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Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T4, levothyroxine) sodium or triiodothyronine (T3, liothyronine) sodium or both. T4 and T3 are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T4 contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine (DIT). T3 contains three atoms of iodine and is formed by the coupling of one molecule of DIT with one molecule of monoiodotyrosine (MIT). Both hormones are stored in the thyroid colloid as thyroglobulin.
Thyroid hormone preparations belong to two categories: (1) natural hormonal preparations derived from animal thyroid, and (2) synthetic preparations. Natural preparations include desiccated thyroid and thyroglobulin. Desiccated thyroid is derived from domesticated animals that are used for food by man (either beef or hog thyroid), and thyroglobulin is derived from thyroid glands of the hog. The United States Pharmacopeia (USP) has standardized the total iodine content of natural preparations. Thyroid USP contains not less than (NLT) 0.17 percent and not more than (NMT) 0.23 percent iodine, and thyroglobulin contains not less than (NLT) 0.7 percent of organically bound iodine. Iodine content is only an indirect indicator of true hormonal biologic activity.
Cytomel (liothyronine sodium) Tablets contain liothyronine (L-triiodothyronine or LT3), a synthetic form of a natural thyroid hormone, and is available as the sodium salt.
The structural and empirical formulas and molecular weight of liothyronine sodium are given below.
 |
L-Tyrosine, O-(4-hydroxy-3-iodophenyl)-3,5-diiodo-, monosodium salt
Twenty-five mcg of liothyronine is equivalent to approximately 1 grain of desiccated thyroid or thyroglobulin and 0.1 mg of L-thyroxine.
Each round, white to off-white Cytomel (liothyronine sodium) tablet contains liothyronine sodium equivalent to liothyronine as follows: 5 mcg debossed KPI and 115; 25 mcg scored and debossed KPI and 116; 50 mcg scored and debossed KPI and 117. Inactive ingredients consist of calcium sulfate, gelatin, corn starch, stearic acid, sucrose and talc.
CYTOMEL is indicated as a replacement therapy in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism.
CYTOMEL is indicated as an adjunct to surgery and radioiodine therapy in the management of welldifferentiated thyroid cancer.
CYTOMEL is indicated as a diagnostic agent in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.
The dose of CYTOMEL for hypothyroidism or pituitary 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 Recommended Dosage For Hypothyroidism, Recommended Dosage For TSH Suppression In Well-Differentiated Thyroid Cancer, Recommended Dosage For Thyroid Suppression Test, WARNINGS AND PRECAUTIONS, and DRUG INTERACTIONS]. 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 Recommended Dosage For Thyroid Suppression Test].
Administer CYTOMEL tablets orally once daily.
The recommended starting dosage is 25 mcg orally once daily. Increase the dose by 25 mcg daily every 1 or 2 weeks, if needed. The usual maintenance dose is 25 mcg to 75 mcg once daily.
For elderly patients or patients with underlying cardiac disease, start with CYTOMEL 5 mcg once daily and increase by 5 mcg increments at the recommended intervals.
Serum TSH is not a reliable measure of CYTOMEL dose adequacy in patients with secondary or tertiary hypothyroidism and should not be used to monitor therapy. Use the serum T3 level to monitor adequacy of therapy in this patient population.
The recommended starting dosage is 5 mcg once daily, with a 5 mcg increase every 3 to 4 days until the desired response is achieved. Infants a few months old may require 20 mcg once daily for maintenance. At 1 year of age, 50 mcg once daily may be required. Above 3 years of age, the full adult dosage may be necessary [see Use In Specific Populations].
Newborns (0 to 3 months) at Risk for Cardiac Failure
Consider a lower starting dose in infants at risk for cardiac failure. Increase the dose as needed based on clinical and laboratory response.
Pediatric Patients at Risk for Hyperactivity
To minimize the risk of hyperactivity in pediatric patients, start at one-fourth the recommended full replacement dose, and increase on a weekly basis by one-fourth the full recommended replacement dose until the full recommended replacement dose is reached.
Pre-existing Hypothyroidism
Thyroid hormone dose requirements may increase during pregnancy. Measure serum TSH and free-T4 as soon as pregnancy is confirmed and, at minimum, during each trimester of pregnancy. In patients with primary hypothyroidism, maintain serum TSH in the trimesterspecific reference range. For patients with serum TSH above the normal trimester-specific range, increase the dose of thyroid hormone and measure TSH every 4 weeks until a stable dose is reached and serum TSH is within the normal trimester-specific range. Reduce thyroid hormone dosage to prepregnancy levels immediately after delivery and measure serum TSH levels 4 to 8 weeks postpartum to ensure thyroid hormone dose is appropriate.
The dose of CYTOMEL should target TSH levels within the desired therapeutic range. This may require higher doses, depending on the target level for TSH suppression.
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 CYTOMEL. 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.
CYTOMEL has a rapid onset of action and residual effects of the other thyroid preparation may persist for the first several weeks after initiating CYTOMEL therapy. When switching a patient to CYTOMEL, discontinue levothyroxine therapy and initiate CYTOMEL at a low dosage. Gradually increase the CYTOMEL dose according to the patient's response.
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 CYTOMEL may be evidence of inadequate absorption, poor compliance, drug interactions, or a combination of these factors.
In adult patients with primary hypothyroidism, monitor serum TSH periodically after initiation of the therapy or any change in dose. To check the immediate response to therapy before the TSH has had a chance to respond or if your patient's status needs to be assessed prior to that point, measurement of total T3 would be most appropriate. In patients on a stable and appropriate replacement dose, evaluate clinical and biochemical response every 6 to 12 months and whenever there is a change in the patient's clinical status.
In pediatric patients with hypothyroidism, assess the adequacy of replacement therapy by measuring serum TSH and T3 levels. For pediatric patients three years of age and older, the recommended monitoring is every 3 to 12 months thereafter, following dose stabilization until growth and puberty are completed. Poor compliance or abnormal values may necessitate more frequent monitoring. Perform routine clinical examination, including assessment of development, mental and physical growth, and bone maturation, at regular intervals.
While the general aim of therapy is to normalize the serum TSH level, TSH may not normalize in some patients due to in utero hypothyroidism causing a resetting of pituitary-thyroid feedback. Failure of the serum TSH to decrease below 20 IU per liter after initiation of CYTOMEL therapy may indicate the child is not receiving adequate therapy. Assess compliance, dose of medication administered, and method of administration prior to increasing the dose of CYTOMEL [see WARNINGS AND PRECAUTIONS and Use In Specific Populations].
Monitor serum T3 levels and maintain in the normal range.
Tablets (round, white to off-white) available as follows:
CYTOMEL tablets (round, white to off-white) are supplied as follows:
| Strength | Tablet Markings | NDC – bottles of 100 |
| 5 mcg | Debossed with KPI on one side and 115 on the other side | 60793-115-01 |
| 25 mcg | Scored on one side and debossed with KPI and 116 on the other side | 60793-116-01 |
| 50 mcg | Scored on one side and debossed with KPI and 117 on the other side | 60793-117-01 |
Store between 15°C and 30°C (59°F and 86°F).
Manufacture by: Pfizer Inc New York, NY 10017. Revised: Jul 2019
Adverse reactions associated with CYTOMEL therapy are primarily those of hyperthyroidism due to therapeutic overdosage [see WARNINGS AND PRECAUTIONS and OVERDOSE]. 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
Pseudotumor cerebri and slipped capital femoral epiphysis have been reported in pediatric patients receiving thyroid replacement therapy. Overtreatment may result in craniosynostosis in infants and premature closure of the epiphyses in pediatric patients with resultant compromised adult height.
Hypersensitivity reactions to inactive ingredients have occurred in patients treated with thyroid hormone products. These include urticaria, pruritus, skin rash, flushing, angioedema, various gastrointestinal symptoms (abdominal pain, nausea, vomiting and diarrhea), fever, arthralgia, serum sickness and wheezing.
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 CYTOMEL (see Tables 1 – 4).
Table 1: Drugs That May Decrease T3 Absorption (Hypothyroidism)
| Potential impact: Concurrent use may reduce the efficacy of CYTOMEL by binding and delaying or preventing absorption, potentially resulting in hypothyroidism.Effect | |
| Drug or Drug Class | Effect |
Bile Acid Sequestrants
|
Bile acid sequestrants and ion exchange resins are known to decrease thyroid hormones absorption. Administer CYTOMEL at least 4 hours prior to these drugs or monitor TSH levels. |
Table 2: Drugs That May Alter Triiodothyronine (T3) Serum Trans port Without Affecting Free Thyroxine (FT4) Concentration (Euthyroidism)
| Drug or Drug Class | Effect |
| Clofibrate Estrogen containing oral contraceptives Estrogens (oral) Heroin / Methadone 5-Fluorouracil Mitotane Tamoxifen |
These drugs may increase serum thyroxine-binding globulin (TBG) concentration. |
| Androgens / Anabolic Steroids Asparaginase Glucocorticoids Slow-Release Nicotinic Acid |
These drugs may decrease serum TBG concentration. |
| Salicylates (>2 g/day) | Salicylates inhibit binding of T4 and T3 to TBG and transthyretin. An initial increase in serum FT4 is followed by return of FT4 to normal levels with sustained therapeutic serum salicylate concentrations, although total T4 levels may decrease by as much as 30%. |
| Other drugs: Carbamazepine Furosemide (>80 mg IV) Heparin Hydantoins Non- Steroidal Antiinflammatory Drugs - Fenamates |
These drugs may cause protein binding site displacement. Furosemide has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increased free-T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. Phenytoin and carbamazepine reduce serum protein binding of thyroid hormones, and total and FT4 may be reduced by 20% to 40%, but most patients have normal serum TSH levels and are clinically euthyroid. Closely monitor thyroid hormone parameters. |
Table 3: Drugs That May Alter Hepatic Metabolism of Thyroid hormones
| Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of thyroid hormones, resulting in increased CYTOMEL requirements. | |
| Drug or Drug Class | Effect |
| Phenobarbital Rifampin |
Phenobarbital has been shown to reduce the response to thyroxine. Phenobarbital increases L-thyroxine metabolism by inducing uridine 5'-diphospho-glucuronosyltransferase (UGT) and leads to a lower T4 serum levels. Changes in thyroid status may occur if barbiturates are added or withdrawn from patients being treated for hypothyroidism. Rifampin has been shown to accelerate the metabolism of thyroid hormones. |
Table 4: Drugs That May Decrease Conversion of T4 to T3
| Potential impact: Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased. | |
| Drug or Drug Class | Effect |
| Beta-adrenergic antagonists (e.g., Propranolol >160 mg/day) | In patients treated with large doses of propranolol (>160 mg/day), T3 and T4 levels change, TSH levels remain normal, and patients are clinically euthyroid. Actions of particular beta-adrenergic antagonists may be impaired when a hypothyroid patient is converted to the euthyroid state. |
| Glucocorticoids (e.g., Dexamethasone ≥4 mg/day) | Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels. However, long-term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (see above). |
| Other drugs: Amiodarone | Amiodarone inhibits peripheral conversion of levothyroxine (T4) to triiodothyronine (T3) and may cause isolated biochemical changes (increase in serum free-T4, and decreased or normal free-T3) in clinically euthyroid patients. |
Addition of CYTOMEL 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 CYTOMEL is started, changed, or discontinued [see WARNINGS AND PRECAUTIONS].
CYTOMEL 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 CYTOMEL dose is increased. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments.
CYTOMEL 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.
Concurrent use of tricyclic (e.g., amitriptyline) or tetracyclic (e.g., maprotiline) antidepressants and CYTOMEL 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. CYTOMEL may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on CYTOMEL may result in increased CYTOMEL requirements.
Concurrent use of ketamine and CYTOMEL may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients.
Concurrent use of sympathomimetics and CYTOMEL 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.
Concurrent use of tyrosine-kinase inhibitors such as imatinib may cause hypothyroidism. Closely monitor TSH levels in such patients.
Consider changes in TBG concentration when interpreting T4 and T3 values. Measure and evaluate unbound (free) hormone in this circumstance. Pregnancy, infectious hepatitis, estrogens, estrogencontaining 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.
Included as part of the "PRECAUTIONS" Section
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 CYTOMEL therapy in this population at lower doses than those recommended in younger individuals or in patients without cardiac disease [see DOSAGE AND ADMINISTRATION and Use In Specific Populations].
Monitor for cardiac arrhythmias during surgical procedures in patients with coronary artery disease receiving suppressive CYTOMEL therapy. Monitor patients receiving concomitant CYTOMEL and sympathomimetic agents for signs and symptoms of coronary insufficiency. If cardiovascular symptoms develop or worsen, reduce or withhold the CYTOMEL dose for one week and restart at a lower dose.
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.
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 CYTOMEL [see CONTRAINDICATIONS].
CYTOMEL has a narrow therapeutic index. Over- or undertreatment with CYTOMEL 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 CYTOMEL carefully and monitor response to titration to avoid these effects [see DOSAGE AND ADMINISTRATION]. Monitor for the presence of drug or food interactions when using CYTOMEL and adjust the dose as necessary [see DRUG INTERACTIONS and CLINICAL PHARMACOLOGY].
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 CYTOMEL [see DRUG INTERACTIONS].
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 CYTOMEL that achieves the desired clinical and biochemical response to mitigate against this risk.
Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of liothyronine sodium.
Experience with liothyronine use in pregnant women, including data from post-marketing studies, have not reported increased rates of major birth defects or miscarriages (see Data). There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Since TSH levels may increase during pregnancy, TSH should be monitored and CYTOMEL dosage adjusted during pregnancy (see Clinical Considerations). There are no animal studies conducted with liothyronine during pregnancy. CYTOMEL should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated.
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.
Disease-associated maternal and/or embryo/fetal risk
Maternal hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, gestational hypertension, pre-eclampsia, stillbirth, and premature delivery.
Untreated maternal hypothyroidism may have an adverse effect on fetal neurocognitive development.
Dose adjustments during pregnancy and the postpartum period
Pregnancy may increase CYTOMEL requirements. Serum TSH levels should be monitored and the CYTOMEL dosage adjusted during pregnancy. Since postpartum TSH levels are similar to preconception values, the CYTOMEL dosage should return to the pre-pregnancy dose immediately after delivery [see DOSAGE AND ADMINISTRATION].
Human Data
Liothyronine is approved for use as a replacement therapy for hypothyroidism. Data from postmarketing studies have not reported increased rates of fetal malformations, miscarriages, or other adverse maternal or fetal outcomes associated with liothyronine use in pregnant women.
Limited published studies report that liothyronine is present in human milk. However, there is insufficient information to determine the effects of liothyronine on the breastfed infant and no available information on the effects of liothyronine on milk production. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for CYTOMEL and any potential adverse effects on the breastfed infant from CYTOMEL or from the underlying maternal condition.
The initial dose of CYTOMEL 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].
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].
Rapid restoration of normal serum T4 concentrations is essential for preventing the adverse effects of congenital hypothyroidism on intellectual development as well as on overall physical growth and maturation. Therefore, initiate thyroid hormone immediately upon diagnosis. Thyroid hormone is generally continued for life in these patients.
Closely monitor infants during the first 2 weeks of thyroid hormone therapy for cardiac overload, arrhythmias, and aspiration from avid suckling.
Closely monitor patients to avoid undertreatment or overtreatment. Undertreatment may have deleterious effects on intellectual development and linear growth. Overtreatment is associated with craniosynostosis in infants, may adversely affect the tempo of brain maturation, and may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature [see DOSAGE AND ADMINISTRATION and ADVERSE REACTIONS].
Closely monitor patients to avoid undertreatment and overtreatment. Undertreatment may result in poor school performance due to impaired concentration and slowed mentation and in reduced adult height. Overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature.
Treated children may manifest a period of catch-up growth, which may be adequate in some cases to normalize adult height. In children with severe or prolonged hypothyroidism, catch-up growth may not be adequate to normalize adult height [see ADVERSE REACTIONS].
Because of the increased prevalence of cardiovascular disease among the elderly, initiate CYTOMEL at less than the full replacement dose [see DOSAGE AND ADMINISTRATION and WARNINGS AND PRECAUTIONS]. Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with thyroid hormone overtreatment in the elderly.
The signs and symptoms of overdosage are those of hyperthyroidism [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. 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 CYTOMEL 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.
CYTOMEL is contraindicated in patients with uncorrected adrenal insufficiency [see WARNINGS AND PRECAUTIONS].
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.
The onset of activity of liothyronine sodium occurs within a few hours. Maximum pharmacologic response occurs within 2 or 3 days.
T3 is almost totally absorbed, 95 percent in 4 hours. The hormones contained in the natural preparations are absorbed in a manner similar to the synthetic hormones.
Liothyronine sodium (T3) is not firmly bound to serum protein. The higher affinity of levothyroxine (T4) for both thyroid-binding globulin and thyroid-binding prealbumin as compared to triiodothyronine (T3) partially explains the higher serum levels and longer half-life of the former hormone. Both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity.
Metabolism
The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately 80% of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3. T3 is further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation.
Excretion
Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. The biological half-life is about 2–1/2 days.
If patents are taking anticoagulants (blood thinners), their clotting status should be checked frequently.
