Brands, Medical Use, Clinical Data
Brands / Synonyms
Cytomel; L-Liothyronine; Liothyronin; Liothyronine Sodium; Thyrolar; Tresitope; Triiodothyronine; Triostat; Triostat
Used as replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyrodism during the recovery phase of subacute thyroiditis.
Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T4, levothyroxine) or triiodothyronine (T3, liothyronine) or both. T4 and T3 are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. Liothyronine (T3) contains three atoms of iodine and is formed by the coupling of one molecule of diiodotyrosine (DIT) with one molecule of monoiodotyrosine (MIT). These hormones enhance oxygen consumption by most tissues of the body and increase the basal metabolic rate and the metabolism of carbohydrates, lipids and proteins. Thus, they exert a profound influence on every organ system in the body and are of particular importance in the development of the central nervous system.
Mechanism of Action
The thyroid hormones, thyroxine (T4) and triiodothyronine (liothyronine or T3), are tyrosine-based hormones produced by the thyroid gland. An important component in the synthesis is iodine. The major form of thyroid hormone in the blood is thyroxine (T4). This is converted to the active liothyronine within cells by deiodinases. liothyronine acts on the body to increase the basal metabolic rate, affect protein synthesis and increase the body's sensitivity to catecholamines (such as adrenaline). The thyroid hormones are essential to proper development and differentiation of all cells of the human body. To various extents they regulate protein, fat and carbohydrate metabolism. But they have their most pronounced effects on how human cells use energetic compounds.
Almost totally absorbed, 95 percent in 4 hours.
Biotrnasformation / Drug Metabolism
Thyroid hormone preparations are generally contraindicated in patients with diagnosed but as yet uncorrected
adrenal cortical insufficiency, untreated thyrotoxicosis and apparent hypersensitivity to any of their active or
extraneous constituents. There is no well-documented evidence from the literature however, of true allergic or
idiosyncratic reactions to thyroid hormone.
Oral Anticoagulants: Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting
factors. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are
impaired. Patients stabilized on oral anticoagulants who are found to require thyroid replacement therapy should be
watched very closely when thyroid is started. If a patient is truly hypothyroid, it is likely that a reduction in
anticoagulant dosage will be required. No special precautions appear to be necessary when oral anticoagulant therapy
is begun in a patient already stabilized on maintenance thyroid replacement therapy.
Insulin or Oral Hypoglycemics: Initiating thyroid replacement therapy may cause 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 of the patient. Patients receiving insulin or oral
hypoglycemics should be closely watched during initiation of thyroid replacement therapy.
Cholestyramine: Cholestyramine binds both T4 and T3 in the intestine, thus impairing
absorption of these thyroid hormones. In vitro studies indicate that the binding is not easily removed.
Therefore, 4 to 5 hours should elapse between administration of cholestyramine and thyroid hormones.
Estrogen, Oral Contraceptives: Estrogens tend to increase serum thyroxine-binding globulin (TBg). In a
patient with a nonfunctioning thyroid gland who is receiving thyroid replacement therapy, free levothyroxine may be
decreased when estrogens are started thus increasing thyroid requirements. However, if the patient's thyroid gland
has sufficient function, the decreased free thyroxine will result in a compensatory increase in thyroxine output by
the thyroid. Therefore, patients without a functioning thyroid gland who are on thyroid replacement therapy may need
to increase their thyroid dose if estrogens or estrogen-containing oral contraceptives are given.
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.
Digitalis: Thyroid preparations may potentiate the toxic effects of digitalis. Thyroid hormonal replacement
increases metabolic rate, which requires an increase in digitalis dosage.
Ketamine: When administered to patients on a thyroid preparation, this parenteral anesthetic may cause
hypertension and tachycardia. Use with caution and be prepared to treat hypertension, if necessary.
Vasopressors: Thyroxine increases the adrenergic effect of catecholamines such as epinephrine and
norepinephrine. Therefore, injection of these agents into patients receiving thyroid preparations increases the risk
of precipitating coronary insufficiency especially in patients with coronary artery disease. Careful observation is
Drug/Laboratory Test Interactions
The following drugs or moieties are known to interfere with laboratory tests performed in patients on thyroid
hormone therapy: androgens, corticosteroids, estrogens, oral contraceptives containing estrogens, iodine-containing
preparations and the numerous preparations containing salicylates.
- Changes in TBg concentration should be taken into consideration in the interpretation of T4 and
T3 values. In such cases, the unbound (free) hormone should be measured. Pregnancy estrogens and
estrogen-containing oral contraceptives increase TBg concentrations. TBg may also be increased during infectious
hepatitis. Decreases in TBg concentrations are observed in nephrosis, acromegaly and after androgen or
corticosteroid therapy. Familial hyper- or hypo-thyroxine-binding-globulinemias have been described. The incidence
of TBg deficiency approximates 1 in 9000. The binding of thyroxine by thyroxine-binding prealbumin (TBPA) is
inhibited by salicylates.
- Medicinal or dietary iodine interferes with all in vivo tests of radio-iodine uptake producing low
uptakes which may not be reflective of a true decrease in hormone synthesis.
- The persistence of clinical and laboratory evidence of hypothyroidism in spite of adequate dosage replacement
indicates either poor patient compliance, poor absorption, excessive fecal loss, or inactivity of the preparation.
Intracellular resistance to thyroid hormone is quite rare.