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Triostat (Liothyronine Sodium Injection) - Description and Clinical Pharmacology




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.


Thyroid hormones enhance oxygen consumption by most tissues of the body and increase the basal metabolic rate and the metabolism of carbohydrates, lipids and proteins. In vitro studies indicate that T3 increases aerobic mitochondrial function, thereby increasing the rates of synthesis and utilization of myocardial high-energy phosphates. This, in turn, stimulates myosin ATPase and reduces tissue lactic acidosis. Thus, thyroid hormones exert a profound influence on virtually every organ system in the body and are of particular importance in the development of the central nervous system.

While the source of levothyroxine (T4) and some triiodothyronine (T3) is via secretion from the thyroid gland, it is now well-established that approximately 80% of circulating T3 arises predominantly by way of the extrathyroidal conversion of T4. The membrane-bound enzyme responsible for this reaction is iodothyronine 5'-deiodinase. Activity of the enzyme is greatest in the liver and kidney. A second pathway of T4 to T3 conversion occurs via a PTU-insensitive 5'-deiodinase located primarily in the pituitary and central nervous system.

The prohormone T4 must be converted to T3 in the body before it can exert biological effects. During periods of illness or stress, this conversion is often inhibited and can be diverted to the inactive reverse T3 (rT3) moiety. Therefore, correction of the hypothyroid condition in patients with myxedema coma is facilitated by the parenteral administration of triiodothyronine (T3). T3 is bound much less firmly to serum binding proteins and therefore penetrates into the cells much more rapidly than T4. Also, the binding of T3 to a nuclear thyroid hormone receptor seems to initiate most of the effects of thyroid hormone in tissues. Although most thyroid hormone analogs, both natural and synthetic, will bind to this protein, the affinity of T3 for this receptor is roughly 10-fold higher than that of T4. Thus, T3 is the biologically active thyroid hormone.


The clinical features of myxedema coma include depression of the cardiovascular, respiratory, gastrointestinal and central nervous systems, impaired diuresis, and hypothermia. Administration of thyroid hormones reverses or attenuates these conditions. Thyroid hormones increase heart rate, ventricular contractility and cardiac output, as well as decrease total systemic vascular resistance. They also increase the rate and depth of respiration, motilityof the gastrointestinal tract, rapidity of cerebration, and vasodilatation. Thyroid hormones correct hypothermia by markedly increasing the basal metabolic rate, as well as the number and activity of mitochondria in almost all cells of the body.


Since liothyronine sodium (T3) is not firmly bound to serum protein, it is readily available to body tissues.

Liothyronine sodium has a rapid cutoff of activity which permits quick dosage adjustment and facilitates control of the effects of overdosage, should they occur.

The higher affinity of levothyroxine (T4) as compared to triiodothyronine (T3) for both thyroid-binding globulin and thyroid-binding prealbumin partially explains the higher serum levels and longer half-life of the former hormone. Both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity. T4 is deiodinated to T3.

A single dose of liothyronine sodium administered intravenously produces a detectable metabolic response in as little as two to four hours and a maximum therapeutic response within two days. However, no pharmacokinetic studies have been performed with intravenous liothyronine (T3) in myxedema coma or precoma patients.

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