Medically reviewed by Drugs.com. Last updated on Jul 27, 2020.
(lye oh THYE roe neen)
- Liothyronine Sodium
- Sodium L-Triiodothyronine
- T3 Sodium (error-prone abbreviation)
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Triostat: 10 mcg/mL (1 mL) [contains alcohol, usp]
Generic: 10 mcg/mL (1 mL)
Cytomel: 5 mcg
Cytomel: 25 mcg, 50 mcg [scored]
Generic: 5 mcg, 25 mcg, 50 mcg
Brand Names: U.S.
- Thyroid Product
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
Oral: Well absorbed (95% in 4 hours)
Urine (primary); Feces
Onset of Action
Oral: Within a few hours
Peak response: Oral: 2 to 3 days
0.75 days (Brent 2011)
Use: Labeled Indications
Thyroid disorders: Oral: Replacement therapy in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism; adjunct to surgery and radioiodine therapy in the management of well-differentiated thyroid cancer; a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.
Limitations of use: Not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients; not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis.
Myxedema coma: IV: Treatment of myxedema coma.
Note: May be used in patients allergic to desiccated thyroid or thyroid extract derived from pork or beef.
Off Label Uses
Augmentation for treatment resistant depression: Data from a meta-analysis supports the use of liothyronine in depression refractory to tricyclic antidepressants [Aronson 1996]. In a randomized controlled trial, liothyronine was as effective as lithium in achieving remission as augmentation therapy in depression refractory to citalopram, sertraline, venlafaxine, or bupropion [Nierenberg 2006].
Enhancement of antidepressant action at treatment initiation: Data from a meta-analysis supports the use of liothyronine in accelerating clinical response to tricyclic antidepressants (Altchuler 2001). When combined with serotonin reuptake inhibitors, the benefit of liothyronine was inconclusive in a meta-analysis [Cooper-Kazaz 2008] and not observed in a randomized placebo-controlled trial [Garlow 2012].
Based on the American Psychiatric Association (APA) practice guidelines for the treatment of patients with major depressive disorder and the World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for treatment of unipolar depressive disorders, antidepressant augmentation with liothyronine is a suggested treatment option in patients that are partial responders or non-responders to antidepressant therapy [APA 2010], [WFSBP [Bauer 2013]].
Cadaveric organ recovery (hormonal resuscitation)
Initial data from two consecutive retrospective cohort studies of brain-dead donors who successfully donated organs suggested that the use of intravenous liothyronine given concomitantly with a continuous infusion of insulin (goal blood glucose: 120 to 180 mg/dL), methylprednisolone, and vasopressin may be beneficial for hemodynamically unstable brain-dead donors to increase the quantity and quality of organs available for transplantation [Rosendale 2003a], [ Rosendale 2003b]. Another protocol using levothyroxine (T4) has been used with success [Salim 2007]. More recently, data from a large retrospective study demonstrated significantly higher rates of organ procurement with administration of thyroid hormone versus no thyroid hormone [Novitzky 2014]. In a prospective study of 30 brain-dead cardiac donors, 16 received liothyronine infusions, which increased circulating liothyronine levels and expression of mRNA levels in cardiac tissue, but did not improve hemodynamics [James 2010].
Based on a consensus document sponsored by the American Society of Transplant Surgeons and the American Society of Transplantation, the use of liothyronine (in combination with vasopressin, methylprednisolone, and insulin) is effective and recommended for hormonal resuscitation in brain-dead donors [Rosengard 2002], [Zaroff 2002]. Additionally, a consensus statement by the Society of Critical Care Medicine, American College of Chest Physicians, and Association of Organ Procurement Organizations recommends that thyroid replacement therapy (either alone or part of combination hormone therapy) should be considered for hemodynamically unstable donors or potential cardiac donors with left ventricular ejection fraction of <45%.
Prevention of memory deficit with electroconvulsive therapy (ECT)
Results from a double-blind trial suggest that liothyronine may prevent ECT-induced memory impairment in patients with major depressive disorder [Mohagheghi 2015].
Injection: Hypersensitivity to liothyronine sodium or any component of the formulation; uncorrected adrenal insufficiency; untreated thyrotoxicosis; concurrent use with artificial rewarming of patient
Oral: Uncorrected adrenal insufficiency
Canadian labeling: Additional contraindications (not in the US labeling): Acute myocardial infarction
Hypothyroidism: Oral: Initial: 25 mcg once daily; may increase by up to 25 mcg/day every 1 to 2 weeks; usual maintenance dose: 25 to 75 mcg once daily
Patients with cardiovascular disease: Initial: 5 mcg once daily; may increase by 5 mcg/day every 2 weeks.
Conversion to liothyronine from thyroid (desiccated) or levothyroxine: Discontinue the other medication, initiate a low dose of liothyronine, and increase gradually according to response. Liothyronine has a rapid onset of action; residual effects of other thyroid preparation may persist for the first several weeks into therapy.
Myxedema coma: IV:
Adjunctive therapy in combination with levothyroxine: Initial: 5 to 20 mcg loading dose; maintenance: 2.5 to 10 mcg every 8 hours; continue therapy as clinically indicated. Lower dosages should be considered for patients who are small, elderly, or have coronary artery disease or arrhythmia. Avoid high doses due to risks associated with high serum triiodothyronine levels (ATA [Jonklaas 2014]).
Note: Normally, at least 4 hours should be allowed between IV doses to adequately assess therapeutic response and no more than 12 hours should elapse between doses to avoid fluctuations in hormone levels. Oral therapy should be resumed as soon as the clinical situation has been stabilized and the patient is able to take oral medication. If levothyroxine rather than liothyronine sodium is used in initiating oral therapy, the prescriber should bear in mind that there is a delay of several days in the onset of levothyroxine activity and that IV therapy should be discontinued gradually.
Conversion to liothyronine tablets from injectable liothyronine: Discontinue the injectable, initiate oral therapy at a low dosage, and increase gradually according to response.
Suppression test (T3): Oral: 75 to 100 mcg once daily for 7 days. Radioactive iodide uptake is determined before and after administration.
Antidepressant augmentation (off-label use): Oral: Initial: 25 mcg/day; may be increased to 50 mcg/day after ~1 week based on response and tolerability (APA 2010). Dose ranges of 20 to 62.5 mcg/day have been studied in clinical trials (Altshuler 2001; Aronson 1996; Nierenberg 2006). Note: The duration of treatment has not been well studied (APA 2010; Cooper-Kazaz 2008). If the patient has a history of multiple episodes or significant treatment resistance, long-term maintenance treatment is reasonable if there are no symptoms of hyperthyroidism and no known cardiac disease (Rosenthal 2011).
Cadaveric organ recovery (hormonal resuscitation) (off-label use): IV: Initial: 4 mcg bolus followed by a continuous infusion of 3 mcg/hour administered to the brain-dead donor who is hemodynamically unstable requiring significant vasopressor support; give concomitantly with vasopressin, methylprednisolone, and continuous regular insulin infusion (maintain blood glucose 120 to 180 mg/dL) (Rosendale 2003a; Rosendale 2003b; Rosengard 2002; SCCM/ACCP/AOPO [Kotloff 2015]; Zaroff 2002).
Prevention of memory deficit with ECT (off-label use): Oral: 50 mcg once daily administered from the day before beginning of ECT and every morning until the last session (Mohagheghi 2015). Additional data may be necessary to further define the role of liothyronine in this setting.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Hypothyroidism: Oral: 5 mcg once daily; increase by 5 mcg/day every 2 weeks.
Myxedema coma: IV: Refer to adult dosing; use with caution and initiate at the low end of the dosing range.
Suppression test (T3): Oral: Refer to adult dosing; use with caution and initiate at the low end of dosing range.
Congenital hypothyroidism:Note: Guidelines do not recommend routine use of liothyronine over levothyroxine monotherapy in the management of hypothyroidism (AAP 2006; ATA [Jonklaas 2014]). Infants, Children, and Adolescents: Oral: Initial: 5 mcg/day; increase by 5 mcg every 3 to 4 days
Usual maintenance dose:
Infants: 20 mcg/day
Children 1 to 3 years: 50 mcg/day
Children >3 years and Adolescents: 25 to 75 mcg/day
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
IV: For IV use only; do not administer IM or SubQ
Intermittent IV administration: Administer at a rate of 10 mcg/minute (Gahart 2014).
Continuous IV infusion: Cadaveric organ recovery (hormonal resuscitation) (off-label use): After IV bolus administration, may administer as a continuous infusion (Rosengard 2002; Zaroff 2002).
Vials: Store under refrigeration at 2°C to 8°C (36°F to 46°F).
Tablets: Store at 15°C to 30°C (59°F to 86°F).
Amezinium: Thyroid Products may enhance the stimulatory effect of Amezinium. Monitor therapy
Amiodarone: May diminish the therapeutic effect of Thyroid Products. Monitor therapy
Apalutamide: May diminish the therapeutic effect of Thyroid Products. 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. Consider therapy modification
Calcium Polystyrene Sulfonate: May decrease the serum concentration of Thyroid Products. Management: To minimize risk of interaction, separate dosing of oral calcium polystyrene sulfonate and thyroid products (eg, levothyroxine) or administer calcium polystyrene sulfonate rectally. Monitor for signs/symptoms of hypothyroidism with concomitant use (oral). 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. Consider therapy modification
CarBAMazepine: May decrease the serum concentration of Thyroid Products. 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. Monitor therapy
Ciprofloxacin (Systemic): May decrease the serum concentration of Thyroid Products. Monitor therapy
Estrogen Derivatives: May diminish the therapeutic effect of Thyroid Products. Monitor therapy
Fosphenytoin: May decrease the serum concentration of Thyroid Products. Phenytoin may also displace thyroid hormones from protein binding sites. 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. Monitor therapy
Growth Hormone Analogs: May diminish the therapeutic effect of Thyroid Products. 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. Consider therapy modification
Phenytoin: May decrease the serum concentration of Thyroid Products. Phenytoin may also displace thyroid hormones from protein binding sites. 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. Monitor therapy
RifAMPin: May decrease the serum concentration of Thyroid Products. Monitor therapy
Ritonavir: May diminish the therapeutic effect of Thyroid Products. Monitor therapy
Selective Serotonin Reuptake Inhibitors: May diminish the therapeutic effect of Thyroid Products. Thyroid product dose requirements may be increased. 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. Avoid combination
Sodium Polystyrene Sulfonate: May decrease the serum concentration of Thyroid Products. Management: To minimize risk of interaction, separate dosing of oral sodium polystyrene sulfonate and thyroid products (e.g., levothyroxine) or administer sodium polystyrene sulfonate rectally. Monitor for signs/symptoms of hypothyroidism with concomitant use (oral). Consider therapy modification
Theophylline Derivatives: Thyroid Products may increase the metabolism of Theophylline Derivatives. Monitor therapy
Tricyclic Antidepressants: Thyroid Products may enhance the arrhythmogenic effect of Tricyclic Antidepressants. Thyroid Products may enhance the stimulatory effect of Tricyclic Antidepressants. Monitor therapy
Vitamin K Antagonists (eg, warfarin): Thyroid Products may enhance the anticoagulant effect of Vitamin K Antagonists. Monitor therapy
T4-binding globulin (TBG): Factors that alter binding in serum (ATA/AACE [Garber 2012]):
Note: T4 is ~99.97% protein bound. Factors that alter protein binding will affect serum total T4 levels; however, measurement of serum free T4 (the metabolically active moiety) has largely replaced serum total T4 for thyroid status assessment.
Conditions/states that increase TBG binding: Pregnancy, hepatitis, porphyria, neonatal state
Medications that increase TBG binding: Estrogens, 5-fluorouracil, heroin, methadone, mitotane, perphenazine, selective estrogen receptor modulators (eg, tamoxifen, raloxifene)
Conditions/states that decrease TBG binding: Hepatic failure, nephrosis, severe illness
Medications that decrease TBG binding: Androgens, anabolic steroids, glucocorticoids, L-asparaginase, nicotinic acid
Thyroxine (T4) and Triiodothyronine (T3): Serum binding inhibitors (ATA/AACE [Garber 2012]):
Medications that inhibit T4 and T3 binding: Carbamazepine, furosemide, free fatty acids, heparin, NSAIDS (variable, transient), phenytoin, salicylates
Thyroid gland hormone: Interference with production and secretion (ATA/AACE [Garber 2012]):
Medications affecting iodine uptake: Amiodarone, iodinated contrast agents, iodine, ethionamide
Medications affecting hormone production: Amiodarone, ethionamide, iodinated contrast agents, iodine, sulfonylureas, sulfonamides, thionamides (carbimazole, methimazole, propylthiouracil)
Medications affecting secretion: Amiodarone, iodinated contrast agents, iodine, lithium
Medications inducing thyroiditis: Alemtuzumab, amiodarone, antiangiogenic agents (lenalidomide, thalidomide), denileukin diftitox, interferon alpha, interleukins, lithium, tyrosine kinase inhibitors (sunitinib, sorafenib)
Medications potentially causing the development of Graves’: Alemtuzumab, interferon alpha, antiretroviral therapy
Medications potentially ameliorating thyroiditis (if autoimmune) or Graves’: Glucocorticoids
Hypothalamic-pituitary axis and TSH: Interference with secretion (ATA/AACE [Garber 2012]):
Medications decreasing TSH secretion: Bexarotene, dopamine, dopaminergic agonists (bromocriptine, cabergoline), glucocorticoids, interleukin-6, metformin, opiates, somatostatin analogues (octreotide, lanreotide), thyroid hormone analogues
Medications increasing TSH secretion: Amphetamine, interleukin 2, metoclopramide, ritonavir, St John's wort
Medications potentially causing hypophysitis: Ipilimumab
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%: Cardiovascular: Cardiac arrhythmia (6%), tachycardia (3%), hypotension (≤2%), myocardial infarction (≤2%)
<1%, postmarketing, and/or case reports: Allergic skin reaction, angina pectoris, cardiac failure, fever, hypertension, phlebitis, twitching
ALERT: U.S. Boxed WarningWeight reduction:
Thyroid hormones, including liothyronine, 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.
• Adrenal insufficiency: Use with caution in patients with adrenal insufficiency; symptoms may be exaggerated or aggravated. Treatment with glucocorticoids should precede thyroid replacement therapy in patients with adrenal insufficiency. Use is contraindicated in patients with uncorrected adrenal insufficiency.
• 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 (may worsen glycemic control).
• Myxedema: Use with caution in patients with myxedema because symptoms may be exaggerated or aggravated. Initiate therapy at a low dose and increase gradually. Myxedema coma should be treated with injectable thyroid hormone replacement products administered IV.
• Osteoporosis: Long-term therapy can decrease bone mineral density. Postmenopausal women and women using suppressive doses should receive the lowest dose necessary for clinical response.
• Elderly: Use with caution in elderly patients; they may be more likely to have compromised cardiovascular function. Increase dose slowly and monitor for signs/symptoms of angina.
• Weight reduction (off-label use): [US Boxed Warning]: Thyroid hormones, including liothyronine, either alone or with other therapeutic agents, should not be used for the treatment of obesity or for weight loss. Thyroid supplements are ineffective and potentially toxic for weight reduction. High doses may produce serious or even life-threatening toxic effects particularly when used with some anorectic drugs.
Thyroid-stimulating hormone (TSH) 4 to 6 weeks after treatment initiation or dose changes, 4 to 6 months after adequate replacement dose determined, followed by every 12 months thereafter (or more frequently depending on clinical situation) (ATA [Jonklaas 2014]); heart rate, blood pressure, new/worsened cardiac symptoms (eg, chest pain, palpitations, edema); clinical signs of hypo- and hyperthyroidism; bone mineral density (particularly with long-term use in postmenopausal women).
Note: TSH is the most reliable guide for evaluating adequacy of thyroid replacement dosage in primary thyroid dysfunction; however, measurement of TSH is not adequate to guide treatment in patients with central hypothyroidism (ATA/AACE [Garber 2012]; ES [Fleseriu 2016]).
Myxedema coma: Monitor thyroid function tests (FT4 or T4, T3) every 1 to 2 days; serial assessment of TSH trends may also be considered to determine trend towards improvement. Monitor clinical response (eg, mental status, temperature, respiratory function, cardiovascular status, electrolytes [eg, serum sodium]) to ensure adequate parenteral thyroid hormone replacement; monitor also for safety with parenteral therapy (eg, tachycardia, arrhythmia, myocardial infarction) (ATA [Jonklaas 2014]).
Antidepressant augmentation (off-label use): Adults: Free T3, free T4, and TSH (baseline, recheck at 3 months, and then every 6 months to 1 year at minimum). TSH level should be at least at the lower limit of the normal range [~0.4 milliunits/ml] or below in the absence of hyperthyroid symptoms; free T3 can be maintained at the upper limit of the normal range based on the severity of depressive symptoms and response to T3.
Overt hypothyroidism increases the risk of irregular menses and infertility; thyroid replacement is recommended to normalize thyroid function in infertile females with overt hypothyroidism who desire pregnancy. Thyroid replacement may also be used in infertile females with subclinical hypothyroidism using assisted reproductive techniques. However, liothyronine is not the preferred thyroid replacement agent (ATA [Alexander 2017]).
Liothyronine has not been found to increase the risk of teratogenic or adverse effects following maternal use during pregnancy.
Maternal hypothyroidism, however, can be associated with adverse effects in 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 148 2015; ATA [Alexander 2017]).
Thyroid replacement therapy minimizes the risk of adverse pregnancy outcomes in females with overt hypothyroidism and treatment is recommended during pregnancy (ACOG 148 2015; ATA [Alexander 2017]). Thyroid replacement therapy is also recommended in some cases of subclinical hypothyroidism during pregnancy and overt hypothyroidism in females with postpartum thyroiditis (ACOG 148 2015; ATA [Alexander 2017]; ES [De Groot 2012]). However, maternal supplementation with liothyronine does not provide the fetus with sufficient concentrations of T4 required for the developing fetal brain. Therefore, liothyronine is not the preferred treatment of maternal hypothyroidism and should not be used in pregnant females (ACOG 148 2015; ATA [Alexander 2017]; ES [De Groot 2012]).
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]; ES [De Groot 2012]). Close monitoring of pregnant patients is recommended (ATA [Alexander 2017]).
What is this drug used for?
• It is used to add thyroid hormone to the body.
• It is used to manage thyroid cancer.
• It is used to test for thyroid problems.
• It may be given to you for other reasons. Talk with the doctor.
All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away:
• Hair loss
WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your doctor or get medical help right away if you have any of the following signs or symptoms that may be related to a very bad side effect:
• Passing out
• Vision changes
• Increased thyroid hormone like heat sensitivity, shakiness, loss of strength and energy, more or less hungry, anxiety, irritability, weight loss, sweating a lot, headache, anxiety, mood changes, trouble sleeping, muscle weakness, leg cramps, fast heartbeat, abnormal heartbeat, chest pain, shortness of breath, excessive weight gain or loss, swelling of arms or legs, diarrhea, vomiting, abdominal cramps, flushing, bone pain, menstrual changes, or trouble getting pregnant
• Severe headache
• Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing, swallowing, or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat.
Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.
Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a limited summary of general information about the medicine's uses from the patient education leaflet and is not intended to be comprehensive. This limited summary does NOT include all information available about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not intended to provide medical advice, diagnosis or treatment and does not replace information you receive from the healthcare provider. For a more detailed summary of information about the risks and benefits of using this medicine, please speak with your healthcare provider and review the entire patient education leaflet.
More about liothyronine
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- Drug class: thyroid drugs
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- Liothyronine (Advanced Reading)
- Liothyronine Intravenous (Advanced Reading)
- Liothyronine Tablets
- Liothyronine Injection
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