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 substanceDescription of interaction
AkarʙozaFMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; with a joint appointment requires constant monitoring of blood glucose concentrations.
Aminosalicylic acidFKV. Increases plasma levels of free fraction, competitively displacing connection with protein.
AmiodaroneFKV. It may change the level in the blood.
AmitriptylineFMR: 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.
AsparaginaseFKV. Decreases (competition) plasma protein binding.
AtenololFKV. 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.
BetaksololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism), may weaken the effect of.
BetametazonFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
BisoprololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism), may weaken the effect of.
BromocriptineFKV. It changes the content in the blood.
WarfarinFMR: 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.
GidrokortizonFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
GlimepirideFMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced, and it may be necessary to increase the dose.
GlipizideFMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; with a joint appointment requires constant monitoring of blood glucose concentrations.
DesogestrelFKV: antagonizm. Increases fixation on thyroxine binding globulin, and reduces the effect of; the combined appointment may require higher doses.
DexamethasoneFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
DiazepamFKV. Changes in blood levels.
DigoxinFKV. FMR: antagonizm. Against the background of levothyroxine sodium reduced serum levels and weakened the effect.
DoʙutaminFMR: synergism. Strengthens (mutually) effect; while the appointment increases the risk of coronary insufficiency (especially in patients with coronary artery disease).
DopamineFKV. Changes plasma levels.
Iron sulfateFKV. Forming a complex, reduces the absorption of; you need to take levothyroxine, at least, through 4 h after iron sulphate.
ImipramineFMR: 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 aspartFMR: 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-2aFMR. Changes effect; with a joint appointment may require dose adjustment.
Interferon alfa-2b, recombinant humanFMR. Changes effect; with a joint appointment may require dose adjustment.
Interferon beta-1bFMR. Changes effect; the combined appointment may require dose adjustment.
YoheksolFKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
Yoksaglovaya acidFKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
YopamydolFKV. Against the background of levothyroxine sodium increases the risk of thyrotoxic symptoms (Relative overdose).
Calcium carbonateFKV. Delays or stops the absorption; levothyroxine should be taken after 4 h — not before — after these funds.
CarbamazepineFKV. FMR.

Weakens effect (accelerates destruction).

KetamineFMR: synergism. Against the background of levothyroxine sodium increases the likelihood of hypertension and tachycardia.
ClomipramineFMR: 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.
KortizonFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
Lithium carbonateFKV. Blocks mediated release of TSH T4 and T3; the combined appointment may need to take more, than normal dose of levothyroxine.
LovastatinFKV. It can change the plasma levels of.
Magnesium oxideFKV. Delays or stops the absorption; levothyroxine should be taken after 4 h — not before — after these funds.
MaprotilinFMR. Increases (mutually) the risk of arrhythmias.
MerkaptopurinFKV. Changes plasma levels.
MethylprednisoloneFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
MethyltestosteroneFKV. Decreases (competition) binding to plasma proteins and increases the concentration of the free fraction.
MetoclopramideFKV. It changes the content in the blood.
MetoprololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
MetforminFMR: antagonizm. Against the background of the effect of levothyroxine sodium reduced; the combined appointment may be necessary to increase the dose.
NadololFKV. FMR. Changes plasma levels. Against the background of levothyroxine sodium (the normalization of thyroid function in patients with hypothyroidism) may weaken the effect of.
NorepinephrineFMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.
OctreotideFKV. Changes in blood levels.
PerfenazynFKV. It reduces the protein binding.
PindololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
PioglitazoneFMR: antagonizm. Against the background of the effect of levothyroxine sodium is reduced; the combined appointment may be necessary to increase the dose.
Poliestradiola phosphateFKV. Increases fixation on thyroxine binding globulin and weakens the effect; the combined appointment may require higher doses.
PramipexoleFKV. Changes plasma levels.
PropranololFKV. 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.
ProtirelinFKV. Against the background of the effect of levothyroxine sodium is reduced TSH stimulation.
RepaglinideFMR: antagonizm. Against the background of the effect of levothyroxine sodium reduced; with a joint appointment may require an increased dose.
RifampicinFKV. Induces biotransformation, accelerates elimination, lowers blood concentration.
RosiglitazoneFMR: antagonizm. Against the background of reduced effect of levothyroxine; with a joint appointment may be necessary to increase the dose.
SomatropinFMR. Against the background of levothyroxine sodium may accelerate epiphyseal bone closure.
SotalolFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
SulfamethoxazoleFKV. Changes plasma levels.
SulfasalazineFKV. Changes plasma levels.
TheophyllineFKV. Against the background of levothyroxine sodium theophylline clearance (hypothyroidism can decrease) normal.
TimololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
TriamcinoloneFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
PhenylbutazoneFKV. Inhibit the binding of serum proteins.
PhenytoinFKV. FMR.

Weakens effect (accelerates destruction).

PhenobarbitalFKV. FMR.

Weakens effect (accelerates destruction).

FludrokortizonFKV. It reduces the concentration of thyroxine binding globulin and reduces binding to plasma proteins.
FurosemidFKV. Decreases (competition) binding to plasma proteins and increases the free fraction of blood.
EpinephrineFMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.
EsmololFMR: antagonizm. Against the background of levothyroxine sodium (the normalization of the patients with hypothyroidism) may weaken the effect of.
EthionamideFKV. Increases plasma levels of free fraction, displacing with binding sites on proteins.
EphedrineFMR: synergism. Increases (mutually) effect; against the backdrop of levothyroxine sodium increases the risk of coronary insufficiency.

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