Product Monograph - ZDS-Liothyronine

INDICATIONS AND CLINICAL USES

ZDS-Liothyronine is indicated in conditions of inadequate endogenous thyroid production. These: include:

a. HYPOTHYROIDISM: As replacement or supplemental therapy in patients with hypothyroidism of any etiology except transient hypothyroidism during the recovery phase of subacute thyroiditis
b. SIMPLE (non-toxic) GOITER: ZDS-Liothyronine may be tried therapeutically in an attempt to reduce the size of such a goiter, the rationale being that suppression of pituitary thyroid stimulating hormone (TSH) removes at least one of the growth-promoting factors.

ZDS-Liothyronine may be used in the T₃suppression test to differentiate suspected hyperthyroidism from euthyroidism. (See special instructions under ADMINISTRATION AND DOSAGE),

ZDS-Liothyronine can be used in patients allergic to dessicated thyroid or thyroid extract derived from pork or beef.

Use in Pregnancy: See WARNINGS and PRECAUTIONS

Use in Nursing Mothers: See WARNINGS and PRECAUTIONS

Pediatric Use: See WARNINGS and PRECAUTIONS and DOSAGE and ADMINISTRATION

Geriatic Use: See WARNINGS and PRECAUTIONS and DOSAGE and ADMINISTRATION

CONTRAINDICATIONS

Patients with an apparent hypersensitivity to liothyronine sodium or any of the inactive product constituents.
Patients with uncorrected adrenal insufficiency, as thyroid hormones increase tissue demands for adrenocortical hormones and may thereby precipitate acute adrenal crisis (see WARNINGS AND PRECAUTIONS).
Patients with acute myocardial infarction

WARNINGS AND PRECAUTIONS

Serious Warnings and Precautions

The use of ZDS-Liothyronine or other thyroid preparations in the therapy of obesity is unjustified and dangerous. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for anorectic effects.

General

Liothyronine sodium has a narrow therapeutic index and has a relatively short half-life compared to levothyroxine. Regardless of the indication for use, careful dosage titration is necessary to avoid the consequences of over or under treatment. These consequences include, among others, effects on growth and development, cardiovascular function, bone metabolism, reproductive function, emotional state and gastrointestinal function. Many drugs interact with liothyronine sodium, necessitating adjustments in dosing to maintain therapeutic response (See DRUG INTERACTIONS).

Cardiovascular

Since Liothyronine sodium is a metabolic stimulant, it is not recommended for use in patients with compromised cardiovascular systems, particularly the coronary arteries. These include patients with angina pectoris, ischemic states, and the elderly (in whom there is a greater likelihood of occult cardiac disease). However, if it is used in such patients, caution should be exercised and the starting dosage should never be more than 5 mcg daily. If the dosage is increased, it should be in increments of no more than 5 mcg daily at two-week intervals. (See DOSAGE and ADMINISTRATION).

Endocrine and Metabolism

Patients with Nontoxic Diffuse Goiter or Nodular Thyroid Disease

Exercise caution when administering liothyronine sodium to patients with nontoxic diffuse goiter or nodular thyroid disease in order to prevent precipitation of thyrotoxicosis. Based on shared pharmacological effect of thyroid hormones, the below caution may apply to liothyronine:

In those patients, particularly the elderly or those with underlying cardiovascular disease, levothyroxine therapy is contraindicated if the serum TSH level is already suppressed due to the risk of precipitating overt thyrotoxicosis. If the serum TSH level is not suppressed, levothyroxine should be used with caution in conjunction with careful monitoring of thyroid function for evidence of hyperthyroidism and clinical monitoring for potential associated adverse cardiovascular signs and symptoms of hyperthyroidism.

Myxedematous patients are sensitive to thyroid substances; dosage should be started at a very low level and increased gradually (See DOSAGE and ADMINISTRATION).

Diabetes

Patients with diabetes mellitus may require upward adjustments of their antidiabetic therapeutic regimens when treated with liothyronine sodium (see DRUG INTERACTIONS).

Hypothalamic/Pituitary Hormone Deficiencies

In patients with secondary or tertiary hypothyroidism, additional hypothalamic/pituitary hormone deficiencies should be considered, and, if diagnosed, treated (see WARNINGS AND PRECAUTIONS, Autoimmune Polyglandular Syndrome for adrenal insufficiency).

Severe and prolonged hypothyroidism can lead to a decreased level of adrenocortical activity commensurate with the lowered metabolic state. When thyroid replacement therapy is administered, the metabolism increases at a greater rate than adrenocortical activity. This can precipitate adrenocortical insufficiency. Therefore, in severe and prolonged hypothyroidism, supplemental adrenocortical steroids may be necessary.

In rare instances, the administration of thyroid hormone may precipitate a hyperthyroid state or may aggravate existing hyperthyroidism. In infants, excessive doses of thyroid hormone preparations may produce cradiosynostosis.

Morphologic hypogonadism and nephrosis should be ruled out before the drug is administered. If hypopituitarism is present, the adrenal deficiency must be corrected before liothyronine sodium therapy is started.

Bone Mineral Density

In women, long-term thyroid hormones therapy has been associated with increased bone resorption, thereby decreasing bone mineral density, especially in post-menopausal women on greater than replacement doses or in women who are receiving suppressive doses of thyroid hormones. Therefore, it is recommended that patients receiving thyroid hormones be given the minimum dose necessary to achieve the desired clinical and biochemical response.

Immune

Autoimmune Polyglandular Syndrome

Occasionally, chronic autoimmune thyroiditis may occur in association with other autoimmune disorders such as adrenal insufficiency, pernicious anemia, and insulin dependent diabetes mellitus. Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with liothyronine sodium. Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated, due to increased metabolic clearance of glucocorticoids by thyroid hormone.

Special Populations

Pregnancy: Thyroid hormones do not readily cross the placental barrier. The clinical experience to date does not indicate any adverse effect on fetuses when thyroid hormones are administered to pregnant women. Thyroid replacement therapy to hypothyroid women should not be discontinued during pregnancy.

Pregnant women who are maintained on liothyronine sodium should have their TSH measured periodically and liothyronine sodium dose adjusted as necessary. Serum TSH level should be obtained six to eight weeks postpartum to adjust dosage.

There are no available animal data informing the drug-associated risk.

Breast-feeding: Thyroid hormones are excreted in human milk in minimal amounts. Because liothyronine is excreted in human milk, caution should be exercised.

Pediatrics: Clinical assessment of growth, development, and thyroid status should be monitored frequently (See DOSAGE AND ADMINISTRATION).

Geriatrics: Clinical studies of liothyronine sodium did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection and renal function should be monitored. Because of the increased prevalence of cardiovascular disease among the elderly, liothyronine therapy should not be initiated at the full replacement dose (See DOSAGE and ADMINISTRATION).

Monitoring and Laboratory Tests

Periodic measurements of thyroid function tests should be performed guided by the patient’s condition.

ADVERSE REACTIONS

Adverse reactions associated with liothyronine sodium are primarily those of hyperthyroidism, due to therapeutic overdosage (see WARNINGS and PRECAUTIONS, General and Overdosage). They include the following:

General: excessive sweating, fatigue, increased appetite, weight loss, heat intolerance, fever. Cardiovascular: cardiac arrhythmias, angina pectoris, palpitations, tachycardia, increased pulse, increased blood pressure, heart failure

Central Nervous System: headache, nervousness, hyperactivity, anxiety, irritability, emotional lability, insomnia

Hypersensitivity: rare instances of allergic skin reactions have been reported

Endocrine: decreased bone mineral density

Gastrointestinal: diarrhea

Musculoskeletal: tremors, muscle weakness

Reproductive: menstrual irregularities

Respiratory: dyspnea

Medication should be interrupted until symptoms disappear, then resumed in smaller doses. Therapy can usually be resumed after one or two days.

DRUG INTERACTIONS

Overview:

Any agent that alters thyroid hormone synthesis, secretion, distribution, effect on target tissues, metabolism, or elimination may alter the optimal therapeutic dose of ZDS-Liothyronine. A listing of drug-thyroidal axis interactions is contained in the Table below:

Drug or Drug Class	Effect
Drug or Drug Class	Effect
Drug or Drug Class	Effect
Drugs that alter thyroid hormone secretion Drugs that may decrease thyroid hormone secretion, which may result in hypothyroidism
Aminoglutethimide Amiodarone Iodide (including iodine-containing radiographic contrast agents) Lithium Thioamides Methimazole Propylthiouracil (PTU) Carbimazole Sulfonamides Tolbutamide	Long-term lithium therapy can result in goiter in up to 50% of patients, and either subclinical or overt hypothyroidism, each in up to 20% of patients. The fetus, neonate, elderly and euthyroid patients with underlying thyroid disease (e.g., Hashimotos’s thyroiditis or with Grave’s disease previously treated with radioiodine or surgery) are among those individuals who are particularly susceptible to iodine-induced hypothyroidism. Oral cholecystographic agents and amiodarone are slowly excreted, producing more prolonged hypothyroidism than parenterally administered iodinated contrast agents. Long-term aminoglutethimide therapy may minimally decrease T4 and T3 levels and increase TSH, although all values remain within normal limits in most patients.
Drugs that may decrease T3 absorption, which may result in hypothyroidism
Bile Acid Sequestrants Cholestyramine	Cholestyramine binds orally administered thyroid hormones in the intestine, impairing their absorption. In vitro studies indicate that the binding is not easily overcome. Therefore, four to five hours should elapse between administration of cholestyramine and thyroid hormones.
Drugs that may alter T3 serum transport
Drugs that may increase serum TBG Concentration Clofibrate Estrogen-containing Oral Contraceptives Estrogens (oral) Heroin/Methadone 5-Fluorouracil Mitotane Tamoxifen	Drugs that may decrease serum TBG Concentration Androgens/Anabolic Steroids Asparaginase Glucocorticoids Slow-Release Nicotinic Acid
Miscellaneous
Oral Anticoagulants	Thyroid hormones appear to increase the catabolism of vitamin K-dependent clotting factors. Patients stabilized on oral anticoagulants may require dosage adjustment, through close monitoring of Prothrombin time, when thyroid therapy is started. No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid therapy.
Tricyclic Antidepressants	Use of thyroid products with imipramine and other tricyclic antidepressants may increase receptor sensitivity and enhance antidepressant activity; transient cardiac arrhythmias have been observed. Thyroid hormone activity may also be enhanced.
Insulin or Oral Hypoglycemics	Initiating thyroid replacement therapy may require increases in insulin or oral hypoglycemic requirements. The effects seen are poorly understood and depend upon a variety of factors such as dose and type of thyroid preparations and endocrine status on the patient.
Digitalis	Thyroid preparations may potentiate the toxic effects of digitalis. Thyroid hormonal replacement increases metabolic rate, which requires an increase in digitalis dosage.
Cytokines Interferon-alpha Interleukin-2	Therapy with interferon-alpha has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both.
Patients who have antithyroid antibodies before treatment are at higher risk for thyroid dysfunction during treatment. Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients. Interferon- beta and gamma have not been reported to cause thyroid dysfunction.
Growth Hormones Somatrem Somatropin	Excessive use of thyroid hormones with growth hormones may accelerate epiphyseal closure. However, untreated hypothyroidism may interfere with growth response to growth hormone.
HMG-CoA reductase inhibitors (statins) Lovastatin	Some statins may increase thyroid hormone requirements. It is unknown if this occurs with all statins. Close monitoring of thyroid function and appropriate thyroid hormone dose adjustments may be necessary when thyroid hormones and statins are co-prescribed.
Ketamine	When administered to patients on a thyroid preparation, the parenteral anesthetic may cause hypertension and tachycardia. Use with caution and be prepared to treat hypertension, if necessary.
Methylxanthine Bronchodilators (e.g., Theophylline)	Decreased theophylline clearance may occur in hypothyroid patients; clearance returns to normal when the euthyroid state is achieved.
Radiographic agents	Thyroid hormones may reduce the uptake of ¹²³I, ¹³¹I, and ⁹⁹mTc.
Sympathomimetics/Catecholamines	Concurrent use may increase the effects of sympathomimetics, catecholamines or thyroid hormone. Thyroid hormones may increase the risk of coronary insufficiency when sympathomimetic or catecholamine agents are administered to patients with coronary artery disease.
Diazepam Ethionamide Metoclopramide Para-aminosalicylate sodium Perphenazine Resorcinol (excessive topical use)	These agents have been associated with thyroid hormone and/or TSH level alterations by various mechanisms.

DRUG/LABORATORY TEST INTERACTIONS

Since liothyronine is not as firmly bound to serum protein as thyroxine, the PBI usually remains at levels below normal during full replacement therapy. As with all thyroid preparations, thyroid gland-function reflected by ¹³¹I uptake may be depressed by ZDS-Liothyronine, particularly when dosage exceeds 75 mcg daily. This effect disappears rapidly, and useful ¹³¹I uptake values may be obtained usually within two weeks following discontinuance of the drug.

The following drugs or moieties are known to interfere with laboratory tests performed in patients on thyroid hormone therapy: androgens, corticosteroids, estrogens and estrogen- containing oral contraceptives, iodine-containing preparations and salicylates.

Changes in TBG concentration should be taken into consideration in the interpretation of T4 and T3 values, which necessitates measurement and evaluation of unbound (free) hormone and/or determination of the free-T4 index (FT4I). Pregnancy, infectious hepatitis, estrogens and estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentration. Decreases in TBG concentrations are observed in nephrosis, severe hypoproteinemia, severe liver disease, acromegaly and after androgen or corticosteroid therapy. Familial hyper- or hypo-thyroxine binding- globulinemias have been described.

The binding of thyroxine by thyroxine-binding prealbumin (TBPA) is inhibited by salicylates.

Medicinal or dietary iodine interferes with all in vivo tests of radioiodine uptake, producing low uptakes which may not be reflective of a true decrease in hormone synthesis.

Drug-Food Interactions: interactions with food products have not been established.

Drug-Herb Interactions: interactions with herbal products have not been established.

DOSAGE AND ADMINISTRATION

Dosing Considerations

Optimum dosage is usually determined by the patient’s clinical response. Confirmatory tests include: Radioactive Iodine T₃Resin Uptake, ¹³¹I-T3 Red cell Uptake, BMR, and the Achilles Tendon Reflex Test. Comparatively small doses (as little as 5 mcg daily) may be fully effective in some cases; however, in other instances, a satisfactory clinical response may not be achieved until recommended dosage levels have been exceeded. Daily doses of up to 150 mcg may be required in a few resistant patients.

Recommended Dose and Dosage Adjustment

It is not necessary to divide daily maintenance doses. Although ZDS-Liothyronine has a rapid cut-off, its metabolic effects persist for a few days following discontinuance.

Mild Hypothyroidism: Recommended starting dose is 25 mcg daily. Daily dosage then may be increased by 12.5 or 25 mcg every one or two weeks. Usual maintenance dosage is 25 – 75 mcg daily. Smaller doses may be fully effective in some patients, while 100 mcg may be required in others.

Myxedema: Myxedematous patients are very sensitive to thyroid substances; dosage should be started at a very low level and increased gradually.

Recommended starting dosage is 5 mcg daily. This may be increased by 5 or 10 mcg daily every one or two weeks. Usual maintenance dosage is 50 to 100 mcg daily.

Cretinism: Since the mother provides little or no thyroid hormone to the fetus, infants with thyroid dysfunction will require replacement therapy from birth. Treatment should be initiated as early as possible to avoid permanent physical and mental changes.

Recommended starting dosage is 5 mcg daily, with a 5 mcg increment every three to four days until the desired response is achieved. Infants a few months old may require only 20 mcg daily for maintenance. At one year, 50 mcg daily may be required. Above 3 years, full adult dosage may be necessary.

Simple (non-toxic) Goiter: recommended starting dosage is 5 mcg daily. This dosage may be increased by 5 to 10 mcg daily every one to two weeks. When 25 mcg daily is reached, dosage may be increased every week or two by 12.5 or 25 mcg. Usual maintenance dosage is 75 mcg daily.

Special Populations

Pediatrics: Treatment should be initiated immediately upon diagnosis and maintained for life, unless transient hypothyroidism is suspected, in which case, therapy may be interrupted for 2 to 8 weeks after the age of 3 years to reassess the condition. Gradual cessation of therapy is justified in patients who have maintained a normal TSH during those 2 to 8 weeks. Therapy should be started with 5 mcg daily and increased only by 5 mcg increments at the recommended intervals. See WARNINGS and PRECAUTIONS.

Geriatrics: Therapy should be started with 5 mcg daily and increased only by 5 mcg increments at the recommended intervals. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. See WARNINGS and PRECAUTIONS.

Switching to ZDS-Liothyronine from thyroid, L-thyroxine or thyroglobulin medication

When switching a patient to ZDS-Liothyronine from thyroid, L-thyroxine or thyroglobulin, discontinue the other medication, initiate ZDS-Liothyronine at a low dosage, and increase gradually according to the patient’s response. When selecting a starting dose, bear in mind that this drug has a rapid onset of action, and that residual effects of the other thyroid preparation may persist for the first several weeks of therapy.

Special Instruction for T₃Suppression Test: When ¹³¹I thyroid uptake is in the borderline-high range, administer 75-100 mcg of ZDS-Liothyronine daily for 7 days, then repeat ¹³¹I thyroid uptake test. In the hyperthyroid patient, 24-hour ¹³¹I thyroid uptake will not be affected significantly. In the euthyroid patient, 24-hour ¹³¹I thyroid uptake will drop to less than 20%.

Missed Dose

The missed dose should be taken as soon as possible. If it is almost time for the next dose, the missed dose should not be taken. Instead, the next regularly scheduled dose should be taken. Doses should not be doubled.

OVERDOSAGE

For the most recent information in the management of a suspected drug overdose, contact your regional poison control centre or Health Canada's toll-free number, 1-844 POISON-X (1-844-764-7669).

Symptoms: see WARNINGS AND PRECAUTIONS, General and ADVERSE REACTIONS. Angina pectoris or congestive heart failure may be induced or aggravated. Shock may also develop. Massive overdosage may result in symptoms resembling thyroid storm. Chronic excessive dosage will produce the signs and symptoms of hyperthyroidism.

Treatment: Dosage should be reduced or therapy temporarily discontinued if signs and symptoms of overdosage appear. Treatment may be reinstituted at a lower dosage. In normal individuals, normal hypothalamic-pituitary-thyroid axis function is restored in 6 to 8 weeks after thyroid suppression.

Treatment of acute massive thyroid hormone overdosage is aimed at reducing gastrointestinal absorption of the drugs and counteracting central and peripheral effects, mainly those of increased sympathetic activity. Vomiting may be induced initially if further gastrointestinal absorption can reasonably be prevented and barring contraindications such as coma, convulsions, or loss of the gagging reflex. Treatment is symptomatic and supportive. Oxygen may be administered and ventilation maintained. Cardiac glycosides may be indicated if congestive heart failure develops. Measures to control fever, hypoglycemia, or fluid loss should be instituted if needed. Antiadrenergic agents, particularly propranolol, have been used advantageously in the treatment of increased sympathetic activity.

ACTION

There are two principal naturally occurring thyroid hormones, L-tetraiodothyronine (T₄, levothyroxine, L-thyroxine) and L-triiodothyronine (T₃, liothyronine).

The mechanisms by which thyroid hormones exert their physiologic actions are not well understood. It is generally believed that they exert most, if not all, of their actions through control of protein synthesis.

At moderate concentrations, thyroid hormones increase the synthesis of RNA and protein, followed by an increase in basal metabolic rate (BMR). They stimulate oxidative enzyme systems generally, and enhance the release of free fatty acids from adipose tissue. They also increase the intestinal absorption and peripheral utilization of glucose.

At higher concentrations, thyroid hormones decrease protein synthesis, uncouple oxidative phosphorylation and increase breakdown of glycogen, lipids and protein.

CLINICAL PHARMACOLOGY

Liothyronine is the synthetic levo form of triiodothyronine, with all pharmacologic activities of the natural substance. Its onset of action is rapid, occurring within a few hours. Maximum pharmacologic response occurs within two or three days, providing early clinical response.

Following oral administration, about 95% of the dose of thyronine is absorbed from the gastrointestinal tract in four hours. Liothyronine, not firmly bound to serum protein, is readily available to body tissues. Its biologic half-life is about 2 ½ days.

Liothyronine has a rapid cut-off of activity which permits quick dosage adjustment and facilitates control of the effects of overdosage should they occur.

Comparative Bioavailability Studies

A randomized, two-treatment, single-dose (4 x 25 mcg), four -period, fully replicated crossover comparative bioavailability study of ZDS-Liothyronine (Zydus Pharmaceuticals (Canada) Inc.) and CYTOMEL® (Pfizer Canada Inc.) was conducted in healthy, adult male subjects under fasting conditions. A summary of the comparative bioavailability data from the 26 subjects included in the statistical analysis are presented in the following table.

SUMMARY TABLE OF THE COMPARATIVE BIOAVAILABILITY DATA

Liothyronine 4 x 25 mcg Geometric Mean Arithmetic Mean (CV %)
Parameter	Test¹	Reference²	% Ratio of Geometric Means	90% Confidence Interval
AUC0-48h (ng·h/mL)	73.26 74.84 (17.75)	71.81 73.14 (16.46)	102.0	98.8 - 105.3
AUC_I (ng·h/mL)	84.72 86.63 (19.87)	82.33 83.41 (15.48)	102.9	98.9 - 107.0
Cmax (ng/mL)	7.06 7.17 (15.67)	6.86 6.99 (17.52)	102.9	99.3 - 106.6
Tmax3 (h)	2.33 (1.67 - 4.50)	2.67 (1.67 - 4.50)
T½ 4 (h)	19.49 (34.61)	18.56 (31.44)

¹ZDS-Liothyronine (liothyronine as liothyronine sodium) tablets 25 mcg (Zydus Pharmaceuticals (Canada) Inc.)

²CYTOMEL® (liothyronine as liothyronine sodium) tablets 25 mcg (Pfizer Canada Inc.)

³Expressed as the median (range) only

⁴Expressed as the arithmetic mean (CV %) only

A randomized, two-treatment, single-dose (4 x 25 mcg), four -period, fully replicated crossover comparative bioavailability study of ZDS-Liothyronine (Zydus Pharmaceuticals (Canada) Inc.) and CYTOMEL® (Pfizer Canada Inc.) was conducted in healthy, adult male subjects under high-fat/high-calorie fed conditions. A summary of the comparative bioavailability data from the 28 subjects included in the statistical analysis are presented in the following table.

SUMMARY TABLE OF THE COMPARATIVE BIOVAILABILITY DATA

Liothyronine 4 x 25 mcg Geometric Mean Arithmetic Mean (CV %)
Parameter	Test¹	Reference²	% Ratio of Geometric Means	90% Confidence Interval
AUC0-48h (ng·h/mL)	54.92 56.11 (20.06)	53.25 54.67 (23.74)	103.1	99.3 - 107.1
AUC_I (ng·h/mL)	62.68 64.45 (22.74)	61.09 63.54 (29.73)	102.6	96.7 - 108.9
Cmax (ng/mL)	4.45 4.54 (18.73)	4.27 4.37 (23.36)	104.3	99.9 - 108.9
Tmax3 (h)	4.33 (2.00 - 6.00)	3.67 (2.00 - 5.50)
T½ 4 (h)	17.40 (33.64)	17.87 (71.12)

¹ZDS-Liothyronine (liothyronine as liothyronine sodium) tablets 25 mcg (Zydus Pharmaceuticals (Canada) Inc.)

²CYTOMEL® (liothyronine as liothyronine sodium) tablets 25 mcg (Pfizer Canada Inc.)

³Expressed as the median (range) only

⁴Expressed as the arithmetic mean (CV %) only

SUPPLY

ZDS-Liothyronine is supplied as follows:

5 mcg: White to off white, round, flat faced beveled edge, uncoated tablets, debossed with ‘582’ on one side and plain on the other side.

Bottles of 100 tablets

Bottles of 1000 tablets

25 mcg: White to off white, oval shaped, uncoated tablets, debossed with ‘583’ on one side and scored on the other side.

Bottles of 100 tablets

Bottles of 1000 tablets

COMPOSITION

Each ZDS-Liothyronine tablet contains liothyronine 5 mcg (present as liothyronine sodium 5.17 mcg) or 25 mcg (present as liothyronine sodium 25.84 mcg); 25 mcg of liothyronine is equivalent to approximately 65 mg of dessicated thyroid or thyroglobulin and 0.1 mg of L-thyronine. The non medicinal ingredients are: calcium sulfate dihydrate, corn starch, gelatin, stearic acid, sucrose and talc.

REFERENCES

1. ^PrCYTOMEL^®Tablets, 5 mcg and 25 mcg, control 206002, product monograph, Pfizer Canada ULC. 2017-07-07

ZDS-Liothyronine Product Monograph