L-Tyroxine, tablets 100 mcg 50 pcs

L-Tyroxine is a synthetic left-handed isomer of thyroxine. In its action it is identical to the naturally occurring thyroid hormone. In small doses it has an anabolic effect. In medium doses it stimulates growth and development of the body, increases the need forSynthetic left-hand-rotating isomer of thyroxine. After partial conversion to triiodothyronine (in the liver and kidneys) and transfer to body cells, it affects development and growth of tissues and metabolism. In low doses it has an anabolic effect on protein and fat metabolism. In medium doses it stimulates growth and development, increases tissue oxygen demand, stimulates metabolism of proteins, fats and carbohydrates, increases functional activity of the cardiovascular system and the central nervous system. At high doses it inhibits the production of thyrotropin-releasing hormone of the hypothalamus and thyrotropic hormone of the pituitary gland.

Therapeutic effect is observed after 7-12 days, during the same time the action lasts after discontinuation of the drug. The clinical effect in hypothyroidism is seen after 3-5 days. Diffuse goiter decreases or disappears within 3-6 months. At high doses it inhibits production of thyrotropin-releasing hormone of hypothalamus and thyrotropic hormone of pituitary.
After the start of therapy the action comes after 3-5 days.

Pharmacokinetics

In oral administration levothyroxine sodium is absorbed almost exclusively in the upper small intestine. Up to 80% of the taken dose of the drug is absorbed. Food intake reduces the absorption of levothyroxine sodium. Cmax is reached approximately 5-6 hours after oral administration. After absorption, more than 99% of the drug is bound to serum proteins (thyroxine-binding globulin, thyroxine-binding prealbumin and albumin). In various tissues, approximately 80% levothyroxine sodium is monodeiodinated to form triiodothyronine (T3) and inactive products. Thyroid hormones are metabolized primarily in the liver, kidneys, brain, and muscles. A small amount of the drug undergoes deamination and decarboxylation, as well as conjugation with sulfuric and glucuronic acids (in the liver). Metabolites are excreted by the kidneys and through the intestine. The half-life of the drug is 6-7 days. In thyrotoxicosis the half-life is shortened to 3-4 days, and in hypothyroidism it is prolonged to 9-10 days.

Indications

• Hypothyroid conditions of various etiologies (including.
• Hypothyroid conditions of various etiologies (including those caused by surgery or medication);
• preventing recurrence of nodular goiter after thyroid resection;
• diffuse toxic goiter – after creating an euthyroid state with thyreostatics (as combined or monotherapy);
• thyroid cancer after surgical treatment (in order to suppress tumor recurrence and as replacement therapy);
• as a diagnostic tool for thyroid suppression test.

In the complex therapy: Graves’ disease, autoimmune thyroiditis.

Active ingredient

Levothyroxine sodium

Composition

How to take, the dosage

The daily dose is determined individually depending on the indication.

The daily dose of L-thyroxine is taken orally in the morning on an empty stomach at least 30 minutes before a meal, with a small amount of liquid (half a glass of water) and without chewing.

In substitution therapy of hypothyroidism in patients younger than 55 years old in the absence of cardiovascular disease, L-thyroxine is prescribed in a daily dose of 1.6-1.8 mkg/kg body weight; in patients over 55 years or with cardiovascular disease – 0.9 mkg/kg body weight. In severe obesity (BMI ≥ 30 kg/m²) calculation should be made for “ideal weight”.

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Infants and children under 3 years of age take a daily dose of L-thyroxine at a single dose 30 minutes before the first feeding. The tablet is dissolved in water to a fine suspension, which is prepared just before taking the drug.

In hypothyroidism, L-thyroxine is usually taken for life. In thyrotoxicosis L-thyroxine is used in combination therapy with antithyroid drugs after achieving euthyroidism. In all cases, the duration of treatment with the drug is determined by the doctor.

Interaction

Sodium levothyroxine increases the effect of indirect anticoagulants, which may require reducing their dose. The use of tricyclic antidepressants with levothyroxine sodium may lead to increased effect of antidepressants. Thyroid hormones may increase the need for insulin and oral hypoglycemic drugs. More frequent monitoring of blood glucose concentrations is recommended during periods of initiation of treatment with sodium levothyroxine, as well as during changes in its dosing regimen. Sodium levothyroxine reduces the effect of cardiac glycosides. When concomitant use colestyramine, colestipol and aluminum hydroxide reduce the plasma concentration of sodium levothyroxine due to inhibition of its absorption in the intestine. When concomitant use with anabolic steroids, asparaginase, tamoxifen possible pharmacokinetic interaction at the level of protein binding. Concomitant use with phenytoin, salicylates, clofibrate, furosemide in high doses increases unbound plasma protein levels of sodium levothyroxine and thyroxine (T4). Taking estrogen-containing medications increases thyroxine-binding globulin, which may increase the need for sodium levothyroxine in some patients. Somatotropin, when used concomitantly with sodium levothyroxine, may accelerate the closure of epiphyseal growth zones. Taking phenobarbital, carbamazepine and rifampicin may increase the clearance of sodium levothyroxine and require increasing the dose.

The distribution and metabolism of the drug are affected by amiodarone, aminoglutethimide, PASC, etionamide, antithyroid drugs, beta-adrenoblockers, carbamazepine, chloral hydrate, diazepam, levodopa, dopamine, metoclopramide, lovastatin, somatostatin.

Concomitant use with phenytoin, salicylates, furosemide (in high doses), clofibrate increases the blood concentration of the drug.

Phenytoin reduces protein-bound levothyroxine and T4 concentration by 15 and 25%, respectively.

Special Instructions

In hypothyroidism caused by pituitary lesions, it is necessary to find out whether there is simultaneously insufficiency of the adrenal cortex. In this case, glucocorticosteroid replacement therapy should be started before starting treatment of hypothyroidism with thyroid hormones to avoid the development of acute adrenal insufficiency.

It is recommended that thyrotropic hormone (TSH) concentrations be determined periodically in the blood, an increase of which indicates inadequate dosing.

The drug has no effect on activities associated with driving and operating machinery.

Contraindications

• Hypersensitivity;
• untreated thyrotoxicosis;
• acute myocardial infarction;
• .
• acute myocarditis;
• untreated insufficiency of the adrenal cortex (must be compensated for before therapy).

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Side effects

• Tachycardia;
• Disorder of heart rhythm;
• Pain in the chest;
• Tremor;
• restlessness;
• insomnia;
• hyperhidrosis;
• weight loss;

diarrhea;

• alopecia;
• adrenal dysfunction (in hypophysial or hypothalamic hypothyroidism);
• renal dysfunction in children, allergic reactions (skin rash, skin itching).

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Overdose

In case of overdose of the drug the symptoms typical for thyrotoxicosis are observed:
• heart palpitations;
• disorder of heart rhythm;
• pains in the heart;
• restlessness;
• tremors;

sleep disturbance;

• high sweating;
• increased appetite;
• decreased body weight;
• diarrhea.

Depending on the severity of symptoms, the physician may recommend reducing the daily dose of the drug, a break in treatment for several days, and prescribing beta-adrenoblockers. After the side effects have disappeared, treatment should be started with caution at a lower dose.

Similarities

Euthyrox 100, Euthyrox