Liothyronine Sodium BP
Liothyronine Sodium BP Uses, Dosage, Side Effects, Food Interaction and all others data.
Liothyronine Sodium BP is a thyroidal hormone T3 which is normally produced by the thyroid gland in a ratio 4:1 when compared with T4: T3. Liothyronine Sodium BP is the active form of thyroxine which is composed in a basic chemical structure by a tyrosine with bound iodine. The exogenous liothyronine product was developed by King Pharmaceuticals and FDA approved in 1956.
In hormonal replacement, liothyronine is more potent and present a faster action when compared to levothyroxine but the time of action is significantly shorter. The type of treatment needs to be well evaluated as the fast correction of thyroid hormones in certain diseases presents additional risks such as heart failure. The onset of activity is observed a few hours after administration and the maximum effect is observed after 2-3 days.
Treatment with liothyronine has been shown to produce normal plasma levels of T3 hormone but to have no effect on the T4 plasma concentration.
| Trade Name | Liothyronine Sodium BP |
| Availability | Prescription only |
| Generic | Liothyronine |
| Liothyronine Other Names | L-T3, Liothyronine, Liothyroninum, Liotironina, Triiodothyronine |
| Related Drugs | levothyroxine, Synthroid, Armour Thyroid, Euthyrox, Tirosint, Levoxyl, Cytomel, Triostat |
| Type | Tablet |
| Formula | C15H12I3NO4 |
| Weight | Average: 650.9735 Monoisotopic: 650.790038137 |
| Protein binding | Liothyronine presents a very large binding to plasma proteins and around 99.7% of the administered dose can be found bound. Liothyronine is found to be bound to thyroxine-binding globulin, thyroxine-binding prealbumin and albumin. It is important to consider that only the little unbound portion of liothyronine is metabolically active. |
| Groups | Approved, Vet approved |
| Therapeutic Class | |
| Manufacturer | ADVANZ Pharma |
| Available Country | United Kingdom |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Liothyronine Sodium BP is a thyroid hormone replacement therapy used to treat hypothyroidism, to suppress TSH, and to help in the diagnosis of hyperthyroidism.
Liothyronine Sodium BP is officially approved for the following indications:
Replacement therapy in primary (thyroidal), secondary (pituitary) and tertiary (hypothalamic) congenital or acquired hypothyroidism.
As an adjunct therapy to surgery and radioiodine in the management of thyroid cancer.
As a diagnostic agent in suppression tests for mild hyperthyroidism or thyroid gland autonomy.
In general terms, exogenous liothyronine is used to replace insufficient hormonal production and restore T3 plasma levels.
The lack of liothyronine can be presented as a pale and puffy face, coarse, brittle hair, dry skin, croaky voice and constipation as well as irregular periods, drowsiness, and lethargy.
Liothyronine Sodium BP should never be used in the suppression of benign nodules and nontoxic diffuse goiter in iodine-sufficient patients nor in the treatment of hyperthyroidism during the recovery phase of subacute thyroiditis.
Liothyronine Sodium BP is also used to associated treatment for these conditions: Autonomy of thyroid gland, Hyperthyroidism, Hypothyroidism, Myxedema coma, Thyroid Cancers, Euthyroid Goitre, Myxedema pre-coma, Supplemental or replacement therapy
How Liothyronine Sodium BP works
Liothyronine Sodium BP replaces endogenous thyroid hormone and then exerts its physiologic effects by controlling DNA transcription and protein synthesis. This effect on DNA is obtained by the binding of liothyronine to the thyroid receptors attached to DNA. Exogenous liothyronine exerts all the normal effects of the endogenous thyroid T3 hormone. Hence, it increases energy expenditure, accelerates the rate of cellular oxidation stimulating growth, maturation, and metabolism of the body tissues, aids in myelination of nerves and development of synaptic processes in the nervous system and enhances carbohydrate and protein metabolism.
Toxicity
The reported oral LD50 of liothyronine in the rat is higher than 4540 mg/kg. When overdosage is registered, symptoms of hyperthyroidism are reported as well as confusion, disorientation, cerebral embolism, seizure, shock, coma, and death. The symptoms of overdose can be presented immediately or several days after overdose ingestion. In an overdose state, reduce the dose of liothyronine and do supportive treatment.
There are no reports studying the carcinogenic, and mutagenic potential nor on the effects of liothyronine on fertility.
Food Interaction
- Take with or without food.
Liothyronine Sodium BP Hypertension interaction
[Major] Thyroid hormones cause increases in myocardial contractility and heart rate as a result of increased metabolic demands and oxygen consumption.
Therapy with thyroid hormones should be administered cautiously and initiated at reduced dosages in patients with cardiovascular disorders such as angina, coronary artery disease, and hypertension.
Clinical monitoring of cardiovascular function is recommended.
If chest pain or exacerbation of cardiovascular disease occurs, the dosage of thyroid hormone should be reduced, even at the expense of achieving euthyroid state.
Thyroid hormones should not be administered to patients with an acute myocardial infarction that is not complicated by hypothyroidism.
Liothyronine Sodium BP multivitamins interaction
[Moderate] ADJUST DOSING INTERVAL: Concurrent administration of calcium-containing products may decrease the oral bioavailability of levothyroxine by one-third in some patients.
Pharmacologic effects of levothyroxine may be reduced.
The exact mechanism of interaction is unknown but may involve nonspecific adsorption of levothyroxine to calcium at acidic pH levels, resulting in an insoluble complex that is poorly absorbed from the gastrointestinal tract.
In one study, 20 patients with hypothyroidism who were taking a stable long-term regimen of levothyroxine demonstrated modest but significant decreases in mean free and total thyroxine (T4) levels as well as a corresponding increase in mean thyrotropin (thyroid-stimulating hormone, or TSH) level following the addition of calcium carbonate (1200 mg Four patients had serum TSH levels that were higher than the normal range. Both T4 and TSH levels returned to near-baseline 2 months after discontinuation of calcium, which further supported the likelihood of an interaction. In addition, there have been case reports suggesting decreased efficacy of levothyroxine during calcium coadministration. It is not known whether this interaction occurs with other thyroid hormone preparations. Monitoring of serum TSH levels is recommended. Patients with gastrointestinal or malabsorption disorders may be at a greater risk of developing clinical or subclinical hypothyroidism due to this interaction.
Some experts recommend separating the times of administration of levothyroxine and calcium-containing preparations by at least 4 hours.
Liothyronine Sodium BP Drug Interaction
Moderate: amphetamine / dextroamphetamine, amphetamine / dextroamphetamineUnknown: diphenhydramine, diphenhydramine, ubiquinone, ubiquinone, duloxetine, duloxetine, omega-3 polyunsaturated fatty acids, omega-3 polyunsaturated fatty acids, levothyroxine, levothyroxine, cyanocobalamin, cyanocobalamin, ascorbic acid, ascorbic acid, cholecalciferol, cholecalciferol, cetirizine, cetirizine
Liothyronine Sodium BP Disease Interaction
Major: adrenal insufficiency, cardiovascular disease, thyrotoxicosisModerate: diabetes, seizures
Volume of Distribution
The reported volume of distribution of liothyronine is reported to be of 0.1-0.2 L/kg.
Elimination Route
Thyroid hormones are well absorbed orally. From these hormones, liothyronine is almost completely absorbed and it does not present changes in the absorption rate due to concomitant administration of food.liothyronin Multiple administration of 50 mcg of liothyronine provided a maximal plasma concentration of total T3 of 346 ng/dL in about 2.5 hours with an AUC of 4740 ng.h/dL.
Half Life
The half-life of liothyronine is reported to be between 1 and 2 days.
Clearance
There are no reports obtaining this value specifically.
Elimination Route
The main elimination of thyroid hormones is known to be done via the kidneys from which less than 2.5% of the excreted drug is represented by the unchanged drug. This elimination route is reduced with age. A portion of the metabolic products of liothyronine is excreted to the bile and gut where they can be part of enterohepatic recirculation.
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