Description Cytomel T3April 16, 2022
Properties of Liothyronine Sodium (T3)
The Greek pharmaceutical company Uni-pharma produces liothyronine, or the thyroid hormone T3. It is used to treat various diseases caused by a deficiency of this substance, triiodothyronine. It is successfully used in sports pharmacology.
Effects of Uni-pharma Liothyronine sodium
Scientists have not yet been able to determine exactly how liothyronine works in the body. Since it affects metabolism, it is used by athletes participating in drying courses because it helps them to get rid of excess weight. The drug affects the CNS, the hypothalamus, the pituitary gland and the thyroid gland itself.
The half-life is one day. In medicine, it is used in hypothyroidism, thyroid hernia. Athletes use it for weight loss and strength training. The drug improves metabolism quite quickly, but the preparation has a characteristic feature: in the absence of physical activity, the loss of fat mass is minimal, because it cannot be called a miracle pill slimming drug.
Contraindications and side effects of UNI-PHARMA liothyronine sodium salt (T3)
Not to be used in the presence of hypersensitivity to drugs, hyperthyroidism, ischaemia and myocardial infarction, and many other cardiovascular diseases. It should also not be used in acute and chronic renal failure, diabetes mellitus.
Side effects are relatively rare and more often due to overdose or intolerance. These may include:
- Cardiovascular problems;
- Partial or complete alopecia;
- False brain tumours (pseudotumours);
- Rash, other skin eruptions.
- If these symptoms occur, the medicine should be stopped completely or the dose reduced.
Doses are individually determined and therapeutic, therapeutic doses are generally much lower than those used in sports pharmacology. They may range from twenty-five milligrams to one hundred milligrams per day.
Hypothyroidism of any origin. Treatment of thyroid hyperplasia: benign hernia with normal function, prevention of recurrence of hernia after surgery or after treatment with radioactive iodine. As part of complex toxic stroke treatment with thyreostatic drugs (once metabolic compensation of the drug has been achieved).
Thyroid hormones are not indicated for the correction of hypothyroid symptoms (dry skin, fatigue, constipation, reproductive disorders, exhaustion or obesity) in the absence of laboratory confirmation of hypothyroidism, as they can cause hyperthyroidism in euthyroid patients.
The dose should be adjusted individually for each patient according to clinical response and thyroid function tests.
Treatment with thyroid hormones is usually started with low doses, which are gradually increased until a euthyroid state is reached, followed by maintenance doses. However, this is not necessary for neonates for whom it is important to reach euthyroidism quickly; their treatment can be started with a full replacement dose. The incidence of side-effects (e.g. hyperactivity) in older children is reduced by starting treatment at ¼ of the usual replacement dose and gradually increasing by 25% every 1 week until the full replacement dose is reached.
The risk of rapid dose escalation is lower in younger patients than in older patients.
In hypothyroid patients with adrenal insufficiency or pangiopituitarism, correction of adrenocortical insufficiency is required prior to initiation of thyroid hormone replacement therapy, as acute adrenal insufficiency with accelerated metabolism is possible. In the case of prolonged or severe hypothyroidism, including myxedema, maintenance treatment with glucocorticoids may also be necessary.
In hypothyroid patients with myxedema or cardiovascular disease, the initial dose of thyroid hormones should be very low and gradually increased, taking into account the possibility of angina pectoris, coronary artery blockage or stroke. If cardiovascular reactions occur, it may be necessary to reduce the dose of thyroid hormones.
β-blockers – possible reduction in conversion of thyroxine to triiodothyronine in the periphery.
Anabolic steroids, asparaginase, furosemide, salicylates, tamoxifen – possible pharmacokinetic interaction at protein binding level with concomitant use; salicylates, furosemide (high dose), clofibrate, levothyroxine increase blood levels.
Anticoagulants, coumarin or indandione derivatives – possible changes in anticoagulant effects depending on thyroid function status; increase in thyroid hormone dose may require reduction in oral anticoagulant dose.
Tricyclic antidepressants – therapeutic and toxic effects of both drugs (proarrhythmogenic and CNS stimulation) may be enhanced with concomitant use, possibly due to increased sensitivity of catecholamine receptors; tricyclic antidepressants may have earlier onset of action. Thimerosal glycosides – possible increased risk of digitalis poisoning in hypothyroidism; thyroid hormone replacement therapy increases metabolic rate, so higher dose of glycosides may be needed.
Cytochrome P450 inducers [barbiturates, especially phenobarbital, griseofulvin, carbamazepine, nevirapine, oxcarbazepine, primidone, rifabutin, St John’s wort, phenylbutazone (mixed inhibitory and inductive effects), phenytoin and possibly other hydantoins, ethanol (with prolonged use), efavirenz] – increase the breakdown of levothyroxine in the liver, which may increase the need for it; dose adjustment may be necessary; phenytoin also reduces levothyroxine binding to plasma proteins and plasma total and free thyroxine concentrations by 15-25%, but most patients remain euthyroid and do not require thyroid hormone dose adjustment.
Symptoms: Changes in appetite, changes in menstrual cycle, chest pain, diarrhoea, frequent or irregular pulse, fever, chills, headache, irritability, cramps in the lower limbs, nervousness, hypersensitivity to heat, breathing difficulties, sweating, sleep disturbances, vomiting, weight loss, symptoms of thyrotoxic crisis (confusion, fever, jaundice, mood changes, loss of muscle strength, psychosis, extreme fatigue, severe weakness – in case of severe overdose).
Depending on the severity of the symptoms, the doctor may recommend a reduction in the daily dose, discontinuation of treatment for a few days or the use of beta-blockers. Once the side effects have disappeared, treatment should be started cautiously with a lower dose.