Levothyroxine sodium

When ATH:
H03AA01

Pharmacological action.
Fill the shortage of thyroid hormones.

Application.

Hypothyroid state of different etiologies (incl. due to surgical or the influence of medication), thyroid suppressive therapy is simple (non-toxic) goiter, autoimmunnogo Hashimoto thyroiditis, mnohouzlovoho goiter, thyrostatic treatment of hyperthyroidism (complex therapy after achieving euthyroid state, tireotropinzavisimye highly differentiated papillary or follicular thyroid carcinoma (combined treatment), prevention of relapse weeks after resection, holding supressionnogo scintigraphic thyroid test.

Contraindications.

Hypersensitivity, Untreated hyperthyroidism, acute myocardial infarction, angina, miokardit, tachysystolic arrhythmias, heart failure, severe hypertension, neskorrigirovannoe dysfunction of the adrenal cortex, advanced age (senior 65 years).

Pregnancy and breast-feeding.

Category actions result in FDA - A. (As a result, adequate and well-controlled studies have found the risk of adverse effects on the fetus in the I trimester of pregnancy and there is no data, evidence of such a risk in subsequent trimesters.)

Side effects.

Tachycardia, arrhythmias, chest pain, tremor, anxiety, insomnia, hyperhidrosis, weight loss, diarrhea, alopecia, dysfunction of the adrenal glands (pituitary or hypothalamic when hypothyroidism), Disorder of renal function in children.

Cooperation.

It reduces the effect of insulin and oral antidiabetic drugs, cardiac glycosides, enhances — indirect anticoagulants, tricyclic antidepressants. Cholestyramine, colestipol, aluminum hydroxide reduces the plasma concentration due to inhibition of intestinal absorption. Phenobarbital and phenytoin accelerate metabolic clearance, without increasing the proportion of free T3 and T4 in blood. Estrogens increase the concentration associated with thyroglobulin fraction (effectiveness is reduced). Protein binding change anabolic steroids, asparaginase, clofibrate, furosemid, salicilaty, Tamoxifen. Amiodarone, aminoglutethimide, aminosalicylic acid, ethionamide, antithyroid drugs, beta-blockers, Carbamazepine, khloralgidrat, diazepam, levodopa, dofamin, metoclopramide, lovastatin, somatostatin, etc.. can alter the levels of thyroid and thyroid-stimulating hormone, usually, affecting the synthesis of, secretion, distribution, metabolism, action or elimination of thyroid hormones or altering the secretion of TSH.

Overdose.

Symptoms: thyrotoxic crisis, sometimes delayed for several days after administration.

Treatment: appointment of beta-blockers, / in the administration of corticosteroids, plasmapheresis.

Dosing and Administration.

Inside, morning, fasting, drinking a small amount of liquid. If hypothyroidism is the initial dose of 25-100 µg per day, gradually increasing (on 25-50 mcg every 2-3 weeks) to support — 125-250 mcg per day, after surgery for malignant tumors of the thyroid gland is to 300 mcg per day.

Children initial dose of 12.5-50 mcg, supports 100-150 mcg per day.

In the complex treatment of hyperthyroidism-5-100 micrograms per day.

To conduct test for supressing 14 days 200 micrograms per day or 3 mg 1 time for 7 days before re scintigrams.

Euthyroid goiter and prevention of its recurrence after resection: adults-75-200 micrograms per day, children-12.5-150 mcg per day.

Precautions.

It is recommended to periodically determine the blood content of TSH, elevated level which indicates failure dose. The adequacy of thyroid suppressive therapy is evaluated as to suppress the capture of radioactive iodine. When long-existing multinodular goiter before treatment should be stimulus test with thyrotropin-releasing hormone. In most cases, hypothyroidism, metabolic status should recover gradually, especially in elderly patients and patients with cardiovascular disease. For older patients initial dose should not exceed 50 g. When applied in the II and III trimester of pregnancy tend to increase the dose to 25%. With caution is prescribed for severe long-existing hypothyroidism. Before treatment should eliminate the possibility of pituitary or hypothalamic hypothyroidism.

Cooperation

Active substance Description of interaction
Akarʙoza FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; with a joint appointment requires constant monitoring of blood glucose concentrations.
Aminosalicylic acid FKV. Increases plasma levels of free fraction, competitively displacing connection with protein.
Amiodarone FKV. It may change the level in the blood.
Amitriptyline FMR: synergism. Against the background of levothyroxine sodium increases the sensitivity of the receptors to catecholamines; with a joint appointment may accelerate and strengthen the therapeutic, and the toxic effects of both agents, incl. increasing the risk of arrhythmias and CNS stimulation.
Asparaginase FKV. Decreases (competition) plasma protein binding.
Atenolol FKV. FMR. Changes in blood concentration. Against the background of levothyroxine sodium (the normalization of thyroid function in patients with hypothyroidism) may weaken the effect of.
Betaksolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism), may weaken the effect of.
Betametazon FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Bisoprolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism), may weaken the effect of.
Bromocriptine FKV. It changes the content in the blood.
Warfarin FMR: synergism. Against the background of levothyroxine sodium, increasing the catabolism of vitamin K-dependent coagulation factors, enhanced effect; the combined use of a dose reduction is needed.
Gidrokortizon FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Glimepiride FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced, and it may be necessary to increase the dose.
Glipizide FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; with a joint appointment requires constant monitoring of blood glucose concentrations.
Desogestrel FKV: antagonizm. Increases fixation on thyroxine binding globulin, and reduces the effect of; the combined appointment may require higher doses.
Dexamethasone FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Diazepam FKV. Changes in blood levels.
Digoxin FKV. FMR: antagonizm. Against the background of levothyroxine sodium reduced serum levels and weakened the effect.
Doʙutamin FMR: synergism. Strengthens (mutually) effect; while the appointment increases the risk of coronary insufficiency (especially in patients with coronary artery disease).
Dopamine FKV. Changes plasma levels.
Iron sulfate FKV. Forming a complex, reduces the absorption of; you need to take levothyroxine, at least, through 4 h after iron sulphate.
Imipramine FMR: synergism. Against the background of levothyroxine sodium increases the sensitivity of the receptors to catecholamines; with a joint appointment could accelerate and increase the therapeutic and toxic effects of both agents, incl. the risk of arrhythmias and CNS stimulation.
Insulin aspart FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; the combined appointment may need to increase the dose.
Insulin dvuhfaznыy [human genetic engineering] FMR. Against the background of the effect of levothyroxine sodium is reduced; the combined appointment is necessary to increase the dose.
Insulin soluble [pork monocomponent] FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; the combined appointment is necessary to increase the dose.
Interferon alfa-2a FMR. Changes effect; with a joint appointment may require dose adjustment.
Interferon alfa-2b, recombinant human FMR. Changes effect; with a joint appointment may require dose adjustment.
Interferon beta-1b FMR. Changes effect; the combined appointment may require dose adjustment.
Yoheksol FKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
Yoksaglovaya acid FKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
Yopamydol FKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
Calcium carbonate FKV. Delays or stops the absorption; levothyroxine should be taken after 4 h — not before — after these funds.
Carbamazepine FKV. FMR.

Weakens effect (accelerates destruction).

Ketamine FMR: synergism. Against the background of levothyroxine sodium increases the likelihood of hypertension and tachycardia.
Clomipramine FMR: synergism. Against the background of levothyroxine sodium increases the sensitivity of the receptors to catecholamines; concomitant use can accelerate and enhance the therapeutic and toxic effects of both agents, incl. the risk of arrhythmias and CNS stimulation.
Kortizon FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Lithium carbonate FKV. Blocks mediated release of TSH T4 and T3; the combined appointment may need to take more, than normal dose of levothyroxine.
Lovastatin FKV. It can change the plasma levels of.
Magnesium oxide FKV. Delays or stops the absorption; levothyroxine should be taken after 4 h — not before — after these funds.
Maprotilin FMR. Increases (mutually) the risk of arrhythmias.
Merkaptopurin FKV. Changes plasma levels.
Methylprednisolone FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Methyltestosterone FKV. Decreases (competition) binding to plasma proteins and increases the concentration of the free fraction.
Metoclopramide FKV. It changes the content in the blood.
Metoprolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
Metformin FMR: antagonizm. Against the background of the effect of levothyroxine sodium reduced; the combined appointment may be necessary to increase the dose.
Nadolol FKV. FMR. Changes plasma levels. Against the background of levothyroxine sodium (the normalization of thyroid function in patients with hypothyroidism) may weaken the effect of.
Norepinephrine FMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.
Octreotide FKV. Changes in blood levels.
Perfenazyn FKV. It reduces the protein binding.
Pindolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
Pioglitazone FMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; the combined appointment may be necessary to increase the dose.
Poliestradiola phosphate FKV. Increases fixation on thyroxine binding globulin and weakens the effect; the combined appointment may require higher doses.
Pramipexole FKV. Changes plasma levels.
Propranolol FKV. FMR. It reduces the activity of T4 5-deiodinase, although the levels of T3 and T4 changes slightly. Against the background of levothyroxine sodium (the conversion of hypothyroidism in euthyroid state) may weaken the effect of.
Protirelin FKV. Against the background of the effect of levothyroxine sodium is reduced TSH stimulation.
Repaglinide FMR: antagonizm. Against the background of the effect of levothyroxine sodium reduced; with a joint appointment may require an increased dose.
Rifampicin FKV. Induces biotransformation, accelerates elimination, lowers blood concentration.
Rosiglitazone FMR: antagonizm. Against the background of reduced effect of levothyroxine; with a joint appointment may be necessary to increase the dose.
Somatropin FMR. Against the background of levothyroxine sodium may accelerate epiphyseal bone closure.
Sotalol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
Sulfamethoxazole FKV. Changes plasma levels.
Sulfasalazine FKV. Changes plasma levels.
Theophylline FKV. Against the background of levothyroxine sodium theophylline clearance (hypothyroidism can decrease) normal.
Timolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
Triamcinolone FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Phenylbutazone FKV. Inhibit the binding of serum proteins.
Phenytoin FKV. FMR.

Weakens effect (accelerates destruction).

Phenobarbital FKV. FMR.

Weakens effect (accelerates destruction).

Fludrokortizon FKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Furosemid FKV. Decreases (competition) binding to plasma proteins and increases the free fraction of blood.
Epinephrine FMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.
Esmolol FMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
Ethionamide FKV. Increases plasma levels of free fraction, displacing with binding sites on proteins.
Ephedrine FMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.

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