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Side Effects & Adverse Reactions
Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity. 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 their anorectic effects.
The use of thyroid hormones in the therapy of obesity, alone or combined with other drugs, is unjustified and has been shown to be ineffective. Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism.
Thyroid hormones should be used with great caution in a number of circumstances where the integrity of the cardiovascular system, particularly the coronary arteries, is suspect. These include patients with angina pectoris or the elderly, in whom there is a greater likelihood of occult cardiac disease. Therefore, in patients with compromised cardiac function, use thyroid hormones in conjunction with careful cardiac monitoring. Although the specific dosage of Triostat depends upon individual circumstances, in patients with known or suspected cardiovascular disease the extremely rapid onset of action of Triostat may warrant initiating therapy at a dose of 10 mcg to 20 mcg. (See DOSAGE AND ADMINISTRATION.)
Myxedematous patients are very sensitive to thyroid hormones; dosage should be started at a low level and increased gradually as acute changes may precipitate adverse cardiovascular events.
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.
Extreme caution is advised when administering thyroid hormones with digitalis or vasopressors. (See PRECAUTIONS–Drug Interactions.)
Fluid therapy should be administered with great care to prevent cardiac decompensation. (See PRECAUTIONS–Adjunctive Therapy.)
Legal Issues
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FDA Safety Alerts
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Manufacturer Warnings
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FDA Labeling Changes
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Uses
Triostat (liothyronine sodium injection) (T3) is indicated in the treatment of myxedema coma/precoma.
Triostat can be used in patients allergic to desiccated thyroid or thyroid extract derived from pork or beef.
History
There is currently no drug history available for this drug.
Other Information
Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T4, levothyroxine) sodium or triiodothyronine (T3, liothyronine) sodium or both. T4 and T3 are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T4 contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine (DIT). T3 contains three atoms of iodine and is formed by the coupling of one molecule of DIT with one molecule of monoiodotyrosine (MIT). Both hormones are stored in the thyroid colloid as thyroglobulin and released into the circulation. The major source of T3 has been shown to be peripheral deiodination of T4. T3 is bound less firmly than T4 in the serum, enters peripheral tissues more readily, and binds to specific nuclear receptor(s) to initiate hormonal, metabolic effects. T4 is the prohormone which is deiodinated to T3 for hormone activity.
Thyroid hormone preparations belong to two categories: (1) natural hormonal preparations derived from animal thyroid, and (2) synthetic preparations. Natural preparations include desiccated thyroid and thyroglobulin. Desiccated thyroid is derived from domesticated animals that are used for food by man (either beef or hog thyroid), and thyroglobulin is derived from thyroid glands of the hog.
Triostat (liothyronine sodium injection) (T3) contains liothyronine (L-triiodothyronine or L-T3), a synthetic form of a natural thyroid hormone, as the sodium salt.
The structural and empirical formulas and molecular weight of liothyronine sodium are given below.
L-Tyrosine, 0-(4-hydroxy-3-iodophenyl)-3,5-diiodo-, monosodium salt
In euthyroid patients, 25 mcg of liothyronine is equivalent to approximately 1 grain of desiccated thyroid or thyroglobulin and 0.1 mg of L-thyroxine.
Each mL of Triostat in amber-glass vials contains, in sterile non-pyrogenic aqueous solution, liothyronine sodium equivalent to 10 mcg of liothyronine; alcohol, 6.8% by volume; anhydrous citric acid, 0.175 mg; ammonia, 2.19 mg, as ammonium hydroxide.
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Triostat Manufacturers
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Jhp Pharmaceuticals Llc
Triostat | Jhp Pharmaceuticals Llc
AdultsMyxedema coma is usually precipitated in the hypothyroid patient of long standing by intercurrent illness or drugs such as sedatives and anesthetics and should be considered a medical emergency. Therapy should be directed at the correction of electrolyte disturbances, possible infection, or other intercurrent illness in addition to the administration of intravenous liothyronine (T3). Simultaneous glucocorticosteroids are required.
Triostat (liothyronine sodium injection) (T3) is for intravenous administration only. It should not be given intramuscularly or subcutaneously.
Prompt administration of an adequate dose of intravenous liothyronine (T3) is important in determining clinical outcome.
Initial and subsequent doses of Triostat should be based on continuous monitoring of the patient's clinical status and response to therapy.
Triostat doses should normally be administered at least four hours–and not more than 12 hours–apart.
Administration of at least 65 mcg/day of intravenous liothyronine (T3) in the initial days of therapy was associated with lower mortality.
There is limited clinical experience with intravenous liothyronine (T3) at total daily doses exceeding 100 mcg/day.
No controlled clinical studies have been done with Triostat. The following dosing guidelines have been derived from data analysis of myxedema coma/precoma case reports collected by SmithKline Beecham Pharmaceuticals since 1963 and from scientific literature since 1956.
An initial intravenous Triostat dose ranging from 25 mcg to 50 mcg is recommended in the emergency treatment of myxedema coma/precoma in adults. In patients with known or suspected cardiovascular disease, an initial dose of 10 mcg to 20 mcg is suggested (see WARNINGS). However, both the initial dose and subsequent doses should be determined on the basis of continuous monitoring of the patient's clinical condition and response to Triostat therapy. Normally at least four hours should be allowed between doses to adequately assess therapeutic response and no more than 12 hours should elapse between doses to avoid fluctuations in hormone levels. Caution should be exercised in adjusting the dose due to the potential of large changes to precipitate adverse cardiovascular events. Review of the myxedema case reports indicates decreased mortality in patients receiving at least 65 mcg/day in the initial days of treatment. However, there is limited clinical experience at total daily doses above 100 mcg. See PRECAUTIONS–Drug Interactions for potential interactions between thyroid hormones and digitalis and vasopressors.
Pediatric UseThere is limited experience with Triostat in the pediatric population. Safety and effectiveness in pediatric patients have not been established.
Switching to Oral TherapyOral therapy should be resumed as soon as the clinical situation has been stabilized and the patient is able to take oral medication. When switching a patient to liothyronine sodium tablets from Triostat, discontinue Triostat, initiate oral therapy at a low dosage, and increase gradually according to the patient's response.
If L-thyroxine rather than liothyronine sodium is used in initiating oral therapy, the physician should bear in mind that there is a delay of several days in the onset of L-thyroxine activity and that intravenous therapy should be discontinued gradually.
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