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t3 100 liothyronine
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T3 100

 
COMPOSITION
Each uncoated tablet contains:
Liothyronine Sodium USP   100mcg
 
CHEMICAL INFORMATION
Chemical: 3,3',5-triiodo-L-thyronine
Molecular Formula: C15H12I3NO4
Molecular Weight: 650.97 g/mol
 
 
COA
 
Chem Structure
DESCRIPTION
T3 100 is a synthetic thyroid preparation containing triiodothyronine (T3) as a sodium salt. Thyroid hormones enhance oxygen consumption by most tissues in the body, increasing the basal metabolic rate and the rate of metabolism of carbohydrates, lipids, and proteins. Thyroid hormones have a profound influence on every organ in the human body.
CLINICAL PHARMACOLOGY
Liothyronine sodium (T3) is weakly bound to serum protein, leaving it readily available for use in body tissues. The onset of T3 100 is rapid, occurring within a few hours. Maximum pharmacological response occurs within 2 or 3 days, providing an early clinical response. The biological half-life is about 2.5 days.
T3 is absorbed 95% within 4 hours of oral administration. T3 has a rapid inaction of activity which allows for quick dosage titration and allows better control of overdose effects, should they occur.
The higher affinity of T4 for both thyroid-binding globulin and thyroid binding prealbumin versus T3 explains the greater serum levels and longer half-life of the T4 vs. T3. Both protein bound hormones exist in reverse equilibrium with a small amount of free hormones which account for the metabolic activity.
INDICATIONS
Thyroid hormone drugs are used for:
Replacement or supplementation therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. This includes cretinism, myxedema, and ordinary hypothyroidism in patients of any age or state; primary hypothyroidism from function deficiency, primary atrophy, partial or total absence of the thyroid gland, or the effects of surgery, radiation, or drugs, with or without the presence of goiter; and secondary (pituitary), or tertiary (hypothalamic) hypothyroidism.
As pituitary thyroid stimulating hormones (TSH) suppressants, in the treatment or prevention of various types of euthyroid goiters, thyroid nodules, subacute or chronic lymphocytic thyroiditis, and multinodular goiter.
As diagnostic agents in diagnosing mild hyperthyroidism vs. thyroid gland autonomy. <
DRUG INTERACTIONS
Patients on oral anticoagulant therapy require close monitoring especially when T3 is started or stopped. Dosages of anticoagulants may require adjustment to re-titrate PT and INR to clinically desirable state.
Diabetics: T3 may alter the metabolism of oral hypoglycemic agents or may change insulin sensitivity in patients with diabetes mellitus which may require adjustment of dosage of insulin and other hypoglycemic drugs.
Avoid concomitant use with other CNS stimulants; particularly sympathomimetic amines.
Cholestyramine dosing must be 4-5 hours apart from T3 dosing due to its ability to block T3 and T4 intestinal binding.
Oral contraceptives/Estrogen: May increase serum thyroxine-binding globulin. Thyroid requirements may change in female patients receiving estrogen therapy. Women without a functioning thyroid gland who are on replacement therapy may need to increase thyroid dosage if estrogens are administered.
Tricyclic Antidepressants (TCA): Use of thyroid products with imipramine and other TCAs may increase receptor sensitivity and enhance antidepressant activity. Transient cardiac arrhythmias have been observed in these patients and well as enhancement of thyroid hormone activity.
T3 may potentiate the toxic effects of digitalis.
Ketamine use by patients on thyroid therapy may result in severe hypertension and tachycardia. Be prepared to treat hypertension in these patients.
Vasopressors: T3 increases the adrenergic effect of catecholamines such as epinephrine and norepinephrine. Injection of these drugs in patients receiving T3 therapy may increase risk of coronary insufficiency. Careful observation is required.
PRECAUTIONS
Drugs with thyroid hormone activity have been used in the treatment of obesity. In euthyroid patients, doses within the normal range of hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given with sympathomimetic amines concomitantly.
Thyroid hormones should not be used without verification of the integrity of the cardiovascular system, particular coronary arteries; especially in patients with angina pectoris and in the elderly where occult cardiac disease is more probable.
Patients with greater risk profiles should begin treatment with doses of 5mcg per day and titration at 2-week intervals until the desired clinical range is achieved Myxedematous patients are very sensitize to thyroid hormones and must be started at a very low dose. If achieving a euthyroid state requires exacerbation of cardiovascular disease, dosage should be reduced,
Nephrosis and morphological hypogonadism should be ruled out prior to treatment.
Hypopituitarism and adrenal deficiency must be corrected prior to T3 use.
Prolonged hypothyroidism can result in decreased adrenocortical activity commensurate with lowered metabolic rate. When thyroid replacement therapy in initiated, metabolism increases at a greater rate than adrenocortical activity; which may trigger adrenocortical insufficiency. In these severe and prolonged hypothyroidism cases; supplementation with adrenocortical steroids may be necessary.
Thyroid hormones may trigger a hyperthyroid state or may aggravate existing hyperthyroidism.
Thyroid therapy in patients with diabetes mellitus or insipidus or adrenal cortical insufficiency may aggravate the intensity of their symptoms. Dosage adjustments and other measures may be required to control these endocrine diseases. If thyroid medication is stopped, a downward readjustment of insulin or other hypoglycemic agents may be necessary to avoid hypoglycemia. Monitor urinary and serum glucose during treatment.
Myxedema coma requires simultaneous administration of glucocorticoids.
Hypothyroidism decreases and hyperthyroidism increases the sensitivity to oral anticoagulants. PT should be closely monitored in these patients when treated with thyroid hormones and dosage adjustment of oral anticoagulants may be required in accordance with serum PT in INR requirements.
Excessive doses of thyroid hormones in infants may produce craniosynostosis.
T3 is excreted primarily by the kidneys; patients with impaired renal functions should be monitored.
Caution should be used with nursing mothers as limited amounts of thyroid hormones are excreted in human milk.
Dosage should be reduced or temporarily discontinued upon signs and symptoms of overdose. In normal patients, the hypothalamic-pituitary thyroid-axis is restored in 6 to 8 weeks are thyroid suppression.
ADVERSE REACTIONS
Chest pain, increased pulse rate, palpitations, excessive sweating, cardiac arrhythmias, hypertension, heat intolerance, nervousness, or any other unusual event. Rarely, congestive heart failure.
PATIENT MONITORING
Thyroid hormones treatment should be preceded by a full clinical analysis with appropriate laboratory tests as determined by the treating physician. TSH suppression testing may be used to evaluate the effectiveness of any thyroid preparation. Bound T3 and Bound T4 serum assays are less clinically useful than Free T3 and Free T4 testing; particularly in patients on concomitant androgen treatment which may alter bound T3 and bound T4 serum concentrations.
Serum testing should include at a minimum: Free T3, Free T4, TSH, FTI, RT3, and anti-TPO.
Laboratory tests should be repeated and dosages titrated until the clinically desirable euthyroid state is reached.
Many drugs are known to interfere with thyroid laboratory testing including but not limited to: androgens, corticosteroids, estrogens, oral contraceptives, iodine-containing preparations, and preparations contains salicylates.
OVERDOSAGE
Treatment of acute massive thyroid hormone overdose is focused on reducing gastrointestinal absorption of the drug and counteracting central and peripheral effects; principally those of increased sympathetic activity. Vomiting may be induced initially if further gastrointestinal absorption can be reasonably 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, and fluid loss should be instituted if needed. Antiadrenergic agents, such as propranolol, have been used in the treatment of increased sympathetic activity. Propranolol may be administered intravenously at a dose of 1 to 3 mg over a 10-minute period or orally, 80 to 160 mg/day, especially when no contraindications exist for its use.
DOSAGE AND ADMINISTRATION
Dosage of T3 is determined based on indications, laboratory findings, and individual patient response.
Mild hypothyroidism: Typical starting oral dosage of 25mcg daily. Dosage may be increased by up to 25 mcg every 1 or 2 weeks thereafter. Usual maintenance dosage is 25 to 75 mcg daily.
Special Populations/Other Indications: As directed by physician.
PRESENTATION
100 uncoated tablets in blisters.
STORAGE
Protect from light. Store at 15 - 25oC.
 
 
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