Tablets (round, white to off-white) available as follows:
- 5 mcg: debossed with KPI on one side and 115 on the other side
- 25 mcg: scored on one side and debossed with KPI and 116 on the other side
- 50 mcg: scored on one side and debossed with KPI and 117 on the other side
Liothyronine sodium is contraindicated in patients with uncorrected adrenal insufficiency [see Warnings and Precautions (5.3)].
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 liothyronine sodium therapy in this population at lower doses than those recommended in younger individuals or in patients without cardiac disease [see Dosage and Administration (2.3) and Use in Specific Populations (8.5)].
Monitor for cardiac arrhythmias during surgical procedures in patients with coronary artery disease receiving suppressive liothyronine sodium therapy. Monitor patients receiving concomitant liothyronine sodium and sympathomimetic agents for signs and symptoms of coronary insufficiency. If cardiovascular symptoms develop or worsen, reduce or withhold the liothyronine sodium 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 liothyronine sodium [see Contraindications (4)].
Liothyronine sodium has a narrow therapeutic index. Over- or undertreatment with liothyronine sodium 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 liothyronine sodium carefully and monitor response to titration to avoid these effects [see Dosage and Administration (2.4)]. Monitor for the presence of drug or food interactions when using liothyronine sodium and adjust the dose as necessary [see Drug Interactions (7) and Clinical Pharmacology (12.3)].
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 liothyronine sodium [see Drug Interactions (7.2)].
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 liothyronine sodium that achieves the desired clinical and biochemical response to mitigate against this risk.
Adverse reactions associated with liothyronine sodium therapy are primarily those of hyperthyroidism due to therapeutic overdosage [see Warnings and Precautions (5.4) and Overdosage (10)]. 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
Gastrointestinal: diarrhea, vomiting, abdominal cramps, elevations in liver function tests
Dermatologic: hair loss, flushing
Endocrine: decreased bone mineral density
Reproductive: menstrual irregularities, impaired fertility
Adverse Reactions in Pediatric Patients
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 liothyronine sodium (see Tables 1 – 4).
|Potential impact: Concurrent use may reduce the efficacy of liothyronine sodium by binding and delaying or preventing absorption, potentially resulting in hypothyroidism.|
|Drug or Drug Class||Effect|
|Bile Acid Sequestrants-Colesevelam-Cholestyramine-ColestipolIon Exchange Resins-Kayexalate-Sevelamer||Bile acid sequestrants and ion exchange resins are known to decrease thyroid hormones absorption. Administer liothyronine sodium at least 4 hours prior to these drugs or monitor TSH levels.|
|Drug or Drug Class||Effect|
|ClofibrateEstrogen-containing oral contraceptivesEstrogens (oral)Heroin/Methadone5-FluorouracilMitotaneTamoxifen||These drugs may increase serum thyroxine-binding globulin (TBG) concentration.|
|Androgens/Anabolic SteroidsAsparaginaseGlucocorticoidsSlow-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:CarbamazepineFurosemide (>80 mg IV)HeparinHydantoinsNon-Steroidal Anti-inflammatory DrugsFenamates||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.|
|Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of thyroid hormones, resulting in increased liothyronine sodium requirements.|
|Drug or Drug Class||Effect|
|PhenobarbitalRifampin||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.|
|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.|
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