
Pharmacy Quality Alliance (PQA): Desiccated thyroid is identified as a high-risk medication in patients 65 years and older on the PQA’s, Use of High-Risk Medications in the Elderly (HRM) performance measure, a safety measure used by the Centers for Medicare and Medicaid Services (CMS) for Medicare plans (PQA 2017).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions are often indicative of excess thyroid replacement and/or hyperthyroidism.
<1%, postmarketing, and/or case reports: Abdominal cramps, alopecia, ataxia, cardiac arrhythmia, chest pain, constipation, diaphoresis, diarrhea, dyspnea, fever, headache, heat intolerance, increased appetite, insomnia, menstrual disease, myalgia, nervousness, palpitations, tachycardia, tremor, tremor of hands, vomiting, weight loss
Hypersensitivity to any component of the formulation; untreated thyrotoxicosis; uncorrected adrenal insufficiency
Disease-related concerns:
• Adrenal insufficiency: Use with caution in patients with adrenal insufficiency; symptoms may be exaggerated or aggravated; contraindicated in patients with uncorrected adrenal insufficiency. Treatment with glucocorticoids should precede thyroid replacement therapy in patients with adrenal insufficiency (ATA/AACE [Garber 2012]).
• Cardiovascular disease: Use reduced initial dosage and conservative dose titration in patients with cardiovascular disease. Overtreatment may increase risk of adverse cardiovascular events, including angina and arrhythmia; patients with developing or worsening cardiac symptoms should have their dose reduced or therapy withheld for 7 days and then resumed at a reduced dose. Chronic untreated hypothyroidism predisposes patients to cardiovascular disease (ATA [Jonklaas 2014]; Razvi 2018).
• Diabetes: Use with caution in patients with diabetes mellitus and diabetes insipidus; symptoms may be exaggerated or aggravated.
• Myxedema: Use with caution in patients with myxedema; symptoms may be exaggerated or aggravated; initial dosage reduction is recommended in patients with long-standing myxedema.
Dosage form specific issues:
• Desiccated thyroid: Contains variable amounts of T3, T4, and other triiodothyronine compounds which are more likely to cause cardiac signs or symptoms due to fluctuating thyroid hormone levels.
Other warnings/precautions:
• Infertility (unapproved use): Thyroid supplements are not recommended for the treatment of female or male infertility, unless associated with hypothyroidism.
• Porcine derived: Some desiccated thyroid products are acquired from porcine thyroid glands of pigs processed for human food; production also occurs at a facility that handles bovine tissues from cows processed for human food. Contamination with porcine or bovine viruses, or other novel or unidentified viruses, is potentially a risk; however, there have been no reported cases of transmission of an infectious illness.
• Weight reduction (unapproved use): [US Boxed Warning]: In euthyroid patients, thyroid supplements within the range of daily hormonal requirements are ineffective for weight reduction. High doses may produce serious or even life-threatening toxic effects particularly when used with some anorectic drugs (eg, sympathomimetic amines).
Overtreatment may result in craniosynostosis in infants and premature closure of epiphyses in children; monitor use closely. May cause transient alopecia in children during the first few months of therapy. In neonates and infants, cardiac overload, arrhythmias, and aspiration from avid suckling may occur during initiation of therapy (eg, first 2 weeks); monitor closely.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Amezinium: Thyroid Products may enhance the stimulatory effect of Amezinium. Risk C: Monitor therapy
Amiodarone: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
Apalutamide: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the serum concentration of Thyroid Products. Management: Administer oral thyroid products at least 4 h prior to colesevelam, and at least 1 h before or 4-6 h after cholestyramine. Specific recommendations for colestipol are not available. Monitor for decreased concentrations/effects of the thyroid product. Risk D: Consider therapy modification
Calcium Polystyrene Sulfonate: May decrease the serum concentration of Thyroid Products. Management: Consider administering thyroid products at least 4 hours prior to calcium polystyrene sulfonate. Monitor for signs and symptoms of hypothyroidism with concomitant use. Risk D: Consider therapy modification
Calcium Salts: May diminish the therapeutic effect of Thyroid Products. Management: Separate the doses of the thyroid product and the oral calcium supplement by at least 4 hours. Monitor for decreased therapeutic effects of thyroid products if an oral calcium supplement is initiated/dose increased. Risk D: Consider therapy modification
CarBAMazepine: May decrease the serum concentration of Thyroid Products. Risk C: Monitor therapy
Cardiac Glycosides: Thyroid Products may decrease the serum concentration of Cardiac Glycosides. Specifically, returning to a euthyroid state from a hypothyroid state may decrease the serum concentration of cardiac glycosides. Risk C: Monitor therapy
Ciprofloxacin (Systemic): May decrease the serum concentration of Thyroid Products. Risk C: Monitor therapy
Estrogen Derivatives: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
Fosphenytoin: May decrease the serum concentration of Thyroid Products. Phenytoin may also displace thyroid hormones from protein binding sites. Risk C: Monitor therapy
Furosemide: May decrease the protein binding of Thyroid Products. This may lead to a transient increase in free thyroid hormone concentrations and to a later decrease in total thyroid hormone concentrations. Risk C: Monitor therapy
Lanthanum: May decrease the serum concentration of Thyroid Products. Management: Separate the administration of thyroid products and lanthanum by at least 4 hours. Risk D: Consider therapy modification
Nirmatrelvir and Ritonavir: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
PHENobarbital: May decrease the serum concentration of Thyroid Products. Risk C: Monitor therapy
Phenytoin: May decrease the serum concentration of Thyroid Products. Phenytoin may also displace thyroid hormones from protein binding sites. Risk C: Monitor therapy
Piracetam: May enhance the adverse/toxic effect of Thyroid Products. Specifically, symptoms including confusion, irritability, and sleep disorder have been described during concomitant use. Risk C: Monitor therapy
Primidone: May decrease the serum concentration of Thyroid Products. Risk C: Monitor therapy
RifAMPin: May decrease the serum concentration of Thyroid Products. Risk C: Monitor therapy
Ritonavir: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
Selective Serotonin Reuptake Inhibitors: May diminish the therapeutic effect of Thyroid Products. Thyroid product dose requirements may be increased. Risk C: Monitor therapy
Sodium Iodide I131: Thyroid Products may diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue thyroid products before sodium iodide I-131 administration, and avoid concurrent use. Stop triiodothyronine (T3) 2 weeks before, and stop thyroxine (T4) 4 weeks before, sodium iodide I-131 administration. Risk X: Avoid combination
Sodium Polystyrene Sulfonate: May decrease the serum concentration of Thyroid Products. Management: Consider administering thyroid products at least 4 hours prior to sodium polystyrene sulfonate. Monitor for signs and symptoms of hypothyroidism with concomitant use. Risk D: Consider therapy modification
Somatropin: May diminish the therapeutic effect of Thyroid Products. Risk C: Monitor therapy
Theophylline Derivatives: Thyroid Products may increase the metabolism of Theophylline Derivatives. Risk C: Monitor therapy
Tricyclic Antidepressants: Thyroid Products may enhance the arrhythmogenic effect of Tricyclic Antidepressants. Thyroid Products may enhance the stimulatory effect of Tricyclic Antidepressants. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Thyroid Products may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Overt hypothyroidism increases the risk of irregular menses and infertility; thyroid replacement is recommended to normalize thyroid function in infertile patients with overt hypothyroidism who desire to become pregnant. Thyroid replacement may also be used in infertile patients with subclinical hypothyroidism using assisted reproductive techniques to become pregnant; however, desiccated thyroid is not the preferred thyroid replacement agent (ATA [Alexander 2017]).
Endogenous thyroid hormones minimally cross the placenta. Desiccated thyroid has not been found to adversely affect the fetus following maternal use during pregnancy; however, normal levels of maternal thyroid hormones are required for fetal development. Untreated maternal hypothyroidism can be associated with adverse effects in both the mother and fetus, including spontaneous abortion, stillbirth, premature birth, low birth weight, impaired neurocognitive development in the offspring, abruptio placentae, gestational hypertension, and preeclampsia (ACOG 2020; ATA [Alexander 2017]).
Thyroid replacement therapy minimizes the risk of adverse pregnancy outcomes in patients with overt hypothyroidism and treatment is recommended for all patients with overt hypothyroidism during pregnancy (ACOG 2020; ATA [Alexander 2017]); however, maternal supplementation with desiccated thyroid does not provide the fetus with sufficient concentrations of T4 required for the developing fetal brain. Therefore, desiccated thyroid is not the preferred treatment of maternal hypothyroidism and should not be used in pregnant patients (ACOG 2020; ATA [Alexander 2017]).
Due to alterations of endogenous maternal thyroid hormones, hypothyroid patients treated with a thyroid replacement product prior to pregnancy require a dose increase as soon as pregnancy is confirmed (ATA [Alexander 2017]). Close monitoring of pregnant patients is recommended (ATA [Alexander 2017]).
Endogenous thyroid hormones are minimally present in breast milk and are not associated with adverse events.
The manufacturer recommends caution be used if desiccated thyroid is administered to a patient who is breastfeeding. When thyroid replacement therapy is needed in patients who are breastfeeding, desiccated thyroid is not the preferred thyroid replacement agent (ATA [Alexander 2017]).
Heart rate, BP, new/worsened cardiac symptoms (eg, chest pain, palpitations, edema), clinical signs of hypo- and hyperthyroidism.
Primary hypothyroidism: Measure TSH levels every 6 weeks and adjust therapy as needed until the TSH is within the goal range (ATA [Jonklaas 2014]). Free T4 (FT4) measurements may be misleading (eg, low FT4 levels despite normal TSH levels) due to the low T4 to T3 ratio (eg, 4:1) of desiccated thyroid products (Hoang 2013).
Note: Measurement of TSH is not adequate to guide treatment in patients with secondary hypothyroidism (eg, due to hypopituitarism) (ES [Fleseriu 2016]).
T4 (thyroxine) serum concentrations: Adults: ~4 to 12 mcg/dL (SI: 51 to 154 nmol/L). Note: Normal range in pregnancy: ~5.5 to 16 mcg/dL (SI: ~71 to 206 nmol/L)
T4 free (free thyroxine; free T4) serum concentrations: Adults: 0.7 to 1.8 ng/dL (SI: 9 to 23 pmol/L).
T3 total (triiodothyronine; total T3) serum concentrations: Adults: 80 to 230 ng/dL (SI: 1.2 to 3.5 nmol/L). Note: T3 levels may vary substantially throughout the day in patients taking desiccated thyroid, and therefore cannot be easily monitored (ATA/AACE [Garber 2012].
Thyroid-stimulating hormone (TSH) serum concentrations: Adults: Varies by laboratory and assay used; refer to laboratory provided reference range. If an upper and lower limit of normal for a third generation TSH assay is not available, a reference range of 0.45 to 4.12 milliunits/L should be considered (ATA/AACE [Garber 2012]). A higher target range of 4 to 6 milliunits/L has been suggested in patients >70 years (ATA [Jonklaas 2014]).
Subclinical hypothyroidism (elevated TSH; free T4 within normal range):
Severe (TSH ≥10 milliunits/L): These patients are at increased risk for heart failure and cardiovascular mortality and should be considered for treatment with L-thyroxine (ATA/AACE [Garber 2012]; ETA [Pearce 2013])
Mild to moderate (TSH 4 to 10 milliunits/L): Decision for when to treat should be tailored to individual patient based on age, symptoms, and cardiovascular risk (ATA/AACE [Garber 2012]; ETA [Pearce 2013])
The primary active compound is T3 (triiodothyronine), which may be converted from T4 (thyroxine) and then circulates throughout the body to influence growth and maturation of various tissues; exact mechanism of action is unknown; however, it is believed the thyroid hormone exerts its many metabolic effects through control of DNA transcription and protein synthesis; involved in normal metabolism, growth, and development; promotes gluconeogenesis, increases utilization and mobilization of glycogen stores and stimulates protein synthesis, increases basal metabolic rate
Onset of action: Liothyronine (T3): ~3 hours
Absorption: Thyroxine (T4): 40% to 80%; T3: 95%; desiccated thyroid contains T4, T3, and iodine (primarily bound)
Protein binding: T4: >99% bound to plasma proteins including thyroxine-binding globulin, thyroxine-binding prealbumin, and albumin
Metabolism: Hepatic to triiodothyronine (active); ~80% T4 deiodinated in kidney and periphery; glucuronidation/conjugation also occurs; undergoes enterohepatic recirculation
Half-life elimination:
T4: Euthyroid: 6 to 7 days; Hyperthyroid: 3 to 4 days; Hypothyroid: 9 to 10 days
T3: 0.75 days (Brent, 2011)
Time to peak: Serum: T4: 2 to 4 hours; T3: 2 to 3 days
Excretion: Urine (major route of elimination); partially feces
Tablets (Armour Thyroid Oral)
15 mg (per each): $0.89
30 mg (per each): $1.05
60 mg (per each): $1.16
90 mg (per each): $1.82
120 mg (per each): $2.13
180 mg (per each): $1.60
240 mg (per each): $1.94
300 mg (per each): $2.28
Tablets (NP Thyroid Oral)
15 mg (per each): $0.85
30 mg (per each): $1.00
60 mg (per each): $1.11
90 mg (per each): $1.73
120 mg (per each): $2.03
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