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Drug overview for CYTOMEL (liothyronine sodium):
Generic name: LIOTHYRONINE SODIUM (LYE-oh-THYE-roe-neen)
Drug class: Thyroid Hormones
Therapeutic class: Endocrine
Liothyronine sodium, the sodium salt of the l-isomer of 3,3',5-triiodothyronine, is a thyroid agent.
Liothyronine sodium may be used for replacement or substitution of diminished or absent thyroid function resulting from primary causes including functional deficiency, primary atrophy, or partial or complete absence of the gland or the effects of surgery, radiation, or antithyroid agents; however, levothyroxine sodium is generally preferred for long-term therapy in these conditions. Liothyronine sodium also may be used for replacement or supplemental therapy in patients with secondary (pituitary) or tertiary (hypothalamic) hypothyroidism. Therapy must be maintained continuously to control the symptoms of hypothyroidism.
Because liothyronine sodium has a rapid onset and short duration of action, some clinicians prefer its use to levothyroxine sodium when a rapid effect or rapidly reversible effect is desired (e.g., diagnostic procedures requiring short-term thyrotropin suppression, myxedema coma); however, the fact that liothyronine produces wide swings in serum triiodothyronine concentrations and the possibility of more pronounced adverse cardiovascular effects generally make the drug unsatisfactory for long-term use. Liothyronine sodium may be useful when absorption of levothyroxine sodium is questionable or impairment of peripheral conversion of thyroxine to triiodothyronine is suspected. Liothyronine sodium may also be used therapeutically in patients with simple (nontoxic) goiter to reduce the size of the goiter.
Liothyronine sodium is used IV in the treatment of myxedema coma or precoma. Simultaneous administration of corticosteroids is required. Myxedema coma should be considered a medical emergency, and therapy should be directed at the correction of electrolyte disturbances, possible infection, or other intercurrent illness in addition to the administration of IV liothyronine sodium. Liothyronine sodium is used principally in the T3 suppression test to differentiate suspected hyperthyroidism from euthyroidism in patients with I 131 thyroid uptake values in the borderline-high range.
Generic name: LIOTHYRONINE SODIUM (LYE-oh-THYE-roe-neen)
Drug class: Thyroid Hormones
Therapeutic class: Endocrine
Liothyronine sodium, the sodium salt of the l-isomer of 3,3',5-triiodothyronine, is a thyroid agent.
Liothyronine sodium may be used for replacement or substitution of diminished or absent thyroid function resulting from primary causes including functional deficiency, primary atrophy, or partial or complete absence of the gland or the effects of surgery, radiation, or antithyroid agents; however, levothyroxine sodium is generally preferred for long-term therapy in these conditions. Liothyronine sodium also may be used for replacement or supplemental therapy in patients with secondary (pituitary) or tertiary (hypothalamic) hypothyroidism. Therapy must be maintained continuously to control the symptoms of hypothyroidism.
Because liothyronine sodium has a rapid onset and short duration of action, some clinicians prefer its use to levothyroxine sodium when a rapid effect or rapidly reversible effect is desired (e.g., diagnostic procedures requiring short-term thyrotropin suppression, myxedema coma); however, the fact that liothyronine produces wide swings in serum triiodothyronine concentrations and the possibility of more pronounced adverse cardiovascular effects generally make the drug unsatisfactory for long-term use. Liothyronine sodium may be useful when absorption of levothyroxine sodium is questionable or impairment of peripheral conversion of thyroxine to triiodothyronine is suspected. Liothyronine sodium may also be used therapeutically in patients with simple (nontoxic) goiter to reduce the size of the goiter.
Liothyronine sodium is used IV in the treatment of myxedema coma or precoma. Simultaneous administration of corticosteroids is required. Myxedema coma should be considered a medical emergency, and therapy should be directed at the correction of electrolyte disturbances, possible infection, or other intercurrent illness in addition to the administration of IV liothyronine sodium. Liothyronine sodium is used principally in the T3 suppression test to differentiate suspected hyperthyroidism from euthyroidism in patients with I 131 thyroid uptake values in the borderline-high range.
DRUG IMAGES
- CYTOMEL 50 MCG TABLET
- CYTOMEL 5 MCG TABLET
- CYTOMEL 25 MCG TABLET
The following indications for CYTOMEL (liothyronine sodium) have been approved by the FDA:
Indications:
Adjunct to surgery or radiotherapy for thyroid carcinoma
Hypothyroidism
T3 suppression for thyroid function test
Professional Synonyms:
None.
Indications:
Adjunct to surgery or radiotherapy for thyroid carcinoma
Hypothyroidism
T3 suppression for thyroid function test
Professional Synonyms:
None.
The following dosing information is available for CYTOMEL (liothyronine sodium):
Dosage of liothyronine sodium is expressed in terms of liothyronine. Dosage of liothyronine must be carefully adjusted according to individual requirements and response. The age and general physical condition of the patient and the severity and duration of hypothyroid symptoms determine the initial dosage and the rate at which dosage may be increased to the eventual maintenance dosage.
Dosage should be initiated at a lower level in geriatric patients; in patients with long-standing disease, other endocrinopathies, or functional or ECG evidence of cardiovascular disease; and in patients with severe hypothyroidism. Adjustment of thyroid replacement therapy should be determined mainly by the patient's clinical response and confirmed by appropriate laboratory tests.
Prompt administration of an adequate dose of IV liothyronine sodium is important in determining clinical outcome of myxedema coma. Initial and subsequent doses of liothyronine sodium should be based on continuous monitoring of the patient's clinical status and response to therapy. Myxedematous patients are very sensitive to the effects of thyroid hormones; therefore, dosage in such patients should be initiated at a low level and increased gradually since acute changes may precipitate adverse cardiovascular events.
For the management of mild hypothyroidism in adults, the usual initial oral dosage of liothyronine is 25 mcg daily given as a single dose; dosage is increased by increments of 12.5 or 25 mcg daily at intervals of 1-2 weeks until the desired response is obtained. The usual maintenance dosage is 25-75 mcg daily; some patients may require higher or lower dosages.
For the management of severe hypothyroidism in adults, the usual initial oral dosage is 5 mcg daily given as a single dose; dosage is increased by increments of 5-10 mcg daily at intervals of 1-2 weeks until the desired response is obtained. The usual maintenance dosage is 50-100 mcg daily. For geriatric patients with hypothyroidism, the usual initial oral dosage of liothyronine is 5 mcg daily given as a single dose; dosage is increased by increments of 5 mcg daily at intervals of 1-2 weeks until the desired response is obtained.
In infants and children, it is essential to achieve rapid and complete thyroid replacement because of the critical importance of thyroid hormone in sustaining growth and maturation. In general, despite the smaller body size, the dosage (on a weight basis) required to sustain a full rate of growth, development, and general thriving is higher in children than in adults. Although levothyroxine sodium is considered the drug of choice for the treatment of congenital hypothyroidism (cretinism), liothyronine has been used.
The initial oral dosage of liothyronine recommended by the manufacturer for the treatment of congenital hypothyroidism is 5 mcg daily given as a single dose; dosage is increased by increments of 5 mcg daily at intervals of 3-4 days until the desired response is obtained. For additional information on the use of thyroid agents in the treatment of congenital hypothyroidism, see Cautions: Pediatric Precautions, in the Thyroid Agents General Statement 68:36.04.
For the management of simple (nontoxic) goiter in adults, the usual initial oral dosage of liothyronine is 5 mcg daily; dosage is increased by increments of 5-10 mcg daily at intervals of 1-2 weeks until a dosage of 25 mcg daily is reached. Thereafter, dosage may be increased by increments of 12.5 or 25 mcg daily at intervals of 1-2 weeks until the desired response is obtained.
The usual maintenance dosage is 75 mcg daily.
When a patient is transferred from another thyroid preparation to liothyronine, the other thyroid preparation should be discontinued and liothyronine therapy initiated at a low dosage. Liothyronine dosage may be increased in small increments after residual effects of the previous thyroid preparation have subsided. When a patient is transferred from liothyronine to another thyroid preparation, it must be kept in mind that the onset and dissipation of effects of liothyronine are relatively rapid, and, to avoid relapse, it is necessary to start therapy with the replacement thyroid preparation several days before complete withdrawal of liothyronine.
Although levothyroxine sodium is generally considered the drug of choice in the treatment of myxedema coma, some clinicians prefer liothyronine because of its rapid onset of action. Liothyronine has been given orally via a nasogastric tube, but the IV route of administration is preferred. The usual initial adult IV dose of liothyronine recommended by the manufacturer for the emergency treatment of myxedema coma or precoma is 25-50 mcg.
In patients with known or suspected cardiovascular disease, the manufacturer suggests an initial dose of 10-20 mcg of liothyronine. The manufacturer states that additional doses of liothyronine should be administered at least 4 hours after the initial dose to allow for adequate assessment of therapeutic response, but no more than 12 hours should elapse between doses to avoid fluctuations in hormone levels. However, both the initial and subsequent doses of the drug should be determined based on continuous monitoring of the patient's clinical condition and response to liothyronine sodium therapy.
Administration of at least 65 mcg daily of IV liothyronine in the initial days of therapy reportedly has been associated with lower mortality. However, clinical experience with liothyronine dosages exceeding 100 mcg daily is limited. Oral therapy with thyroid hormones should be resumed as soon as the patient's condition stabilizes and the drug can be given orally.
Oral therapy with liothyronine sodium should be initiated at a low dosage following discontinuance of the IV drug, and dosage should be increased gradually according to the patient's response. If levothyroxine sodium rather than liothyronine sodium is used in initiating oral therapy, the clinician should consider the delay in onset of activity of levothyroxine sodium and IV liothyronine sodium should be discontinued gradually.
When used in the T3 suppression test to differentiate suspected hyperthyroidism from euthyroidism, liothyronine is given in a dosage of 75-100 mcg daily for 7 days. Radioactive I 131 uptake test is performed before and after administration of the 7-day course of liothyronine. In patients with hyperthyroidism, the radioactive iodine thyroid uptake will not be substantially affected, while in the euthyroid patient, it will decrease to less than 20% of the baseline value.
For further information on chemistry, pharmacology, pharmacokinetics, uses, toxicity, cautions, acute toxicity, drug interactions, laboratory test interferences, and dosage and administration of liothyronine sodium, see the Thyroid Agents General Statement 68:36.04.
Dosage should be initiated at a lower level in geriatric patients; in patients with long-standing disease, other endocrinopathies, or functional or ECG evidence of cardiovascular disease; and in patients with severe hypothyroidism. Adjustment of thyroid replacement therapy should be determined mainly by the patient's clinical response and confirmed by appropriate laboratory tests.
Prompt administration of an adequate dose of IV liothyronine sodium is important in determining clinical outcome of myxedema coma. Initial and subsequent doses of liothyronine sodium should be based on continuous monitoring of the patient's clinical status and response to therapy. Myxedematous patients are very sensitive to the effects of thyroid hormones; therefore, dosage in such patients should be initiated at a low level and increased gradually since acute changes may precipitate adverse cardiovascular events.
For the management of mild hypothyroidism in adults, the usual initial oral dosage of liothyronine is 25 mcg daily given as a single dose; dosage is increased by increments of 12.5 or 25 mcg daily at intervals of 1-2 weeks until the desired response is obtained. The usual maintenance dosage is 25-75 mcg daily; some patients may require higher or lower dosages.
For the management of severe hypothyroidism in adults, the usual initial oral dosage is 5 mcg daily given as a single dose; dosage is increased by increments of 5-10 mcg daily at intervals of 1-2 weeks until the desired response is obtained. The usual maintenance dosage is 50-100 mcg daily. For geriatric patients with hypothyroidism, the usual initial oral dosage of liothyronine is 5 mcg daily given as a single dose; dosage is increased by increments of 5 mcg daily at intervals of 1-2 weeks until the desired response is obtained.
In infants and children, it is essential to achieve rapid and complete thyroid replacement because of the critical importance of thyroid hormone in sustaining growth and maturation. In general, despite the smaller body size, the dosage (on a weight basis) required to sustain a full rate of growth, development, and general thriving is higher in children than in adults. Although levothyroxine sodium is considered the drug of choice for the treatment of congenital hypothyroidism (cretinism), liothyronine has been used.
The initial oral dosage of liothyronine recommended by the manufacturer for the treatment of congenital hypothyroidism is 5 mcg daily given as a single dose; dosage is increased by increments of 5 mcg daily at intervals of 3-4 days until the desired response is obtained. For additional information on the use of thyroid agents in the treatment of congenital hypothyroidism, see Cautions: Pediatric Precautions, in the Thyroid Agents General Statement 68:36.04.
For the management of simple (nontoxic) goiter in adults, the usual initial oral dosage of liothyronine is 5 mcg daily; dosage is increased by increments of 5-10 mcg daily at intervals of 1-2 weeks until a dosage of 25 mcg daily is reached. Thereafter, dosage may be increased by increments of 12.5 or 25 mcg daily at intervals of 1-2 weeks until the desired response is obtained.
The usual maintenance dosage is 75 mcg daily.
When a patient is transferred from another thyroid preparation to liothyronine, the other thyroid preparation should be discontinued and liothyronine therapy initiated at a low dosage. Liothyronine dosage may be increased in small increments after residual effects of the previous thyroid preparation have subsided. When a patient is transferred from liothyronine to another thyroid preparation, it must be kept in mind that the onset and dissipation of effects of liothyronine are relatively rapid, and, to avoid relapse, it is necessary to start therapy with the replacement thyroid preparation several days before complete withdrawal of liothyronine.
Although levothyroxine sodium is generally considered the drug of choice in the treatment of myxedema coma, some clinicians prefer liothyronine because of its rapid onset of action. Liothyronine has been given orally via a nasogastric tube, but the IV route of administration is preferred. The usual initial adult IV dose of liothyronine recommended by the manufacturer for the emergency treatment of myxedema coma or precoma is 25-50 mcg.
In patients with known or suspected cardiovascular disease, the manufacturer suggests an initial dose of 10-20 mcg of liothyronine. The manufacturer states that additional doses of liothyronine should be administered at least 4 hours after the initial dose to allow for adequate assessment of therapeutic response, but no more than 12 hours should elapse between doses to avoid fluctuations in hormone levels. However, both the initial and subsequent doses of the drug should be determined based on continuous monitoring of the patient's clinical condition and response to liothyronine sodium therapy.
Administration of at least 65 mcg daily of IV liothyronine in the initial days of therapy reportedly has been associated with lower mortality. However, clinical experience with liothyronine dosages exceeding 100 mcg daily is limited. Oral therapy with thyroid hormones should be resumed as soon as the patient's condition stabilizes and the drug can be given orally.
Oral therapy with liothyronine sodium should be initiated at a low dosage following discontinuance of the IV drug, and dosage should be increased gradually according to the patient's response. If levothyroxine sodium rather than liothyronine sodium is used in initiating oral therapy, the clinician should consider the delay in onset of activity of levothyroxine sodium and IV liothyronine sodium should be discontinued gradually.
When used in the T3 suppression test to differentiate suspected hyperthyroidism from euthyroidism, liothyronine is given in a dosage of 75-100 mcg daily for 7 days. Radioactive I 131 uptake test is performed before and after administration of the 7-day course of liothyronine. In patients with hyperthyroidism, the radioactive iodine thyroid uptake will not be substantially affected, while in the euthyroid patient, it will decrease to less than 20% of the baseline value.
For further information on chemistry, pharmacology, pharmacokinetics, uses, toxicity, cautions, acute toxicity, drug interactions, laboratory test interferences, and dosage and administration of liothyronine sodium, see the Thyroid Agents General Statement 68:36.04.
Liothyronine sodium is administered orally. The drug also is administered by IV injection in the treatment of myxedema coma or precoma. The manufacturer states that liothyronine sodium injection should not be administered IM or subcutaneously.
DRUG LABEL | DOSING TYPE | DOSING INSTRUCTIONS |
---|---|---|
CYTOMEL 5 MCG TABLET | Maintenance | Adults take 1 tablet (5 mcg) by oral route once daily |
CYTOMEL 25 MCG TABLET | Maintenance | Adults take 1 tablet (25 mcg) by oral route once daily |
CYTOMEL 50 MCG TABLET | Maintenance | Adults take 1 tablet (50 mcg) by oral route once daily |
DRUG LABEL | DOSING TYPE | DOSING INSTRUCTIONS |
---|---|---|
LIOTHYRONINE SOD 25 MCG TAB | Maintenance | Adults take 1 tablet (25 mcg) by oral route once daily |
LIOTHYRONINE SOD 5 MCG TAB | Maintenance | Adults take 1 tablet (5 mcg) by oral route once daily |
LIOTHYRONINE SOD 50 MCG TAB | Maintenance | Adults take 1 tablet (50 mcg) by oral route once daily |
The following drug interaction information is available for CYTOMEL (liothyronine sodium):
There are 0 contraindications.
There are 2 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
Drug Interaction | Drug Names |
---|---|
Radioactive Iodide/Agents that Affect Iodide SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Many compounds can affect iodide protein binding and alter iodide pharmacokinetics and pharmacodynamics.(1) CLINICAL EFFECTS: Compounds that affect iodide pharmacokinetics and pharmacodynamics may impact the effectiveness of radioactive iodide.(1) PREDISPOSING FACTORS: Compounds that affect iodide pharmacokinetics and pharmacodynamics are expected to have the most impact during therapy using radioactive iodide. Diagnostic procedures would be expected to be impacted less. PATIENT MANAGEMENT: Discuss the use of agents that affect iodide pharmacokinetics and pharmacodynamics with the patient's oncologist.(1) Because indocyanine green contains sodium iodide, the iodine-binding capacity of thyroid tissue may be reduced for at least one week following administration. Do not perform radioactive iodine uptake studies for at least one week following administration of indocyanine green.(2) The manufacturer of iopamidol states administration may interfere with thyroid uptake of radioactive iodine and decrease therapeutic and diagnostic efficacy. Avoid thyroid therapy or testing for up to 6 weeks post administration of iopamidol.(3) DISCUSSION: Many agents interact with radioactive iodine. The average duration of effect is: anticoagulants - 1 week antihistamines - 1 week anti-thyroid drugs, e.g: carbimazole, methimazole, propylthiouracil - 3-5 days corticosteroids - 1 week iodide-containing medications, e.g: amiodarone - 1-6 months expectorants - 2 weeks Lugol solution - 3 weeks saturated solution of potassium iodine - 3 weeks vitamins - 10-14 days iodide-containing X-ray contrast agents - up to 1 year lithium - 4 weeks phenylbutazone - 1-2 weeks sulfonamides - 1 week thyroid hormones (natural or synthetic), e.g.: thyroxine - 4 weeks tri-iodothyronine - 2 weeks tolbutamide - 1 week topical iodide - 1-9 months (1) |
ADREVIEW, JEANATOPE, MEGATOPE, SODIUM IODIDE I-123 |
Sodium Iodide I 131/Agents that Affect Iodide SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Many compounds can affect iodide protein binding and alter iodide pharmacokinetics and pharmacodynamics.(1,2) CLINICAL EFFECTS: Compounds that affect iodide pharmacokinetics and pharmacodynamics may impact the effectiveness of radioactive iodide.(1,2) PREDISPOSING FACTORS: Compounds that affect iodide pharmacokinetics and pharmacodynamics are expected to have the most impact during therapy using radioactive iodide. Diagnostic procedures would be expected to be impacted less. PATIENT MANAGEMENT: Discuss the use of agents that affect iodide pharmacokinetics and pharmacodynamics with the patient's oncologist.(1,2) Because indocyanine green contains sodium iodide, the iodine-binding capacity of thyroid tissue may be reduced for at least one week following administration. Do not perform radioactive iodine uptake studies for at least one week following administration of indocyanine green.(3) The manufacturer of iopamidol states administration may interfere with thyroid uptake of radioactive iodine and decrease therapeutic and diagnostic efficacy. Avoid thyroid therapy or testing for up to 6 weeks post administration of iopamidol.(4) DISCUSSION: Many agents interact with radioactive iodine. The average duration of effect is: anticoagulants - 1 week antihistamines - 1 week anti-thyroid drugs, e.g: carbimazole, methimazole, propylthiouracil - 3-5 days corticosteroids - 1 week iodide-containing medications, e.g: amiodarone - 1-6 months expectorants - 2 weeks Lugol solution - 3 weeks saturated solution of potassium iodine - 3 weeks vitamins - 10-14 days iodide-containing X-ray contrast agents - up to 1 year lithium - 4 weeks phenylbutazone - 1-2 weeks sulfonamides - 1 week thyroid hormones (natural or synthetic), e.g.: thyroxine - 4 weeks tri-iodothyronine - 2 weeks tolbutamide - 1 week topical iodide - 1-9 months (1,2) |
HICON, SODIUM IODIDE I-131 |
There are 13 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
Drug Interaction | Drug Names |
---|---|
Thyroid Preps/Bile Acid Sequestrants; Lanthanum; Sevelamer SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Bile acid sequestrants, lanthanum and sevelamer may decrease the gastrointestinal absorption of thyroid drugs.(1) CLINICAL EFFECTS: Simultaneous administration of a bile acid sequestrant, lanthanum or sevelamer may result in decreased absorption and effectiveness of thyroid drugs.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: For maximal bioavailability, thyroid preparations should be taken on an empty stomach at least 4 hours apart from bile acid sequestrants and sevelamer.(1-3) Thyroid preparations should be taken at least 2 hours apart from lanthanum.(4) DISCUSSION: The effect of cholestyramine on the absorption of thyroid drugs appears to be clinically significant, resulting in approximately a 50% decrease in thyroid absorption. Cholestyramine has been used to treat thyroid overdoses. When administered with colesevelam (3.75 g), the area-under-curve (AUC) and maximum concentration (Cmax) of levothyroxine (600 mcg) decreased by 22% and by 33%, respectively. When administered 1 hour prior to colesevelam, the AUC of levothyroxine increased by 6% and the Cmax of levothyroxine decreased by 2%, respectively. When administered 4 hours prior to colesevelam, the AUC and Cmax of levothyroxine increased by 1% and 8%, respectively. Although used for hyperphosphatemia, sevelamer is linked to this monograph due to its structural and pharmacologic similarities to colesevelam. Both agents are non-absorbed cross linked polymers with a high affinity for bile acids.(2,3) An in vivo study in healthy subjects evaluated the bioavailability of levothyroxine 1 mg when given with or without sevelamer 800 mg. Concomitant administration of sevelamer decreased levothyroxine AUC by 46%.(13) One case report described a newly diagnosed hypothyroid patient with a TSH of 297 mU/L (reference 0.03 - 4.20 mU/L). She took her daily levothyroxine with her morning blood pressure medications, acetaminophen, B-vitamins and sevelamer 3200 mg. Over 3 months of treatment her levothyroxine dose was increased to 150 mcg daily but the TSH remained high at 196 mU/L. Her levothyroxine dose was changed to an evening dose taken at least 4 hours after medications. Three weeks later she was symptomatically improved and TSH had decreased to 19 mU/L. She was inadvertently rechallenged on the morning levothyroxine and sevelamer regimen due to a hospitalization. After the hospital stay her TSH risen to 76 mU/L; on return to her evening regimen her TSH again normalized.(14) |
CHOLESTYRAMINE, CHOLESTYRAMINE LIGHT, CHOLESTYRAMINE RESIN, COLESEVELAM HCL, COLESTID, COLESTIPOL HCL, FOSRENOL, LANTHANUM CARBONATE, PREVALITE, QUESTRAN, QUESTRAN LIGHT, RENVELA, SEVELAMER CARBONATE, SEVELAMER HCL, WELCHOL |
Thyroid Preparations/Calcium; Iron; Sucralfate SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The mechanism by which malabsorption of thyroid preparations occurs from calcium-containing products is presumed to be a binding of the medication to the thyroid hormone, forming an insoluble or nonabsorbable complex.(1-3) Iron may form a ferric-thyroxine complex with thyroid agents, preventing their absorption from the gastrointestinal tract.(1,4) Sucralfate binds to other agents in the gastrointestinal tract and alters absorption of other drugs, including thyroid agents.(1,5) CLINICAL EFFECTS: The simultaneous administration of thyroid preparations with calcium, iron, or sucralfate may result in decreased levels and clinical effects of thyroid preparations.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Instruct patients to separate the administration time of thyroid preparations from calcium or iron by as much time as possible, preferably by at least four hours.(1) Administer thyroid preparations at least 2 hours before sucralfate.(5) Patients taking thyroid preparations and calcium- or iron-containing products or sucralfate should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased. Separating the administration times of the thyroid preparation and the calcium- or iron-containing products or sucralfate may decrease the effects of the interaction.(1-5) DISCUSSION: In a pharmacokinetic study 8 healthy, euthyroid adults were given levothyroxine alone and levothyroxine coadministered with calcium carbonate, calcium citrate, or calcium acetate in doses containing 500 mg elemental calcium. The coadministration of each of the three calcium preparations significantly reduced levothyroxine absorption by about 20%-25% compared with levothyroxine given alone.(3) In a study in 14 subjects, the simultaneous administration of thyroxine with ferrous sulfate for 12 weeks resulted in an increase in the mean level of thyroid stimulating hormone (TSH) from 1.6+/-0.4 mU/L to 5.4+/-2.8 mU/L. Mixing thyroxine with ferrous sulfate in vitro resulted in a poorly soluble complex.(4) In a study in 20 hypothyroid patients, the simultaneous administration of levothyroxine and calcium carbonate (1200 mg) daily for three months resulted in reductions in the mean free T4 and total T4 levels. These values increased in most patients following the discontinuation of calcium carbonate. A concurrent in-vitro study found that calcium carbonate adsorbed levothyroxine in solution at a pH of 2, gastric pH, but not at a pH of 7.4.(6) One author reported three cases of decreased levothyroxine efficacy following the addition of calcium carbonate to therapy.(7) In a study in 5 healthy subjects, levothyroxine (five 200 mcg tablets) was administered in 3 different dosing regimens: after an overnight fast, with the fifth and final dose of sucralfate (1 gram every 6 hours) and 8 hours after the second and final dose of sucralfate (2 grams every 12 hours). When administered alone, 80% of levothyroxine was absorbed within 6 hours of administration, compared to 23% when administered concurrently with sucralfate. There was no difference in levothyroxine absorption when administered alone or 8 hours after sucralfate.(8) There are several case reports documenting decreased effects of thyroid supplementation as the result of simultaneous administration of sucralfate.(9,10) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
ACCRUFER, AUROVELA 24 FE, AUROVELA FE, AURYXIA, BALCOLTRA, BLISOVI 24 FE, BLISOVI FE, CALCIUM ACETATE, CALCIUM CHLORIDE, CALCIUM GLUCONATE, CALCIUM GLUCONATE MONOHYDRATE, CARAFATE, CHARLOTTE 24 FE, FINZALA, GEMMILY, HAILEY 24 FE, HAILEY FE, JOYEAUX, JUNEL FE, JUNEL FE 24, KAITLIB FE, LARIN 24 FE, LARIN FE, LAYOLIS FE, LEVONORG-ETH ESTRAD-FE BISGLYC, LO LOESTRIN FE, LOESTRIN FE, MERZEE, MIBELAS 24 FE, MICROGESTIN FE, MINZOYA, NORETHIN-ETH ESTRA-FERROUS FUM, NORETHINDRONE-E.ESTRADIOL-IRON, SUCRALFATE, TARINA 24 FE, TARINA FE, TARINA FE 1-20 EQ, TAYTULLA, TILIA FE, TRI-LEGEST FE, VELPHORO, WYMZYA FE |
Thyroid Preparations/Polystyrene Sulfonate SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Polystyrene sulfonate may bind and delay or prevent the absorption of thyroid preparations from the gastrointestinal tract.(1) CLINICAL EFFECTS: Simultaneous administration of polystyrene sulfonate may result in decreased levels of and effectiveness from thyroid preparations.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of levothyroxine states that levothyroxine should be administered at least 4 hours apart from polystyrene sulfonate.(1) DISCUSSION: Because polystyrene sulfonate may bind and delay or prevent the absorption of levothyroxine from the gastrointestinal tract, the US manufacturer of levothyroxine states that levothyroxine should be administered at least 4 hours apart from polystyrene sulfonate.(1) |
KIONEX, SODIUM POLYSTYRENE SULFONATE, SPS |
Thyroid Preparations/Orlistat SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Orlistat may bind to the thyroid preparation in the small intestine, decreasing systemic absorption.(1-4) CLINICAL EFFECTS: Concurrent administration of orlistat and thyroid preparations may decrease the clinical effects of the thyroid agent.(1-4) Hypothyroidism has been reported.(3) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Separate the administration times of orlistat and thyroid preparations by at least 4 hours. Patients receiving concurrent therapy should be monitored for changes in thyroid function.(1-3) DISCUSSION: In a case report, a post-thyroidectomy patient on a stable dose of levothyroxine (250 mcg daily) started concurrent orlistat therapy. Within two weeks of starting orlistat therapy, she felt experienced cold intolerance and felt lethargic and tired. She was found be severely hypothyroid and the orlistat was discontinued. Within two weeks, her symptoms improved and, within 4 weeks, her thyroid levels normalized.(4) |
ORLISTAT, XENICAL |
Thyroid Preparations/Ciprofloxacin SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Ciprofloxacin may inhibit organic anion transporting polypeptide (OATP) 1A2 in the intestines, either through competitive or direct inhibition.(1) CLINICAL EFFECTS: The simultaneous administration of thyroid preparations and ciprofloxacin may result in decreased levels and clinical effects of thyroid hormones.(1) PREDISPOSING FACTORS: This interaction may be more significant in patients receiving long term courses of ciprofloxacin. PATIENT MANAGEMENT: Patients taking thyroid preparations and ciprofloxacin should be monitored for changes in thyroid function. Separating the administration times of the thyroid preparation and ciprofloxacin by 6 hours, may decrease the effects of the interaction.(1,2) DISCUSSION: In a study, 8 healthy individuals received single doses of levothyroxine (100 mcg) combined with placebo or ciprofloxacin (750 mg). The simultaneous administration of ciprofloxacin significantly decreased the T4 AUC by 39% (p=0.035). The reduction in T4 AUC after coadministration of ciprofloxacin with levothyroxine is consistent with inhibition of an intestinal T4 uptake transport.(1) In a case report, two patients with hypothyroidism and receiving levothyroxine developed decreased T4 levels after taking ciprofloxacin for 3-4 weeks.(2) |
CIPRO, CIPROFLOXACIN, CIPROFLOXACIN HCL |
Thyroid Preparations/Imatinib;Sunitinib SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The suspected mechanism responsible for this phenomenon is an induction of non-deiodination clearance. The induction of uridine diphosphate-glucuronyl transferases (UGTs) by imatinib and sunitinib decreases levels of the thyroid preparations.(1) CLINICAL EFFECTS: The coadministration of thyroid preparations and imatinib and sunitinib may result in decreased levels and clinical effects of thyroid hormones.(1-3) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients taking thyroid preparations and imatinib or sunitinib should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased.(1-3) DISCUSSION: In a case report, 8 patients had undergone thyroidectomy and used levothyroxine and imatinib. These patients had an increase need for levothyroxine levels and were monitored for elevations in thyrotropin indicating worsening hypothyroidism.(2) A case report of a 73 year old man who was treated with imatinib and levothyroxine developed worsening hypothyroidism. An increase in levothyroxine dosage was needed.(3) In a case report, a 59 year old woman was taking levothyroxine therapy for hypothyroidism secondary to subtotal thyroidectomy and was recently started on imatinib for chronic myeloid leukemia. The patient developed clinical signs of hypothyroidism and required an increased dose of levothyroxine.(4) In a case report, a 73 year old woman was taking levothyroxine and developed fatigue, nausea, cold-intolerance, hair-loss, brittle nails, progressive weakness, and impressive facial oedema 6 months after starting imatinib. The patient levothyroxine was increased and she remained euthyroid, but the imatinib was discontinued due to extreme fatigue and periorbital oedema. Five months later the patient was stared on sunitinib and her levothyroxine dose was increased. The patient developed similar symptoms to imatinib reaction.(5) In a case report, a patient receiving sunitinib for metastatic papillary renal cell cancer developed high thyroid stimulating hormone levels and severe symptoms despite receiving L-thyroxine.(6) |
GLEEVEC, IMATINIB MESYLATE, IMKELDI, SUNITINIB MALATE, SUTENT |
Thyroid Preparations/Rifampin SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Rifampin is an organic anion transporting polypeptide (OATP) inhibitor and has been found to decrease measured free T4 when taking thyroid replacements. The mechanism for the rifampin effect may be due to induction of hepatic metabolic and biliary clearance. It is also possible that rifampin may have increased net intestinal absorption of L-T4 through inhibition of P-glycoprotein, an intestinal efflux transporter. CLINICAL EFFECTS: The concurrent or recent use of rifampin may result in altered levels and clinical effects of thyroid hormones. Some patients may experience increased thyroid hormone effects, while others may experience decreased effects.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients taking thyroid preparations and rifampin should be monitored for changes in thyroid function. Symptoms of hyperthyroidism include weight loss, rapid heartbeat, nervousness, sweating, tremor, fatigue, and difficulty sleeping. Symptoms of hypothyroidism include fatigue, sluggishness, constipation, stiffness, muscle cramps, loss of appetite, excessive weight gain, or dry skin. The dosage of levothyroxine may need to be adjusted accordingly. DISCUSSION: In a study, 8 healthy individuals received 100 mcg of levothyroxine combined with placebo or rifampin 600 mg. The coadministration of rifampin significantly increased the 4 AUC by 25% (p=0.003). Levothyroxine absorptions with rifampin was 125% compared to controls.(1) In contrast to this study, two case reports exist documenting decreased effects of levothyroxine during concurrent rifampin. In a case report, a 31 year old woman had a total thyroidectomy and was receiving levothyroxine and was recently started on rifampin. The patient did not develop symptoms of hypothyroidism, but had a decrease in serum thyroxine levels and free thyroxine index during rifampin therapy and an increase in serum thyrotropin levels.(2) In a case report of a 50 year old male, stable on levothyroxine, who exhibited significantly elevated TSH levels during therapy with rifampin. The patient's TSH levels returned to baseline 9 days after discontinuing rifampin.(3) |
RIFADIN, RIFAMPIN |
Patiromer/Thyroid Preparations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Patiromer may bind to thyroid preparations.(1) CLINICAL EFFECTS: Concurrent use may result in decreased gastrointestinal absorption and loss of efficacy of the thyroid preparation.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of patiromer recommends that you administer patiromer at least 3 hours before or 3 hours after levothyroxine.(1) DISCUSSION: A study in healthy volunteers showed that patiromer decreased the systemic exposure of coadministered levothyroxine. No interaction was seen when these drugs were taken 3 hours apart.(1) |
VELTASSA |
Thyroid Preparations/Ritonavir SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Thyroid preparations are substrates for uridine diphosphate glucuronosyltransferase (UGT). Also, levothyroxine is converted to the thyroid hormone triiodothyronine (T3) which is further metabolized via UGT.(1) Ritonavir may induce UGT and may increase metabolism of levothyroxine and T3.(1) CLINICAL EFFECTS: The concurrent use of ritonavir may result in decreased levels and clinical effects of the thyroid preparation. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients taking thyroid preparations and ritonavir should be monitored for changes in thyroid function. Symptoms of hypothyroidism include fatigue, sluggishness, constipation, stiffness, muscle cramps, loss of appetite, excessive weight gain, or dry skin. The dosage of the thyroid preparation may need to be adjusted accordingly. DISCUSSION: A case report of a 29 year old male with auto-immune thyroiditis was stabilized on levothyroxine 125 mcg daily for one year when concurrent therapy with stavudine 40 mg twice daily, lamivudine 150 mg twice daily, ritonavir 600 mg twice daily, and saquinavir 400 mg twice daily was started. One month after concurrent therapy, the patient's thyroid stimulating hormone (TSH) increased to 18.47 mIU/L (a 2.7-fold increase) requiring a dose increase of levothyroxine to 250 mcg daily. Subsequently, ritonavir was discontinued with a decrease in levothyroxine dose to 125 mcg daily with stabilization of TSH at 7.32 mIU/L.(2) A case report of a 58 year old female on zidovudine, lamivudine, and lopinavir/ritonavir underwent a total thyroidectomy with subsequent introduction of levothyroxine. Levothyroxine was titrated to 225 mcg daily along with the addition of liothyronine. Due to persistently elevated TSH values (range 47.6 - 85.1 mIU/L), lopinavir/ritonavir was then withdrawn and two months later TSH and T4 levels returned to normal, 4.1 mIU/L and 12.1 pmol/L, respectively. Eight months later lopinavir/ritonavir was reintroduced and 1 month later TSH and T4 increased to 42.9 mIU/L and 10.6 mIU/L, respectively. Again, lopinavir/ritonavir was withdrawn and TSH and T4 values returned to normal, 1.1 mIU/L and 13.4 pmol/L, respectively.(3) A case report of a 37 year old female on abacavir/lamivudine and lopinavir/ritonavir details the management course of hypothyroidism over a six year period, including during 3 pregnancies. After a total thyroidectomy, the patient was started on levothyroxine 75 mcg daily. Post-surgical levels of TSH and T4 (during patient's second pregnancy) increased to 94.3 mIU/L and 6.1 mIU/L, respectively, and peaked at 125.89 mIU/L and 7.7 mIU/L, respectively. Levothyroxine doses were increased to 175 mcg daily over the following year (during the patient's second and third pregnancies) to achieve decreased TSH and T4 values of 8.58 mIU/L and 12.8 mIU/L, respectively. TSH values rose again to 17.23 mIU/L and ritonavir was withdrawn from therapy. The patient was then maintained on levothyroxine 125 mcg daily with a TSH of 0.12 - 0.42 mIU/L over the next 2 years.(1) |
KALETRA, LOPINAVIR-RITONAVIR, NORVIR, RITONAVIR |
Thyroid Preparations/Sertraline SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The mechanism by which sertraline lowers serum thyroid hormone concentrations is uncertain. One reported case in which sertraline caused a low serum total thyroxine concentration is believed to be caused by sertraline increasing the clearance of the thyroxine.(1) CLINICAL EFFECTS: The coadministration of thyroid preparations and sertraline may result in decreased levels and clinical effects of thyroid hormones.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients taking thyroid preparations and sertraline should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased. DISCUSSION: In a case report of 9 levothyroxine treated patients with hypothyroidism, who were treated with sertraline, all were found to have elevated serum thyrotropin concentrations. Elevated thyrotropin levels are indicative of a decrease in the efficacy of levothyroxine. The dose of levothyroxine was increased for all patients. Required dosage adjustments ranged from 11% to 50%.(1) In a study, patients with major depression and hypothyroidism on adequate levothyroxine therapy were treated with either fluoxetine or sertraline. The results of this study showed no change in thyroid levels among hypothyroid patients on levothyroxine therapy who were treated with either fluoxetine or sertraline.(2) |
SERTRALINE HCL, ZOLOFT |
Thyroid Preparations/Estrogens SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Estrogens increase thyroxine-binding globulin (TBG) levels by increasing its biosynthesis and decreasing its clearance.(1) Hypothyroid patients who start estrogens may be unable to compensate for this increase and may have decreased serum free T4 (FT4) concentrations and increased TSH.(1,2) CLINICAL EFFECTS: The coadministration of thyroid preparations and estrogens may result in decreased levels and clinical effects of thyroid hormones.(1-4) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients taking thyroid preparations and who start or stop estrogens should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased.(1-4) DISCUSSION: In a prospective observational study, 25 post-menopausal women with hypothyroidism on stable levothyroxine therapy for at least 9 months started on estrogen replacement therapy. After 12 weeks, mean serum FT4 levels decreased significantly from 1.7 +/- 0.4 ng/dL to 1.4 +/-0.3 mg/dL and TSH increased significantly from 0.9 +/-1.1 to 3.2 +/- 3.1 milli-units/L.(1) |
2-METHOXYESTRADIOL, ACTIVELLA, AFIRMELLE, ALTAVERA, ALYACEN, AMETHIA, AMETHYST, ANGELIQ, ANNOVERA, APRI, ARANELLE, ASHLYNA, AUBRA, AUBRA EQ, AUROVELA, AUROVELA 24 FE, AUROVELA FE, AVIANE, AYUNA, AZURETTE, BALCOLTRA, BALZIVA, BEYAZ, BIJUVA, BLISOVI 24 FE, BLISOVI FE, BRIELLYN, CAMRESE, CAMRESE LO, CAZIANT, CHARLOTTE 24 FE, CHATEAL EQ, CLIMARA, CLIMARA PRO, COMBIPATCH, COVARYX, COVARYX H.S., CRYSELLE, CYRED, CYRED EQ, DASETTA, DAYSEE, DELESTROGEN, DEPO-ESTRADIOL, DESOGESTR-ETH ESTRAD ETH ESTRA, DIETHYLSTILBESTROL, DIVIGEL, DOLISHALE, DOTTI, DROSPIRENONE-ETH ESTRA-LEVOMEF, DROSPIRENONE-ETHINYL ESTRADIOL, DUAVEE, EEMT, EEMT H.S., ELESTRIN, ELINEST, ELURYNG, ENILLORING, ENPRESSE, ENSKYCE, ESTARYLLA, ESTRACE, ESTRADIOL, ESTRADIOL (ONCE WEEKLY), ESTRADIOL (TWICE WEEKLY), ESTRADIOL BENZOATE, ESTRADIOL CYPIONATE, ESTRADIOL HEMIHYDRATE, ESTRADIOL HEMIHYDRATE MICRO, ESTRADIOL MICRONIZED, ESTRADIOL VALERATE, ESTRADIOL-NORETHINDRONE ACETAT, ESTRATEST F.S., ESTRATEST H.S., ESTRING, ESTRIOL, ESTRIOL MICRONIZED, ESTROGEL, ESTROGEN-METHYLTESTOSTERONE, ESTRONE, ETHINYL ESTRADIOL, ETHYNODIOL-ETHINYL ESTRADIOL, ETONOGESTREL-ETHINYL ESTRADIOL, EVAMIST, FALMINA, FEMLYV, FEMRING, FINZALA, FYAVOLV, GEMMILY, HAILEY, HAILEY 24 FE, HAILEY FE, HALOETTE, ICLEVIA, IMVEXXY, ISIBLOOM, JAIMIESS, JASMIEL, JINTELI, JOLESSA, JOYEAUX, JULEBER, JUNEL, JUNEL FE, JUNEL FE 24, KAITLIB FE, KALLIGA, KARIVA, KELNOR 1-35, KELNOR 1-50, KURVELO, LARIN, LARIN 24 FE, LARIN FE, LAYOLIS FE, LEENA, LESSINA, LEVONEST, LEVONORG-ETH ESTRAD ETH ESTRAD, LEVONORG-ETH ESTRAD-FE BISGLYC, LEVONORGESTREL-ETH ESTRADIOL, LEVORA-28, LO LOESTRIN FE, LO-ZUMANDIMINE, LOESTRIN, LOESTRIN FE, LOJAIMIESS, LORYNA, LOW-OGESTREL, LUTERA, LYLLANA, MARLISSA, MENEST, MENOSTAR, MERZEE, MIBELAS 24 FE, MICROGESTIN, MICROGESTIN FE, MILI, MIMVEY, MINIVELLE, MINZOYA, MONO-LINYAH, MYFEMBREE, NATAZIA, NECON, NEXTSTELLIS, NIKKI, NORELGESTROMIN-ETH ESTRADIOL, NORETHIN-ETH ESTRA-FERROUS FUM, NORETHINDRON-ETHINYL ESTRADIOL, NORETHINDRONE-E.ESTRADIOL-IRON, NORGESTIMATE-ETHINYL ESTRADIOL, NORTREL, NUVARING, NYLIA, OCELLA, ORIAHNN, ORTHO TRI-CYCLEN, ORTHO-NOVUM, PHILITH, PIMTREA, PORTIA, PREMARIN, PREMPHASE, PREMPRO, RECLIPSEN, RIVELSA, SAFYRAL, SETLAKIN, SIMLIYA, SIMPESSE, SPRINTEC, SRONYX, SYEDA, TARINA 24 FE, TARINA FE, TARINA FE 1-20 EQ, TAYTULLA, TILIA FE, TRI-ESTARYLLA, TRI-LEGEST FE, TRI-LINYAH, TRI-LO-ESTARYLLA, TRI-LO-MARZIA, TRI-LO-MILI, TRI-LO-SPRINTEC, TRI-MILI, TRI-SPRINTEC, TRI-VYLIBRA, TRI-VYLIBRA LO, TRIVORA-28, TURQOZ, TWIRLA, TYBLUME, VAGIFEM, VELIVET, VESTURA, VIENVA, VIORELE, VIVELLE-DOT, VOLNEA, VYFEMLA, VYLIBRA, WERA, WYMZYA FE, XULANE, YASMIN 28, YAZ, YUVAFEM, ZAFEMY, ZARAH, ZOVIA 1-35, ZUMANDIMINE |
Carbimazole; Methimazole/Thyroid Preparations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Methimazole can affect the therapeutic response to thyroid hormone therapy. It decreases thyroid hormone secretion. Thyroid hormone therapy can antagonize the pharmacologic effects of methimazole by supplying an exogenous source of thyroid hormone. Carbimazole is a prodrug of methimazole.(1) CLINICAL EFFECTS: Concurrent use of carbimazole or methimazole and thyroid hormones may result in opposing effects. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Concurrent use of carbimazole or methimazole and thyroid hormones should be avoided. DISCUSSION: The 2016 American Thyroid Association guidelines recommended avoiding the concurrent use of methimazole and thyroid preparations for "block and replace" therapy to make a patient euthyroid. Meta-analyses have shown that a higher prevalence of adverse events occurs with block-and-replace regimens than dose titration.(2) The 2018 European Thyroid Association guidelines state that methimazole (30 mg) may be given combined with levothyroxine supplement ion for block-and-replace therapy to avoid drug-induced hypothyroidism but methimazole dose titration is the preferred therapy.(3) |
CARBIMAZOLE, METHIMAZOLE |
Selected Anticoagulants/Thyroid SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Unknown. However, thyroid hormones may influence concentrations of vitamin K-dependent clotting factors. CLINICAL EFFECTS: Concurrent use of vitamin K antagonists and thyroid hormones may increase the risk for bleeding. Hypothyroidism may increase the oral anticoagulant requirements. Administration of thyroid hormones or hyperthyroidism may decrease oral anticoagulant requirements. PREDISPOSING FACTORS: The risk for bleeding episodes may be greater in patients with disease-associated factors (e.g. thrombocytopenia). Drug associated risk factors include concurrent use of multiple drugs which inhibit anticoagulant/antiplatelet metabolism and/or have an inherent risk for bleeding (e.g. NSAIDs). PATIENT MANAGEMENT: Monitor prothrombin activity and adjust the anticoagulant dosage accordingly during initiation of warfarin therapy in patients receiving thyroid replacement therapy, during the initiation or titration of thyroid replacement therapy in patients receiving warfarin, or if any changes in thyroid function occur. If concurrent therapy is warranted, monitor patients receiving concurrent therapy for signs of blood loss, including decreased hemoglobin, hematocrit, fecal occult blood, and/or decreased blood pressure and promptly evaluate patients with any symptoms. When applicable, perform agent-specific laboratory test (e.g. INR, aPTT) to monitor efficacy and safety of anticoagulation. Discontinue anticoagulation in patients with active pathologic bleeding. Instruct patients to report any signs and symptoms of bleeding, such as unusual bleeding from the gums or nose; unusual bruising; red or black, tarry stools; red, pink or dark brown urine; acute abdominal or joint pain and/or swelling. The time of highest risk for a coumarin-type drug interaction is when the precipitant drug is initiated or discontinued. Contact the prescriber before initiating, altering the dose or discontinuing either drug. DISCUSSION: Any change in thyroid status in patients stabilized on warfarin may necessitate a change in warfarin dosage requirements. Initiation of thyroid replacement therapy in patients stabilized on warfarin may result in increases in the effects of warfarin. A decrease in the dose of warfarin usually becomes necessary within one to four weeks after starting therapy with thyroid compounds. Warfarin therapy should be initiated in low doses in patients who are hyperthyroid. In a 16 year population based nested matched case control study, 10,532 hospitalizations for hemorrhage were evaluated and matched to 40,595 controls. The primary analysis showed no increase in risk of hemorrhage in older patients on warfarin initiated on levothyroxine in previous 30 days (OR 1.11, 95% CI 0.67-1.86). When patients were matched up to 90 days prior to the hemorrhage event, there was no significant association with levothyroxine 31-60 days prior to index date (OR 0.75 95% CI 0.26-2.25) or 61-90 days prior to index date (OR 0.67 95% CI 0.15-3.01). A retrospective, self-controlled study of 102 patients on chronic warfarin therapy were included if the patient had INR results 90 days before and after starting levothyroxine. The mean warfarin dose/INR ratio in the pre-period and post-period had no significant change (p=0.825). In patients who achieved euthyroid during post-period, warfarin dose/INR ratio was numerically lower in the post-period but not statistically significant (13.42 versus 12.7, respectively; p=0.338). In patients initiated on levothyroxine doses greater than 50 mcg, pre-period and post-period warfarin dose/INR ratio also had no significant difference (p>0.2). |
ANISINDIONE, DICUMAROL, JANTOVEN, PHENINDIONE, WARFARIN SODIUM |
The following contraindication information is available for CYTOMEL (liothyronine sodium):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 2 contraindications.
Absolute contraindication.
Contraindication List |
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Primary adrenocortical insufficiency |
Thyrotoxicosis crisis |
There are 2 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
Severe List |
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Hyperthyroidism |
Pituitary insufficiency |
There are 7 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
Moderate List |
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Angina |
Cardiac arrhythmia |
Coronary artery disease |
Diabetes mellitus |
Hypertension |
Osteopenia |
Osteoporosis |
The following adverse reaction information is available for CYTOMEL (liothyronine sodium):
Adverse reaction overview.
No enhanced Common Adverse Effects information available for this drug.
No enhanced Common Adverse Effects information available for this drug.
There are 15 severe adverse reactions.
More Frequent | Less Frequent |
---|---|
None. |
Osteopenia |
Rare/Very Rare |
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Abnormal hepatic function tests Acute myocardial infarction Angina Angioedema Cardiac arrest Cardiac arrhythmia Dyspnea Heart failure Idiopathic intracranial hypertension Mood changes Seizure disorder Skin rash Tachycardia Urticaria |
There are 26 less severe adverse reactions.
More Frequent | Less Frequent |
---|---|
Female infertility |
Hypertension Weight loss |
Rare/Very Rare |
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Abdominal pain with cramps Alopecia Chest pain Diarrhea Fatigue Fever Flushing Headache disorder Heat intolerance Hyperhidrosis Increased appetite Increased pulse rate Insomnia Irregular menstrual periods Irritability Menstrual disorder Muscle spasm Muscle weakness Nervousness Palpitations Symptoms of anxiety Tremor Vomiting |
The following precautions are available for CYTOMEL (liothyronine sodium):
No enhanced Pediatric Use information available for this drug.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Contraindicated
None |
Severe Precaution
None |
Management or Monitoring Precaution
None |
No enhanced Pregnancy information available for this drug.
No enhanced Lactation information available for this drug.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for CYTOMEL (liothyronine sodium):
WARNING: This medication should not be used for weight loss. Normal doses of this medication will not work for weight loss, and large doses may cause serious, possibly fatal side effects, especially when taken with diet pills.
WARNING: This medication should not be used for weight loss. Normal doses of this medication will not work for weight loss, and large doses may cause serious, possibly fatal side effects, especially when taken with diet pills.
The following icd codes are available for CYTOMEL (liothyronine sodium)'s list of indications:
Adjunct to surgery or radiotherapy for thyroid carcinoma | |
C73 | Malignant neoplasm of thyroid gland |
Hypothyroidism | |
E03 | Other hypothyroidism |
E03.0 | Congenital hypothyroidism with diffuse goiter |
E03.1 | Congenital hypothyroidism without goiter |
E03.2 | Hypothyroidism due to medicaments and other exogenous substances |
E03.3 | Postinfectious hypothyroidism |
E03.4 | Atrophy of thyroid (acquired) |
E03.8 | Other specified hypothyroidism |
E03.9 | Hypothyroidism, unspecified |
E89.0 | Postprocedural hypothyroidism |
Formulary Reference Tool